'■&*£•' tf.W? SB /.- ft "v' 't,«V\ Mr: 8#&v-... •tf.Jh.V, ''VVfri.-' .' .' • ft* /»;■>. MO 3ft ^ i' m 1ST" /7\ T£i /r\/ ^. SURGEON GENERAL'S OFFICE LIBRARY. n, jvo. iq & $T6. nBUKIVJEli..X7f: .ysu.^rj..r.?r..-w:.T.....!~*'....r...^.,... — .^-T....... By''Gift Of.............................................................--*:, fa r ^v « p K t ff". If A TEXT-BOOK PRACTICAL MEDICINE, WITH PARTICULAR REFERENCE TO PHYSIOLOGY AND PATHOLOGICAL AXATOMY. DR. FELIX vox XTEMEYER, PROFESSOR OP PATHOLOGY AND THERAPEUTICS, DI. ^'TiB OP THE MEDICAL CLINIC OF TUB UNIVERSITY OF TUBINliEN. TRANSLATED FROM THE SEVENTH GERMAN EDITION, BY SPECIAL PERMISSION OF THE AUTHOR, I5Y GEORGE II. HUMPHREYS, M. D., ONE OP THE PHYSICIANS TO THE BUREAU OP MEDICAL AND SURGICAL RELIEF AT BELLEVUE HOSPITAL FOR THE OUT-DOOR POOR, FELLOW OF THE NEW-YORK ACADEMY OF MEDICINE, ETC., CHARLES E. IIACKLEY, M.D., ONE OP THE PHYSICIANS TO THE NEW-YORK HOSPITAL, ONE OF THE SURGEONS TO THE NEW-YORK EYE AND EAR INFIRMARY, FELLOW OP THE NEW YORK ACADEMY OF MEDICINE, ETC. VOLUME II. FOURTH AMERICAN EDITIok NEW YORK D . A P P L E T 0 X A X -p 90, 92 & 94 GR-VSD. STREET. 18 10. #J**',XK" UMBRA /1 5? K~t* ^ NN2 v. 2. ftlinno. \)\3P), 0(rp 2- Entered, according to Act of Congress, in the year 1869. by D. APPLETON & CO., In the Clerk's Office of the District Court of the United States for the Southern District of New York. t TABLE OF CONTENTS OF YOL. II. DISEASES OF THE URINARY ORGANS. SECTION I. DISEASES OF THE KIDNEYS. pag a Chap. I.—Hyperaemia of the Kidney,.........7 II.—Haemorrhage from the Kidney,........13 III.—Acute Bright's Disease—Croupous Nephritis,......16 IV.—Chronic Bright's Disease—Parenchymatous Nephritis, ... 20 V.—Nephritis Vera—Interstitial Nephritis—Eenal Abscess—Metastatic De- posits in the Kidney,......\ ... 36 VI.—Perinephritis,...........40 VII.—Amyloid Degeneration of the Kidney,.......41 VIII.—Parenchymatous Degeneration of the Kidney,.....43 IX.—Carcinoma of the Kidney,.........45 X.—Tuberculosis of the Kidney,.........46 XI.—Parasites in the Kidney,..........47 XII.—Deformities of the Kidney—Irregularities of its shape and position, . 48 Appendix.—Diseases of the Suprarenal Capsules—Addison's Disease—Bronzed Skin, .............49 SECTION II. DISEASES OF THE PELVIS OF THE KIDNEYS AND URETERS. Chap. I.—Hydronephrosis—Dilatation of the Pelvis of the Kidney, with Atrophy of the Eenal Substance,.........54 II.—Pyelitis—Inflammation of the Pelvis of the Kidney, .... 56 III.—Stony Concretions in the Pelvis of the Kidney, and Eenal Colic, . . 59 IV.—Carcinoma and Tuberculosis of the Pelvis of the Kidneys and of the Ureters,............62 SECTION III. DISEASES OF THE BLADDER. Chap. I.—Catarrh of the Bladder—Cystitis Catarrhalis,......64 II.—Croupous and Diphtheritic Cystitis,.......TO III.—Pericystitis,............TO IV.—Tuberculosis and Carcinoma of the Bladder,.....71 V.—Haemorrhage from the Bladder—Haematuria Vesicalis, .... 72 VI.—St<">ny Concretions in the Bladder,.......73 iv TABLE OF CONTENTS OF VOL. II. XEUEOSES OF THE BLADDEK. PAGB Chap. VII.—Hyperesthesia of the Bladder,........78 VIII.—Anaesthesia of the Bladder,........78 IX.—Hypercinesis of the Bladder—Spasm of the Bladder—Cystospasmus. . SO X.—Acinesis of the Bladder—Vesical Palsy—Cystoplegia, ... 82 SECTION IV. DISEASES OF THE URETHRA. Chap. I.—Virulent Catarrh of the Male Urethra—Clap—Gonorrhoea, . . .86 II.—Non-virulent Catarrh, of the Urethra,.......96 DISEASES OF THE SEXUAL ORGANS. J.—DISEASES OF THE MALE SEXUAL OEGANS. Chap. I.—Nocturnal and Diurnal Pollutions—Spermatorrhoea, .... 98 II.—Impotence and Irritability, with "Weakness of the Male Sexual Organs, 102 5.—DISEASES OF THE FEMALE SEXUAL OEGANS. SECTION I. DISEASES OF THE OVARIES. Chap. I.—Inflammation of the Ovary—Oophoritis (Ovaritis), .... 10T II.—Formation of Cysts in the Ovaries—Hydrops Ovarii, .... 109 III.—Complicated Tumors, Neoplasia, and Solid Tumors in the Ovary, . 115 SECTION II. DISEASES OF THE UTERUS. Chap. I.—Catarrh of the Uterus, and Catarrhal Ulcers of the Cervix Uteri, . . 116 II.—Parenchymatous Metritis—Acute and Chronic Infarction of the Uterus, 124 III.—Perimetritis and Parametritis,........127 IV.—Contractions and Closures of the Uterus—Haemometra and Hydrometra, 129 V.—Curvatures of the Uterus—Flexions and Infarctions, . . . .131 VI.—Changes of Position of the Uterus,.......135 VII.—Tumors of the Uterus,........... 137 VIII.—Anomalies of Menstruation, ... .... 140 IX.—Ectro-Uterhie Hematocele, .... .... 144 SECTION III. DISEASES OF THE VAGINA. Chap. I.—Virulent Catarrh of the Vagina,........147 II.—Non-virulent Catarrh of the Vagina,.......148 III.—Croupous and Diphtheritic Inflammation of the Vagina, . . . 150 TABLE OF CONTENTS OF VOL. II. v DISEASES OF THE NERVOUS SYSTEM. SECTION I. DISEASES OF THE BRAIN. PAGS 1'hap. I.—Hyperemia of the Brain and its Membranes,......151 II.—Partial Hyperaemia and Partial GEdema of the Brain, .... 161 III.—Anaemia of the Brain and its Membranes,......169 IV.—Partial Anemia and Partial Necrosis of the Brain—Thrombosis and Em- bolism of the Cerebral Arteries—Softening,.....175 V.—Cerebral Hemorrhage—Apoplectic Stroke—Apoplexy Sanguinea, . . 189 VI.—Hemorrhages of the Cerebral Membranes — Apoplexia Meningea— Hematoma of the Dura Mater,.......202 INFLAMMATIONS OF THE BRAIN AND ITS MEMBEANES. VII.—Inflammation of the Dura Mater—Inflammation and Thrombosis of the Cerebral Sinus,...........205 VIII.—Inflammation of the Pia Mater, with Puro-fibrinous Exudation—Menin- gitis of the Convexity—Meningitis Simplex,.....208 IX.—Basilar Meningitis, Tuberculous Inflammation, and Simple Miliary Tu- berculosis of the Pia Mater—Acute Hydrocephalus, .... 211 X.—Epidemic Cerebro-spinal Meningitis,.......218 XI.—Inflammation of the Brain—Encephalitis,......223 XII.—Partial Sclerosis of the Brain,........231 XIII.—Tumors sf the Brain and its Membranes,......233 XIV.—Serous Effusions in the Mature Skull—Hydrocephalus Acquisitus, . 246 XV.—Serous Effusions in the Incomplete Skull—Hydrocephalus Congenitus, . 249 XVI.—Hypertrophy of the Brain,.........251 XVII.—Atrophy of the Brain,..........253 SECTION II. DISEASES OF TEE SPINAL MARROW AND ITS MEMBRANES. Chap. I.—Hyperemia of the Spinal Marrow and its Membranes, . . . .257 II.—Hemorrhage of the Spinal Marrow and its Membranes —Spinal Apoplexy,............258 III.—Inflammation of the Membranes of the Spinal Marrow —Meningitis Spinalis,............260 IV.—Inflammation of the Spinal Marrow—Myelitis,.....263 V.—Growths and Parasites of the Spinal Medulla and its Membranes, . . 2G7 VI.—Hydrorhachis Congenita—Spina Bifida,......268 VII.—Consumption of the Spinal Cord—Tabes Dorsualis—Ataxie Locomotrice Progressive (Duehenne)—Gray Degeneration of the Posterior Columns of the Spinal Cord (Leyden)—Locomotor Ataxy, .... 270 SECTION III. DISEASES OF THE PERIPHERAL NERVES. Chap. I.—Inflammation of the Nerves—Neuritis,.......2>r8 II.—Neuroma,............280 III.—Neuralgia,.............282 IV.—Neuralgia of the Trigeminus—Prosopalgia—Tic Douloureux—Fother- gill's Faceache,..... .....292 vi TABLE OF CONTENTS OF VOL. II. PAGB Jhap.V.—Hemicrania—Migraine,.......... 290 VI.—Cervico-Occipital Neuralgia,...... • • 298 VII.—Cervico-Braohial Neuralgia,.........299 VIII.—Intercostal Neuralgia,..........301 IX.—Mastodynia—Irritable Breast {Cooper), ........302 X.—Lumbo-Abdominal Neuralgia,........303 XI.—Neuralgia Ischiadica—Ischias—Ischias Nervosa Postica Cotunnii—Sci- atica—Hip-Gout,...........303 XII.—Crural Neuralgia—Ischias Antica Cotunnii,.....307 XIII.—Anesthesia of the Cutaneous Nerves,.......307 XIV.—Anesthesia of the Trigeminus,........313 SPASM INVOLVING PARTICULAR PERIPHERAL NERVES. XV.—Spasm of the Facial Nerve—Mimic Spasm of the Face—Tic Convulsif, . 316 XVI.—Spasm in the region of the Spinal Accessory Nerve of "Willis, . . 318 XVII.—Scrivener's Spasm—Mogigraphia,........320 XVIII.—Idiopathic Cramp of the Muscles of the Extremities—Arthrogryposis, 322 XIX.—Peripheral Palsy,...........324 XX.—Palsy of the Facial Nerve—Mimic Facial Palsy—Bell's Palsy, . . 331 XXL—Palsy of the Serratus Muscle, . :......335 XXII.—Progressive Palsy of the Cerebral Nerves, Tongue, Velum-Palati, and Lips,.............337 XXIII.—Essential Palsy of Children—Spinal Infantile Palsy {Heine), . . 338 SECTION IV. GENERAL NEUROSES OF UNKNOWN ANATOMICAL ORIGIN. Chap. I.—Chorea—Chorea St. Vita—St. Vitus's Dance,......342 II.—Lockjaw—Trismus—Tetanus,........348 III.—Epilepsy—Falling Sickness,.........354 IV.—Eclampsia Infantum,..........368 V.—Hysteria,.............372 VI.—Catalepsy,............386 VII.—Hypochondriasis,...........389 DISEASES OF THE SKIN. I.—Hypertrophy of the Skin, ...... 394 Chap. I.—Diffuse Hypertrophy of the Papillary Layer and Epidermis—Ichthyosis, 398 II.—Diffuse Hypertrophy of the Skin and Subcutaneous Connective Tissue —Pachydermia—Elephantiasis Arabum, . . - . . . 400 II.—Atrophy of the Skin,.......401 III.—Hyperemia and Anaemia of the Skin, . . . 404 IV.—Inflammation of the Skin,......406 III.—The Slighter Form of Acute Inflammation of the Skin without Vesi- cation—Erythematous Dermatitis—Erythema, . . . . 407 IV.—Erysipelatous Dermatitis—Erysipelas,.......410 V.—Herpes—Acute Superficial Dermatitis, with Formation of Groups of Vesicles upon the Skin,.........416 VL—Urticaria—Nettle-Eash—Acute Superficial Dermatitis, with Formation of "Weals,............418 VII.—Eczema—Diffuse Superficial Dermatitis, with Serous Exudation upon the Free Surface, and without Typical Course,.....420 VHL—Impetigo —Diffuse Superficial Dermatitis,, with Formation of Small Pustules, . ........433 TABLE OF CONTENTS OF VOL. II. vii FAGS Chap. IX.—Ecthyma—Dermatitis, with Formation of Large, Isolated, Permanent Pustules,............435 X.—Pemphigus—Pompholyx—Superficial Dermatitis, with Formation of Large, Isolated Blebs,.........436 XL—Eupia—Dermatitis, with Formation of Isolated Flat Vesicles, from which. Scabs of a peculiar Shape are formed,.....438 XII.—Psoriasis—Chronic Dermatitis, with Infiltration of the Corium, and Abnormal Growth of Epidermis, ......439 XIII.—Lichen—Dermatitis forming Groups of Persistent Conical Nodules, . 443 XIV.—Prurigo—Dermatitis with Small, Scattered, Itching Nodules, . 444 XV.—Acne, Acne Vulgaris, Acne Disseminata—Inflammation and Sup- puration of Obstructed Sebaceous Follicles,.....447 XVI.—Mentagra—Sycosis—Inflammation and Suppuration of the Sebaceous Glands and Hair Follicles of the Beard,.....449 XVII.—Acne Eosacea—Gutta Eosacea—Chronic Inflammation of the Seba- ceous Glands of the Face, with Dilatation of the Blood-vessels and Growth of the Connective Tissue about them,.....451 V.—Hemorrhages of the Skin—Purpura, . . . 452 VI.—Growths in the Skin,.......454 XVIII.—Lupus—Lupus Exedens,.........454 VII.—Parasites in the Skin,.......459 XIX.—Favus—Porrigo Favosa, Lupinosa,.......459 XX.—Herpes Tondens, .......... . .462 XXI.—Pityriasis Versicolor,..........4H4 XXII.—Scabies—Itch,............464 VIII.—Derangements of Secretion in the Skin, . . 469 DISEASES OF THE ORGANS OF LOCOMOTION. RHEUMATISM. Chap. 1.—Acute Articular Eheumatism—Eheumarthritis Acuta—Flying Gout, . 477 II.—Chronic Articular Eheumatism—Eheumarthritis Chronica, . . 485 III.—Deforming Articular Inflammation—Arthritis Deformans, Arthritis Pauperum—Arthrite Chronique Seche,......490 IV.—Muscular Eheumatism—Eheumatismus Muscularis, .... 492 V.—Gout—Podagra—Arthritis,.........495 VI.—Eachitis—Eickets,..........507 VII.—Osteomalacia,............515 VIII.—Progressive Muscular Atrophy—Atrophie Musculaire Graisseuse Pro- gressive—Paralysie Musculaire Progressive Atrophique, . . 517 IX.—Progressive Muscular Paralysis as a Eesult of Hypertrophy of the In- terstitial Fatty Tissue,.........519 CONSTITUTIONAL DISEASES. SECTION I. ACUTE irWECTIOUS DISEASES. Chap. I.— Measles—Morbilli—Eubeol. —Eougeole,......521 II.—Scarlet Fever—Scarlatina,.........533 III.—Eose-Eash—Eoseola Febrilis, . .......543 IV.—Small-Pox—Variola—Petite Verole,.......54-' mi TABLE OF CONTENTS OF VOL. II. PAGE Chap. V.—Cow-Pox—Vaccina,..........556 VI.—"Wind-Pox, Water-Pox, Sheep-Pox, Varicella, Chicken-Pox, . . 560 VII.—Typhus Fever—Exanthematic Typhus, Petechial Typhus, Spotted Fever,............• 562 VIII.—Abdominal Typhus—Ileotyphus, Typhoid Fever, .... 571 IX.—Epidemic Diphtheritis—Malignant Pharyngitis—Angina Maligna, . 602 MALARIAL FEVERS. X.—Intermittent Fever,..........607 XL—Eemittent and Continued Malarial Fever,......623 XII.—Asiatic Cholera,...........625 XIII.—Bloody Flux—Dysentery,.........648 XIV.—Trichina Disease—Trichinosis,........657 SECTION II. CHRONIC INFECTIOUS DISEASES. Chap. 1.—Syphilis,.............665 II.—Congenital and Hereditary Syphilis,.......706 APPENDIX. infectious diseases transmissible from brutes to human beings. Chap. I.—Human Glanders,...........709 II.—Hydrophobia—Lyssa—Eabies,........714 SECTION III. GENERAL DISORDERS OF NUTRITION WHICH DO NOT DEPEND UPON INFECTION. "hap. I.—Chlorosis,............720 II.—Scorbutus—Scurvy,..........72S III.—Purpura Hemorrhagica, the " Morbus Maculosus " of "Werlhof, . . 733 IV.—Hemophilia (Hemorrhagic Diathesis),......735 V.—Scrofula,.............736 VI.—Diabetes Mellitus—Mellituria,........748 VII.—Diabetes Insipidus,...........759 DISEASES OF THE URINARY ORGANS. SECTION I. DISEASES OF THE KIDXEY. CHAPTER I. HYPEREMIA OF THE KIDXEY. Hyperemia of the kidney and its consequences are not to be con- founded with inflammation of the kidney, although during life it is some- times quite impossible to distinguish between the two, and notwith- standing that similar symptoms appear in both disorders, such as the presence of blood and albumen in the urine, as well as the appearance in it of peculiar objects, generally called fibrinous casts (although it is probable that they are not composed of fibrin, and certainly are not pure fibrin, but consist in great part of mucin). Etiology.—A thorough knowledge of the normal circulation of the kidney is indispensable to a proper understanding, not only of the physiology, pathogeny, and etiology, but also of the symptoms of hy- peremia of this organ. To Virchow the credit is due of having cor- rected some of our former ideas upon this subject, and of having ren- dered others more complete. According to the result of his researches, the branches of one par- ticular portion of the renal artery (that, namely, which belongs to the middle and outer part of the cortical substance) go exclusively to form the afferent vessels, and, entering the Malpighian capsules as such, these divide to form the vessels of the glomeruli. Then, leaving the Malpighian capsule as efferent vessels, they again break up into branches, once more to reunite as renal veins. On the boundary be- tween the cortical and pyramidal substances there is a sort of " neutral ground." Here there are arteries from which branches arise, some forming afferent vessels, glomeruli, and efferent vessels, with long off- 8 DISEASE3 OF THE KIDNEY. shoots running into the cortical and medullary substance, and others which act directly as nutrient vessels for the medullary substance. Finally, the renal artery has branches upon which there are no glome- ruli at all, and whose function is simply nutrition of the medullary substance. The resistance encountered by the blood which passes through the glomeruli is far greater than that met by the blood which merely flows directly from the arteries into the capillaries. Even under normal conditions the blood-pressure in the renal arteries is a very consider- able one, that vessel being both short and of disproportionately large calibre. When the pressure within these arteries is increased, hyper- emia of course will first arise in that portion of the kidney where the blood encounters the greatest resistance, namely, in the cortical sub- stance, and, above all, in the glomeruli. "Where the resistance is less, as in the medullary substance, although the circulation is accelerated there, the actual amount of blood which the part contains is not ma- terially increased. It is very different, however, when the escape of the blood from the renal veins is impeded. In such a case the quan- tity of blood in the veins and capillaries is augmented, but the en- gorgement cannot extend through the narrow efferent vessels into the glomeruli; and, as the contents of the arteries are abnormally reduced in most of the disorders in which there is an obstruction of the renal veins (as in cardiac and pulmonary diseases), the reason at once be- comes apparent why, even in cases of extreme obstructive hyperemia of the kidney, the glomeruli are scantily supplied with blood, and the secretion of urine is proportionately small. Perhaps, too, nervous in- fluence may not be without effect in bringing about this condition, since it is possible that in the kidneys, just as in other organs, the ar- teries of the various vascular systems are not subject to the same kind of innervation. The causes which induce fluxion to the kidney are: 1. The transient plethora induced by every copious draught of liquid. This hyperemia is most pronounced in the secretory portion of the kidney, and the profuse transudation which takes place out of the overloaded glomeruli is the principal step in the process by which the general plethora of the system is relieved. 2. There is a second cause of renal hyperemia, which is closely analogous to the first, and which occurs when the left side of the heart is hypertrophied, and which also is confined to the arterial system, in- cluding the glomeruli. 3. Collateral fluxion to the kidney may result from compression of the abdominal aorta, or iliac arteries, by a tumor or gravid uterus, as well as from derangement of the circulation in the capillaries of the HYPEREMIA OF THE KIDNEY. 9 skin in the cold stage of intermittent fever. In the second stage of Bright's disease, compression of the vessels of the cortical substance, by the distended urinary tubules, also gives rise to collateral fluxion in the medullary substance of the kidney ( Virchow). 4. Dilatation of the afferent vessels, from palsy of then- muscular elements, seems to be the principal cause of that arterial hyperemia of the kidney, the existence of which is revealed by the discharge of a large quantity of limpid urine in certain spasmodic diseases (urina spastica). 5. Fluxionary hyperemia is found in the vicinity of inflamed regions and deposits of morbid product. This form of hyperemia we have already endeavored to account for, in treating of an analogous condi- tion in other organs, ascribing it to a loss of tone in the tissues, and to a dilatation of their capillaries, whose walls are ill supported by the surrounding relaxed parts. 6. Renal hyperemia complicates inflammatory disease of the urinary passages, especially disease of the pelvis of the kidney. 7. The renal hyperemia which sometimes attends the use of can- tharides, balsam of copaiba, and similar drugs, as well as that which accompanies certain infectious diseases, especially scarlatina, measles, typhus, and cholera, seems to be of similar origin. However, the affec- tions of the kidney which arise from the diseases above named cannot all be attributed to hyperemia. Many of them belong to the class of maladies which we shall describe as parenchymatous degeneration of the kidney, in Chapter VII., and which, undoubtedly, are capable of de- veloping without the occurrence of hyperemia. This is equally true of the renal affections which so often accompany pregnancy. Obstructive engorgement of the kidney arises from causes similar to those which induce engorgement of the liver (see Volume I.), so that the two diseases often accompany one another; but it will readily be understood, from what has already been said as to the peculiar character of the hepatic circulation, that engorgement of the liver usually is of earlier occurrence and greater intensity than engorgement in the kidnej-s. Engorgement of the kidney arises : 1. In uncompen- sated valvular disease of the heart; 2. In structural disease of the heart, which depresses the functional energy of the organ; 3. When the vigor of the heart is impaired by a condition of marasmus; 4. In disease of the lungs, which causes compression or wasting of the pul- monary capillaries; 5. In conditions in which the aspiration of the blood to the thorax is arrested; 6. In rare instances, contraction and closure of the vena cava or emulgent veins, by compression or throm- bosis, give rise to engorgement of the kidney, but the hyperemia yrising in such cases is of very great intensity. 10 DISEASES OF THE KIDNEY. Anatomical Appearances.—A kidney in a state of recent hy- peremia is of a more or less dark-red color. Sometimes it is enlarged, owing either to dilatation of its vessels or to serous infiltration. The oedema of its parenchyma and subcapsular connective tissue renders the hyperemia organ unnaturally moist and soft, and loosens its capsule. When cut into, and when the vessels of the glomeruli are much dis- tended by blood, the Malpighian coils dot the surface of the section, as dark-red points. When the hyperemia is of long standing, particularly when there is habitual engorgement, as occurs in chronic disease of the heart and lung, the changes which arise are of a different kind. The kidney is then but little enlarged, or remains of its normal magnitude, or may even be somewhat smaller than natural. It is more resistent in texture, and is of a uniform red color. Upon microscopic examination, the epithelium of the urinary tubules of the cortical substance is found to be swollen, the contour of the cells is ill-defined, and they are filled with finely-granular contents, which clear up upon the addition of acetic acid. Sometimes there is a desquamation of the degenerated epithelium here and there; and the tubules collapse after the epithe- lium is expelled, causing the surface of the kidney to become uneven by depressions of varying depth. Traube and Beckman have called particular attention to the difference between this condition and the degenerative chronic inflammation of the kidney, which we shall de- scribe in Chapter IV. as chronic Bright's disease. While the alterations above described are going on in the epithe- lium of the cortical substance, the straight tubules of the medullary substance are usually found filled with a material which is sometimes transparent and pale, and sometimes of a more yellow color. By mod- erate pressure upon the pyramids, a large quantity of an opaque creamy liquid is discharged from the papille, which contains a great deal of epithelium and a few of those casts of the tubuli, in the form of homo- geneous transparent tolerably firm cylinders. Symptoms axd Course.—The kidney has so few nerves of sensa- tion, and its capsule is so distensible, that hyperemic swelling of the organ is never accompanied by pain. As the amount of urine secreted depends chiefly upon the degree of pressure within the vessels of the glomeruli, its secretion necessarily becomes more profuse in that form of renal hyperemia which involves the arterial system of the kidney, including the vessels of the Malpighian tufts. This is almost the only symptom caused by fluxion to the kidney, which arises from copious drinking, hypertrophy of the left heart, compression of the aorta or iliac arteries, and dilatation of the renal arteries. The urine is copi- ous in quantity, dilute in quality, of low specific gravity, and of a pale HYPEREMIA OF THE KIDNEY. 11 color. In such cases, the pressure in the glomeruli hardly ever is suf- ficient to occasion transudation of albumen, or to rupture the vessels, and cause extravasation of blood into the Malpighian capsules. This fact is in accordance with the results of physiological experimenta- tion. Ligation of the abdominal aorta below the origin of the renal arteries, in spite of the increase of pressure which ensues in those arte- ries, never results in albuminuria. A very different train of symptoms follows upon a moderate de gree of obstructive engorgement of the kidney. Since, as we have just shown, in almost every case of obstruction of the renal veins the degree of tension within its arteries is very small, there is a diminution instead of an increase of the secretion of urine. On the other hand, the strain upon the capillaries becomes exceedingly severe, since they cannot discharge their contents into the already overloaded veins until the pressure within them exceeds that within the veins. Hence, not only does the plasma of the blood readily escape from the capillaries into the urinary tubules, so that the scanty, concentrated, dark-colored urine contains albumen, and the so-called fibrinous casts (or, more properly speaking, exudation casts),.but the delicate walls of the capil- laries give way before the strain, so that the urine is also full of blood- corpuscles. According to the recent observations of Liebermetstcr, the simultaneous appearance of blood and albumen is so usual in obstruc- tive hyperemia of the kidney, that the appearance of albumen alone, without a trace of blood, almost excludes the idea of simple engorge- ment from the diagnosis, and indicates the existence of inflammation. This fact in pathology, which may be verified in almost every case of chronic disease of the heart, and traced through all its phases, agrees with the results of physiological experiment. Albuminuria and hema- turia are the never-failing consequence of ligation of the renal veins, or of the vena cava above their point of entrance. The escape of plasma from the capillaries of the kidneys, in obstructive congestion, into the uriniferous tubules is analogous to the extravasation from the pulmonary capillaries into the air-vesicles, which occurs in engorgement of the lungs, and which is there called hypostasis. The so-called hypostatic pneumonia is quite as independent of genuine inflammatory action as is the disorder of the kidney at present under consider- ation. The form of renal hyperemia which apparently proceeds from re- laxation of the tissues of the kidney and consequent dilatation of its capillaries, has no effect either in augmenting or diminishing the quan- tity of urine secreted. It is attended, however, by a more or less pro- fuse transudation of blood-plasma, as well as by a greater degree of snedding, and probably too by a more active reproduction of the eel- 12 DISEASES OF THE KIDNEY. lular contents of the uriniferous tubules. Hence, when, after the abuse of irritating diuretics, or in disease which we know to be frequently complicated with this form of renal hyperemia, we find the urine to be albuminous and full of casts thickly studded with epithelial cells, our diagnosis may be renal catarrh. This name, which has been applied to the form of hyperemia in question by most modern pathologists, is not quite appropriate, it is true, as the tubules have no mucous mem- brane, and as the term catarrh itself means an affection peculiar to such a membrane. However, it is quite as appropriate as is the term catar- rhal pneumonia. (See Vol. I.) The course of both fluxionary and obstructive hyperemia of the kidney, when the exciting cause is of a transient character, usually is favorable, and the disease in itself probably never causes death. Al- though, during the last few weeks of a case of heart-disease, this affec- tion appears in its most intense form, yet it is not renal hyperemia of which the patient finally dies, but the respiratory derangement, the dropsy, and other symptoms which proceed immediately from the cardiac disorder. However, it cannot be denied that the albuminuria aggravates the dropsy and hydremia, and aids in undermining the strength of the patient. The renal catarrh also runs a favorable course as a rule, and, when the primary disease tends toward recovery, usually terminates in complete restoration to health. Far more rarely, diffuse parenchymatous inflammation of the kidney may develop from renal catarrh. Treatment.—The measures called for in treatment of the cause of hyperemia of the kidney may be inferred from the account above given of the causes themselves. When the hyperemia of the kidney is but a symptom of a more wide-spread and grave disease, it is to the latter rather than to the hyperemia to which the treatment should be directed. Where it has arisen from the abuse of irritating diuretics, their employment must be discontinued, and all application of vesi- cants, and use of irritating salves upon suppurating surfaces (a very common cause of fluxion to the kidney), must be abstained from. Be- sides this, large quantities of drink must be administered, in order as much as possible to dilute the acrid matter which has been secreted in the kidneys. Pure water or the dilute acids are the most suitable for the purpose. The old practice of using barley-water, linseed-tea, milk of almonds, and the like, mucilaginous or oleaginous liquids, must be regarded as obsolete, as it is well known that such articles have no effect upon the character of the urine. General and local blood-letting, and derivatives to the skin or intes- tines, are only to be resorted to in fulfilling the indications from the disease itself, when such remedies are indicated for other reasons, or HEMORRHAGE FROM THE KIDNEY. 13 when the hyperemia is extreme, and there are no counter-indications against blood-letting. CHAPTER II. hemorrhage from the kidney. Etiology.—The causes of hemorrhage from the kidney are: 1. Wounds, contusions, and other injuries of the organ. The presence of calculi in the pelvis of the kidney is one of the most common sources of such injury. Bayer tells about a patient with renal calculus who had hematuria whenever he was compelled to ride. 2. Hemorrhage from the kidney may proceed from intense hyperemia, and rupture of the overloaded renal capillaries, and especially from that form of hyperemia which accompanies the first stage of inflammation of the kidney, and which ensues after the employment of irritating diuretics, as well as in that form of the affection which follows scarlatina, small- pox, typhus, malarial fevers, and other infectious diseases. The hyper- emia which exists about the seat of a parasite, or a neoplastic growth, especially cancer, often gives rise to hematuria. Finally, the exces- sive obstructive engorgement of the kidney, produced by disease of the heart and lungs, often results in an escape of blood from the renal capillaries. 3. In rare instances renal hemorrhage depends upon a hmmorrhaglG diathesis, that unknown disorder of the blood-vessels from which scorbutus and purpura hemorrhagia proceed. 4. In cer- tain tropical regions—the Isle of France, in Brazil, and elsewhere— hemorrhage from the kidney is endemic, there being no known cause for the disease. A peculiar form of renal hemorrhage, hemorrhagic infarction, arises under conditions similar to those under which hemorrhagic infarction takes place in the spleen. This can be traced in most cases, but not in all, to embolism. Genuine renal apoplexy is usually the result of severe injury, but in children may also proceed from severe hyperemia (BokitansJcy). Anatomical Appearances.—In hemorrhage from the kidney, the blood may be effused into the normal interstices of the tissues, without detriment to the latter. In this way ecchymoses arise, in which there are spots of varying size stained of a deep red, and from which blood flows freely when they are cut into. They are situated sometimes under the albuginea, and sometimes within the tissues of the kidneys themselves. When recent, hemorrhagic infarction has the appearance of a dark- red deposit of a cuneiform shape, the point of the wedge being directed toward the lulus of the kidney. When of longer standing, the deposit 14 DISEASES OF THE KIDNEY. loses its color, beginning at the middle, and becomes converted into a yellow caseous mass, or else breaks down, forming a renal abscess, with yellow puruloid contents, which at first consist of detritus alone, but which afterward are mixed with pus. The seat of renal apoplexy is generally the medullary portion of the kidney. Collections, of varying size, form in the lacerated paren- chyma, their contents consisting partly of clotted blood, and in part of crushed and broken-down debris of the tubules. It would seem that the contents, both of apoplectic extravasations and of hemor- rhagic infarctions, may undergo fatty degeneration and absorption, and that recovery may take place, leaving a depressed cicatrix. Part of the blood effused into the tubules coagulates, forming cylinders, which are densely studded with blood-corpuscles. Sometimes we find pig- ment in the tubules, and Malpighian capsules, as the residue of some former extravasation of blood. Symptoms and Course.—The occurrence of renal hemorrhage does not become recognizable unless the blood be effused into the tubules, and discharged with the urine. Hence it not unfrequently happens, in post-mortem examinations, that hemorrhagic infarctions and apoplectic extravasations are discovered, which were quite undis- coverable during life, because the blood did not enter the uriniferous tubules. If the amount of blood mingled with the urine be very small, the color of the latter is a peculiar dirty red, when viewed by reflected light, while by transmitted light it is a pure red, of greater or less depth. After standing for some time, a somewhat characteristic, slightly flocculent, brownish sediment is precipitated. When urine containing blood is exposed to the action of heat and nitric acid, the albumen of the serum of the blood coagulates. If the sediment be examined microscopically, blood-corpuscles are found, some of which are well preserved, while others are somewhat altered. There are also the casts above described, studded with blood-corpuscles, which are peculiarly characteristic of renal hemorrhage. I strongly recommend Heller's test for blood as very simple and convenient, and by means of which, as I have often satisfied myself, the faintest trace of blood may be discovered. The urine is to be heated, then caustic potash is to be added, and it must be heated anew. The phosphates are thus precipitated, taking with them the coloring matter of the blood, which imparts a dirty yellowish-red color to the sediment, when viewed by reflected light, and, when seen by transmitted light, makes it appear of a splendid blood-red color. Neither the coloring matter of the urine nor that of the bile is precipitated with the phosphates, so that col- oration of urine which shows this reaction cannot be ascribed to the presence of the latter pigments. When the quantity of blood in the HAEMORRHAGE FROM THE KIDNEY. 15 urine is very large, it is of a dark or brownish red, and, after standing, forms a cake of blood at the bottom of the vessel. Not unfrequently, a partial coagulation of the blood takes place in the bladder, and the coagula thus formed can only be got rid of after great suffering on the part of the patient. Sometimes the blood coagulates while in the ureters. In such instances, the symptoms of renal colic, hereafter to be described, may arise, and long, worm-like coagula (casts of the ureters) may be voided. The course of renal hemorrhage necessarily depends upon the na- ture of the disease which causes the hemorrhage. When induced by renal calculus, bleeding occurs regularly after every violent exertion. Hemorrhage arising from the presence of a tumor, especially cancer, is usually very profuse and persistent. The bleeding which accompa- nies inflammation of the kidney and the infectious diseases, or which results from venous obstruction or scorbutus, is not often very severe. In the endemic hematuria of the tropics there are periodical profuse flows of blood from the kidneys. In hemorrhagic infarction, if there be hematuria at all, it is always slight. It is usually ushered in by a chill, and is attended by pain in the region of the kidney, and by violent sympathetic vomiting. The occurrence of such a train of symptoms—a chill, lumbar pain, vomiting, and hematuria—in a case of heart-disease, would warrant the diagnosis of a renal infarction, which otherwise generally escapes detection. Renal apoplexy is marked by similar symptoms, which, however, are of much greater intensity. The results of renal hemorrhage cannot be described in detail until after a more thorough discussion of the diseases whereon they depend. The hematuria arising from cancer, from renal calculus, and from the tropical disease, acts chiefly by producing exhaustion from loss of blood. Treatment.—The main point in the management of a case of renaL, hemorrhage is the treatment of any hyperemia, inflammation, or other constitutional disease from which it proceeds. In most instances, Avhen the main disease is susceptible of efficient treatment, the hemorrhage does not require any especial attention. Sometimes, however, the danger of exhaustion arising from repeated attacks of profuse and per- sistent hemorrhage, such as occur in cancer and renal calculus, may require relief. Cold, in the form of a bladder of ice laid over the re- gion of the kidney, cold sitz-baths, or cold injections, should then be resorted to. Internal administration of styptics has been recommended, and the whole list has been given seriatim in many cases, each failing in its turn. Articles containing tannin, especially tannic acid itself, which is eliminated through the kidneys in the form of gallic acid, and thus is enabled to act directly upon the bleeding point, deserve the 48 1G DISEASES OF THE KIDNEY. greatest amount of confidence. Next to it, secale cornutum, or ergotiue, may be given, but the doses must be large. The only effect to be ex- pected from the preparations of iron is the beneficial action which they exert upon the deterioration of the blood. CHAPTER III. ACUTE BRIGHT'S DISEASE—CROUPOUS NEPHRITIS. Etiology.—The name Bright's disease is generally applied to two forms of inflammation of the kidney. The first, which is the subject of the present chapter, is closely allied to croup of the larynx and air- vesicles, not only in its anatomical lesions—consisting of a coagulating exudation, containing epithelial cells, and often extravasated blood- cells, and which fills up and occludes the urinary tubules—but in its course, which is always acute, like that of the other croupous diseases above mentioned, and nearly always terminates either in recovery or death within a few days. It is rare for the disease to pass into the second form of Bright's disease, which we shall describe in the next chapter, under the name of " parenchymatous nephritis." This latter circumstance, indeed, seems to me to indicate that it is both right and practical to regard acute and chronic Bright's disease as independent and distinct affections. I attach little value to the term " croupous nephritis," applied to acute Bright's disease, in the previous editions of this work, as I must acknowledge that it is a matter of doubt whether the exudation which fills up and obstructs the uriniferous tubules consists of fibrin like the exudation of croupous laryngitis and croupous pneumonia, and as it cannot be denied that the epithelium of the uriniferous tubules takes a more active part in the nutritive disor- ders attending acute Bright's disease than is taken by the epithelial cells of the larynx and air-vesicles in croupous laryngitis and croupous pneumonia. 1. Croupous nephritis is a frequent complication of scarlatina. There is a prevalent notion among the laity that a child who dies of dropsy, after scarlet fever, "has not been well taken care of;" and many an unhappy mother, who has lost her child from this cause, re- proaches herself for years for having changed its linen too soon, or im- prudently opened a door, and thus brought about her child's death. It is possible that chilling of the skin during scarlet fever may sometimes favor the occurrence of croupous inflammation, and may even actually produce it, but it is certainly not the case in the majority of instances. Besides the disturbance of the skin which it occasions, scarlatinous vrirus constantly induces disorders of the fauces and kidneys. Tn most ACUTE BRIGHT'S DISEASE—CROUPOUS NEPHRITIS. 17 epidemics they are of a hyperemic nature, and give rise to the well- known symptoms of catarrhal angina in the throat, and in the kidneys cause renal catarrh, as described in the foregoing chapter. There are malignant epidemics of scarlatina, however, which give rise to much graver disorder of these organs. Instead of simple catarrh, there is nearly always a diphtheritic inflammation of the fauces, and, instead of a simple renal hyperemia, the urinary tubules are attacked by croupous inflammation. In such epidemics, many children die of dropsy who have received the best possible care, while many, who have been actually neglected, escape unscathed. The virus of measles, typhus fever, and the poison of malaria, may also induce croupous nephritis, but they are far less frequent causes of the disease than is scarlatina. 2. Croupous nephritis arises during the typhoid stage of cholera, and, by many authors, is regarded as a constant complication, if not the actual cause, of this very common and obscure sequel of cholera. Although we cannot subscribe to this latter opinion, having witnessed the death of many patients from cholera typhoid, whose urine was abundant and free from albumen, yet the frequence of croupous ne- phritis, as a sequel to cholera, cannot be denied. It remains an open question whether the vascular engorgement and inspissation of the blood, which take place in the algid stages of cholera, induce obstruc- tion of the renal capillaries from crowding together of the blood-cor- puscles, and extravasation of plasma and blood into the tubules, or whether the inflammation of the kidneys, like the other inflammatory affections of the typhoid stage of cholera, be ascribable to infection of the blood. It, undoubtedly, is very rare for croupous nephritis, in healthy subjects, to proceed from contusions, the misuse of irritating diuretics, exposure to cold, or other unknown exciting causes. Anatomical Appearances.—The anatomical alterations found post mortem after croupous nephritis are identical with those so ad- mirably described by Frerichs as the first stage of Bright's disease, the " stage of hyperemia and incipient exudation." The kidney is often enlarged to twice its proper size, and its surface is smooth. The tunica albuginea is opaque, injected, and is easily detached. The cortical substance, to whose swelling the increase in volume of the kidney is mainly due, is of a more or less dark-brown color, soft, and easily torn. When cut into, a bloody adhesive liquid bathes the face of the section. Both the superficial and deeper parts of the cortical substance are dotted with dark-red points. The pyramids also are hy- peremic, and striped with red, and an opaque and often bloody liquid is usually found in the calices and pelvis of the kidney, which like- wise are injected with blood. Microscopic examination does not IS DISEASES OF THE KIDNEY. exhibit any important change in the texture of the kidney. The glomeruli, being overloaded with blood, are very distinct. Extravasa- tions of blood are almost always found in the Malpighian capsules and tubules, which account for the blood-red points above alluded to. There are likewise extravasations between the albuginea and the tu- bules. The uriniferous tubules, especially those of the cortical sub- stance, are filled with coagulated exudation. Upon microscopic ex- amination of the liquid expressed from the cut surface of the diseased kidney, we find the cylindrical masses of exudation covered with epi- thelium and blood-corpuscles, so often referred to, and which form casts of the tubules. The epithelium itself is not materially altered. Symptoms and Course.—Sometimes croupous nephritis is ushered in by a rigor, followed by fever and a sharp pain in the region of the kidney. In addition to this, there is almost always more or less violent (sympathetic) vomiting; indeed, vomiting is a more constant token of incipient disease of the kidney than either fever or pain, and it is well to warn parents of children with scarlatina of the serious nature of this symptom, and to require them to seek medical aid should it arise. The patient feels a constant inclination to pass water, but is unable to expel more than a few drops with each effort. The suppression of urine may be so complete that the whole amount se- creted in course of a day may not exceed an ounce or two. Its spe- cific gravity is high. Sometimes, and for a short time, it may be of the eolor of pure blood; more usually it is opaque, and of a peculiar dirty reddish-brown hue, and looks as though it really contained dirt. Both urine and sediment have this dirty appearance, which alone, to the eye of an expert, is a tolerably sure sign of acute Bright's disease. There is a very large quantity of albumen in the urine, and, upon the application of heat and nitric acid, the half or even three-quarters of the liquid will coagulate. Upon microscopic examination of the sedi- ment, we find large quantities of epithelium from the tubules and urinary passages, as well as many blood-corpuscles, and casts, studded with blood-corpuscles. Dropsical symptoms soon set in, and in most cases the dropsy soon becomes very severe. The face, hands, legs, and scrotum swell up, and the skin is so tensely swollen that an impres- sion made upon it by the finger is soon effaced. The dropsy of croup- ous nephritis, like that of parenchymatous nephritis, as we shall pres- ently see, shows a great tendency to shift its position; the swelling increasing in one part of the body, while it diminishes in another. When the progress of the disease is favorable, the coagula, which block up the uriniferous tubules, are washed away, the urine becomes freer and more abundant, and the albumen diminishes. At the same time there is an abatement of the dropsy, which, in this disease, seems ACUTE BRIGHT'S DISEASE—CROUPOUS NEPHRITIS. 19 rather to depend upon suppression of the secretion of urine than upon that leakage of the albumen of the blood which takes place in acute hydremia. In the most fortunate cases, the disease may terminate in from eight to fourteen days, recovery being complete and without sequele. In very many instances the nephritis is accompanied by acute inflammation of the lung, pleura, pericardium, or peritoneum, and it is to one of these complications that the patient usually suc- cumbs in fatal cases. It happens much more rarely that croupous nephritis, instead of terminating in the above manner, gives rise to the so-called uremic in- toxication. It is easy to comprehend that, in consequence of the sup- pression of the urinary secretion, substances may accumulate in the blood which act perniciously upon the nutrition and functions of the various organs. It used formerly to be supposed that the urea, which is the most abundant of the solid constituents of the urine, and which is the best known of all its organic ingredients, by accumulating in the blood, induced convulsions, coma, and ultimate palsy of the entire nervous system, and, when such symptoms accompanied suppression of urine, they were called uremic symptoms, or uremic poisoning. Frerichs afterward supposed that this toxic effect was due to the presence of carbonate of ammonia, resulting from decomposition of the urea, rather than to the urea itself. This theory, however, cannot, by any means, be regarded as proved, and we must acknowledge that we are unacquainted with the excrementitious material retained in the blood, which exerts so pernicious an influence upon the organism in cases of suppression of urine. However, notwithstanding the rarity of uremic poisoning in croupous nephritis, yet it is of great importance, as regards both the prognosis and treatment of the disease, not rashly to ascribe any convulsions or stupor which may arise to inflammation and exuda- tion in the brain. Cases occur in which the convulsions and coma sub- side as the free secretion of urine is reestablished, and the attack termi- nates favorably. (For further details of the so-called uremia, and of the frequent dependence of cerebral symptoms upon oedema of the brain see Chapter IV.) I should finally state that cases of croupous nephritis occur in which the disease improves somewhat, but does not subside completely ; the albuminuria continues, and the character of the acute croupous nephritis (acute Bright's disease) runs into that of parenchymatous nephritis (chronic Bright's disease). I have never seen such a case, and they must be very rare. Treatment.—In recent cases, and in tolerably robust subjects, it is advisable to resort to local depletion over the region of the kidneys, by means of leeches or cups. The effect of the first application will decide as to the propriety of its repetition in case of recurrence of the 20 DISEASES OF THE KIDNEY. symptoms. General blood-letting should be rejected, as liable to ag- gravate the already existing tendency to deterioration of the blood. The use of calomel and other so-called antiphlogistics is equally im- proper. Warm baths, followed by envelopment of the body in woollen blankets, are much preferable to the internal exhibition of diaphoretics. In treating of parenchymatous nephritis, we shall go more into detail upon this subject, and upon the brilliant results which are sometimes obtained from diaphoresis. If the bowels be confined, a few powerful doses of drastic medicine should be given—jalap, senna, or even colo- cynth. The profuse serous transudation into the intestine, caused by these medicines, may have a beneficial effect upon the dropsy; but it sometimes happens that the patient has a violent diarrhoea, and yet the dropsy continues to increase rapidly. Mineral waters containing carbonic acid are the most suitable beverage. We should not be too sparing in their administration, as the increase of pressure in the glom- eruli, and the augmented transudation, may assist in washing away the obstructing coagula. On the other hand, drastic diuretics are con- traindicated, owing to the inflamed condition of the kidney. During convalescence, and in tedious cases even prior to convalescence, the tendency to deterioration of the blood must be combated by the ad- ministration of quinine and iron, and a plentiful supply of albuminous food. CHAPTER IV. chronic bright's disease—parenchymatous nephritis. Etiology.—In parenchymatous nephritis the epithelium of the uriniferous tubules exhibits the alterations which we have repeatedly described as characteristic of all parenchymatous inflammations. Its cells first increase considerably in bulk, through imbibition of an al- buminous liquid; their contents then undergo fatty metamorphosis, by which the epithelial cells gradually become converted into cells of fatty granules. Finally, the cell-membrane perishes, and the fat globules emerge free into the urinary tubules. While these are the essential changes which the kidney undergoes, in the majority of cases coagulating exudations are also formed in the tubules, and in many instances proliferation of the insterstitial connec- tive tissue occurs. Atrophy of the kidney, which sets in afterward, is the natural and necessary consequence of the inflammatory process above described. Parenchymatous nephritis is a very common disease. Predisposi- tion to it is far less in childhood than in more advanced life. Men are CHRONIC BRIGHT'S DISEASE—PARENCHYMATOUS .NEPHRITIS. 21 attacked by it somewhat more frequently than women; persons of debilitated and depressed constitution more readily than those who are robust. Hence the poorer part of the community are more afflicted by the disease than the well-to-do class, being more exposed to the evils which produce it. 1. Chief among the predisposing causes of Bright's disease is the temporary, and in a still greater degree the continual exposure of the skin to the effect of cold and moisture. This accounts for the great frequence of the disease in England, Holland, Sweden, as well as on the German coasts; and not only upon that of the North Sea as Frerichs has assumed, but also upon the eastern shore. In the very moderate number of beds in the Greifswalder clinic, there used always to be many cases of Bright's disease. 2. It would seem that the misuse of irritating diuretics and the incautious exhibition of cubebs and copaiba may sometimes lead to parenchymatous nephritis, although, perhaps, this does not occur very frequently. 3. On the other hand, the abuse of ardent spirits unmistakably plays a most important role in the etiology of the disorder, so that Bright's disease appears almost as frequently among hard drinkers as does cirrhosis of the liver. We have no physiological explanation of this circumstance; but as recent researches have proved that alcohol taken into the system is not all consumed in the blood, as used for- merly to be supposed, but that at least a portion of it, passing through the urinary organs, is eliminated from the system unaltered, it is con- ceivable that the alcohol may act locally upon the kidney, just as we have shown it to act in cirrhosis of the liver. 4. Parenchymatous nephritis very frequently is associated with tedious suppuration, with caries, and necrosis of the bones, the surgical wards of the hospitals always furnishing a rich contingent of this mal- ady ; although the latter causative agents lead to amyloid degenera- tion of the kidney with equal if not greater frequence. The connec- tion between these exhausting affections and Bright's disease is ob- scure. However, just as in other cachectic conditions, so the appear- ance of inflammation in the most diverse organs is so common an occurrence in these depressing maladies, that it becomes a question whether nephritis holds a closer relationship to such conditions than is held by pleuritis, pericarditis, peritonitis, and the like. 5. Finally, parenchymatous nephritis often attends conditions of dyscrasia, from gout, rachitis, syphilis, scrofula, malarial cachexia, in which, however, besides the inflammatory degeneration, the lardaceous metamorphosis hereafter to be described is often observable. I agree with Traube, that it is improbable that simple obstructive' 22 DISEASES OF THE KIDNEY. hyperemia, from disease of the heart and the like, can give rise to inflammation of the kidney, and I believe that, hitherto, there has been a great deal of confusion of this malady with that described in the preceding chapter. Nor can I regard pregnancy as one of the remote causes of parenchymatous nephritis. The albuminuria so com- mon among pregnant women is not generally a result of inflammation, but is rather due to a parenchymatous degeneration of the kidney, to be described in Chapter VII. Anatomical Appearances.—A review of the anatomical changes occurring in the kidney during this disease will be materially facili- tated by grouping them according to their three stages of progress after Frerichs. The first stage seldom comes under observation of the pathological anatomist. At this period the kidney is enlarged, hyperemic, and in- filtrated. The epithelium as yet is but little changed; but the urinif- erous tubules contain cylinders of exudation, so that the diseased organ bears a very similar appearance to that presented by croupous nephri- tis, excepting that the various lesions are less pronounced. In the second stage, " that of exudation and incipient conversion of the exudation," the dimensions and weight of the kidney have in- creased still further. Its surface is still smooth, excepting where a few " granulations " project above the general level here and there. The consistence of the organ is less firm; its tunica albuginea is opaque and loosened. In color, the former dark red, or reddish brown, gives place to a more yellowjsh, or even distinctly yellow hue; the amount of blood contained in it is small; and the red points represent- ing the vascular coils of the Malpighian capsules are no longer visible to the naked eye. Upon section, it is found that the enlargement of the kidney is due solely to the swollen condition of the cortical sub- stance, which may attain a thickness of from half an inch to an inch. The pyramids do not participate in the yellow discoloration, and their red color forms an abrupt contrast to the hue of the cortical substance. Microscopic examination reveals an enormous dilatation, and vari- cose sacculation of the tubules. Within them, in some places we still find intact though swollen epithelial cells, whose contents are in a state of incipient fatty metamorphosis; elsewhere they contain exuda- tion cylinders which are similarly degenerating; while at other points we find dark granular masses of fat, the residua of degenerate and extinct epithelium. While here and there single Malpighian capsules remain normal, others are found to be considerably enlarged, and their epithelium swollen and clouded by the presence of fatty molee Jes. The glomeruli are almost bloodless, and their cavity is filled with an amorphous exudation, which renders their outline very indistinct. CHRONIC BRIGHT'S DISEASE—PARENCHYMATOUS NEPHRITIS. 23 The dilatation of the urinary tubules, which is a necessary result oi compression of the vessels, and the appearance of fat within the tubules, fully account for the appearance presented by the kidney to the naked eye at this stage; for the thickening of the cortical portion within whose tubules the process is going on, for the obscuration of the glomeruli, and for the small granulations upon the surface, which consist of single uriniferous tubules that have become greatly dilated. In the third stage, the stage of degeneration and atrophy, the kid- ney, which hitherto has been enlarged, is now reduced both in weight and bulk. Not unfrequently it is considerably smaller and lighter than a normal kidney. Its surface, heretofore smooth and uniform, is now lobulated and studded with " granulations," and elevations sepa- rated by narrow clefts. Its consistence is no longer soft and tender, but is exceedingly firm and tough. The tunica albuginea, which is opaque and much thickened, has grown fast to the parenchyma, from which it is difficult to detach it. The color of the organ is a dirty yellow, changing to a more whitish hue in the clefts. Upon section, the cortical portion is found, in a great measure, to have disappeared. Its thickness is often so slight as merely to form a narrow border around the pyramids. Upon microscopic examination we still find the urinary tubules and Malpighian capsules enlarged and filled with fatty matter, at points corresponding to the elevations and granulations; but in the contracted spots the tubules are empty, and shrivelled or collapsed ; or there may be nothing remaining of them, excepting an ill-defined fibrous mass. The Malpighian capsules are wasted, and now present the appearance of small balls, filled with a few fat glob- ules, in which the glomeruli are no longer recognizable. In this stage, too, the microscope fully explains what is seen by the naked eye, and accounts for the shrinking of the kidney, the disappearance of the cor- tical substance, and the depression between the points where there still remain dilated tubules filled with fatty contents. The appearances are somewhat different when, besides these altera- tions of the epithelium, there is a proliferation of the interstitial con- nective tissue of the kidney. The Malpighian capsules are then not unfrequently surrounded by concentric layers of connective-tissue cells, or even by perfect connective tissue, the uriniferous tubules also being enclosed by recently-formed tissue, and separated from one another by wide intervals. Sometimes the tunica propria of the Malpighian cap- sule and tubules is converted into a broad homogeneous lryaline border. Among the less constant changes which occur in parenchymatous ne- phritis, Frerichs, whose excellent description we have here repeated as briefly and accurately as possible, describes the traces of former apoplexies, in the form of round spots, varying in size from that of a 21 DISEASES OF THE KIDNEY. poppy-seed to that of a pea, of a blackish or ochre-yellow color, and which are the results of some former violent hyperemia. In rare in- stances small abscesses are seen; and, finally, there may be cysts, which are tolerably common, and which vary from the size of a pea to that of a hazel-nut, and which probably are actually obstructed canals in a state of enormous dilatation by the liquid exuded into them from the glomeruli and surrounding vessels above the point of obstruction. In many instances the above alterations are neither so extensive nor so much advanced as those which we have just described. The lesions are often limited to the convoluted tubules in the immediate vicinity of the pyramids. Just at that region there is a yellowish discoloration, and it is only by means of the microscope that the in- cipient degeneration of the epithelium can be ascertained. This lesser degree of the malady forms a connecting link with the form of disease to be described in Chapter VII., and usually accompanies tedious sup- puration, chronic cachexia, and dyscrasia; although in these affections parenchymatous nephritis often attains the extent and intensity above described. Symptoms and Course.—Pain in the region of the kidney, which has been reckoned by most authors as among the most constant symp- toms of morbus Brightii, according to my observation, is wanting in the majority of cases throughout the entire course of the disease. It is true, that if we press with great force upon the kidney, the patients complain that the procedure is uncomfortable and distressing, but we shall hear a like complaint from well folk, whom we may subject to similar infliction. It is as unusual for the attention of the patient to be called to the grave nature of his disease by any marked diminution in the amount of urine which he passes, as it is for him to suffer pain in the renal region. After the dropsy and the albuminuria have placed the diagnosis beyond a doubt, most patients, if asked whether they have passed too little urine in the course of their disease, will not only deny it, but will even declare that throughout the entire duration of their dropsy they have made a great deal of water. Such an account as this, from a patient with chronic dropsy, is in itself suggestive of the probable dependence of the dropsy upon chronic renal disease. On the other hand, if a patient assert that his dropsy has developed grad- ually, and that since its commencement he has always passed remark- ably little urine, there is a certain amount of presumption that the dropsy is of cardiac or pulmonary origin, and that it does not proceed from disease of the kidney. However, we must not ignore the fact that such statements from patients, as to their passing an unusual quantity of water, are often the result of a delusion upon their part. An inclination to pass water frequently, a symptom due to sympathy of CHRONIC BRIGHT'S DISEASE—PARENCHYMATOUS NEPHRITIS. 25 the urinary bladder, and common both to chronic and to acute Bright's disease, but which is never very severe, impresses the patient with the idea that, in his frequent acts of micturition, he has discharged a large quantity of water. Accurate measurement of the amount passed in twenty-four hours shows that, in many cases, it does not quite reach the normal flow. In others it is normal; while in others, again, the proper quantum is really exceeded. A considerable diminution of the normal secretion or actual suppression of urine seldom occurs, and then merely forms, as it were, a short episode in the disease. This peculiar behavior of the urinary secretion, in chronic Bright's disease, is alto- gether enigmatical. The slighter degree of suppression, which is the most frequently observed, admits of the easiest explanation; as the obstruction of numerous tubules by swollen and degenerated epithe- lium would obviously impede the outflow of the urine, and the com- pression of many of the glomeruli must effect a diminution in the amount of urine secreted. But how shall we explain the fact that, in many instances, in spite of this hinderance to the discharge, and in spite of the limitation of the secreting surface, the flow of urine still remains normal, or even is abnormally profuse ? How account for the fact that the increase in this secretion is peculiarly common in the third stage of the disease, at a period when the kidney is atrophied^ and when many of its tubules and Malpighian capsules have collapsed and wasted away ? We admit that the hypertrophy of the left ventricle of the heart may perhaps assist in augmenting the secretion of urine by increasing the pressure within the glomeruli, which still remain intact, thus hastening the filtration of liquid through them; but its influence is by no means to be so highly rated as to suppose that the absence of many defunct glomeruli can be more than compensated for by in- crease of internal pressure upon those which remain. Nor does the collateral fluxion to the remaining glomeruli, induced by obliteration of the blood-vessels in the affected portion of the kidney, do more than to explain why there is not a material decrease in the secretion of urine, and by no means accounts for its augmentation. There is some probability that privation of the blood of its albumen may have some effect in increasing the secretion from the kidney. As is well known, a .liquid will pass more freely through an animal membrane from a dilute solution of albumen, than from a solution which is more concen- trated, the pressure being the same. But even this does not seem to account for the increased production of urine which we so often observe in the third stage of Bright's disease. Although, as before said, neither pain in the region of the kidney, nor any unusual flow of urine, calls attention to the grave disease which is going on, yet its recognition is no longer difficult, since it has 26 DISEASES OF THE KIDNEY. become the practice of the better class of physicians to make careful examination of the urine. Hospital patients do not generally apply for aid until the dropsy has appeared. Exclusion of other causes of dropsy will establish a strong presumption that we have a case of Bright's disease to deal with. Examination of the urine places the diagnosis beyond a doubt. In private practice, the observant and ex- perienced practitioner will have recognized the disease before the dropsy sets in. The history of the case is almost invariably as follows: The patients have long remarked a failure of their strength, and a pallor and anemic aspect of their skin, and visible mucous membranes. As all their functions are apparently normal, they are unable to ac- count for this paleness and debility. The physician, after careful ex- amination of all other organs, can find no appearance of disease to which the loss of strength and impoverishment of the blood can be ascribed. He examines the urine, and finds it to be loaded with albu- men, and the symptoms are accounted for. No elaborate demonstra- tion is required to show that, in addition to the other expenditures of the blood, a daily loss from the blood of large quantities of albumen, which may amount to from twelve to twenty grammes in the twenty- four hours, cannot be made good by the daily supply of nourishment; or, in other words, a person subject to a daily drain from his blood of from twelve to twenty grammes of albumen necessarily becomes pale, bloodless, and enfeebled. As an examination of the urine reveals the existence of the disease before the occurrence of the dropsy as well as after it, it will be well to give a more detailed account of the charac- teristics of the urine secreted in parenchymatous nephritis. It is gen- erally of a pale-yellow color, and often exhibits a somewhat opalescent reflection. As it is more viscid than common urine, on account of the albumen which it contains, it is more easily made frothy than urine free from albumen, and the froth lasts longer. When there is no in- tercurrent febrile disease, its specific gravity is remarkably low, and may sink to 1005. This is principally on account of a decrease in its urea, and in a lesser degree owing to a diminution of the salts, especial- ly the alkaline chlorides. The reduction in the amount of urea cannot at first be ascribed to retention of it in the blood. It would seem rather that, just as in other hydremic conditions in which the urine *is abnormally light, the metamorphosis of material in the body is going on more slowly than is natural, thus retarding the production of urea. The explanation of Schmidt as to the decrease in the saline constitu- ents of the urine, especially its alkaline chlorides, is less satisfactory, namely, that the saline ingredients of the blood augment as its albu- men diminishes, and vice versa. When the patients are already drop- sical, the transfer of the chlorides into their dropsical effusion is a CHRONIC BRIGHT'S DISEASE—PARENCHYMATOUS NEPHRITIS. 27 phenomenon of far greater importance. The significance of this cir- cumstance consists in the fact that, as long as the dropsy keeps in- creasing, the saline contents of the urine are very small, but whenever any rapid diminution of the effusion takes place, the salts are elimi- nated into the urine more freely, much more freely, indeed, than under normal conditions. If a portion of the urine be heated, after addition of a few drops of acetic acid, in case its reaction should be alkaline, or if nitric acid be added, the albumen coagulates. According to Frerichs, its quan- tity ranges from about 2.5 to 15.0 p. M. This presence of albuminuria, which usually persists throughout the whole course of the disease, and only disappears now and then, for short periods, unfortunately cannot be satisfactorily accounted for. One might be led into mistaking the albumen and the exudation cylinders for the products of inflammation, excreted from the free surface of the tubules, were it not that, in other and non-inflammatory diseases of the kidney, the urine contains both tube-casts and large amounts of albumen. I believe the presence of albumen in the urine to depend upon the destruction or degeneration of the epithelium. That normal urine should not contain albumen is confessedly extremely perplexing to the physiologists. They are al- most forced to suppose that the albumen does transude into the kidney, together with the water and salts; and they are reduced to the hy- pothesis that its absence from normal urine is in some way connected with the epithelial lining of the uriniferous tubules, the transuded albumen either becoming assimilated for the nutrition of the epithe- lium, or else its diffusion into the tubules, receiving some other modifi- cation, as yet unknown to us, from the epithelium. The observation that albuminuria exists in all diseases of the kidney, in which its epi- thelium is either degenerated or destroyed, fully confirms this physio- logical hypothesis. After the urine has been allowed to stand for a while, a light, whitish, flocculent precipitate falls to the bottom of the vessel. If this sediment be placed under the microscope (for this purpose it is best to let it deposit in the bottom of a pointed champagne-glass), the well- known casts are found. At the commencement of the disease they are covered by epithelium, in a state of fatty metamorphosis; at a later period, they seem quite bare, or are merely covered with granules and globules of fat. Besides this, the sediment contains common epithe- lial cells from the urinary passages, and smaller round, slightly-gran- ular cells. Dropsy is one of the most characteristic signs of Bright's disease, excepting in a few rare instances, in which it has been absent through- out the entire course of the malady. It generally begins as anasarca. 28 DISEASES OF THE KIDNEY. At first the face and feet swell, the upper extremities, abdomen, and scrotum not becoming affected until a later period. The cedema often shifts its position in a peculiar manner, so that at one time the face or upper extremities may be the more swollen, at another the feet, ab- dominal walls, or scrotum, while the tumefaction subsides in the region at first affected. Moreover, if the patient be out of bed, the feet gen- erally show the greatest amount of swelling in the evening, while in the morning the feet are smaller again, and the swelling involves the hips, back, and hands. The more slowly the anasarca develops, so much the more does the skin lose its elasticity, and so much more slowly is the imprint of the finger effaced from the cedematous surface. The addition of ascites and hydrothorax to the anasarca does not take place until a more advanced period. In one exceptional instance, I have witnessed the appearance of hydrothorax and cedema of the lungs early in the disease, where previously there had only been a slight cedema of the integument, a condition of apparent security thus sud- denly becoming one of great danger. In cases which advance rapidly, the dropsy may attain great magnitude in a few weeks. I have seen a patient who weighed a hundred kilogrammes, i. e., two hundred pounds, who affirmed that, eight weeks before, he did not weigh one hundred. Such extreme dropsical swelling, from the strain which it exerts, may be the cause of inflammation and gangrene of the skin, especially of the scrotum and labia majora. In the worst cases, the skin often bursts at several points, and the liquid trickles copiously from the rents. The pathogeny of the dropsy of parenchymatous nephritis is ex- ceedingly difficult of explanation. As is already stated, the dropsy often develops in the midst of a copious excretion of liquid from the kidneys, and hence cannot be ascribed to any increase of pressure upon the veins of this organ, although this must be regarded as the main cause of the dropsy of acute croupous nephritis, in which disease there is always a suppression of urine. It is true that, during any check to the secretion of urine which may occur in this disease, the dropsy makes rapid headway; and when the urine is scanty through- out the entire course of the malady, the dropsy soon becomes exces- sive, and the malady runs a subacute course. There is no doubt but that a " hydremic crasis," a lack of albumen in the blood, favors the occurrence of dropsy. Owing to the continual loss of albumen, which the blood is suffering, in Bright's disease, a liquid which contains but little albumen flows through the capillaries of the system. Hence, an abnormal transudation takes place from the capillaries into the inter- stices of the tissues, and hence, too, the amount of serum returned to the veins is abnormally small. It is not to be doubted that the ab- CHRONIC BRIGHT'S DISEASE—PARENCHYMATOUS NEPHRITIS. 29 sorption of liquid from the interstices of the tissues into the vessels is more active, in proportion as the difference in concentration in the liquid contained in the vessels, and that without them, is greater. Now, as, in parenchymatous nephritis, this difference is abnormally small, it follows, of course, that not only more liquid should leave the vessels, but that less should return to them. I have observed cases at my clinic which confirmed the correctness of this in the most strik- ing manner. A girl, who had been suffering for a year from paren- chymatous nephritis, stated that, some time before the appearance of the cedema, she had felt exceedingly dull and miserable. Being con- sidered plethoric, she was advised to get bled. A week after the blood-letting, the first symptoms of anasarca showed themselves, and since then have never entirely disappeared. It may be inferred in this case that the hydremia, which, though extant in moderation, still had not as yet produced dropsy, was so much aggravated by the blood- letting as to cause the dropsical symptoms to appear. In another case, the patient became anasarcous after a hemorrhage, but the ana- sarca afterward disappeared for a while, and set in anew after the es- tablishment of profuse suppuration. Nevertheless, hydremia is not the sole cause of Bright's disease, and probably not even its chief cause. Dropsy, as severe as that seen in Bright's disease, is hardly ever observed in any other form of hydremia. It often occurs early, but does not keep pace with the privation of the blood of its albumen. The peculiar manner in which the cedema shifts from one region to another is another argument against its dependence upon simple hydremia. If we abstract blood from an animal, and inject a corre- sponding amount of water into its veins in its stead, the animal does not become dropsical. Finally, the dropsy is so very often accompa- nied by attacks of inflammation as to indicate that, besides the thin- ning of the blood, there is another source both of the transudation and exudation, consisting in some disorder of the tissues as yet unknown to us. It sometimes happens that the continual aggravation of the symp- toms above described, and the excessive dropsy, which finally may in- volve the serous sacs and alveoli of the lungs, cause death without further complication. In most cases, however, remissions occur, in which the condition of the patient improves, the albumen in the urine diminishes, and the dropsy subsides. After a while he grows worse again, perhaps once more to improve at a later period, and thus the disease will fluctuate. In such protracted cases the above symptoms are seldom the only ones, but are accompanied by others which arise in part as complications of the main disease, and in part are immediate consequences of it. 30 DISEASES OF THE KIDNEY. Of these, inflammation of the lungs, of the pleura, pericardium, perito- neum, and meninges, deserve the first mention, as they are extremely frequent complications of Bright's disease, and because it is of these intercurrent affections that the patient most frequently dies, far more frequently, indeed, than of the so-called uremic symptoms—to be de- scribed presently—or even of excessive dropsy. Such inflammations of the lungs, pleura, etc., do not differ from similar inflammations in other conditions of anemia. The patient seldom succumbs at once to the first attack; and we not uncommonly find vestiges of previous inflammation, such as adhesions of the pleura, pericardium, and peri- toneum, besides the marks of the final seizure. Parenchymatous nephritis is often complicated by catarrh, particularly by catarrh of the bronchi and intestine. There is nothing peculiar about the for- mer, although in some cases the secretion is tolerably copious. The latter, however, is almost always characterized by a very abundant serous transudation, and by its extreme obstinacy. It would seem that the same cause which induces the escape of such large quantities of liquid into the subcutaneous connective tissue also gives rise to this immense transudation upon the free surface of the bronchial and in- testinal mucous membrane. Nevertheless, since the dropsy is not in- variably accompanied by catarrh, it must be admitted that its origin is somewhat obscure. According to my experience, chronic oedema of the lung is of very common occurrence in Bright's disease. It gives rise to great dyspnoea, to a tormenting cough, and, at the climax of the coughing-fit, not unfre- quently induces vomiting. I have had repeated opportunity of observing, whenever the vomiting caused the patient to eject much secretion, that his breath became freer for a while, his cough ceased, and that the fine subcrepitant rales subsided. Paroxysms of so-called urinous asthma, which are said to occur in Bright's disease, are probably de- pendent in a great degree upon oedema of the lung. Many patients with parenchymatous nephritis suffer from disease of the heart. Besides the adhesions of the heart and pericardium from former pericarditis, and the valvular derangement resulting from endocarditis, none of which are uncommon in Bright's disease, we very often find a hypertrophy of the heart, and more especially a hypertrophy of its left ventricle. Traube has advanced the theory that this hypertrophy is a result of derangement of the circulation of the kidney, which he claims should augment the labor of the heart. This theory is disputed by Bamberger and others, who reply that the hypertrophy develops in a stage of the disease when no obstruction of any importance to the circulation of the kidney ex- ists. A more extensive collation of facts will be necessary to decide CHRONIC BRIGHT'S DISEASE—PARENCHYMATOUS NEPHRITIS. 31 this disputed point; but, at all events, enormous hypertrophy of the heart sometimes occurs even in the second stage of Bright's dis- ease, and assuredly the circulatory disturbance of the kidney is not the sole cause of it. As is well known, the signs of the enlargement are not very striking, but, by paying attention, we can often detect an augmented heart-shock, or, in its absence, hear remarkably loud car- diac sounds. In a great number of cases, the symptoms of the so-called uremic poisoning do not appear at all throughout the entire course of the com- plaint. Sometimes they develop slowly and gradually; sometimes they come on very suddenly. At times (but not always), the attack is preceded by a decrease in the secretion of urine, and in rare instances it has happened that, during or immediately prior to the appear- ance of the uremic phenomena, the normal flow of urine has been largely exceeded (Ziebermeister). It is a suspicious sign when pa- tients complain of severe headache, and become languid and apathetic, and still more so, if these symptoms be accompanied by vomiting, which occasionally is so very obstinate as to awaken apprehension of serious disorder of the gastric mucous membrane. All these symp- toms may subside again, without evil consequence; in other cases, however, the drowsiness increases to a deep stupor, or convulsions of an epileptic or more rarely of a tetanic character may arise. Even when the convulsions have not been preceded by drowsiness, they are usually followed by a condition of deep coma with stertorous breathing. The fits recur at longer or shorter intervals, the stupor meanwhile con- tinuing to grow deeper; and the patient may finally succumb to gen- eral paralysis. It is not at all rare, however, for the fits gradually to become less frequent, the intervening stupor less profound, and for the signs of " uremia" to disappear, perhaps not to recur for weeks or months. In a previous section, we have already acknowledged that we are unacquainted with the nature of the poison causing uremic intoxication. There is a. second difficulty in explaining the uremia of parenchymatous nephritis, since certain well-attested cases of uraemic poisoning have been observed, in which there was no suppression of urine. If the urea and other material to be eliminated from the blood pass into the tubules by a process of pure endosmosis, it remains in- explicable how these materials can accumulate in the blood when the urine is secreted freely; hence we must assume that the epithelium of the urinary tubules has some important influence over the secretion of urine, and therefore that its disease or death may occasion antib- normal state of the blood, even though the kidneys continue to dis- charge a sufficient quantity of liquid. Moreover, I think that it would be going too far to attribute all the grave nervous symptoms which' 49 39 DISEASES OF THE KIDNEY. arise in parenchymatous nephritis—the headache, the convulsions, the coma, etc.—simply to a poisoning of the blood; and for many cases at least I agree to the equally one-sided views of Traube, according to whom the so-called uremic symptoms depend upon oedema of the brain and cerebral anemia. Since the first appearance of my text- book, I have been much gratified at the steady advance made by the doctrine which I propounded long ago, that the symptoms of the so- called cerebral pressure, due to encroachment upon the cavity of the cranium, whether by a depression of the skull, hemorrhage, tumor, abscess, inflammatory exudation, or serous transudation, all depend upon an arrest or obstruction to the flow of blood to the ganglion-cells and nerve-fibres of the brain. But, in spite of the experiments of Munh, I hold it to be unproved, and even improbable, that the acute cedema of the brain of Bright's disease should have an origin different from that of cedema of other regions, or that it should be ascribable to an increase of pressure within the cerebral arteries. Moreover, it seems to me to be extravagant to endeavor to ascribe all cases of so-called uremia to compression of the cerebral capillaries, and to anemia of the brain. My position in this question is as follows: In chronic parenchymatous nephritis, various organs are subject to oedema, the precise cause of which is unknown. It is characteristic of this cedema, that it shifts its position. It may attack the lungs at any period, either early or late in the disease, sometimes causing death, and sometimes subsiding again after a short duration. In a manner precisely similar, and for the same unknown reason, the brain may become the seat of an acute or subacute cedema, to which many succumb, while in others the cedema changes its position, and the patients are restored to a state of tolera- ble comfort for a period of variable duration. Many cases of so-called uremic intoxication, but by no means all, are the result of oedema of the brain, and consequent anemia of the cerebral capillaries. We may infer that an attack of this kind depends upon such an cedema, and not upon blood-poisoning: 1. When the seizure takes the form of deep coma, with intercurrent eclamptic spasms. 2. When, at the time of its occurrence, the secretion of urine is normal or increased. 3. When the attack is accompanied by marked oedema of the face. 4. When the carotids pulsate strongly during the attack. As we shall see directly, this is a valuable but often ill-appreciated sign of repletion of the cranial space with blood, and of impediment to the exit of the blood from the same. In many cases of parenchymatous nephritis, the patients observe a gradual failure of their power of vision; in others, blindness, more or less complete, sets in suddenly. I have seen a patient, after coming to himself, after a uremic convulsion followed by coma, ask to have CHRONIC BRIGHT'S DISEASE—PARENCHYMATOUS NEPHRITIS. 33 the gas lit, although it was burning brightly at the time. This par- tial or total extinction of vision, too, used formerly to be referred to uremic intoxication, and was called uremic amblyopia, or amaurosis. Latterly, however, the real source of this disorder has been found to be an extravasation into the retina, accompanied by inflammation. A diagnosis of Bright's disease has repeatedly been made by means of the ophthalmoscope alone. In one case which I have watched, the impairment and subsequent improvement of vision which occurred manifestly coincided with the formation and absorption of such extrava- sations. In respect to the duration and results of parenchymatous nephritis, it may be said that there are cases which run their entire course in a period of from six weeks to three months, and others in which the malady drags on for years. I used to know a physician of large practice in Altmark, who only died within a few years, although he had all the symptoms of Bright's disease as long as twenty years ago. We have already alluded to the fluctuations in the intensity of the symptoms, which take place in protracted cases. The most frequent termination of Bright's disease is death; although patients more com- monly die of the intercurrent inflammations than directly of the dis- ease itself. Complete recovery may possibly take place, but it is extraordinarily rare. The longer the duration of the malady, so much the less is a favorable result to be looked for. In recent cases, the question always arises, whether we have not to do with a croupous nephritis, which, as we have explained, admits of a better prognosis. Treatment.—The causal indications require that a patient with parenchymatous nephritis should wear flannel next his skin, and ex- change his dwelling, if damp and cold, for a dry and warm one ; and that he should be forbidden to go out at night or in bad weather, even during any temporary improvement. Well-to-do people, who dwell in bleak, damp, windy, seaside neighborhoods, should be induced to change their abode. Excesses in spirituous liquors, and the use of diuretics, cubebs, copaiba, and spices, are to be strictly prohibited. The discovery that Bright's disease is an inflammatory affection has done but little toward an efficient treatment of it. The so-called anti- phlogistic method is inapplicable to any of its stages. In fulfilment of the indications from the disease itself, derivation from the intestines by drastics, and from the skin by diaphoretics, has been proposed. We shall recur to the employment of this measure while treating of the management of the symptoms, as it often acts favorably upon the dropsy; but we do not believe that the inflammation of the kidney can be arrested or allayed by such deri- vation. Frerichs speaks favorably of tannic acid, which he gives three times daily, in doses of from two to six grains, in combination 34 DISEASES OF THE KIDNEY. with aloes and in the form of a pill. The elimination of tannic acid through the urine in the form of gallic acid and pyrogallic acid, to which we have alluded elsewhere, warrants this treatment from a theoretical point of view. Frerichs himself admits that, although he has observed a diminution in the quantity of albumen excreted, yet, in chronic cases, he has but seldom seen a complete disappear- ance of it. My own experience does not speak at all in favor of tannic acid. Bad as we have represented the prognosis of parenchymatous ne- phritis to be, we have often succeeded quite brilliantly in palliative treatment, and, in fulfilling the symptomatic indications, the therapeu- tics of Bright's disease are by no means to be regarded as powerless. We have recognized the loss of albumen from the blood as the imme- diate cause of most of the symptoms of the disease, and hence our most important task by far is to cover the loss of albumen by a diet rich in protein substances, and by appropriate medication. Soft-boiled eggs, milk, strong meat-broths, and roast-beef, in as large quantity as the patient is able to digest, are probably the best preventives of the dropsy; and, while patients in comfortable circumstances often with- stand the loss of albumen with impunity for years, the poor, on the other hand, succumb to it far more speedily, because the former have better means than the latter to supply the daily losses which they suffer. Besides this, a moderate amount of beer or good wine should be prescribed, as by the use of these articles the waste of tissue is retarded and the nutrition promoted. Quinine and iron are the most suitable medicines. The former was thrown overboard by many phy- sicians during the time of a generally prevailing nihilism in therapeu- tics, and its supposed tonic action upon the fibres has been much de- rided. But, in these days of reaction against such nihilism, tonics, and especially the preparations of quinia, have once more come into repute, and, indeed, it would seem that they do exert a beneficial action upon the state of nutrition by diminishing the consumption of material. Preparations of iron are equally appropriate, since their effect upon the formation of blood is most decided, and it is not the albumen of the blood alone but also the red blood-corpuscles which are reduced in quantity in this disease. Neglect of such directions as the above, a blind groping in search of a specific remedy, and a vague, planless ex- hibition of diuretics after the dropsy has set in, are merely so many tokens of incapacity on the part of the physician. In a series of cases, which have been described by Dr. Schmidt, in his inaugural thesis, I have obtained most brilliant results where all other treatment had failed, by putting the patients upon an exclusive diet of milk. The patients did not take a grain of any medicine whatever, but drank CHRONIC BRIGHT'S DISEASE—PARENCHYMATOUS NEPHRITIS. 35 from five to six pints of cows' milk daily. After the " cure " had been continued in this manner for about four weeks, some of the patients who, prior to the treatment, had been in the most wretched condition, had got rid of their dropsy, recovered an appearance.of health, and re- gained so much of their strength as to be able to resume their business and even to perform hard labor. The albuminous character of the urine, however, has disappeared in but one case; in all the others it persisted. I am unable to account for the eminently beneficial action of milk upon Bright's disease. I propose to try whether it be possible to obtain a physiological explanation of these results by a careful analysis of the phenomena attending an exclusively milk diet, during health as well as disease, especially by careful weighing of the body and by taking accurate account of every thing taken into and ejected from the system. If the above measures prove unsuccessful in averting the dropsy, or in allaying that which already exists, the establishment of active dia- phoresis is strongly to be recommended. No benefit, however, is to be expected from the use of spiritus mindereri, the antimonials, and other so-called diaphoretics. I have known patients in an advanced stage of dropsy to rid themselves of it completely, in a few weeks, by the daily use of a hot bath, of a temperature of 80° to 100° F., fol- lowed by sweating for two hours in woollen blankets. The diaphoresis was so great in one case, that as much as 800 cubic centimetres of the sweat which had soaked through was collected in a wash-basin placed under the bed. All these patients were weighed before and after the sweating, and the clinical journals show that, during the sweating, they had lost two, three, and even four pounds in weight. However, it cannot be denied that, in some cases, this procedure also failed, nor that debilitated patients sometimes suffered so much from the process that I was obliged to desist from it. Finally, I may state that, in one instance, the abatement of the patient's dropsy was coincident with the first appearance of uremic convulsions. The profuse drain of liquid from the skin naturally makes the blood more concentrated, and this accounts for the absorption of the interstitial effusion. Since, however, in parenchymatous nephritis, the effusion contains urea and perhaps other salts, it is readily conceivable that an active abstraction of liquid from the system Avould have the effect of overcharging the blood with these materials, and might thus give rise to uremia. However, a closer investigation of the cases above mentioned has led to the con- clusion that the supposed connection between diaphoretic treatment and the uremic symptoms is improbable. Whatever the theoretical objections against the employment of diuretics may be, yet, in desperate cases, recourse should always be 36 DISEASES OF THE KIDNEY. had to them. Squills and other stimulating diuretics must not be em- ployed without the utmost caution, on account of the irritating action which they exert upon the kidneys; but there are certain salts, espe- cially cream of tartar, and the tartarus boraxatus (soluble cream of tartar), which are decidedly beneficial in their effect. The physician above alluded to has repeatedly freed himself of his dropsy through the free use of buttermilk, and the employment of cream of tartar and small doses of Dover's powder. We have yet to mention the drastics as remedies against the dropsj'. Observations upon cholera have taught us that a heavy drain of water from the intestinal capillaries will render the blood more concentrated, and thereby promote absorption of dropsical collections. There was a very instructive case at the clinic of Tubingen, which has been de- scribed by Liebermeister, where a patient with Bright's disease was attacked by dysentery and died. In consequence of the thin, copious diarrhoea, the extensive general dropsy, from which this patient had long suffered, was reduced to a minimum a few days before his death. It may also be said in favor of the drastics that, during their employ- ment, the kidneys are saved from irritation. Nevertheless, we should never have recourse to them save in time of extreme need, since the patient is Hable to be intensely affected by them, and since, by their persistent use, the digestion becomes impaired. The drastics most frequently employed in treatment of Bright's disease are, elaterium, gr. \—\, colocynth, in form of decoction, 3 j— 3 ij, to water, § vj, or else in the form of tincture. As remedies against uremic intoxication, Frerichs, who ascribes this condition to surcharge of the blood with carbonate of ammonia, has proposed the acids, especially benzoic acid, in order to form harm- less ammoniacal combinations. In the cases observed by me, I have not been able to perceive any effect from this treatment which is based purely upon theory; whereas strong drastics, and iced applications to the head, always seem to produce a favorable impression. CHAPTER V. NEPHRITIS VERA—INTERSTITIAL NEPHRITIS—RENAL ABSCESS—METAS- TATIC DEPOSITS IN THE KIDNEY. Etiology.—While in acute and chronic Bright's disease the chief pathological changes take place in the uriniferous tubules, the altera- tions which occur in the intervening substance being altogether of a subordinate and secondary character, in the variety of renal inflamma- tion which forms the subject of the present chapter, the disease lies INTERSTITIAL NEPHRITIS—RENAL aBSCESS. 37 mainly in the scanty connective tissue which binds the tubules together. The most common causes of true nephritis are as follows: 1. Wounds and contusions. The kidney is seldom subjected to external violence, owing to its sheltered position. It is far more liable to injury from the presence of stones within the pelvis of the kidney. 2. Collections of decomposed ammoniacal urine in the pelvis of the kidney, the result of urethral stricture, enlargement of the prostate, palsy of the bladder, from injury of the spine, and so forth. Here the irritation to Avhich the kidney is subject is of a chemical instead of a mechanical nature. 3. Propagation of inflammation from the urinary passages to the kidney. It is easy to comprehend that an inflammation of the pelvis of the kidney, a pyelitis, might readily extend into the parenchyma of the organ, and cause nephritis; but the fact that nephritis is sometimes associated with gonorrhoea, but is not a result of extension of the latter disease by contiguity, and where there is no accumulation of urine in the pelvis of the kidney, is altogether enigmatical. 4. Propagation of the inflammation from the connective tissue of surrounding parts, the peritoneum and other organs. This is the rarest of all the modes of origin. 5. Embolism of small arteries of the kidney, and the introduction of septic or miasmatic material into the blood. This is the source of the so-called metastatic nephritis, observed in endocarditis, valvular disease of the heart, and in the various disorders classed under the general title of pyemia, as well as in the infectious diseases. There is usually no doubt as to the embolic origin of the cuneiform deposits, which, in the disease of the heart above alluded to, occur almost as frequently in the kidney as in the spleen; but it is sometimes extremely difficult to trace the origin of the small metastatic deposits which form in the kidney during the later stages of septicemia, puer- peral fever, typhus, etc., to the action of embolism. It is questionable whether interstitial nephritis ever arises from the effect of cold, or from that of acrid diuretics. Anatomical Appearances.—In traumatic nephritis, or in ne- phritis arising from an extension of inflammation from the pelvis of the kidney, or from other organs, the kidney at first is enlarged, and is of a deep-red hue, which is either diffused over its whole substance, or else is confined to single spots in the cortical or medullary portion. Its consistence is much less firm. The albuginea is injected, thickened by infiltration, and easily detached. Upon section, the structure is indistinct, and the boundary between the cortical and pyramidal sub- stance is effaced. A bloody, thick liquid can be expressed from the surface of the cut. At a more advanced sj:age the redness subsides. 38 DISEASES OF THE KIDNEY. The color of the renal substance becomes of a dirty brown or gray, owing to compression of its vessels by the interstitial exudation, which already, here and there, contains pus. The discoloration usually begins at detached points, of the size of a hemp-seed. As it increases, these spots soften, until they finally break down into a purulent liquid. In this way small abscesses form, by the melting down of the renal substance, under the pressure of the con- stantly-accumulating pus-cells. In the cortical substance, the form of the abscess is more rounded; in the pyramidal, more elongated. The abscesses enlarge and coalesce, finally forming a great sac of matter, which may occupy one-half or even two-thirds of the kidney. Such an abscess may become incapsulated, and long remain embedded in condensed cellular tissue. In other cases, the deposits discharge in various directions, as into the pelvis of the kidney, the cavity of the abdomen, externally through long fistulous tracks, into neighboring parts of the intestine, which have become adherent to the wall of the abscess, or even, through the diaphragm, into an adherent portion of the lung. When the disease runs a more chronic course, it sometimes terminates differently. In such cases the interstitial substance of the kidney undergoes proliferation, while the peculiar tissues of the organ perish. At the close of such an attack of chronic interstitial nephritis, the kidney is irregular, and nodulated in shape. The elevations are more marked than those of the third stage of Bright's disease, and the albuginea is firmly adherent in the sulci between them. Upon cutting into one of these depressed spots, instead of renal-tissue proper, we find nothing except the indurated substance of a cicatrice. The metastatic nephritis, which accompanies disease of the heart, shows no tendency to suppuration. In recent cases, distinctly circum- scribed, dark-red cuneiform spots are found in the kidney. The base of the wedge lies toward the periphery of the organ, the apex toward its hilus. Microscopic examination shows an intense engorgement of the vessels with dark masses of blood, blood being also effused into and between the tubules. Hemorrhagic infarction of the kidney, when of longer standing, undergoes metamorphosis similar to that already described as occurring in hemorrhagic infarction of the spleen. A dis- coloration commences in the middle of the point of infarction, which, having undergone a complete fatty metamorphosis, and all the fat having been absorbed, cicatrizes, leaving a depressed scar. The me- tastatic deposits which form in the kidney in infectious disease, and in consequence of the absorption of putrid matter into the blood, are generally much smaller, and far more numerous, than the infarctions which occur in disease of the heart. Moreover, their tendency to break , down is very great, so that, upon examination, it is not usual to find INTERSTITIAL NEPHRITIS—RENAL ABSCESS. 39 solid spots, but merely abscesses in the kidney, surrounded by an area of redness. Symptoms and Course.—When not of metastatic origin, acute in- terstitial nephritis, like acute inflammation of other important organs, sometimes commences with a rigor. At the same time there are vio- lent pains in the region of the kidney, and, in this form of renal in flammation, there is a pain, which is hardly ever absent, which becomes almost intolerable upon the most moderate pressure, and shoots along the ureters to the bladder, and toward the testicle and thigh of the affected side. The sympathetic vomiting, which we have described as an almost constant accompaniment of acute parenchymatous nephritis, is nearly always present also in this form of nephritis. Owing to com- pression of the urinary tubules and Malpighian capsules by the inter- stitial exudation, the secretion of urine is repressed. That which is passed is concentrated, dark, and is often mingled with blood. The fever which accompanies this disease from the outset is very apt to assume a typhoid character. The patients become disturbed in mind, delirious, somnolent, and fall into a state of stupor, with convulsions; symptoms which are to be ascribed to a suppression of the urine, and to a surcharge of the blood with excrementitial matter. The disease may terminate fatally, in the course of a few days, through general pa- ralysis of the nervous system. The occurrence of suppuration in the kidney may be suspected when the disease continues without remission, and when its course is marked by numerous chills, and, above all, when pus is discharged with the urine. "When an abscess forms in one part of the kidney, the rest of which has not been affected, or has regained its healthy condition, the disease takes a more chronic course; but the fever continues, and consumes the patient gradually, who almost always dies sooner or later of a phthisis renalis. To detail the various modi- fications of symptoms which arise from the complications of pyelitis, cystitis, and the bursting of renal abscesses in various directions, would lead us too far. The different courses which the matter may take have already been mentioned above. There is a form of inter- stitial nephritis, which is very difficult of recognition, in which the substance of the kidney gradually perishes, and is replaced by a new growth of connective tissue. A permanent derangement of the urinary secretion, a constant desire to pass water, dull pains in the region of the kidney, dropsy, great listlessness, which gradually increases to coma, with other indications of the so-called uremic poisoning, are the symptoms of this form of disease, but they are very rarely properly interpreted. Metastatic interstitial nephritis, not having any characteristic symp 40 DISEASES OF IHE KIDNEY. toms, is usually overlooked during life. However, I have sometimes noticed that the formation of a large hemorrhagic infarction in the kid- ney is accompanied by a chill, that the patient complains of severe pain in the kidney affected, and that the urine is scanty and contains blood. When we encounter symptoms like these, in a case of disease of the heart, we may confidently diagnosticate the existence of an in- farction of the kidney, particularly when there is or has been evidence of embolism elsewhere. Renal metastases, which form during septi- cemia, puerperal fever, etc., are usually mere "accidental" discov- eries upon the dissecting-table. • We cannot even suspect their exist- ence during life. Treatment.—As, in most cases of interstitial nephritis, it is im- possible to meet the causal indication when the affection proceeds from the presence of a stone, or from a collection of putrid urine in the pelvis of the kidney, or from embolism or infectious disease, we must confine our efforts to an antiphlogistic treatment, which is much more appropriate in this case than in those heretofore described. The repeat- ed application of leeches, cut cups, and of cold over the kidney, with the subsequent use of long-continued warm baths and warm poul- tices, and the exhibition of drinks containing carbonic acid, are the most approved measures. The sequele, especially the abscesses and fistule which may form, must be treated according to the symptoms. CHAPTER VI. PERINEPHRITIS. Etiology.—In rare instances the adipose tissue, in which the kid- ney is enclosed, becomes the seat of a primary, independent inflamma- tion, which is usually the result of an injury, or, as has been claimed now and then, of exposure to cold. Much more frequently the inflam- mation is secondary to a suppurative action within the pelvis or sub- stance of the kidney. I have seen one case in which a pericystitis extended along the ureter to the fat around the kidney. Anatomical Appearances.—As a rule, inflammation of the areolar envelope of the kidney soon results in suppuration. The tis- sues then become discolored, and their meshes are filled with pus. The small collections of pus coalesce and an abscess forms, often of very considerable magnitude, and which may point in almost any direction. In other cases there is no suppuration, but the loose cellular tissue be- comes condensed and indurated, and is converted into a thick fibrous rind. Symptoms and Course.—When perinephritis is acute, its symp- PERINEPHRITIS. 41 toms bear n strong similarity to those of acute interstitial nephritis. A violent fever, which sometimes is ushered in by one or more rigors, and by severe pain in the region of the kidney, which becomes intoler- able whenever the adjacent muscles of the body contract, or are sub- jected to any strain by movement of the body, is a symptom common to both diseases. There is one important distinctive point between the two; in pure uncomplicated perinephritis, there is no suppres- sion of urine, nor does the urine contain either blood, albumen, or pus. If the disease goes on so as to give rise to a large abscess, a tu- mor appears in the renal region, which fluctuates with greater or less distinctness. If the abscess break into the cavity of the abdomen, it occasions an acute peritonitis, which speedily terminates in death. Recovery may take place where the abscess discharges into the intes- tine, or where it points externally, or is opened artificially. External opening of the abscess generally occurs in the back, below the false ribs, and is usually preceded by an excessive aggravation of the pain upon movement of the body, and by a more or less extensive oedema of the skin over the region affected. In other cases the pus descends along the psoas muscle, giving rise to a symptomatic abscess, which usually makes its appearance below Poupart's ligament. Treatment.—The most appropriate treatment of a recent case of perinephritis is local blood-letting, and, in a later stage of the disease, the systematic application of cataplasms and, the use of lukewarm baths. Abscesses must be opened as soon as possible, according to surgical rules, and should be kept open for a while. CHAPTER VII. AMYLOID DEGENERATION OF THE KIDNEY--PARENCHYMATOUS NE- PHRITIS, WITH AMYLOID DEGENERATION. The kidney, like the liver and the spleen, not unfrequently under- goes a degeneration, by the deposit in the elements of its tissues of a material, whose reaction against iodine and sulphuric acid resembles that of the cellulose of plants, but whose chemical constitution is more like that of the protein substances. Amyloid degeneration of the kid- ney takes place under conditions similar to those under which it oc- curs in the liver and spleen, its causes being severe chronic disease, such as syphilis, mercurial poisoning, rachitis, consumption of the lungs, and long-standing suppuration, such as occurs in caries and necrosis. The degeneration probably always commences in the walls of the blood-vessels, particularly in those of the glomeruli, to which it usuallv 42 DISEASES OF THE KIDNEY. remains limited; while, at the same time, the epithelium of the tubules undergoes the changes already described in Chapter IV. The name " parenchymatous nephritis, with amyloid degeneration," is, therefore, more appropriate for this form of disease than the term " amyloid or lardaceous degeneration of the kidney." Even microscopic examina- tion is not by itself sufficient to enable us to distinguish between the affection in question and simple parenchymatous nephritis. But, if a thin slice of the specimen be treated for a few moments with a solution of iodine, the red color of the glomeruli becomes so distinct even to the naked eye, that, even before resorting to the microscope, the appear- ance of a multitude of small red dots, standing out in contrast to the surrounding yellow ground, makes the diagnosis almost certain. Under the microscope the loops of the glomeruli seem remarkably large, and present a peculiar dead lustre. The Malpighian capsules, too, often ex- hibit a broad, homogeneous, dull outline. If, prior to the examination, the preparation have been laid for a time in a dilute solution of iodine, the bodies above described will assume the characteristic yellowish- red color. Upon the subsequent addition of a few drops of sulphuric acid, they become of an indistinct violet or dark blue. It is very un- usual for the tunica propria, and still more so for the epithelium of the urinary tubules, to participate in the amyloid degeneration. When an individual, who hitherto has enjoyed good health, is affected by albuminuria, dropsy, and deterioration of the blood, it is so very improbable that he is suffering from amyloid degeneration of the kidney, that that disease may confidently be excluded from the diagnosis. On the other hand, the appearance of similar symptoms in a person who has long been afflicted by syphilis, consumption, tedious suppuration, or any other exhausting malady, makes it extremely prob- able that we have to deal with an amyloid degeneration of the kidney, or, more properly speaking, with a parenchymatous nephritis with amyloid degeneration of the walls of the renal vessels. If the patient also have an enlargement of the liver and spleen, and if the portions of these organs accessible to palpation present the characteristic resistance of amyloid degeneration, the diagnosis is still more sure. In distinguishing between amyloid degeneration and simple parenchy- matous nephritis, Traube lays great stress upon the high specific grav- ity and dark color of the urine in the former disease. My own obser- vations fully confirm the truth of Traube's views, and I may add that I have been struck, not only by the darkness of the urine, in amyloid renal degeneration, but also by its unnatural, yellowish-brown color ; moreover, my colleague, Hoppe-Seller, has shown that such urine con- tains extraordinary quantities of indican. There is nothing in the quality of the exudation-casts, or in the degree of frequence of uremic PARENCHYMATOUS DEGENERATION OF- THE KIDNEY. 43 symptoms, whereon to base a differential diagnosis between a simple parenchymatous nephritis and one which is complicated by amyloid degeneration. Moreover, the difference between the two conditions is a matter of but little practical interest. The treatment recommended for amyloid degeneration of the liver and spleen is equally appropriate in amyloid disease of the kidney. It is questionable whether a retrogression of the disease be possible. The preparations of iron and of iodide of iron, which have been pro- posed, may perhaps act beneficially upon the primary disease, but can hardly cure a degeneration of the kidney. CHAPTER VIII. PARENCHYMATOUS DEGENERATION OP THE KIDNEY. Upon post-mortem examination, the epithelial cells of the urinary tubules are very often found to be more or less enlarged by albumi- nous exudation; their contents being opaque, and the cells themselves being in a state of molecular disintegration. Such a condition is not to be ascribed either to pure parenchymatous inflammation or to simple renal hyperemia. It is true, that the epithelium of the tubules swells, undergoes fatty degeneration, and breaks down in parenchym- atous nephritis; but the latter differs so greatly from the affection now under consideration, not only in the intensity and extent of the process, but also in its independent character, and its unmistakably inflammatory nature, that it is impossible to regard the diseases as identical. In like manner, it is equally improbable and unproved that hyperemia should be the cause of parenchymatous degeneration of the kidney—as this affection is called, for want of a better name. When we consider that the disease may occur as early as the fifth or sixth month of pregnancy, it is quite beyond my comprehension that the attempt should have been made to ascribe the very frequent occur- rence of this complaint during pregnancy to a compression of the renal arteries, and to consequent obstructive hyperemia of the kidney (Bosenstein). As this morbid condition of the epithelium is only found in the bodies of persons who have died of severe disease, and in those of pregnant or puerperal women, we are justified in supposing that grave disease, and pregnancy (which, from the powerful impression which it makes upon the general economy, bears a strong analogy to disease), may exercise a pernicious influence upon the nutrition and upon the minuter structure of the tissues. It is not improbable that the entire system is under the same pernicious influence, although at present we 11 DISEASES OF THE KIDNEY. have only a more intimate knowledge of its existence and effects in the kidney. And although we have not any very definite knowledge as to how disease and how pregnancy affect the minuter structure of the kidneys and of other organs, yet such nutritive derangement will not surprise us if we take into consideration the grave derange- ments both of innervation and of the general health, which are also attributable to material alteration. The most common and frequently the sole symptom of parenchym- atous degeneration of the kidney is the presence of albumen in the urine. We may say, too, that whenever there has been albuminuria, during pregnancy or during grave disease, the renal epithelium will be found to be in a more or less advanced state of degeneration after death. How often the question is asked by the anatomist during the autopsy, whether the patient had albuminous urine! On the other hand, I will not venture to state positively that the albuminuria, which so often accompanies the conditions above referred to, is always the result of degeneration of the epithelium of the kidney, or that degen- eration of the renal epithelium is always attended by albuminuria. The quantity of albumen which the urine contains is probably never so great in parenchymatous degeneration as in amyloid degeneration, and parenchymatous inflammation of the kidney. When it arises after acute febrile disease, it never produces dropsy. This symptom is often absent, too, during pregnancy accompanied by parenchymatous renal degeneration and albuminuria. Sometimes, however, there is a mod- erate degree of dropsy, and in rare instances a very large one. When it accompanies pregnancy, it is sometimes a source of danger, owing to the eclamptic attacks which it provokes during and immediately after parturition, and of which we shall have more to say when we come to treat of diseases of the nerves. If the original disease terminate in recovery, the nutritive disorders of the renal epithelium to which it has given rise are also completely repaired. Soon after delivery the albuminuria and dropsy disappear in almost all cases, another proof that the malady in question is not to be confounded with interstitial nephritis. We are quite ready to admit that in most cases of eclampsia puerperarum there is renal dis- ease ; but we deem it quite inadmissible to attribute the albuminuria, dropsy, and eclampsia to " Bright's disease." After what has been said already regarding parenchymatous degen- eration, further discussion of its treatment becomes superfluous. We shall treat hereafter of the proper management of the eclampsia. CARCINOMA OF THE KIDNEY 45 CHAPTER IX. CARCINOMA OF THE KIDNEY. Of the malignant neoplastic growths, carcinoma is the one most frequently seen in the kidney. Renal cancer is sometimes primary; sometimes it accompanies carcinoma of other organs, as a secondary formation. Young persons, and even children, are quite frequently at- tacked, although it is somewhat more common in advanced age. Cancer of the kidney generally assumes the medullary form. Scirrhus and colloid are far more rare. The former sometimes de- velops in the form of circumscribed nodules of varying size, which gradually replace the parenchyma of the kidney. Sometimes the can- cerous degeneration spreads farther and farther into the surrounding tissues from its original point of development, so that the kidney gradually becomes transformed into cancer [BoJcitansJcy, infiltrated cancer). A carcinomatous kidney may attain an enormous bulk some- times, forming a nodular tumor of the size of a child's head. The de- generation often involves the lymphatic glands in the hilus of the kid- ney, whence it spreads to the retroperitoneal and mesenteric lym- phatics, and to the ligaments and periosteum of the spinal column; or else it may grow inward into the cavity of the organ, and thence into that of the adjoining veins. The frequency with which cancer of the kidney is complicated with cancer of the testis, is a matter of impor- tance, which calls to mind the still more common coincidence of tuber- culosis of these organs. Hemorrhages both within the tumor and on its periphery are very apt to occur. In the latter case, the blood is effused either into the peritoneum or else into the urinary passages. The disease often remains latent for a long time. It is usually by the gradual advance of a marasmus, for which no other cause can be assigned, that suspicion is awakened of the existence of a malignant tumor in a region inaccessible to palpation. There may be no pain at all in the lumbar region, and, when it does exist, it is not character- istic. The renal secretion may go on undisturbed, and the urine may be quite free of blood and albumen. As the disease advances, the tumor formed by the cancerous kidney, which is often of enormous size, can generally be felt through the abdominal walls, especially when the latter have become wasted and relaxed. The form of the tumor, and especially its immobility, will prevent our mistaking the enlarged kidney for an enlargement of the liver or spleen. It cannot be moved from side to side, nor does it follow the motions of the diaphragm. Very large cancers of the right kidney sometimes produce a remarkable and peculiar displacement of the liver inward, causing it to turn upon its 46 DISEASES OF THE KIDNEY. long axis, so as to bring a large part of its convex surface in contact with the abdominal wall. Hematuria and albuminuria are absent about as frequently as they occur. As already stated, part of the bleeding proceeds from the vessels .of the growths which push into the urinary passages, while another part is the result of excessive hyper- emia of the surrounding tissues. Owing to the large quantity of blood thus discharged, the hematuria often forms one of the most prominent symptoms of this disease. The complexion of the patient assumes the dirty hue so common in cancer, and he dies of exhaustion which progresses all the more rapidly when the hemorrhages are frequent and profuse; unless, indeed, death ensue in consequence of some intercurrent disorder, or from the invasion of other vital organs by secondary cancer. Treatment is ineffectual, and must be limited to husbanding the patient's strength, repression of the hemorrhages, and removal of coagula from the bladder, according to surgical rules, CHAPTER X. TUBERCULOSIS OF THE KIDNEY. Rokitansky recognizes two forms of renal tubercle. The first form is symptomatic of a tuberculosis involving several or even the majority of the organs. In acute miliary tuberculosis, gray nodules, sim- ilar to those found studding the lungs, pleura, peritoneum, etc., are also found in the albuginea and parenchyma of the kidney. In extensive chronic tuberculosis, tolerably large, yellow, cheesy deposits of tubercle are sometimes met with in the kidneys, but they rarely contain collec- tions of softened tubercular matter or tubercular cavities. The first of these forms has but little effect upon the action of the organ. It is unrecognizable during life, and is of more moment in a pathological than in a clinical point of view. The second form of renal tubercle is generally complicated with tuberculosis of the testicle, prostate, seminal vesicles, and urinary pas- sages. It is not constantly preceded by pulmonary tubercle; but this disease almost always sets in at a more advanced period of renal dis- order. In this second form the deposit is very copious, and the indi- vidual nodules soon coalesce into large tubercular masses. The organ becomes enlarged, assumes an irregular, knobby shape, and within it we find large cheesy collections, some of which are filled with tubercu- lous pus. This form of renal tuberculosis, too, would likewise frequently escape observation, were not the diagnosis almost always aided by the complications above mentioned. The longer a chronic disease of the urinary passages has coexisted with the admixture of pus, and now and PARASITES IN THE KIDNEY. 47 then of blood in the urine, the tuberculous character of which is in- dicated by the coexistence of an enlargement of the testicle, so much the more likely will it be that the kidney itself has become involved in the disease. The diagnosis receives further confirmation if we are able to feel an uneven tumor in the region of the kidney, through the flaccid walls of the abdomen. CHAPTER XI. PARASITES IN THE KIDNEY. The echinococcus is the parasite most frequently found in the kid- ney, although even there it is met with less frequently than in the liver. Its presence in this organ is originally due to the existence of the embryo of the tenia echinococcus in the intestinal canal (see Vol. I.). We have no knowledge as to why the young brood, in their emigra- tion from the bowel into the other organs of the body, should some- times enter the kidney. The echinococcus sacs, which occasionally attain the size of a fist or of a child's head, are quite like those found in the liver and spleen. They are embedded in a fibrous capsule be- longing to the kidney. They may atrophy and burst, discharging their contents in different directions. They may also occasion inflammation and suppuration in the parts about them, and the renal abscess thus re- sulting may burst into the peritoneum, intestine, or pelvis of the kidney. The development of echinococci in the kidney may be entirely un- attended by symptoms. In some instances, however, the patients com- plain of a dull pain in the lumbar region, which we cannot well account for. A tolerably sure diagnosis may be made out if we can feel an irregular nodular tumor in the region of the kidney, and at the same time can exclude carcinoma, tuberculosis, and hydronephrosis, to be treated of hereafter. Certainty is only possible when cysts of the echinococci or traces of them are discharged with the urine. The hyaline walls of the daughter cysts, consisting of concentric layers, distinctly recognizable under the microscope, are not easily mistaken. Symptoms of renal colic may arise during their passage through the ureters, and their discharge from the bladder is often attended by the utmost distress, especially in men. The cysticercus cellulosus and the strongylus gigas are of much rarer occurrence in the kidney. The latter somewhat resembles the round worm, is from six inches to three feet long, and some lines thick. Its form is cylindrical, and, when fresh, it is of a blood-red color. Its cephalic end is blunt, and has six papille surrounding its small mouth. In the tail of the male there is a funnel-shaped hollow 50 48 DISEASES OF THE KIDNEY. from which the penis projects distinctly. The symptoms to which these parasites give rise, and even the manner in which they become embedded in the kidney, are obscure. CHAPTER XII. DEFORMITIES OF THE KIDNEY—IRREGULARITIES OF ITS SHAPE AND POSITION. Absence of one kidney usually is accompanied by abnormal mag- nitude of the ether, and the secretion of urine remains normal. Union of the two kidneys, which then are generally connected by a narrow bridge of renal substance at their lower ends—the so-called horseshoe- kidney—are matters of mere anatomical interest, and of no clinical importance. The same is true also of lobulation of the kidney, which depends upon a persistence after birth of the foetal condition of the organ, and is distinguishable from an acquired lobular state of the kidney by the healthy condition of the renal parenchyma and capsule at the depressed points. Irregularity of position is most common in cases of horseshoe-kidney; the united organs then usually lie much deeper than natural, sometimes as low down as the last lumbar vertebre. But even without the coexistence of this malformation, an unnaturally deep position of the kidneys is not an uncommon congenital deformity, and is usually accompanied by irregularity in the origin and number of the renal vessels, as well as by anomaly in the lengths of the ureters. Misplacement of the kidney, with abnormal mobility, is a matter of greater importance. Quite a considerable number of cases of this anomaly have been observed since attention was first called to it. In Greifswald alone I know of three cases of movable kidney. The kidney (and almost always the right one) lies embedded in a loose areolar tissue. Its vessels are elongated, and have a sort of mesentery formed out of the reduplication of their peritoneal coat. Such anom- alies are most common among women whose abdominal integuments have become greatly relaxed by repeated child-bearing. According to Bayer, it may also result from violent concussion of the body—as from a fall from a great height. In other cases there is no other anomaly, nor is there any apparent cause for the mobility of the viscus. When the patient stands erect, the movable kidney may be felt usually below the liver, or even still deeper. Its characteristic bean-shape is distinctly recognizable, and it often can be pushed a con- siderable distance to the right or left, but more easily upward and downward. A patient in my ward, by moving and shaking his body, was able to get his kidney into a great variety of. positions. There DISEASES OF THE SUPRARENAL CAPSULES. 49 are either no evil results whatever attending the affection, or they de- pend upon complications, although colics and slight inflammations of the peritoneum may result from pressure of the movable organ upon the other viscera. The knowledge that she has a tumor in her abdo- men often acts very injuriously upon the spirits of the patient, who sometimes becomes hypochondriac. Little can be done by way of treatment for a movable kidney; but the patient (particularly if she have very flabby abdominal walls) generally feels better when she wears an elastic bandage of gum elastic or knit cotton. APPENDIX. DISEASES OF THE SUPEARENAL CAPSULES—ADDISON'S DISEASE- BRONZED SKIN. Etiology.—In 1855, when Addison, depending upon a small number of cases (some of which have been imperfectly observed), de- scribed a new disease, which he attributed to a degeneration of the su- prarenal capsules, his views soon found numerous adherents, although their correctness was doubted and controverted by many well-known investigators. " Positive " and " negative " observations were collect- ed. Keeping in view the most striking symptom of the malady—the dark hue of the skin—the cases reported by Addison and others, in which degeneration of the suprarenal capsules coexisted with a bronzed color of the integument, were contrasted, first, with cases in which there was degeneration of the capsules Avithout bronzed skin; and, secondly, with cases wherein the skin was bronzed, but where there was no disease of the capsules. It is true that the latter class could disprove nothing, unless Addison had made the false and unwarrant- able assertion that disease of the suprarenal capsules was the sole cause of an excessive deposit of pigment in the rete Malpighii, which is contrary to all experience ; and even the first class of cases utterly failed to disprove their point, as a description of the symptoms and course of the affection will show. The question as to the existence or non-existence of Addisorts dis- ease may now be regarded as decided, although our knowledge of the physiological connection between the symptoms of the malady and the anatomical changes which take place in the suprarenal capsules is still very imperfect. The nature of the disorder in the suprarenal cap- sules, which most commonly results in Addison's disease, is a chronic .nflammation, terminating in caseous degeneration of the inflammatory products, and of the elements of the tissues themselves. The source 50 DISEASES OF THE KIDNEY. of this inflammation is altogether unknown. It comes on without ap- preciable cause, often appearing in persons in whom we have no rea- son to suspect a predisposition to caseous degeneration. Genuine tubercle of the capsule, forming one of the symptoms of general tu- berculosis, is less common. Cancer is somewhat more frequent, usu- ally coexisting with cancer of other organs, although it sometimes appears as a primary independent affection. Lastly, some cases of apoplexy, of simple fatty degeneration, and of amyloid degeneration of the suprarenal capsules, have been recorded. Anatomical Appearances.—But two cases, published by Vir- chow, have presented themselves as yet, in which the suprarenal cap- sules were greatly swollen, thickened, of dark color, and studded with extravasations of blood, and whi^Ii ^seem to represent the first stage of an inflammation, the consequences of which have so often been re- corded. The cases reported -by Wdtlman,f other changes of structure which induce the catarrh of the uterus. Where the uterine catarrh depends on constitutional disease, it is not *122 DISEASES OF THE UTERUS. always possible to remove the cause; but frequently the original dis- ease is so important, or other dangerous results of it are so prominent, that Ave cannot attend to the uterine catarrh. This is particularly true of tuberculosis. Finally, it is not ahvays possible to say Avhether anemia and chlo- rosis are the results or cause of this disease. If we think that the sequence in which the symptoms occur and other causes justify us in the latter supposition, we may often obtain the best results from the use of iron, quinine, a moderate amount of wine, and nutritious diet. Moreover, the good result of cold-Avater treatment, sea-bathing, and different mineral Avaters in uterine catarrh, is due to the fact that they have fulfilled the causal indication. Any practitioner Avill bear Avitness that the constitution suffers in many cases without our being able to discover the cause; and that anomalies of the constitution, Avhich shoAv themselves by a change in the secretion and function of different or- gans, cannot ahvays be cured by preparations of iron and nourishing diet, even if there are evident coexistent signs of anemia and hydre- mia. Under such circumstances, all we can do is, to change and im- prove the constitution by placing the patient under the most different circumstances, changing the entire mode of life, and particularly by modifying as much as possible the exchange of tissue by baths and douches, by giving quantities of water with or without the addition of salts, and by other means. Among the anomalies of secretion that occur in the different organs of such patients, catarrh of the uterus is very frequent; and it often disappears very quickly when we succeed in improving the constitution, while it does not yield to exclusively local treatment. I have seen the most surprising results from such treatment in the Greifswalder clinic, where the arrangements to some extent replaced the treatment by mineral waters and baths, and where Professor liebermeister, at that time assistant physician of the medi- cal clinic, kept account of the effect of the changed diet, increased ex- ercise, and copious supply of salty liquids, of the baths and douches, by weighing the body and examining the urine. The indications from the disease may be far more readily fulfilled in catarrh of the uterus than in catarrh of other organs that are less accessible. The uncertainty of internal remedies for catarrh has been repeatedly mentioned. They may be dispensed with in the treatment of uterine catarrh, and muriate of ammonia (which many physicians consider just as efficacious foi bronchial catarrh as for gastric and in- testinal catarrh) is not used in uterine catarrh because we have better and more certain remedies for it. I should be entirely misunderstood if it were supposed that I considered the local treatment of uterine catarrh as superfluous, or underrated its results; in what Avas said CATARRH OF THE UTERUS. 123 above, I only intended to show that one indication should not be fol- lowed to the neglect of the others. In all cases where the cause of the catarrh cannot be discovered, as is most frequently the case, local treatment must be used, and where it has existed for a long time and is complicated with ulcers, particularly granulating ulcers, local treat- ment should be used Avith that for fulfilling the causal indications. Among the local remedies we shall first mention injections into the vagina. It is not long since these constituted the only local treatment for " leucorrhea," no matter AA'hether it came from the uterus or vagina. They aid the treatment and are required for cleanliness, although they are of far less use than the procedures to be hereafter mentioned. In acute catarrh Ave inject lukeAvarm AAater; in chronic catarrh, at first lukeAvarm, and afterward cold water, or solutions of sulphate of zinc, tannin, or alum. Instead of using an enema syringe with a uterine nozzle, it is well to employ a clysopompe [Davison's syringe], so that we may throw in a large amount of liquid without irritating the vagina by frequent introduction of the nozzle. The application of leeches to the os uteri in acute catarrh is indicated when it begins with great severity, and in chronic catarrh when the substance of the uterus par- ticipates in the inflammation, or when there is acute exacerbation of the disease with symptoms of severe congestion in the pelvis. Sean- zoni also recommends them when there are granulating ulcers on the os uteri. We should apply leeches to the os uteri ourselves, or have it done by a nurse skilled in the operation. Gynecologists of the present day are refraining more and more from the "use of leeches in the treatment of catarrh of the uterus and ulcers of the os, while for- merly they were used far too often. The local application of nitrate of silver, in substance or in strong solution, is by far the most effective treatment for chronic uterine catarrh, and particularly for catarrhal erosions and follicular ulcers of the vaginal portion of the uterus. To prevent the caustic from breaking off in the cervical canal, we should employ sticks of double annealed nitrate of silver, or have it hardened by the addition of a few grains of nitrate of potash. When thus pre- pared, we may push it boldly into the cervical canal. If cauterizations with solid nitrate of silver cause hemorrhage, which is often the case even in simple ulcer, Ave should use in its place concentrated solutions (one part to two or four of water), which should be poured in through the speculum rather than used on a brush. I should employ these solu- tions much oftener, if it were not so difficult to protect the fingers and clothes from being soiled. The application should be repeated once a week or oftener, till the discharge diminishes and the portio vaginalis has regained its normal appearance. The result of this treatment is so striking, that touching the os uteri and itsXervical canal, in chronic 124 DISEASES OF THE UTERUS. catarrh of the organ, must be classed among the most gratifying opera- tions in medicine. The pain induced by the cauterization is usually very insignificant, but in some cases it is quite severe. If the nitrate of silver be passed far into the cervical canal, some women will have painful contractions of the uterus, that may continue for hours. Be- sides nitrate of silver, the remedies most frequently used for catarrhal erosions and follicular ulcers of the os uteri are pyroligneous acid, liquor hydrargyri nitrici and cuprum alumina turn (lapis divinus). Pyroligneous acid is particularly beneficial where the ulcers have a great tendency to bleed; the liquor hydrargyri nitrici, and still more the lapis divinus, are to be tried when the nitrate of silver has failed. In such cases the actual cautery is a very effective remedy, and the opposition to its use is ascribable to its psychical effect rather than to the pain or danger accompanying it. Pyroligneous acid poured through the speculum is an invaluable remedy for the granulating ulcers of the os uteri that bleed readily. In most cases it arrests the hemorrhage more certainly than sesquichloride of iron or alum; the latter is applied to the os uteri in substance more readily than in solution. We should only use injections into the cavity of the uterus in cases of absolute necessity, i. e., only when the above treatment fails, and we are forced to believe that the cavity of the uterus chiefly is diseased. In such cases we should use the ordinary solutions of nitrate of silver (3 ss. to water § j). The effect of these injections is much more severe than touching the os uteri with nitrate of silver; they not unfrequently induce severe inflammatory symptoms; where the cervi- cal canal is contracted, they should never be employed. CHAPTER II. PARENCHYMATOUS METRITIS—ACUTE AND CHRONIC INFARCTION OF THE UTERUS. Etiology.—The changes of the substance of the uterus in acute and chronic parenchymatous inflammation rarely go beyond excessive hyperemia, inflammatory edema and proliferation of its connective- tissue elements, in which the muscular elements usually participate but little or not at all. There is rarely suppuration or formation of abscesses. We do not include the puerperal form here. For the etiology of parenchymatous metritis we may refer to that of the catarrhal form. The injurious influences there mentioned some- times cause inflammation of the substance of the uterus; at others of its mucous membrane, but most frequently of both. These influences also cause parenchymatous metritis more readily if they act while the METRITIS. 125 uterus is in a state of physiological congestion. Lastly, the paren chymatous metritis of an unimpregnated uterus must often be regarded as the continuation of a puerperal metritis, or at least that a large number of cases date from the period of a confinement or of an abortion. Anatomical Appearances.—In acute parenchymatous metritis, Ave find the uterus increased in size, particularly in thickness. It may attain the volume of a hen's egg or larger. The over-filling of the blood-vessels causes its substance to appear more or less dark, and usually irregularly reddened. These changes are most marked in the layers lying next the mucous membrane. Occasionally there are effu- sions of blood into the parenchyma. The mucous membrane almost ahvays shows the signs of acute catarrh. The serous coat also often participates in the inflammation, and is covered Avith deposits of fibrin. In chronic infarction, the uterus is often enlarged to three or four times its normal size ; its cavity increases, particularly in the long diam- eter ; its walls may become an inch thick. The hyperemia, Avhich is at first present, subsequently disappears, as the vessels are confessed by the neoplastic shrinking connective tissue. Then the substance appears very pale and dry, and becomes denser and harder, often to such an extent that it creaks under the knife. In rare cases Ave find hyperemic spots and veins that have become dilated as a result of the obstructed flow of blood. If the vaginal portion be chiefly affected, the os uteri is greatly swollen, and occasionally elongated like a snout. The mucous membrane almost invariably shows the changes described in the previous chapter. On the peritoneal surface we often find firm adhesions to neighboring organs. Symptoms and Course.—Acute parenchymatous metritis begins with a chill more frequently than the catarrhal form does, and is more apt to be accompanied by symptoms of feAer in its subsequent course. The pain in the sacral and inguinal regions, the feeling of pressure in the pelvis, the sensitiveness of the lower part of the abdomen, the dysuria and tenesmus, are present in the former as well as in the latter, and almost ahvays attain a higher grade than they do in the simple catarrh. The uterus can rarely be felt above the symphysis pubis, but through the vagina we may usually detect enlargement and tenderness of the inferior segment, and a moderate shortening and thickening of the portio vaginalis. There are also anomalies of men- struation. If, as is usually the case, the disease begins during men- struation, the bleeding usually ceases suddenly; if the time for men- struation occurs during the progress of the disease, we either have metrorrhagia (metritis hemorrhagica) or, as more frequently occurs, there is no bleeding. Except during the period of menstruation, the 126 DISEASES OF THE UTERUS. discharge characteristic of uterine catarrh (the constant companion of parenchymatous metritis) is present. In favorable cases the disease runs its course in from eight to fourteen days, the symptoms subside gradually and the disease ends in perfect recovery ; in unfavorable cases, chronic infarction remains. There are some very rare instances where an abscess formed and perforated into the abdomen, and the disease thus terminated fatally. Except at the menstrual periods, the symptoms of chronic infarc- tion of the uterus are often not very prominent. Frequently the patient complains only of a feeling of weight in the pelvis and a sen- sation of " bearing down." The pressure of the enlarged uterus on the rectum and bladder usually causes constipation as well as a fre- quent and annoying inclination to go to stool and to urinate. At the commencement of the disease, menstruation is often free and pro- longed ; but the more the vessels of the uterus are compressed by the neoplastic connective tissue, the more difficult menstruation becomes and the scantier the flow. Finally, the menses are often absent for months or years, while the regularly recurring molimina seem to indi- cate that the ripening and throAving off of the egg takes place regu- larly. In this form of metritis also, which, moreover, is ahvays accom- panied by the catarrhal form, the nutritive state of the patient usually suffers after a time, and the hyperesthesia and other disturbances of innervation, mentioned in a previous chapter, usually develop. On physical examination Ave may often feel the enlarged uterus through the abdominal walls above the symphysis pubis, particularly if we push it up a little with the finger introduced into the vagina. On ATaginal examination, we also discover that the vaginal portion is enlarged, indurated, and more or less painful. On introducing the uterine sound (AA'hich should not be employed unless the practitioner is skilled and experienced in its use), the increase in the long diameter may be ascertained. Although not dangerous, the disease is very obstinate and tedious. Even in its advanced stages it cannot be regarded as absolutely incurable; the decrease, after confinement, of the uterus, AA-hich had been greatly enlarged during pregnancy, renders it not im- probable that there may also be a retrocession of the pathologically increased tissues of the uterus. Occasionally improvement and cure of infarction of the uterus have been seen directly after pregnancy, and in such cases it seemed as if, with the involution of the uterus after confinement, there had been at the same time a diminution of the physiologically and pathologically increased tissue. Treatment.—According to the variety of the exciting cause, the causal indications are fulfilled by the different rules prescribed in the preceding chapters. In many cases the continued use of slight laxa- PERIMETRITIS AND PARIMETRITIS. 127 tives is very beneficial, particularly the laxative waters of Marienbad, Franzenbad, Kissengen, etc. The indications from the disease are best answered by the repeated application of leeches (four to six) to the portio vaginalis. Although I have seen a most favorable effect from this treatment, in my OAvn practice and in that of others, Avhere the disease was recent, it has seemed of little use in protracted cases. Theoretically, also, Ave may expect better results from abstraction of blood while the connective- tissue formation is still new, and the catamenia are plentiful and con- tinued, than Avhen the capillaries have been compressed, the uterus deprived of blood, and the menses have ceased. Before convincing ourselves by personal observation of the brilliant results of abstraction of blood in the first stages of parenchymatous metritis, and finding how well the patients bear the loss, it is usually difficult to make up our minds to increase the copious loss of blood by applying leeches to .the vaginal portion of the uterus every week or tAvo. A more irritat- ing treatment, particularly the continued use of warm douches to the uterus, seems preferable in the later stages of the disease. These douches should be used about ten minutes every day; the Avater em- ployed should not be over 99° or 103° F. It is also worth Avhile try- ing the use of Kreuznach and other saline baths, as Avell as the baths and waters of Krankenheil. The internal administration of iodide of potassium and of bromide of potassium, as recommended by Simp- son, is also beneficial. CHAPTER III. PERIMETRITIS AND PARAMETRITIS. Inflammations of the parts about the uterus occur very frequently just after confinement, and not unfrequently at other times. In the latter case they usually depend on disturbance of the menses. If the inflammation start from the serous coat of the uterus and its append- ao-es, and the case is one of partial peritonitis, the disease is called perimetritis; if, on the contrary, the inflammation be in the subperi- toneal connective tissue, it is called phlegmon periuterina, or, accord- ing to Virchow, parametritis. Perimetritis leads to more or less copious exudation on the free surface of the peritoneum. Scanty, fibrinous exudations cause adhe- sions Avith the neighboring organs. Even large fluid exudations are usually capsulated by adhesions at their edges. After absorption of the exudation, adhesions to the pelvic organs often remain. In para- metritis there is infiltration of the subperitoneal tissue, Avhich is firm 55 12S DISEASES OF THE UTERUS. from the first. The infiltration may be reabsorbed; but a firm indu- ration often remains as the result of connective-tissue proliferation. In other cases the inflammation goes on to suppuration, and abscesses form, whose contents may perforate into the rectum, vagina, bladder, or abdomen. It is often difficult to distinguish between peri- and para-metritis during life; they begin and run their course Avith more or less severe subjective and objective symptoms of fever. The patients complain of pain deep in the pelvis, which is increased by pressure on the lower part of the abdomen. Generally, also, there are symptoms of com- pression of the pelvic organs, the bladder, rectum, and, according to my experience, of the nerves along the walls of the pelvis. The pres- ence or absence, and the degree of severity and obstinacy, of dysuria and difficult defecation, as well as of the pain extending along the sacral, sciatic, and crural nerves, depend in each case on the seat and amount of the exudation. Where there has been extensive exudation, on examination we may find a tumor of variable size above the pubis. Examination through the vagina or rectum usually shoAvs that the uterus is displaced and firmly wedged in. Intraperitoneal exudations usually fill Douglas's cul-de-sac, and may be readily felt. Subperi- toneal infiltrations and abscesses are generally somewhat higher, but they also can mostly be reached by the finger. The disease may con- tinue for weeks, and greatly exhaust the patient by the accompanying fever. The perforation of subperitoneal abscesses, or of intraperitoneal exudations into the intestines or bladder, is marked by the sudden de- crease in size of the tumor, and by the evacuation of purulent masses Avith the stools or urine; perforation into the abdomen causes severe general peritonitis, which quickly proves fatal. Even in favorable cases the patients generally recover slowly. In many of the patients under my observation the neuralgic pains lasted for months. Local abstraction of blood and the application of cataplasms to the lower part of the abdomen act well in the treatment of recent cases of perimetritis and parametritis. We should continue the use of the latter as long as there is any swelling left, even if there be no pain. In protracted cases I have found great benefit from the use of Avarm salt baths, with an addition of mother liquid, and the internal admin- istration of iodide of iron. At the same time we must keep up the nu- trition and strength by proper diet, and treat any existing fever by antipjTetics. CONTRACTIONS AND CLOSURES OF THE UTERUS. CHAPTER IV. CONTRACTIONS AND CLOSURES OF THE UTERUS—HAEMOMETRA, HY- DROMETRA. In young persons, Avho develop late, moderate degrees of contrac- tion of the os uteri are quite frequent. They hinder conception, Avith- out rendering it impossible. Moreover, they impede the escape of the menstrual blood, and cause it to collect temporarily in the uterus, and to be expelled by painful contractions (uterine colic). I have fre- quently knoAvn women to menstruate without difficulty after their first confinement, Avho, during their maidenhood and the first years of their married life, had severe uterine colic during menstruation. Great flexions and angular curvatures cause contraction of the cavity of the uterus at the point of flexion, which also impede conception, and occa- sion uterine colic during menstruation. Finally, neoplasia, which in- fringe on the calibre of the uterine cavity and the cervical canal, have the same effect. Perfect closure, atresia of the uterus, is Aery rare. It is sometimes congenital, sometimes the result of erosions and ulcers, which, in cicatrizing, have caused adhesions. The seat of congenital closure of the uterus is usually at the external orifice, that of the de- veloped form at the internal orifice. As long as the women continue to menstruate, the menstrual blood collects behind the point of closure, causing haemometra. If the closure does not take place till the menses have ceased, the catarrhal secretion from the mucous membrane occasionally collects in the closed cavity, and distends the uterus. Sometimes this secretion resembles serum or synovia, doubtless because the excessive tension destroys the secreting glands in the mucous membrane, and the latter becomes like a serous membrane. The above state is called hydrometra. In hmnometra, which, moreover, depends on atresia of the vagina oftener than on atresia of the uterus, the uterus may be gradually dis- tended till it becomes as large as it does in the later months of preg- nancy, and the blood contained in it, which is usually black and tarry, may amount to eight or ten pounds. According to the observations of Scanzoni and Veit, Avhen the distention takes, place rapidly, the walls of the uterus are thinned; if it comes on slowly, they are thick- ened by hypertrophy. In the early stages it is difficult to diagnose hemometra. During childhood closure of the uterus or vagina is hardly ever discovered. The first morbid symptoms occur about the commencement of puberty. At intervals of four weeks there is severe uterine colic, with a feeling of pressure and Aveight in the pelvis, and signs of severe congestion of the other pelvic organs, or of perimetritis. 130 DISEASES OF THE UTERUS. At first the patients feel well again after these symptoms have con- tinued a few days; till after four weeks there is a relapse. After a time the intervals are no longer free from pain. The abdomen increases in size; the uterus rises above the symphysis pubis, and may rise as high as the navel. In the monthly attacks the pains become very severe. The patients emaciate, and may become marasmic, or, if no mode of escape be furnished for the blood, the uterus may rupture, or they may die of peritonitis. The latter disease is particularly apt to occur if the tubes be also filled with blood, and their contents escape into the abdomen. Hemometra cannot be recognized with certainty, or distinguished from other forms of amenorrhea, or dysmenorrhea, particu- larly at its commencement, without a careful local examination. If, at the commencement of puberty, there be uterine colic at regular intervals of four weeks, while there is no escape of blood, and if there be, at the same time, a distention of the abdomen, Avhich periodically increases slightly, we should suspect the development of a hemometra, and urge an ex- amination. If the hemometra depend on atresia of the vagina, Ave find the latter distended to a tense tumor, AAThose lower end extends into the vestibule. If the external os uteri be closed, the vaginal por- tion is often entirely obliterated, and the position of the os uteri may not be recognizable. If, on the other hand, the internal os uteri be closed, the vaginal portion may retain its normal length. Besides this, we find the uterus distended to a considerable size; sometimes, but not always, there is fluctuation. The treatment of hemometra is purely surgical. Of course, hydrometra can only result from acquired closure of the os uteri or vagina, and after the menses have ceased. Mild cases of the disease are seen quite often; severer cases, where the uterus is distended to the size of a head or larger, are rare. The most impor- tant symptom of hydrometra is an enlargement of the uterus, which usually occurs gradually, and Avithout exciting attention, while in some feAV cases it is quite rapid and decided. This may be detected on physical examination, and is often even perceived by the patient. If the Avails of the distended uterus be thinned, there is occasionally dis- tinct fluctuation; if they be hypertrophied, we do not find this most important sign for distinguishing hydrometra from almost all other uterine tumors. Occasionally there is uterine colic, particularly durino- severe congestions of the uterus. If the closure be incomplete, these contractions sometimes force out the collected fluid, and, according to Scanzoni, occasionally also gases that have formed from them. The treatment of hydrometra consists in surgically making a passage for the liquid, and in attempting, by astringent injections, to limit the secretion of the mucous membrane. CURVATURES OF THE UTERUS. 131 CHAPTER V. CURVATURES OF THE UTERUS—FLEXIONS AND INFARCTIONS. Etiology.—Inflexions and infarctions indicate anomalies of form— not of position—of the uterus. Usually all distortions of the axis of the uterus, whether curved or angular, are termed flexions. If we wish to designate the variety of the distortion more distinctly, Ave call the former inflexions, the latter infarctions. If the uterus be so curved that its concavity lies anteriorly, its convexity posteriorly, there'is an anteflexion. If, on the other hand, the fundus be bent over backAvard, so as to approach the posterior Avail of the portio vaginalis, there is a retroflexion. The lateral flexions of the uterus are less important. There are various views regarding the pathogeny of these distor- tions. Most authors think that the causes of the distortion lie in the uterus itself, and support their vieAV on the fact that, at the point of distortion, the wall of the uterus is ahvays flattened, and its parenchyma loose and reflexed. Virchow considers the changes at the point of distortion as secondary symptoms, due to the pressure on the Avails of the uterus at this point, and to the anemia of the parenchyma caused by this pressure. It is his opinion that most distortions of the uterus, particularly anteflexions, are caused by congenital or developed short- ening of the ligament of the uterus, and by its consequent fixation on distention of the bladder and rectum. It is most probable that the causes of flexions are not always the same—that they are sometimes within, sometimes outside of the uterus. Betrofle^zions—the most frequent form in Avomen Avho have had children—are, on the other hand, rare in those Avho have had none; they almost always date from the time of a confinement or an abortion. If the involution of the uterus go on sloAvly after its con- tents have been evacuated; if it remain enlarged and relaxed, the fundus readily sinks doAvn on account of its weight, or is pressed doAvn by the other contents of the abdomen. As the greater part of the uterus remains in the posterior Avail after delivery, it is natural that it should most frequently sink backAvard; but we cannot Avonder if there are deviations from this, as they may readily be induced by different positions of the distended intestines in the vicinity, and by other acci- dental causes. At this period a complete return to the normal state is certainly possible. The bending of the uterus is straightened out Avhen it contracts early. But, if this do not take place soon, the paren- chyma, at the point of curvature, becomes anemic and atrophied from the continued pressure, or the fundus uteri forms some abnormal at- tachment. In either case Ave have a permanent anomaly—a distortion 132 DISEASES OF THE UTERUS. in the strict sense. Scanzoni mentions, as the most frequent causes, the slow and incomplete involution of the uterus, and, as the most important etiological factors of the retroversion, early marriages, frequent and quickly-repeated pregnancies, abortion, artificial de- livery, etc. Antefiexlons chiefly occur in those aat1io have had no children. In young persons the most frequent cause seems to be a relaxation of the substance of the uterus by chronic catarrh; in aged persons it is a senile atrophy of the uterus, at the point where these distortions ahvays occur, that is, near the internal os uteri. It is easy to under- stand that anteflexion should be the more frequent form of distortion in women who have had no children, if we remember that a virgin uterus has normally a slight inclination forward. In this case also it seems to me there is no doubt that the flattening of the wall of the uterus, and the atrophy of the tissue, at the point of flexion, Avhich takes place after a time, are due to the pressure and anemia. Besides these flexions, caused by anomalies of the substance of the uterus, there are others which are undoubtedly caused by shortening of the uterine ligaments, as is proved by the cases observed by Virchow, Avhere there were flexions without any structural change in the paren- chyma. In the same Avay, distortion may result from fibroid tumors in the anterior or posterior wall of the uterus, from tense adhesions, or from the pressure of tumors. The more securely the loAver portion of the uterus is held in place by a rigid vagina, the more readily flexions occur; the less firmly it is held the more often displacements will occur instead. Anatomical Appearances.—On autopsy, flexions of the uterus may be readily recognized, as part of the anterior or posterior wall of the body, instead of the fundus, forms the highest part of the uterus. Generally we may readily restore the sunken fundus to its position, but it sinks back again to its former place when Ave let go of it. In some cases it cannot be restored to its normal position on account of peritoneal adhesions with the surrounding parts. Besides the flex- ion, there is almost always a slight anteversion or retroversion. If we cut the uterus out of the body, and hold it erect by the vaginal por- tion, the fundus sinks down, either anteriorly or posteriorly; if it be held horizontally, it not unfrequently holds its weight if the flexed portion be upward, but it bends together if we reverse it. The point of flexion is always near the internal os uteri. Here the flexion is sometimes slight, sometimes at right angles, or even at an acute angle. The os uteri is almost always moderately open, even in women who have had no children; this is a natural result of the tension, on the an- terior lip, in retroflexion, on the posterior lip in anteflexion. The in- CURVATURES OF THE UTERUS. 133 ternal orifice, on the contrary, is contracted partly by the flexion itself, partly by the SAvelling of the mucous membrane. In older Avomen, Ave occasionally find complete atresia of the internal os uteri. The con- traction or closure of the internal os uteri causes more or less hydro- metra. The disturbance of circulation at the point of flexion suffi- ciently explains the almost constant complication Avith catarrh of the uterus, ulcers of the os, and parenchymatous metritis. Symptoms and Cure.—The most constant symptoms of flexion depend on the impeded escape of the contents of the uterus. Hence the patients usually suffer severely from dysmenorrhea as long as they continue to menstruate. Small clots of blood, that has coagulated in the uterus, are often mixed with the menstrual blood, which is evac- uated with severe uterine colic. Uterine colic may also be caused, in the interval between the menses, by the impeded escape of the mu- cous and serous secretions, retained above the point of flexion. In many cases there are also the symptoms of uterine catarrh, as de- scribed in the first chapter, the fluor albus uterinus, decided loss of blood during menstruation, etc. Difficult and painful evacuation of the rectum, desire to urinate, and pain while doing so, the signs of anemia, and bad nutritive condition, and finally the disturbances of innervation that have been so often mentioned, complete the descrip- tion given by many women suffering form flexion of the uterus. But we must add that sometimes Avomen, with very decided flexions of the uterus, never have any, or have but few, of these symptoms, or, if they do occur, they soon pass off Avithout the disappearance of the flexion. Sterility itself, although very frequent, does not constantly accompany flexions of the uterus. Hence it appears that it is not the flexions, but the other anomalies of the uterus which complicate them, that cause the symptoms above described. These complications are so frequent, that their absence is an exception. This is partly because the same inju- rious influences that induce the flexions also excite the different forms of metritis, partly because the disturbances of circulation at the point of flexion cause hyperemia and exudation in the parenchyma, mucous membrane, and serous covering of the uterus. The course of flexions is very tedious. The disappearance of the condition is exceedingly rare, if it ever takes place. Flexion can only disappear completely, if new parenchyma is formed in place of the flattened and atrophied uterine tissue. When, with advancing years, the periodical recurrence of physiological congestion of the uterus ceases, all the symptoms usually moderate; and Avhen, in aged persons, the uterus and part of its blood-vessels become atrophied, the patient may feel pretty well. On physical examination, the finger introduced through the vagina 134 DISEASES OF THE UTERUS. first feels a dislocation, anteriorly or posteriorly, of the portio vaginalis, caused by the coexistent anteversion or retroversion. We also gen erally find the os so patulous that the point of the finger may be readily passed into it, even in women who have had no children. From the vagina, either before or behind the vaginal portion, we may find the body and fundus of the uterus, forming a round, firm, movable tumor. Usually, also, we may reach the point of flexion. The fact that the opposite part of the vagina is empty prevents our mistaking a flexed uterus from one that is enlarged, or diseased in some other way. The introduction of the uterine sound aids the diagnosis, but when the uterus is flexed this operation is peculiarly difficult, and we again re- peat that, in the hands of an unskilful physician, or even in those of a skilful one, the uterine sound is a dangerous instrument, which should be used as little as possible. Treatment.—We have already said that total disappearance of a flexion must to a certain extent be considered as a physiological im- possibility, as it is almost ahvays accompanied by atrophy of the paren- chyma of the uterus at the point of flexion. " Flexion instruments," sounds, redressers, and intra-uterine pessaries, which Avere for a time much used for flexions, do actually no good, but much harm. Scan- zonl has stated plainly that in his large gynecological practice he has never cured a flexion, and that he considers the use of flexion instru- ments as of no use and dangerous. Tonics also, whether used locally or internally, promise no benefit. The advice that patients with ante- flexion should hold their urine as long as#possible, so that the distended bladder may raise up the fundus, and that patients with retroversion should retain the feces for the same reason, is given from theoretical grounds, and has not proved correct. ( Virchow says that anteflexion results from great distention of the bladder Avhile the uterus is fixed.) Most gynecologists advise wearing a firm girdle around the pelvis and loAver part of the abdomen, and many patients praise the results of this treatment. It is difficult to understand that, even in retroflexion, pressure on the lower part of the abdomen should relieve the patient. Perhaps their greater ease may be due to the compression of the uterus and its consequent bloodless state. Little as Ave can do to remove the flexions, Ave may do much to relieve the sufferings of the patient if Ave treat the catarrh and paren- chymatous inflammation of the uterus, which first call attention to the flexion, according to the rules laid doAvn in previous chapters. Oc- casional abstractions of blood from the portio vaginalis are peculiarly beneficial, and are almost always effective in cases of flexion. CHANGES OF POSITION OF THE UTERUS. 135 CHAPTER VI. CHANGES OF POSITION OF THE UTERUS. The uterus, which is very movable, may be dislocated in any direc- tion. The most important deviations in position are anteversion, retro- version, descent, and prolapse. Anteversion most frequently occurs in women with strongly-curved pelvis. The natural inclination forAvard of the uterus may be increased by the pressure from above of fluids in the peritoneal sac or of tumors, and anteversion may thus be caused. More frequently the uterus sinks forAvard from its OAvn Aveight; hence almost always moderate degrees of anteversion accompany infarctions and new formations in the fundus uteri. Anteversion rarely becomes excessive, since each distention of the bladder restores the uterus to place, if some peculiar circumstance does not interfere with the reposition. Corresponding to this, the annoyance caused by the disease is usually slight, and it is only when the uterus is otherwise diseased and enlarged, or when it swells up at the menstrual period, that compression of the pelvic organs and tension of Douglas's ligaments cause pain in the small of the back, pressure in the pelvis, difficult micturition, desire to go to stool, and pain during defecation. On vaginal examination, we find the portio vaginalis directed backward toward the IioIIoav of the sacrum, and passing the finger fonATard we come Avithout interruption upon the body and fundus, which lie against the anterior part of the Aagina. Retroversion depends on the same causes as anteversion; a continued pressure from behind forward, tense adhesions on the posterior surface of the uterus or tumors in its posterior wall, cause a sinking of the fundus uteri into Douglas's space, and a prom- inence of the vaginal portion toward the symphysis pubis. The retroversion that occurs independently during the first months of pregnancy, and soon after confinement, is a very important disease; that occurring at other times is generally only a subordinate result of other diseases of the uterus or other pelvic organs. The symptoms of retroversion are analogous to those of anteversion, and they also de- pend on the pressure of the horizontally-displaced uterus on the pelvic organs, particularly on the rectum and bladder. Descent and prolapse of the uterus depend chiefly on relaxation of the parts that maintain the uterus in position, particularly its liga- ments, the pelvic fascia, and the vagina. If, during this relaxation, a stronger pressure from above doAvnward act on the uterus, the latter is pressed down, inverts the vagina, and passes deeper into it, and the result is a descent. If part of the uterus protrude from the vulva, we 136 DISEASES OF THE UTERUS. speak of a prolapse; when the entire uterus lies outside of the vulva, it is called a prolapsus completus. Relaxation of all the parts that should maintain the uterus in position occurs most frequently in the puerperal state; and it is the abdominal pressure that most often presses the uterus doAvnAvard. Poor women, who cannot take care of themselves after confinement, but are obliged to do hard work, that causes abdominal pressure a few days subsequently, are peculiarly liable to descents and prolapses. As every descent of the uterus in- verts the vagina, and each prolapse of the uterus induces prolapse of the Aragina, so, on the other hand, prolapse of the vagina may give rise to descent or prolapse of the uterus. If the loAver end of the va- gina be prolapsed, as a result of rupture of the perineum during de- livery, or from some other cause, the upper end exercises traction on the uterus, which either results in elongation of the vagina or de- scent of the uterus. Descent or prolapse of the uterus only excep- tionally occurs in women who have had no children. When they do occur, it is because the same conditions exist as after confinement, and particularly because the vagina is relaxed by blennorrhea and vene- real excesses, or the uterus is pressed downward by heavy tumors in the pelvis. If prolapse of the uterus take place suddenly, as occasion- ally happens from lifting heavy weights, from severe coughing, or strong bearing-doAvn efforts, the stretching of the ligaments causes severe pain in the abdomen, and great general disturbance, fainting, nausea, etc. If the descent or prolapse develop slowly, there is usu- ally but little annoyance at first; this consists chiefly in an undecided feeling of pressure dowmvard, and in stretching pain in the lower part of the abdomen and small of the back. The deeper the uterus de- scends, the more annoying these symptoms become; they increase when the patients stand up, Avalk, cough, etc.; they diminish dur- ing rest, and in the horizontal position. There are also inconven- ience and pain during urination and defecation, and there are consti- pation, colic, and other symptoms due to dislocation, pressure, and tension of the abdominal organs. If the uterus project from the vulva, it at first forms a round or oval tumor, as large as a walnut, which may be easily replaced; but soon the uterus covered by the vagina ad- vances, the tumor rapidly increases in size, and is replaced with diffi- culty ; it feels doughy, but on firm pressure we may distinguish a hard body more deeply seated. If, Avith the anterior wall of the vagina, the fundus and posterior wall of the bladder be drawn through the vulva (cystocele), on the anterior wall of the prolapse we may see a tense, sometimes fluctuating, tumor, which swells and subsides again several times during the day, and into which, by exercising some skill, we may introduce a male catheter through the urethra. On intro- TUMORS OF THE UTERUS. 137 ducing the finger into the rectum, we find it bulged forAvard. The os uteri gapes open, because the vaginal portion is averted; it is red- dened and covered with glairy mucus. The prolapsed vagina is dry, parchment-like, thickened; the epithelium resembles epidermis; fre- quently it is excoriated by the friction of the clothes and the irrita- tion of the urine that trickles over it, and not unfrequently deep ulcers form in it. The treatment of dislocations of the uterus is purely surgical. And it would lead us too far to speak even of the choice of certain pessaries, and of the rules for their introduction and employment. CHAPTER VII. TUMORS OF THE UTERUS. A very frequent form of tumor of the uterus is the fibroid or fibromuscular, as it is also called, from containing muscular elements as Avell as connective-tissue filaments. They develop, AAithout per- ceptible cause, chiefly in women between thirty and fifty years old. Their size and number vary. There are very small fibroids, and some that Aveigh tAventy to thirty pounds. There may be one, several, or very many. They are generally round; some, particularly the large ones, are more irregular and nodular in shape. On incision, they ap- pear white or pale red, and their fibrous structure, and the regularly concentric or irregular direction of their filaments, may be distinctly recognized. Fibrous tumors usually have the consistence of fibrous cartilage; exceptionally they are more relaxed and softer, or contain a caAity filled with serum. The tumor is almost ahvays in the base or body of the uterus; occasionally it is embedded in its substance, and enclosed by a loose connective-tissue layer, Avhile sometimes it is at- tached by one or more pedicles. The former are divided into inter- stitial, subserous, and submucous, according as they are located chiefly in the middle of the wall, close under the serous or mucous membrane. The pedunculated submucous fibroids are called fibrous polypi. Occasionally fibroid tumors become bony and cease growing; in other cases the connective-tissue capsule inflames. If suppuration occur in the latter cases, the fibroid may be enucleated and expelled. In all forms, except the subserous fibroid, the parenchyma of the uterus be- comes hypertrophied. They frequently induce displacement and flex- ions of the uterus. At the commencement of the disease the symp- toms are obscure. Anomalies of menstruation and signs of chronic uterine catarrh are common to fibroid and to other diseases of the uterus; still, feAV other affections cause such severe and continued 138 DISEASES OF THE UTERUS. hemorrhage and such decided pain as fibroid. If a woman complain that she has her menses every fortnight, and they often last fourteen days, that she loses a great deal of blood, and, at the same time, has bearing-down pains, we should strongly suspect that she has fibroid of the uterus. The more copious the hemorrhage, the more probable it is that she has a large polypus; on the other hand, the more severe the pain, the more probable it is that she has a fibroid in the substance of the uterus. At the same time there are symptoms of pressure on neighboring organs; dysuria, constipation, difficult defecation, hemor- rhoids, also edema, pain, and formication, or numbness in the lower extremities. Physical examination alone renders the diagnosis cer- tain. By it we may usually make out the increase in size of the ute- rus, its resistance, and its irregular form, when the tumor has attained any considerable size. In subserous fibroid we may often feel distinct, hard, and round tumors above the symphysis pubis, which follow all the movements of the uterus. When the fibroid develops in the wall of the uterus, or projects into its caAity, the shape of the uterus is less irregular, the neck gradually becomes shorter, and is finally obliter- ated, so that on careless examination we may suspect pregnancy. Finally, the os uteri becomes patulous, permits the finger to enter the cavity of the uterus and feel the polypus. It is not unfrequently difficult to determine whether a fibroid has a broad base or is pedun- culated. While the uterus is only moderately enlarged, the sooner the cervix is shortened and obliterated, and the earlier the os becomes patulous, the more probable it is that we have a pedunculated poly- pus. This form alone alloAvs a favorable prognosis, for, in many cases at least, it can be removed by operation. The operation for uterine polypus is one of the most gratifying operations in surgery, for fre- quently women, who had been brought to the edge of the grave by the continued hemorrhage, became fresh and blooming a few months after the operation. In other forms the prognosis is bad in proportion to the hemorrhage. If they be not carried off by some intercurrent disease, many patients die of marasmus and dropsy; others die of peritonitis, and the result of strangulation of the abdominal organs caused by the fibroid. Pregnancy (which occasionally takes place in spite of the fibroid), delivery, and childbed, are accompanied by pecu- liar dangers, that we shall not describe. Mucous polypi originate from proliferation of the mucous mem- brane. In these polypi there is sometimes a preponderance of con- nective tissue; at other times they are very vascular, and again they consist chiefly of dilated follicles. Hence a division is made into cel- lulo-fibrous, cellulo-vascular, and so-called vesicular polypi. Mucous polypi are rarely larger than a hazel-nut, are sometimes spherical at TUMORS OF THE UTERUS. 139 others pear-shaped, and have a rather thick pedicle. They are usually- situated near the cervix, appear in the os uteri, and after a time project out of it. Mucous polypi also frequently cause blennorrhea and se- vere hemorrhages. The source of these symptoms is doubtful till physical examination reAeals it. Carcinoma occurs more frequently in the uterus than in any other organ. In most cases it is of the medullary variety, more rarely scir- rhous or alveolar. The degeneration, Avhich usually consists in a diffuse infiltration, almost ahvays begins in the ceivix, rarely spreads to the fundus, but very often advances anteriorly to the bladder and poste- riorly to the rectum, so that subsequently, Avhen sloughing occurs, there is fearful destruction, and fistulous communications may form with the bladder and rectum, and horrible cloaca may occasionally re- sult. The lymphatic glands of the pelvis and side also usually partici- pate in the degeneration. In one case of cancer of the uterus that I saw, the glands along the front of the spine, as far up as the cervical por- tion, were cancerous, and during life thick, hard, glandular masses could be felt in the supraclavicular fossa. The most important symptoms of cancer of the uterus are pains in the small of the back, womb, and groins, which are at first moderate, but, after a while, become very severe, so that most patients with cancer of the uterus are obliged to take large doses of opium; there are also hemorrhages, at first only at the menstrual periods, but subsequently at other times, and, finally, there is a blennorrheal discharge, which gradually becomes more wa- tery, irritant, and foul-smelling. If we make a vaginal examination at the commencement of the disease, we find an uneven, nodular, very hard swelling of the cervix; subsequently a gaping, funnel-shaped, cancerous ulcer, with everted edges, which bleeds readily on being- touched, but is not sensitive. Death occurs from excessive marasmus; thromboses often form in the femoral veins; occasionally there is per- foration of the peritoneum, or some other accident that hastens death. Cauliflower excrescences are papillary tumors on the os uteri, which, as they become older, are complicated Avith epithelial cancer. Papillary tumors result from great hypertrophy of the papille of the os uteri, and at first look like Avarty or condylomatous tumors; after- ward, when the papillary sprouts have groAvn to be long and shaggy, they look like caulifloAver excrescences. The papille and tags consist of Avidely-dilated capillaries, which contain very little connective tis- sue, and are covered Avith a very thick epithelial layer. Subsequently alveoli, filled Avith the elements of epithelial cancer, occur in the base of these tumors, between the connective-tissue and muscular layers, and cause extensive destruction. After death or removal this cauli- flower groAvth appears whitish, but during life it is very red, bleeds 140 DISEASES OF THE UTERUS. easily, and induces a profuse discharge like the Avashings from meat, which quickly becomes fetid. These symptoms, which are sufficiently explained by the structure of the growth, as well as the severe pain in the small of the back and groin, the exhaustion and impoverishment of the blood, from loss of fluids and hemorrhage, cause the symptoms of cauliflower excrescence to greatly resemble those of cancer of the uterus. In most cases this resemblance continues till death, Avhich occurs in almost all patients with the symptoms of marasmus and dropsy, but is usually delayed longer than in cancer of the uterus. Removal of the tumor at the proper time has resulted in permanent cure in some cases. A woman, from whom Berndt removed a cauli- flower growth, as large as a man's fist, died seventeen years after of tuberculosis of the lungs and intestines, at the Greifswalder clinic; the tumor had not returned. CHAPTER VIII. ANOMALIES OF MENSTRUATION. Anomalies of menstruation are not independent diseases, but are symptoms of affections of the sexual organs, or of other diseases impairing the general health. Hence the discussion of amenorrhea, dysmenorrhea, menorrhagia, etc., does not properly belong in. a text- book of special pathology and therapeutics, but in a work on semeiol- ogy and diagnosis. FolloAving the example of most authors, for prac- tical reasons, we will give a short account of the most important men- strual disturbances. Too early menstruation—menstruatio prcecox—is not frequent, if by this term Ave mean only those cases of hemorrhage from the female genitals before puberty that are accompanied by the expulsion of a ripe ovum. As we have no certain means of finding out Avhether this complication exists or not, Ave must note Avhether the hemorrhage re- curs at regular intervals; AA'hether it is accompanied by disturbance of the general health; by pains in the back, and other symptoms which almost always accompany menstruation proper. Hemorrhage occur- ring once, or at irregular intervals in the course of acute diseases, particularly of acute infectious diseases, as Avell as in chronic dyscrasia and venous congestions, has nothing to do with menstruation. If, in our climate, menstruation begins between the twelfth and fourteenth years, instead of the fourteenth and sixteenth, it is only a morbid symptom, if the girl be undeveloped. Many girls at this age, who still go to school, and wear short clothes, have full breasts, and hair on the pubes. We may say that they have develvoped too early, but not ANOMALIES OF MENSTRUATION. 141 that they have any anomaly of menstruation; in them the absence of the menses would be pathological. But, besides these cases, we not unfrequently find apparently undeveloped girls aged eleven or twelve years, with regularly-recurring hemorrhages from the genitals, and such characteristic symptoms of congestion in the pelvis, that Ave can- not doubt there is a case of early ovulation—a true menstruatio precox. Experience shoAvs that almost all such girls subsequently suffer from obstinate chlorosis. Cases Avhere menstruation has been observed in small children are only partially reliable. It is very rare, indeed, for menstruation to cease several years too late. Among us, women usually menstruate till forty-five or forty-eight years old. If menstruation has begun early, it usually ceases some- Avhat sooner; if the reverse, it continues a feAV years longer. Scanzoni has seen only one case, in his practice, where an unmistakable menstrual hemorrhage continued to the age of fifty-tAvo years. Even very old women are inclined to regard all hemorrhage from their genitals as menstrual. Of course, we can only speak of amenorrhoea when the menses are absent in a woman who has attained the age of puberty, and has not passed the climacteric, and Avho is not pregnant or nursing. Tardy men- struation is one form of amenorrhea; too early cessation is another form. If a girl sixteen or eighteen years old be no more developed than one of ten or twelve years, she can no more be said to have retarded menses, than a fully-developed girl of twelve or thirteen who menstra- ates can be said to have menstruatio precox. Except in cases of tardy menstruation, or too early cessation of the menses, amenorrhea more frequently depends on constitutional disease than on local affections of the genitals. It is chiefly chlorosis, scrofula, and tuberculosis that retard the occurrence of menstruation, or cause its arrest. It is not ahvays easy to determine, in these cases, whether the ovum does not ripen, or whether only the hemorrhage, that usually accompanies the expulsion of the ovum, is absent. If, at intervals of four weeks, we notice more or less decided molimina, accompanied by SAvelling of the breasts and increased discharge of mucus from the genitals, it Avould seem as if only the hemorrhage Avere wanting; in the reverse cases, we may suppose that ovula do not ripen. Among the diseases of the sexual organs, de- generation of the ovaries rarely causes amenorrhea, and only does so Avhen both ovaries are at the same time the seat of organic disease. Among the various diseases of the uterus, chronic catarrh, and espe- cially chronic infarction, in which the blood-vessels are compressed by the shrinking connective tissue, most frequently induce this disease. Amenorrhea occasionally occurs in strong, healthy girls, in Avhom the genitals have not developed so rapidly as the rest of the body. 142 DISEASES OF THE UTERUS'. Lastly, Scanzoni concludes, from the cases where the menses (which had previously been normal) ceased on the occurrence of paraplegia, that amenorrhea may result from abnormal innervation. The sudden arrest of the menstrual flow—suppressio menslum— is most frequently the symptom of acute metritis. It depends on the same injurious influences that we mentioned in the etiology of that disease, and is accompanied by the same symptoms. More rarely the menses cease suddenly, if the amount of blood in the uterine vessels be lessened by a diminution of the entire amount of blood in the body by- venesection, or by excessive fluxion to some other organ. By vicarious menstruation, we mean hemorrhages from mucous membranes, wounds, telangiectasis, etc., which occur at the time of the expulsion of an ovum, instead of the hemorrhage from the genitals, or with a slight amount of the latter. There are numbers of cases where this has been certainly seen, although it is among the " affections not well ex- plained." Scanzoni gives the following explanation of the occurrence of vicarious menstruation: The periodical ripening of an ovum causes a general vascular disturbance; as a consequence of this, AAhere cir- cumstances favor it, there may be a rupture of vessels in some part unconnected Avith the sexual organs; and this bleeding from the locus minoris resistentlai may moderate the hyperemia of the uterine mucous membrane (as a venesection during menstruation does), so that there shall be very little, if any, loss of blood from it. In treating amenor- rhea, the causal indications are to be fulfilled first, or rather, we must, first of all, remove the disease of which the amenorrhea is a symptom. There are cases, however, where the amenorrhea continues,- and re- quires special treatment after the cure of the original disease. In these cases, which are not so frequent as is supposed by the laity (Avho constantly urge us to bring back the menses, thinking that recovery from any existing disease will certainly follow), it is most important to determine Avhether only the hemorrhage be absent, or Avhether no ovra ripen. It is absurd to use foot-baths or emmenagogues when the latter is the case. If signs of congestion in the pelvis, SAvelling of the breasts, increased discharge of mucus from the genitals, indicate that an ovum has ripened, and the uterine mucous membrane is in a state of hyperemia, it is certainly desirable to increase this hyperemia enough to cause a rupture of the vessels; otherwise, changes may be induced in the mucous membrane and parenchyma of the uterus, Avhile by inducing hemorrhage, this danger may be avoided. The most effective emmenagogues are the warm uterus douche, scarification of the os uteri, and the application of leeches to it. If the presence of a hymen prevent the employment of these remedies, we may apply cups to the inside of the thighs, and order warm and irritant hip and foot ANOMALIES OF MENSTRUATION. 143 baths. According to Scanzoni, the only internal emmenagogues that are reliable are aloes, sabine, and ergot; but he very properly Avarns against their employment in all cases Avhere there are signs of con- gestion or inflammation in the pelvic organs. Menorrhagia, or too copious menstrual hemorrhage, has been already mentioned as a symptom of various structural changes and of tumors in the uterus. But they also occur Avithout perceptible dis- turbance of nutrition, Avhere the escape of blood from the uterus is hindered in heart and lung diseases, etc., as well as in fluxions induced by irritation of the uterus from sexual excess, perhaps also by sensual excitement. In very rare cases menorrhagia depends on a hemor- rhagic diathesis, being a symptom of scurvy, purpura hemorrhagica, acute infectious diseases such as hemorrhagic small-pox, or measles, or of typhus, etc.; where it is due to obstructed efflux or increased afflux of blood to the uterus, they are usually preceded by symptoms similar to, but more marked than, those with which normal menstru- ation usually begins. Part of the blood passes off in a fluid state, part coagulates in the vagina, forming irregular clots; rarely it coag- ulates in the uterus, and there forms so-called fibrous polypi, such as frequently occur after abortions. Plethoric patients often bear very decided loss of blood without injury; anemic patients have the symp- toms of increased anemia. The treatment of menorrhagia requires great attention to the original disease. The occasional application of leeches to the cervix is often of surprising benefit in those cases de- pendent on chronic inflammation of the uterus. As soon as the loss of blood is decided and threatens to impair the strength, it is impor- tant to prevent all bodily exertion and mental excitement, and keep the patient in a horizontal position during menstruation. At the same time Ave forbid all stimulating food and drink, and order mineral or vegetable acids. It will only rarely be necessary to employ cold water or ice compresses, or to have recourse to styptics. In some cases, however, the bleeding threatens life, and then it is necessary to act energetically, and even to inject solutions of chloride of iron, etc., into the uterus. Those anomalies of menstruation, Avhere there is particularly severe pain before the commencement of the bleeding and while it lasts, are termed dysmenorrhoea or menstruatio difficilis. We have men- tioned this as a symptom of flexions and other diseases of the uterus, but it also occurs without perceptible organic change, and it may be divided into two forms, nervous and congestive. The former is ob- served in women with morbid excitability of the nervous system. The mental uneasiness that precedes the menses in most Avomen, in them attains an unusual grade, as do the pains in the abdomen, small of the 56 144 DISEASES OF THE UTERUS. back, and thighs, which many other women have during menstruation. The morbid excitement of the sensory nerves of the uterus is often transferred to other parts, causing neuralgia in remote organs, cramps, etc. These symptoms usually exist only during th6 first days of men- struation, and disappear the second or third day; this often happens so regularly, that some women always expect to pass the first day of each menstrua] period in bed. In other cases the annoyances last till the menses are over. It is not improbable that, in the first-mentioned cases, the pain partly depends on a spasmodic contraction of the os uteri, and on contractions of the uterus like labor-pains. In the con- gestive form of dysmenorrhea, the hemorrhage is preceded by unusual congestion to the pelvic organs, increased action of the heart, rush of blood to the head, and a general fever. These troubles do not mod- erate till a copious hemorrhage occurs on the first, second, or third day. This form is not by any means limited to plethoric women, but is not uncommon among the weakly and anemic. It is difficult to determine whether in some cases the hyperemia of the pelvic organs is kept up too long and rendered excessive by the difficulty of the escape of a Graafian follicle vviiich lies deep in the ovary or is covered by thickened peritoneum. In severe congestions to the uterus, an exudation is occasionally deposited between the mucous membrane and the parenchyma, and the mucous membrane is thrown off in pieces of variable size. In nervous dysmenorrhea, besides the treatment of the original disease, narcotics are indicated either by the mouth or as enemata. In the congestive form, on the contrary, we may apply leeches ; bleeding from the foot, as was formerly done in these cases, is rarely indicated. CHAPTER IX. RETRO-UTERINE HEMATOCELE. This affection depends on an effusion of blood into the pelvic cav- ity, or into the subserous connective tissue of the pelvis, particularly between the folds of the broad ligaments of the uterus; this takes place at the menstrual period. In the first case it is most probable that there has been an abnormal amount of hemorrhage from the rup- tured follicle, and that the blood has passed directly into the pelvic cavity. In the latter case, on the other hand, the bleeding seems to depend on a rupture of the vessels in the subserous connective tissue. Under normal circumstances, the excessive fluxionary hyperemia in the pelvic organs, that accompanies the discharge of a ripe ovum, induces rupture of vessels in the uterine mucous membrane, and effusion of blood into the uterus, and occasionally, from unknown causes, it alsc RETRO-UTERINE HEMATOCELE. 145 induces hemorrhage in the subserous connective tissue of the interna] sexual organs. Since the diagnosis made by Professor Breit, in one of the three cases that I have seen during the past three years, was verified by an immediate relief following a copious passage of blood from the bowels, I have come to the conclusion that retro-uterine hematocele is by no means so rare a disease as most authors suppose. I have no doubt that most of the cases, where, in menstruating women, I diagnosed a peritonitis, with capsulated exudation starting from the ovary, Avere caused by an effusion of blood in the pelvic cavity, or into the sub- serous connective tissue of the pelvis—that is, by retro-uterine hema- tocele. In the cases I have seen, the patients were young persons, AA'ho for years had had irregularities of the menses, sometimes severe molimina, sometimes great and long-continued loss of blood; other observers also seem to think that the disease is more frequent in such persons than in Avomen AA'ho menstruate without difficulty and lose little blood. The symptoms of retro-uterine hematocele are essentially those of more or less extensive subacute peritonitis, starting from the pelvic organs. A feeling of pressure and discomfort, deep in the pelvis, occa- sionally precedes the severe peritonitic pain, which is rendered un- bearable by slight pressure. The accompanying fever is of variable intensity, but is not usually excessive. It is rarely ushered in by a single chill; more frequently there are repeated rigors during the course of the disease. Dysuria is an almost constant symptom, and entire retention of urine is very common, so that, for many days, we may be obliged to use the catheter. There is usually constipation also. Most patients complain of nausea; some have obstinate vomit- ing as soon as they take the slightest amount of food or drink into the stomach. If we observe these symptoms in a woman Avho is menstruating, or Avhose menses have ceased within a feAV days, we shall probably be correct in diagnosticating retro-uterine hematocele. Local examination is more certain. If the pain permit us to make deep pressure toAvard the pelvic cavity in the hypogastric region, we find a circumscribed tumor, of variable size, above the symphysis pubis, and usually to one side of the median line, besides which, in the me- dian line, Ave may also find the fundus of the elevated uterus. On vaginal examination, Ave find the cervix very high up, and pressed firmly against the pubis. In the posterior part of the vagina we find a tense, elastic, smooth tumor, which, on superficial examination, might be mistaken for the fundus of a retroverted uterus. Its outlines can usually be more distinctly made out at one side than at the other. Examination per rectum gives the most characteristic signs; by this 146 DISEASES OF THE UTERUS. we can hardly fail to discover a tense elastic tumor, lying betAveen the rectum and uterus, and pressing the latter against the symphysis pubis. The course of the disease varies according as the effusion of blood is gradually absorbed, or is spontaneously or artificially evacuated. In the first case the pains remit in a few days, it is true; they do not en- tirely subside, however, but vary in intensity for several weeks, till finally, Avhile the tumor becomes smaller and less distinct, they entirely disappear. In the cases that I have seen, during this time there was severe uterine catarrh, with a purulent, occasionally bloody, secretion. If, on the other hand, there be perforation of the rectum or vagina, pr an artificial opening be made through them, the pain and tumor disap- pear as if by magic. In rare cases, the effusion of blood leads to sup- puration and abscesses in its vicinity. In the treatment of retro-uterine hematocele, particular attention must be paid to the resulting peritonitis, for we know no remedy to hasten the absorption of the effused blood. One or, if necessary, more applications of leeches, as well as Avarm but light poultices to the ab- domen, and attention to the evacuation of the bladder and rectum, apparently suffice, in most cases, to lead the disease to a favorable termination in a few weeks. Some authorities advise the early evacu- ation of the blood by a puncture through the vagina. But, if the en- trance of air be not very carefully avoided, this operation may readily induce decomposition of the remaining blood, and suppuration in its vicinity. SECTION III. DISEASES OF THE VAGINA. In this section we shall only treat of the inflammations of the vagina, leaAing the congenital anomalies, tumors, and other diseases nf that organ, to the text-books on obstetrics and surgery. CHAPTER I. VIRULENT CATARRH OF THE VAGINA. Etiology.—For the pathogeny and etiology of gonorrheal catarrh of the vagina, Ave may refer to Avhat we have said of virulent catarrh of the male urethra. Anatomically, it is not distinguishable from non- virulent catarrh, but its course and origin are different. The disease is not induced by sexual excess, or any other cause than infection with gonorrheal matter. Anatomical Appearances.—In Avomen the chief seat of virulent catarrh is the mucous membrane of the vulva and vagina; more rarely it extends to that of the uterus. But in almost all cases the catarrh extends to the urethra, and this is important in the diagnosis. The affected mucous membrane at first shoAvs the changes peculiar to the most severe form of acute catarrh; subsequently those of chronic ca- tarrh. The secretion, which, in the beginning, is usually scanty, sub- sequently becomes very copious, purulent, irritates the vulva and inner surface of the thighs, but is only peculiar in that it is the bearer of the contagion. Symptoms and Course.—The first symptoms of gonorrhea in the female, a feeling of itching and warmth in the sexual organs, and a scanty mucous discharge, are not very characteristic, and are often un- noticed. A few days after the commencement of the disease, there are severe burning pain in the genitals, swelling of the vuha, ardor urinaz ; but these troubles rarely become so severe as to interfere greatly with 148 DISEASES OF THE VAGINA. walking, sitting, and moving the body. The secretion, which in this stage is yellowish-green, thick, and purulent, often oozes up in large quantities betAveen the labia; in the vulva and its vicinity, even to the anus, Ave find shallow ulcers, which are not to be confounded with chancres. We may almost always press pus out of the urethra. Af- ter the disease has lasted a fortnight or three weeks, the pain abates and ceases; the discharge loses its purulent appearance, but continues a long while till the secretion, which constantly becomes more mucous, dries up, and loses its power of inoculation. Treatment.—The local treatment, which we preferred to internal remedies for gonorrhea in men, is almost exclusively used for the dis- ease in women. Considering the different seats of gonorrhea in the two sexes, it may be readily understood that copaiba or cubebs, whose active constituents are excreted with the urine, may have an effect on gonorrhea in the male urethra that it cannot have on the disease in the female, where the vagina is chiefly affected. While there is se- vere pain, we prescribe scanty diet, laxatives, long-continued sitz- baths, during Avhich a speculum should be left in the vagina, if its in- troduction be not too painful. If there be no symptoms of inflamma- tion, or if they have been allayed, we may employ injections of solu- tions of tannin, nitrate of silver, alum, sulphate of zinc, acetate of lead, etc. Injections of plumbi acet. crystall. 3 iij-—Aque conj. j, as recommended by Bicord, are very efficacious; instead of being inject- ed, this solution may be poured in through a speculum, and the latter slowly withdrawn, so that the fluid shall come in contact with all parts of the vagina. In very obstinate cases we may introduce wads of charpie, sprinkled with alum, into the vagina, or touch the parts with solid nitrate of silver. CHAPTER II. NON-VIRULENT CATARRH OF THE VAGINA. Etiology.—Kblliker and Scanzoni, avIio have carefully examined the secretion from the vaginal mucous membrane, both in health and disease, found perfectly healthy secretion in very few Avomen, and only in those who had had no children, and had not frequently indulged in coitus. It was so scanty that the surface of the mucous membrane was only lubricated by it; it was nearly as clear as water, fluid, only viscid, white or yelloAvish in spots ; it was almost ahvays acid, and, besides a small amount of pavement epithelium, it contained no noticeable solid constituents. Shortly before and after menstruation the secretion was more copious, ahvays fluid, and almost always acid; at this time it NON-VIRULENT CATARRH OF THE VAGINA. 149 contained more epithelial cells, and, after the cessation of the menses, as long as it retained its red color, there were more or less blood-cor- puscles in it. In catarrhal affections they found the secretion either milky and thin, or more yellowish and thicker. The more opaque, Avhite, or yellow, the secretion appeared, the more numerous were its pavement epithelium and young cells (mucous and pus-corpuscles), often also the infusoria discovered by Donne (trichomonas vaginalis), and some few fungous filaments and vibriones. Hence we see that these observers rarely found a perfectly normal secretion, and that catarrh of the vagina is one of the most common of female diseases. Irritation of the ATagina, by sexual excess, is the chief cause of catarrh of that part, it is true ; but it is often induced by other causes, Avhich Avere mentioned when speaking of uterine catarrh. It is particularly to be borne in mind that catarrh of the vagina, like that of the uterus, depends as often on constitutional as on local causes. A consideration of the exciting causes shoAvs that this disease must be rare during childhood; and this is true, except in the cases where oxyuris have passed over the perineum from the anus to the vagina, and have there caused great irritation. Anatomical Appearances.—In acute catarrh we find the mucous membrane bright red, SAvollen and relaxed; in many cases Ave see small prominences on it, Avhich ghe the membrane a granular appear- ance, and Avhich are not, as Avas formerly supposed, due to distention of the follicles, but to swelling of the mucous papille. Sometimes these changes affect the entire vagina, at others only parts of it. At first the secretion is scanty, but, after the disease has lasted a very short time, it becomes more copious and more or less opaque. In chronic catarrh the walls of the vagina appear distensible and flaccid. The membrane is more bluish red, its surface is more fre- quently granular than in the acute variety, the secretion is sometimes more milky, sometimes more yelloAV and thick. Not unfrequently the relaxation of the vagina induces prolapse, particularly of the anterior wall. Symptoms and Course.—In non-virulent catarrh also, if it begin acutely, the patient complains of prickling and burning in the private parts; but, as the mucous membrane of the urethra is unaffected, she lias no pain on urination. In chronic catarrh the discharge of the ab-. normal secretion, the leucorrhea (fluor albus vaginalis), is often the only symptom of the disease. The chief means of deciding whether the discharge be from the vagina or uterus is by examination with the speculum. Many women bear the drain without any injury; in others it induces anemia, pallidity, weakness, and emaciation. Treatment.—In treating non-virulent vaginal catarrh, just as in 150 DISEASES OF THE VAGINA. uterine catarrh, we must first attend to the causal indications. But we cannot often cure the disease without accompanjing local treat- ment. We would chiefly recommend the hip-baths and injections mentioned in the last chapter; in obstinate cases the introduction of a tampon sprinkled Avith alum, and even the application of solid nitrate of silver. CHAPTER III. CROUPOUS AND DIPHTHERITIC INFLAMMATION OF THE VAGINA. Croupous and diphtheritic inflammations of the vaginal mucous membrane are common during puerperal fever, but are rare except in the puerperal state. They either depend on local irritation or on con- stitutional disease. Thus, the discharge from a sloughing cancer of the uterus, the urine constantly flowing through a vesico-vaginal fis- tula, a bad pessary, a large uterine polypus projecting into the va- gina, may induce croupous or diphtheritic inflammation of the vaginal mucous membrane; while the disease is also often observed in the later stages of typhus, cholera, measles, and small-pox, and accompany- ing similar affections of other mucous membranes. Usually only cer- tain spots of the vagina are covered Avith croup membrane, or changed to diphtheritic sloughs. In the vicinity of these spots the mucous membrane is dark red; after the slough has been throAvn off, irregular losses of substance remain; these are sometimes superficial, at others deep. Our attention is called to the disease by severe pain in the parts, and by a fetid, often bloody, discharge, which begins in a few days ; local examination is the only means of certain diagnosis; Avhere a large or putrefied pessary has caused the inflammation, its removal, and the use of lukewarm, and later of cold and astringent, injections, ordinarily suffice to cure the disease. The affection usually disappears readily also if a large polypus, that has forcibly distended the vagina, be removed. On the other hand, where sloughing cancer or Aesico- vaginal fistula has caused the disease, we must limit ourselves to a palliative treatment. In those cases occurring in the course of infec- tious diseases, it is usually sufficient to attend to cleanliness as the secondary disease generally passes off Avith the primary. f DISEASES OF THE NEKVOUS SYSTEM. "Section l DISEASES OF THE BRAIN. CHAPTER I. HYPEREMIA OF THE BRAIN AND ITS MEMBRANES. Etiology.—For a time the fact was ignored that on autopsy the blood-Aessels within the skull Avere sometimes found distended and at others empty, and it was supposed that the amount of blood contained in the closed cranium of an adult could neither increase nor diminish, but was constant; and that anemia or hyperemia was only supposable when the brain-substance was increased or diminished, that is, when there was hypertrophy or atrophy of the brain. This view was based on the folloAving reasoning: The brain is not compressible, at least not by the pressure to which it is subjected from the contents of the blood-vessels; and it is surrounded by Avails which do not expand; consequently only the same amount of blood can enter the skull as passes out from it, and conversely only as much blood can pass out of the skull as enters it. This reasoning is false, as it starts with the supposition that the contents of the cranium consist only of the mem- branes of the brain, the brain-substance and the blood-vessels with their contents; it leaves the cerebrospinal fluid out of consideration. This, which is a simple transudation, can rapidly increase or diminish, and can at least partly pass into the spinal canal, which is not entirely enclosed by rigid walls. In almost all autopsies it may be seen that the amount of blood contained in the vessels and the amount of cere- brospinal fluid are in inverse proportion ; that a distention of the ves- sels of the meninges is accompanied by a decrease of arachnoid fluid, and conversely that, when the vessels are less full, the meshes of the 152 DISEASES OF THE BRAIN. text us cellulosus subarachnoidealis contain a greater amount of serum. Only when the brain is atrophied do Ave find edema of the membranes with overfilling of the vessels; and only when an effusion of blood, a tumor, or a collection of fluid in the ventricles, has contracted the space in the skull do we find, along Avith anemia, dryness of the membranes, and disappearance of the sulci between the cerebral convolutions. The division of cerebral hyperemia into active and passive, or, to retain the expressions previously used, into fluxionary and congestive, is practically valuable not only on account of the consideration being easier, but because the symptoms ofj^one form differ from those of another. ^ - Fluxionary hyperemia results—1. fjjrm increased heart-action. It is true that, in this case, while the arteries are fuller than usual, the Aeins are less so; hence the entire amount of blood in the vessels of the brain and its membranes is not increased by the stronger action of the heart. But the increased lateral pressure induces increased ful- ness of the capillaries, and it depends chiefly on these (not on the amount of blood in the large vessels) whether or not the brain acts normally and is normally nourished. This form of cerebral hyper- emia occurs temporarily from augmented energy of contraction of a healthy heart, as in fever and great bodily or mental excitement; it is habitual in the permanently increased activity of a hypertrophied heart, but only when the hypertrophy is an independent disease, or in case it accompanies an obstruction to circulation, when it has become greater than is necessary for the compensation. Simple, non-com- plicated hypertrophy of the heart is not frequent, and occurs almost exclusively in topers and persons who continually do hard work. On the other hand, hypertrophy that has become greater than was neces- sary to compensate the obstruction to the circulation is quite frequent. Examples of this are the occasional enormous hypertrophies of the left ventricle Avhen there is insufficience of the aortic valves, and perhaps also the hypertrophy of the heart in morbus Brightii. 2. Fluxionary hyperemia of the brain results from too slight resist- ant power of the afferent blood-vessels, whether this be congenital or acquired. When the cerebral arteries have delicate, thin walls, so that they yield to an increased pressure of the blood sooner than the other arteries of the body do, and hence, when the action of the heart is only moderately increased, fluxionary hyperemia of the brain is in- duced, it is customary to say that the person so affected has a tendency to "rush of blood to the head." 3. Fluxionary hyperemia to the brain results from an increase of the lateral pressure in the carotids as a consequence of obstructed escape of blood from the aorta into other branches. As a type of this HYPEREMIA OF THE BRAIN AND ITS MEMBRANES. '' collateral fluxion " to the brain, we may mention the habitual cere- bral hyperemia AA'here there is contraction or closure of the aorta at the point where the arterial duct terminates in the aorta (Volume I., page 349). It frequently results from compression of the abdominal aorta and its branches, by the distended intestines and by exudations. In the same way obstruction of the cutaneous circulation during the cold stage of intermittent fever, and from the action of severe cold, induces collateral fluxion to the brain. According to Watson, in cold nights many unfortunates are arrested in the streets for being drunk, Avhen they are only suffering from cerebral hyperemia as a result of disturbance of the cutaneous circulation. It is not improbable that severe muscular exertion may also induce increased fulness of the carotids and fluxionary cerebral hyperemia, by the pressure of the con- tracted muscles on the capillaries. 4. A fourth cause is paralysis of the vasomotor nerves of the cere- bral vessels. Physiological experiments show that, if the cervical por- tion of the sympathetic nerve be divided, the vessels on the correspond- ing side of the head become dilated. The cerebral vessels appear to be similarly affected by the use of spirituous liquors, by some poisons, as well as by great emotions and excessive mental activity. I would particularly call attention to the last cause, as I have frequently seen dangerous hyperemia of the brain after too prolonged mental labor, Avhich resulted fatally from the occurrence of edema. We can hardly give any other explanation for these cases, than that the walls of the vessels are paralyzed by the above influences, their calibre dilated, and the supply of blood consequently increased. 5. Lastly, fluxion to the brain results from atrophy of that organ. The space left in the skull by the disappearance of the brain-substance is partly filled by the dilatation of the vessels. We shall find this dilatation of the vessels to be a frequent cause of their rupture; and, as atrophy of the brain often follows apoplexy, it is also a cause of returns of apoplexy. We shall not attempt to say whether or not the fluxionary hyperemia of the brain, occasionally observed during con- valescence from severe disease, is the result of atrophy of the sub- stance of the brain or of the neuroglia and consequent dilatation of the vessels. Passive hyperemia, congestion of blood in the brain, depends— 1. On compression of the jugular veins and vena cava descendens. As a type of this form, we may mention the excessive cerebral con- gestion caused by strangulation. The jugular veins are most fre- quently compressed by enlarged thyroid or lymphatic glands, the vena cava descendens by aneurisms of the aorta. 2. Congestion of the brain results from energetic expiratory move- 154 DISEASES OF THE BRAIN. ments while the glottis is contracted. In coughing, straining, playing wind-instruments, etc., as we have often shown, the flow of blood into the thorax is hindered; the pulmonary circulation contains too little, the general circulation too much blood. Under such circumstances, the brain must suffer far more from hyperemia than other organs sup- plied by the general circulation, particularly the liver, spleen, and kidneys; because the passage of blood through the upper aperture of the thorax is more impeded than it is through the lower, since these abdominal glands undergo the same compression from the abdominal muscles that the veins of the thorax and the heart do. 3. We have cerebral congestion in all those diseases of the heart AA'here the function of that organ is impaired, if they are not compli- cated by other anomalies of opposite effect, and so compensated. In non-compensated valvular disease of the left ventricle, the whole amount of blood in the vessels of the brain and its membranes is not increased, it is true, since, while the veins are overfilled, the arteries are less full; but the overfilling of the veins obstructs the flow of blood from the capillaries, thus inducing capillary hyperemia, which, as we have shown, is the most important cause of the cerebral hyperemia. The affection caused by v7alvular disease of the right heart is far greater than that from valvular disease of the left heart; for, in the former case, not only is the escape of venous blood from the brain impeded, but the entire amount of blood in the skull is increased. 4. The same state of affairs occurs in extensive compression or atrophy of the vessels of the lungs as in pleuritic effusions, emphy- sema, or cirrhosis of the lungs. In these diseases also, when the right ventricle is not hypertrophied in proportion to the impediment to the circulation, the systemic circulation is overloaded at the expense of the pulmonary, and the amount of blood in the skull is increased. Since the contents of the cerebral veins and sinuses cannot pass into the overfilled jugular veins, the same excessive cyanosis occurs in the brain that is so evident in the skin, and which is almost pathognomonic of the diseases in question. The last stage of emphysema gives us an excellent opportunity of studying the gradual development, steady in- crease, and, finally, the severest symptoms of congestion of the brain. Lastly, we must mention a form of cerebral hyperemia which is neither fluxionary nor congestive, and Avhich is peculiarly important as it should be very carefully avoided by persons suffering from disease of the blood-vessels, and having a tendency to apoplexy; I mean those cases of hyperemia that appear as one SA/mptoin of temporary general plethora induced by a very free supply of food and drink. Anatomical Appearances.—On post-mortem examination, it is often difficult to decide whether the vessels of the cerebral membranes. HYPEREMIA OF THE BRAIN AND ITS MEMBRANES. 155 and still more so Avhether those of the cerebral substance, have been more than normally filled Avith blood during life. Mistakes in the account of the autopsy are frequent. The mistakes regarding the amount of blood in the cerebral mem- branes depend partly on the fact that, Avhen unaccustomed observers find the vessels much distended at the dependent parts of the surface of the brain, they diagnose a hyperemia of the cerebral membranes, even if the blood has only sunk dowmvard, and the vessels in the upper part be empty. Still more frequently another error is committed even by practised observers: that is, from a similar distention of the vessels on the convex surface of the cerebrum, hyperemia of the cerebral membranes is decided on without looking further. It should be borne in mind that the arteries supplying the cerebral membranes with blood lie at the base of the brain, and that only very fine arterial twigs reach the convexity of the greater hemispheres. All the large blood-vessels usually seen on the surface of the brain, when the skull is opened, are Aeins. Distention of these veins is a normal appearance, if the indi- vidual has died of an acute disease by Avhich his blood was not con- sumed, or, if he has died suddenly from suffocation, acute poisoning-, or from some other accident involving no loss of blood. Hence it is entirely wrong, in such cases, to decide, from the overfilling of the Aeins, that there has been hyperemia of the brain or its membranes during life, and to' connect this pretended hyperemia Avith the symp- toms that have been observed. In the history of the post mortem, accounts of excessive hyperemia of the brain and its membranes are often combined with others of a similar excessive hyperemia of the lungs, liver, kidneys, etc. If there were no mistake here, did we not have to suppose that, in the body of a previously healthy person, who had died neither from exhausting disease nor loss of blood, the normal amount of blood was often considered pathological, these accounts of post mortem Avould only convey the absurd idea that the entire amount of blood in the body was increased by poisoning, suffocation, etc. We must make it a rule to consider hyperemia of the cerebral membranes as proved only in those cases where the finest vessels also are injected, and where the overloading of the cerebral vessels is not at all in proportion to the amount of blood in other organs. The great difficulty of detecting, in the cadaver, a hyperemia of the substance of the brain, that has existed during life, depends chiefly on the fact that the first fine ramifications of the vessels supplying the brain take place in the pia mater, and that the vessels passing thence to the substance of the brain are mostly capillary (Luschka). As these can scarcely be recognized Avith the naked eye, it is customary to use the size and number of the drops of blood oozing up on a cut 156 DISEASES OF THE BRAIN. surface of the brain as a means of determining the amount of blood contained in the cerebral vessels. I do not deny that this sign has some value, particularly in judging of passive cerebral hyperemia; but I must add that the size and number of these drops of blood de- pend far more on the fluidity of the blood than on the fulness of the vessels. At all events, in cases where there can be no doubt of death having resulted from increased flow of blood to the head, or from its obstructed escape thence, on a section through the brain, its substance is often found very pale, and on its cut surface only a few small blood- drops ooze up. This circumstance, and the symptoms of paralysis occurring in the severer cases of cerebral hyperemia (of which we shall speak more fully in the next paragraph), cause it to appear to me very probable that, Avhen there is increased lateral pressure in the small arteries and veins of the brain, a transudation of serum from them into the perivascular spaces and interstices of the brain may very readily take place, and cause compression of the capillaries. It is only in yielding and distensible organs and tissues, Avhich are not enclosed by firm envelopes, that any considerable edema can coexist with a normal fulness of the capillaries. In all tissues enclosed by fascia or other firm capsule, edema causes anemia of the capillaries. If the size of the brain be not diminished by atrophy, and if the skull be closed, or, it remaining opened, if the dura mater be tense, there is no doubt that a slight transudation of serum will suffice to completely compress the capillaries of the brain. It is true, we cannot be sure, from post-mortem examination, that there is such a secondary edema; but the supposition that such is the case appears to us perfectly justi- fiable when a patient has died with the symptoms of cerebral paralysis, and if, on autopsy, we find that the very white hue of the brain-sub- stance and the slight number of small blood-points appearing on its cut surface contrast strongly Avith the distention of the large vessels in the meninges. Where the hyperemia is often repeated, atrophy of the brain and decided dilatation of the vessels result. The vessels of the meninges, which are unmistakably dilated, run a tortuous course; on section through the brain, we may distinctly see the gaping mouths of the vessels; the dilatation may even be observed in the capillaries on microscopical examination. There is plenty of serum in the sub- arachnoid spaces, the brain-substance is moist and shining. This ap- pearance, which is frequent in topers, is readily understood, if we remember that, in atrophy of the brain, the fluid contents of the skull must increase so as to fill the caAity. It is doubtful AAThether the de- velopment of the Pacchionian bodies can also be considered as a result of repeated hyperemia; they are sometimes solitary, sometimes HYPEILEMIA OF THE BRAIN AND ITS MEMBRANES. 157 grouped as whitish, opaque excrescences of the arachnoid, coming par- ticularly along the sides of the longitudinal sinus. The pressure that they exercise on the dura mater separates its filaments, so that they perforate it; by further pressure they also cause atrophy of the bone, and they are then found embedded in little fosse in the skull. Micro- scopically, they consist of connective tissue; occasionally they contain fat and chalky salts. Symptoms and Course.—Before taking up the symptomatology of hyperemia of the brain, I shall Avarn against the Avide-spread error, so injurious to the patient, of considering all cases of disturbance of function of the brain, where severe structural changes can be excluded, as due to hyperemia (or anemia). Thus, the disturbance of the cerebral functions in fever is not due to increased afflux of blood to the brain from excited action of the heart; but, as Ave have repeatedly pointed out, it depends partly on the high temperature of the blood in the cerebral vessels, partly on its abnormal quality, the " feverish state," a necessary result of the in- creased transformation of tissue during the fever. Delirium and other severe cerebral troubles are most common in the so-called asthenic fevers, just Avhere the increase of bodily temperature and the produc- tion of Avarmth attain the highest grade, AAiiile the heart's action is hastened, but weakened, and there is no fluxion to the brain. According to the observations made during the last war, as Avell as from the valuable investigations and experiments of Obernler, the symptoms of sun-stroke, or insolatio, do not, as Avas formerly sup- posed, depend on hyperemia of the brain, induced by the action of the sun's rays on the head. The symptoms of this disease consist in a paralysis of all the functions of the brain, occurring either suddenly or gradually. In the latter case the paralysis is preceded by excite- ment, delirium, and other symptoms of cerebral irritation. It has been determined that, in our zone at least, the action of the sun's hot rays is not alone sufficient to induce these severe attacks, but that they only occur when individuals are subjected to great fatigue, on a very hot day, particularly if, at the same time, they SAveat very little, be- cause they do not drink enough. We may assume that, under such circumstances, while the radiation of heat is limited on account of the high temperature of the surrounding atmosphere, while the production of heat is increased by the active muscular exercise, and the coolness induced by free perspiration is limited, there is an overheating of the body, an increase of the bodily temperature to a height incompatible with life. We have already sufficiently explained the significance of the fulness of the veins of the meninges, which is found on autopsy in cases of sun-stroke. 15S DISEASES OF THE BRAIN. Lastly, the symptoms of acute alcoholic-poisoning, as well as that from opium and other narcotics, do not depend at all, or, at any rate, depend to a very small extent, on over-fulness of the cerebral vessels, although in them the brain is hyperemic. The case appears to be different in the symptoms induced by the immoderate use of hquor for a length of time, or the continuous misuse of narcotics, a practice AA'hich has greatly increased since the introduction of subcutaneous in- jections of morphine. In such cases cerebral hyperemia plays a more important part, at least, than it does in the symptoms of intoxication and of acute opium-poisoning. Hyperemia of the brain is marked partly by symptoms of increased excitability of the nerve-filaments and ganglion-cells and by their mor- bid excitement (symptoms of irritation), partly by symptoms of dimin- ished or lost excitability of these nerve-elements (symptoms of depres- sion). Usually the symptoms of irritation precede those of depression, in other cases the former do not occur, and the latter begin from the outset. It is commonly supposed that this difference of symptoms depends on difference of pressure on the brain from the more or less distended blood-vessels, and reference is made to the analogous action of the peripheral nerves, which are also irritated by a moderate pressure and paralyzed by a stronger one. This explanation appears very suit- able as regards the symptoms of irritation. Experience shows that nerves, passing through bony canals in company with blood-vessels, are throAvn into a state of increased excitability and morbid excite- ment by overfilling of these vessels ; the nerve-elements of the brain, enclosed by the dura mater and skull, are in a like condition when the cerebral vessels are overfilled. On the other hand, the reference of the symptoms of paralysis to an increase of the " intravascular pres- sure " appears to me erroneous, for even in the severest forms of hy- peremia this pressure does not nearly approach the grade necessary to induce paralysis of a peripheral nerve. In support of the above vieAV, it has been said that paralysis is also caused by the scarcely greater " extravascular pressure " of small extravasations on the brain; but I shall hereafter sIioav that the apoplectic symptoms from cerebral hemorrhage do not depend on contusion of the brain from the extrav- asation. It is much more probable that the symptoms of depression and paralysis arise because the requisite supply of arterial, oxygenated blood to the nerve-filaments and ganglion-cells of the brain is limited or entirely stopped in excessive cerebral hyperemia. In congestive hyperemia the escape of venous blood from the brain is checked; and it is evident that, when the veins finally become filled to a certain point, no new arterial blood can enter the capillaries. It is often as- serted that the symptoms of cerebral hyperemia are very similar to or HYPEREMIA OF THE BRAIN AND ITS MEMBRANES. I59 exactly identical with those of cerebral anemia; this is true in regard to congestive hyperemia and anemia, and the explanation of the cor respondence is easy. In both cases the brain lacks its neAV supply of arterial blood. To explain the symptoms of paralysis occurring in fluxionary hyperemia also, Ave must take the hypothesis that, during its course, there is a secondary edema of the brain, as a result of Avhich Ave have capillary anemia, a condition directly opposite to the original hyperemia. The symptoms of cerebral hyperemia are ren- dered more varied by the fact that, in different cases, the irritation or paralysis is more prominent at one time in the sensory, at another in the motory, and again in psychical functions. We cannot give any satisfactory explanation of this difference. Among the symptoms of irritation in the sensory functions are headache, great sensitiveness to external impressions, and simple sub- jective impressions from the nerves of special sense. The headache, a very frequent symptom in all cerebral diseases, is very difficult to explain; we do not even know if it is of central origin (that is, if it originates in the parts of the brain where irritation causes symptoms of pain after the insensible greater hemispheres have been removed), or whether, as I think is more probable, it depends on irritation of the filaments of the trigeminus going to the dura mater. The great sen- sitiveness to impressions on the senses depends on the increase of ex- citability caused by the, cerebral hyperemia on the hyperesthesia of those portions of the brain through which peripheral irritations are perceived. The patients do not exactly feel, see, and hear more sharply than ordinarily, but they are annoyed by irritations far weaker than such as usually annoy them. Light troubles them; a slight sound, or an insignificant irritation of the nerves of touch, excites disagreeable feelings. Morbid excitation (which must not be identified Avith in- creased excitability) of the same central parts causes the dazzling be- fore the eyes, seeing sparks, roaring and buzzing in the ears, the sen- sation of formication, or of undefined pain, which are not induced by peripheral irritation. Among the motory symptoms of irritation we have restlessness, sudden starting, gnashing the teeth, crying out, Avithout the expression of pain, the automatic movement of the ex- tremities, twitching of single muscles, and lastly the general convul- sions Avhich are observed in the course of cerebral hyperemia. In re- gard to the first of these symptoms, particularly the restlessness, the constant tossing around in bed, Ave may often be doubtful Avhether it depends on increased excitability of those portions of the brain through Avhich the motor nerves and muscles are excited and motions induced,. or on morbid states of excitement in the organs affected. On the other hand, there is no doubt that the twitching of individual muscles,. 57 160 DISEASES OF THE BRAIN occurring independently of mental influences, and convulsions affecting the whole body, are the results of a morbid excitement of the cerebral motor centres. It is very remarkable that general convulsions occur- ring in cerebral hyperemia and other affections of the brain, as well as in epilepsy and eclampsia, are not accompanied by other symptoms of cerebral irritation, but, on the contrary, are constantly combined with symptoms of cerebral paralysis, especially with complete loss of consciousness. By a series of valuable experiments, Kussmaul and Tenner have shown that the same combination of general convulsions, with loss of consciousness, may be induced by artificially obstructing all the arteries supplying the brain with blood; but it is entirely un- explained, and it is enigmatical, how it happens that the same patho- logical process induces a state of the greatest excitement in some parts of the brain and paralysis in others. Until this contradiction is ex- plained, the investigations as to whether the above symptoms depend directly on the lack of oxygenated blood, or indirectly on changes oc- curring in the blood, which remains unrenovated on account of the ob- struction, are of little value. Since these attacks of convulsions are constantly accompanied by symptoms of paralysis, and since we do not believe that the latter can proceed from the pressure of the distended vessels on the nerve-elements of the brain, and, lastly, since Ave may artificially induce loss of consciousness and general convulsions by preventing the flow of arterial blood to the brain, we consider the fol- lowing decisions justifiable: The general convulsions and loss of consciousness occurring during hyperemia of the brain, Avhich are usu- ally termed epileptiform attacks, either occur because in passive hy- peremia the veins become so full that more arterial blood cannot en- ter, or because the hyperemia has induced a transudation of serum into the perivascular spaces and interstitial tissue of the brain, with consequent anemia. Among the symptoms of psychical irritation, there is first such a rapid change and loose connection between the thoughts, that clear thinking is impossible. Along Avith this confusion of ideas, the patient often has false notions about himself and the out- side world, or delirium. Delirium is sometimes so real and intense that the patient cannot distinguish it from true perceptions. This is the origin of hallucina- tions and illusions. By the former Ave understand erroneous impres- sions, AAiiich are considered as the product of direct perceptions, Avith- out there being any actually existing external object corresponding to the impression. The patients think they see animals and other ob- jects Avhich are not present, and that they hear voices Avhen all is quiet. By illusions, on the other hand, Ave understand the misappre- hension or false interpretation of external objects which really exist. HYPEREMIA OF THE BRAIN AND ITS MEMBRANES. As a result of illusion, the most harmless things may become objects of great terror to patients suffering from hyperemia of the brain, par- ticularly to children. Dizziness, Avhich is one of the most frequent symptoms of hyperemia of the brain, and of many other cerebral dis- eases, is, as a rule, a simple hallucination, since it consists in a vivid representation of a movement of the body of the patient himself, or of the bodies of surrounding objects which the patients imagine they see or feel, although they are actually at rest. We shall hereafter speak of other forms of dizziness. Closely related to the symptoms of in- creased mental excitement are sleeplessness and the disturbance of sleep by viAid dreams, symptoms which are very common in liypene- mia of the brain. Among the symptoms of depression observed in the sensibility in cerebral hyperemia, we must first mention a certain insensitiveness, a tolerance to external irritation, bright light, loud noise, etc. There is no reaction to slight irritation. On an increase of this in complete anes- thesia to complete cerebral anesthesia, the patients do not perceive even the severest irritation. The excitability of the portions of the brain through which external impressions are perceived is lost. The motor symptoms of depression are decided slowness and sluggishness in the motions of the patients; " their limbs are as heavy as lead." If this state increases, there is complete inability to make any volun- tary movement (cerebral paralysis). The excitability of the motor centres is extinguished. The psychical symptoms of depression are : loss of interest, and indifference; great sloAvness of thought, and limi- tation of the ideas; inclination to sleep, from which the patient is aroused Avith difficulty, and subsequently cannot be aroused at all. When this state is increased to the highest point, consciousness is com- pletely lost. In hyperemia of the brain there is not unfrequently, also, a devia- tion from the normal in those movements that are excited by the cere- bral nerves, independently of the will. Thus, in states of irritation the pupil is contracted, because the oculo-motor nerve is more excited; in depression it is dilated, because then the sympathetic filaments of the iris act more strongly. In the same Avay, just as, in physiological experiments, increased excitement of the vagus causes the heart to beat sloAver, Avhile in central paralysis of the vagus, as well as after its division, the heart's action is more frequent. In paralytic states of the brain, respiration is often very sIoav, deep, and stertorous. Although we cannot give an exact explanation of this symptom, we may still call attention to the fact that, after division of the vagus in animals, besides other symptoms, there is ahvays retardation of the respiration. Lastly, avc must mention vomiting as a very frequent and important 162 DISEASES OF THE BRAIN. symptom of irritation of the brain. Without understanding the pro- cess in the central organs, by Avhich the motions of vomiting are brought about, we nevertheless know that it is artificially induced in animals by dividing the vagus, and then irritating the central end. The above symptoms of morbid excitement, and of increased, diminished, or lost excitability of the brain, which we shall also meet in many other cerebral diseases, occur in the most varied groups in cerebral hyperemia. When speaking of general convulsions, we called attention to the constant coincidence of this symptom, which is due to morbid increase of excitement in the medulla oblongata, Avith loss of consciousness, which indicates loss of excitability of the other central ganglion-cells and nerve-filaments ; and we must add that, not unfre- quently we meet other complications of symptoms of irritation with those of paralysis, in hyperemia of the brain. For instance, the power of motion is occasionally lessened while the patient is under great mental excitement, complaining of headache, sparks before the eyes, etc. Hence, from the state of the pupil, the slowness or rapidity of the pulse, etc., we may recognize the state of excitement in which the central organs of the nerves governing these states are at the time, but we cannot come to any conclusion regarding the condition of other parts, or of the entire brain. The variety of appearances, resulting from the different combination of symptoms, is so great, that Andral has represented, as different forms, eight different combinations of symp- toms Avhich appear in cerebral hyperemia. We shall only give a short account of the most frequent and important forms. In many cases of hyperemia of the brain, disturbances of sensibility, of an irritating character, are the most prominent symptoms. Such patients complain of the head feeling contracted, of more or less severe headache; they are sensitive to bright light and loud noises ; have flashes of light before the eyes, and noises in the ears. They go to sleep Avith difficulty, and the sleep is disturbed by unquiet dreams. In severer cases, there are often dizziness and a feeling of formication in the extremities. The face and conjunctiva are usually reddened, the pulse full and rapid. But Ave must not consider these symptoms as constant; for, in the most dangerous cases of hyperemia of the brain, in those induced by excessive mental labor, continued night-watching, etc., the amount of blood in the external organs does not at all cor- respond to the supply in the brain; and frequently the conjunctiva is not at all injected in such patients, nor is the face flushed ; on the con- trary, it is pale. Occasionally the above symptoms only last a few minutes. In some patients a few glasses of Avine, or some hot coffee, suffice to induce these symptoms of " congestion in the head;" AA'hile they remain exempt from them if they keep quiet, and avoid excitement. HYPEREMIA OF THE BRAIN AND ITS MEMBRANES. 163 The symptoms of hyperemia of the brain in children, where the motor disturbances are usually greatest, may very much resemble those of meningitis. The two diseases are often confounded, and occasionally they can only be distinguished by their course. Such children have usually suffered from constipation for a few days, have had restless sleep, gnashed their teeth during sleep, or have been frightened out of it by dreams, which disquieted them after waking, and prevented then sleeping again. Then there were vomiting, contraction of the pupil, and twitching of some of the limbs. But these symptoms are often only preliminary to far severer ones, which cause great anxiety. They are followed by general convulsions. In rare cases, these convulsions also occur without premonition, as the first symptoms of great hyper- emia of the brain. The tAvitching usually begins in one extremity, or one half the face, and rapidly spreads over the body. Occasionally the convulsive movements alternate Avith tetanic contractions, or certain muscles, particularly those of the back of the neck, are tetanically con- tracted, while the face tAvitches, and the extremities are tossed about by clonic spasms. The children do not respond Avhen called, or AArhen the strongest irritants are applied to their skin. They are bathed in perspiration, the abdomen is puffed up, the respiration impaired; the saliva, made frothy by the movements of the masticatory muscles, Aoavs from the mouth. Occasionally there is a pause in the severity of the convulsions, and we hope the attack Avill pass off; but, after a short remission, the spasms begin again Avith their former severity, and, in severe cases, the attack may continue, with varying intensity, for many hours. In one child I saw the spasms last over twenty-four hours, with only slight occasional interruptions. Still, in the great majority of cases, the attack ends in half an hour or an hour. In spite of the terror that patients in this state cause the laity and inexperienced physicians, Ave may give a favorable prognosis, if Ave can exclude a meningitis. This can usually be done with certainty. Purulent menin- gitis is, on the Avhole, a rare disease, which, as we shall hereafter show. only exceptionally occurs in previously healthy children without pre- cedent injury of the head, or disease of the cranial bones. Tubercu- lous basilar meningitis, a far more frequent disease, often escapes ob- servation till the children have convulsions; but, if Ave inquire carefully, Ave shall find that the attack has been preceded by a long illness, and by other symptoms that have been overlooked, or at least under- valued, which we shall hereafter describe. If the child has been Avell the day before the attack, except some signs of cerebral hyperemia; if it has had no injury of the head, no otorrhea, etc., Ave may be pretty certain that it AAill be better, if not quite well, the next day. The attack is usually folloAved by a deep sleep, from which the child 164 DISEASES OF THE BRAIN. awakens fatigued, but otherwise free from threatening symptoms. In a moderately extensive practice, there is occasion every year to see cases of cerebral hyperemia in cliildren, which take the above-described very regular course. Not unfrequently several children of the same family will have these attacks at different times, or the same child may have repeated attacks. It is rare for epilepsy to develop from them; but, as we shall hereafter show, repeated hyperemias may induce hydrocephalus. In a third form of cerebral hyperemia the mental symptoms pre- dominate to such a degree that the disease is often mistaken, and, to the great injury of the patient, is sometimes considered as an attack of melancholy; at others, as mania. In the former case, after a few days of headache, disturbance of sensibility, and sleeplessness, the patients are seized with an undefined feeling of anxiety and disquiet. They cannot stay long in one place, go about restlessly, are worried, and are conscience-stricken about slight oversights. There is also delirium, which has the same character as the above-described frame of mind, and results from the attempts to explain it. At first the patients struggle against this delirium, which they occasionally recog- nize as such, and which they fear, as they think they are " out of their minds;" but they soon weary in this struggle, and give it up. In such cases the sleeplessness is almost absolute; opiates, given by ignorant physicians, have no effect, or, after the exhibition of this rem- edy, which is injurious and dangerous to the patient, there is a short, restless sleep, from which the patient awakes with all the symptoms increased. In this form of cerebral hyperemia, which develops chiefly as a result of excessive mental labor, there is usually frequent pulse and other symptoms of fever; but in these very cases a greater amount of blood in the face, etc., does not correspond to the greater amount in the brain; the patients are not high-colored, but are often even pale. From the fever and sleeplessness they rapidly lose strength, emaciate, and, if they do not fall into the right hands, they are in great danger of dying from their disease. Finally, the excitement gives way to apathy, the insomnia to deep sleep, from which the patient cannot be aroused, and in AA'hich they die. Far more rarely, there is permanent mental disease. In other persons, wiiere the psychical disturbance is in excess, it ap- pears in maniacal attacks, with corresponding delirium. This form is especially seen after a long-continued excessive use of spirituous liquors, in that class of topers who for a year will use very little liquor, but when they have begun to drink do not know Avhen to stop. This cannot be easily mistaken for an attack of delirium tremens. The patients are sleepless, run about, fight and bite if they are held, de- HYPEREMIA OF THE BRAIN AND ITS MEMBRANES. 165 stroy any thing that comes in their way, cry, laugh, or sing. There is also delirium of varying character; usually the patients consider them- selves as injured and betrayed, and rage against their enemies and persecutors. The continued muscular exertion throAVS them into a perspiration, the heart-beat and pulse are accelerated and stronger, the face is usually reddened. This form is also very dangerous if it be mistaken and improperly treated, for then an apoplectic attack, a true apoplexy, or an excessive hyperemia of the lung Avith acute edema, causes death. According to my observation, cases exactly like-the following, detailed by Andral, are by no means rare; in the Mag- deburg hospital, and in the Greifswalder clinic, I have seen several of them within a few years: " For several days a middle-aged man kept up a series of cries sufficient to disturb the Avhole hospital-ward. These cries ceased suddenly, and on approaching his bed he Avas found dead. He Avould not have died more suddenly if struck by lightning. On opening tie body, the only lesion found Avas a lively injection of the cerebral substance." Lastly, Ave must mention those forms of cerebral hyperemia A\here symptoms of general depression and paralysis appear, and by their sudden occurrence so resemble an apoplexy than an exact diagnosis is often impossible. In some cases the attack is for a' time preceded by headache, disturbance of sensibility, dizziness, sleeplessness or psychi- cal disturbances; in others, it occurs Avithout premonitory symptoms. The patient suddenly becomes dizzy; " every thing whirls around with him;" he staggers, all looks dark before him; he loses consciousness and sinks to the ground, either Avith or Avithout slight spasm. Such an attack, Avhere all activity of the brain is lost, may cause death by the paralysis extending from the brain to the centres of the organic nervous system. More frequently the patients recover consciousness after a time, with an indistinct remembrance of Avhat has passed or Avithout any recollection of it. These apoplectiform attacks, occurring in the course of hyperemia of the brain, correspond Avith the above- mentioned epileptiform attacks, as regards the cerebral anesthesia and the paralysis of the psychical functions, and like them appear to depend partly on obstructed escape of the venous blood, partly on secondary edema of the brain. As we have preAiously shoAvn, both states prevent the supply of oxygenated arterial blood, which is indis- pensable for the excitability of the brain and the entire nervous sys- tem. Traube, Avho refers the epileptiform attacks in Bright's disease also to edema of the brain, has advanced the theory that an edema, limited to the greater hemispheres, induces simple loss of conscious.-. ness; when it affects both the hemispheres and medulla oblongata there are loss-of consciousness and convulsions. We shall not discuss 166 DISEASES OF THE BRAIN. the correctness of this hypothesis; it has something seducing about it, but opposed to it is the fact that, if it be true, the same pathological change (compression of the capillaries by serous exudation) has a par- alyzing effect on the greater hemispheres and an irritant effect on the medulla oblongata. Treatment.—Although, in the treatment of hyperemia of the brain, general and local blood-letting, cold to the head, and derivation to the skin and bowels justly enjoy a good reputation, we must not use one or the other indifferently, or employ all at the same time, in any case that arises. In fact, there is no disease where it is more im- portant to fulfil the causal indications, and to attend to the causes of the disease when prescribing the remedies required by the indications. In those forms where increased action of the heart and a coincident diminution of resistance in the vessels of the brain have induced fluxion to that organ, the same regimen must be observed as was recom- mended in the first volume, in the treatment of habitual fluxions to the lungs. If danger threatens, we should bleed; in such cases venesec- tion cannot be replaced by ice-compresses to the head, or by leeching behind the ears. If there be collateral fluxion to the brain, we must first of all attempt to remove the obstructions to the circulation by which the pressure of blood in the carotids is increased. Evacuating the intes- tines, by laxatives or by enemata of Avater and vinegar, often has a marvellous effect, AAThich is induced by nothing else, both in adults who are constipated and suffering from headache, tinnitus, dizziness, etc., and especially in children Avhere constipation is accompanied by con- vulsions, etc. If these remedies are insufficient and symptoms of de- pression occur, from which we fear danger, it is proper to draAV blood here also, in adults by venesection, in children by leeches to the head. The treatment must be quite different when the cerebral hyper- emia has resulted from the continued misuse of alcohol or of narcotics, or from excessive mental excitement. In such cases nothing is to be expected from general bleeding, and large venesections are often in- jurious ; on the other hand, the indications are, to apply a bladder of ice to the head, or else moist compresses, that have laid under a tin vessel filled Avith ice and salt, till they were frozen. In some cases of this variety derivatives are good; by these we attempt to remove the fluxion from the brain by inducing fluxion to the skin, intestines, geni- tals, or rectum. The most common remedies used with this object are irritant foot-baths, among which those of ice-water, in which the patient only passes a short time, are better than those of hot water, Avith mus- tard or salt, and wood-ashes. In acute cases, blisters to the nape of the neck, and in chronic ones the establishment of an issue in the arm— PARTIAL HYPEREMIA AND ffiDEMA OF THE BRAIN. an old remedy, from Avhich I have seen great benefit—and, lastly, the administration of active purges, are also among the more common remedies. In acute threatening hyperemia of the brain, croton-oil is peculiarly in repute, while, in chronic cases, pills of aloes, colocynth, jalap, etc., are usually prescribed. If, as occasionally happens, there be fluxion to the brain, instead of to the pehis, at the menstrual period, Ave may apply leeches to the cervix of the uterus, or cups to the inside of the thighs. Occasionally, also, the application of leeches about the anus lias a Avonderful effect, as is shown by the well-knoAvn histories of the patients that Goethe so much ridicules under the name of " proktophantasmisten." In congestive hyperemia resulting from compression of the jugular veins or vena cava, as well as in that occurring from heart and lung diseases, venesection or leeches behind the ears may be employed, if the obstruction to the flow of blood cannot be removed. We have shown that congestion, by arresting the supply of arterial blood to the brain, diminishes or removes the excitability of the brain filaments and ganglia. The greater freedom of escape Ave give the venous blood, the sooner we shall succeed in removing the symptoms of depression and the paralysis. This may be done by the application of leeches behind the ears, since this moderates the tension in the veins outside of the skull, Avith which the emissaria Santorini communicate; or by Aenesection, by which the tension in the anonymous veins is dimin- ished, because less blood enters them from the arm. In such cases Ave cannot expect any thing from the employment of cold, or from laxatives and blisters. In hyperemia of the brain resulting from too much nourishment, instant diminution of the quantity of blood may be urgently indicated, and a well-timed venesection not unfrequently prevents a threatening apoplexy. It is very important to regulate the mode of life of such patients, to shoAV them the danger of prolonged, luxurious meals, and to let them eat little, drink Avater instead of Avine, and Avalk a great deal. Of course, in each case, peculiar circumstances will require some deviation from the plans of treatment advised, and different directions as to regimen. CHAPTER II. PARTIAL HYPEREMIA AND PARTIAL (EDEMA OF THE BRAIN. A short consideration of partial hyperemia of the brain Avill de cidedly facilitate the comprehension of the symptoms of diseases of the brain limited to circumscribed spots. 16S DISEASES OF THE BRAIN. The causes of the partial hyperemia are to be sought for within the skull. Fluxions and congestions result from extravasations of blood, points of softening and inflammation, tumors, and all other dis- eases of the brain that affect the circulation at circumscribed spots. If an artery or a great number of capillaries be compressed, or other- Avise closed, there is fluxion in the collateral branches; if, on the other hand, a vein be contracted or closed, there is congestion in the capil- laries supplying it. Of course, there will usually be fluxion at one place, congestion at another, and anemia at still others, at the same time. But the circumscribed diseases of the brain not only induce hyperemia by compression of the vessels, but most of them also excite it by irritation of the surrounding parenchyma. Just as we see hyper- emia and edema result in the vicinity of tumors, inflammations, ex- travasations of blood, etc., in all other parts of the body, so they also develop in the brain when it is the seat of these diseases. On autopsy, it is just as difficult to discover a partial hyperemia of the brain as it is to make out a general hyperemia, particularly if the hyperemia has led to edema, without the edema having softened the brain-substance. In some cases, however, in the vicinity of tumors, points of inflammation, etc., Ave see clearly that the parenchyma is more infiltrated and relaxed, or that there have been small extravasa- tions from the vessels. The symptoms of partial hyperemia of the brain are those of irri- tation and depression, but they are much more limited than the symp- toms of general hyperemia of the brain, and come under the head of so-called local symptoms (" Herdsymptome," Grieslnger). Among these are circumscribed headache, glimmering or sparks before one eye, or blindness of one eye, contraction or dilatation of one pupil, noise or deafness in one ear, neuralgia or anesthesia limited to one nerve, but especially spasms, contractions, or paralysis, affecting only one-half of the body, one extremity, or a single group of muscles, and, lastly, partial disturbance of the mind. The grade and extent of the partial hyperemia of the brain vary Avith the greater or less amount of blood contained in the organ, and AAith the phases and stages of development of the point of disease that they surround. This explains why the local symptoms depending on partial hyperemia of the brain are sometimes more prominent than at others, or may even disappear and return again. Since, in all severe structural disease of the brain, there is complete loss of function of the affected part, Avhether the trouble there be the development of a tumor, or that the nerve-filaments and ganglion-cells have been broken down or destroyed by an extravasation of blood, the only symptoms that we can consider as immediately due to severe local disease of the brain AN.EMIA OF THE BRAIN AND ITS MEMBRANES. 169 are partial anesthesia, partial paralysis, and the loss of certain menta] functions. If, in the course of an apoplexy, of an abscess of the brain, or of a cerebral tumor, etc., Ave have symptoms of partial irritation, as Avell as those of partial paralysis, the former cannot possibly depend on the disease itself, but must be due to the anomalies of circulation in its vicinity. Moreover, all temporary symptoms of paralysis occurring in the course of local destructive diseases do not depend on the disease itself, but mostly on the disturbances of circulation around it. (When speaking of diseases encroaching on the space in the skull, Ave shall shoAV that temporary paralysis may also result in other ways.) The fact that in apoplexies, tumors, abscesses, etc., where complete or even partial restitutio ad integrum is not conceivable, paralysis not unfrequently decreases or entirely disappears, seems at first difficult to explain, but the explanation is simple when we bear in mind that the symptoms of paralysis may depend on a collateral edema in the vi- cinity of the disease, and that the extent of this edema varies greatly. Lastly, the most varied diseases of the brain would induce the same symptoms, if they had similar locations and extent, if the dis- turbances of circulation in the vicinity of the different diseases did not vary. But the disturbances of circulation in the vicinity of a tumor are different from those in the vicinity of an abscess, and these again differ from those about a portion of brain broken doAvn by an extrava- sation of blood. This, to some degree, explains the difference of symptoms in different diseases of the brain that have the same seat and extent. The treatment of partial hyperemia is to be conducted on the same plan as that for general hyperemia of the brain. If Ave lessen the supply of blood, or facilitate its escape, we moderate the local fluxion or congestion. CHAPTER III. ANAEMIA OF THE BRAIN AND ITS MEMBRANES. Etiology.—For a time the possibility of anemia of the brain Avas denied, just as that of hyperemia Avas, and on the same grounds which were given in the first chapter. We haAe aheady called attention to the errors in these conclusions, and shall only mention here that, inde- pendently of the numerous autopsies where the brain has been found anemic, Donders, Kussmaul and Tenner have observed excessive anemia through an opening (covered by a glass plate) in the skull of living animals. The causes of anemia of the brain are— LTO DISEASES OF THE BRAIN. 1. Those that diminish the entire amount of blood in the organ Among these belong not only abstractions of blood and spontaneous hemorrhages, but extensive losses of fluid, considerable exudations, and tedious, particularly feverish, diseases. Unfortunately, it occasion- ally happens that, in internal hemorrhage, anemia of the brain is mis- taken for hyperemia, and treated accordingly. The form of the dis- ease which, since the time of Marshall Hall, has been known as hy- drocephaloid, is particularly common in children who have suffered from continued diarrhea. Typical examples of this are not unfre- quently seen as a result of extensive hepatization in weak persons with pneumonia. But protracted fevers also consume the flesh and blood of the patient, induce general poverty of the blood, and, as one symptom of it, anemia of the brain. In all of these diseases, blood and the fluids of the body are lost or used up too rapidly; on the other hand, the amount of blood may be diminished by its formation being limited from insufficient supply of nourishment. Thus, in per- sons wiio have died of starvation, the most marked symptoms of ane- mia of the brain have been observed before death (as Gerstenberg has described in his " Ugolino," in very vivid terms, it is true, but still quite accurately). 2. This affection not unfrequently results from the overloading of other organs with blood. The best example of this form are the cases where it is induced by the application of Junod's cupping-boot, by the injudicious use of which the anemia may readily become dangerous. This also explains Avhy, when the heart's action is weak, a person faints more readily when standing up than Avhen lying down. It is evident that, in the upright position, the lower extremities will become overloaded with blood, if the propelling power is insufficient to over- come the obstruction caused by the weight of the venous blood in this long course. On the other hand, in diminished action of the heart, the obstruction from the weight of blood in the short carotid artery must have a very inferior influence on the occurrence of anemia of the brain in the upright position. 3. Another cause is compression or obstruction of the arteries sup- plying the brain. In almost all of the cases of this class that have been reported, the obstruction Avas artificially caused by ligation of the carotid. In a few cases only the carotid or vertebral arteries were compressed by tumors or closed by emboli. 4. Cases where, from mental excitement, without lessening of the heart's action, there are paleness of the cheeks and even loss of con- sciousness and other symptoms of insufficient supply of blood to the brain, seem to indicate that anemia of the brain may also be caused by abnormal innervation or spasmodic contraction of the arteries. AN.EMIA OF THE BRAIN AND ITS MEMBRANES. 171 5. Anemia of the brain is the necessary result of diminution of the space in the skull by exudations, extravasations, or tumors of the brain and its membranes. Under this form would come a variety which does not belong in our domain, that is, the cases of anemia which necessarily result from depressed fractures of the skull. We lay pe- culiar stress on the anemia of the brain resulting from encroachment on the cranial cavity, which is the most frequent form of the disease, because we believe that the so-called symptoms of pressure in apo- plexy, tumors, the various forms of hydrocephalus, and other diseases encroaching on the intercranial space, are not immediately referable to the pressure on the brain-substance, but to the consequent anemia. Other observers also, among them Traube and Ley den, have recently come to my conclusion. Since it is not merely the presence of blood in the vessels of the brain, but the supply of oxygenated arterial blood that is indispensa- ble for the normal functions of the organ, it is evident that, even Avhere the absolute amount of blood in the brain is not diminished, but Avhere its circulation and distribution are changed so that only a small amount of blood enters through the arteries, and but little es- capes through the veins, the same symptoms must arise as in true anemia. And the experiments of Kussmaul and Tenner entirely con- firm the experience of pathologists, that, in degeneration of the heart from non-compensated valvular obstruction, and in other diseases im- pairing its action, there is an overloading of the veins at the expense of the arteries, and a retardation of the circulation, that is, the same symptoms that occur in anemia of the brain. Lastly, Ave must mention that, without a diminution of the amount of blood in the brain, and Avhere that fluid is normally distributed in the arteries and veins, symptoms very similar to those of anemia may result from the blood being too poor in red corpuscles. This symptom also is readily explained, for we are fully justified in considering the red corpuscles as the " bearers of oxygen." Noav, if this be so, a dim- inution of red corpuscles Avill affect the supply of oxygen to the brain, just as a diminution of the blood would. Anatomical Appearances.—The substance of the brain is dis- colored ; the gray substance appears paler and more resembles the Avhite. The latter is very milky and shining. On section, few if any blood-points are seen on the cut surface. The vessels of the cerebral membranes are empty and collapsed. We do not ahvays find a con- siderable amount of fluid in the subarachnoid space. Kussmaul and Tenner could not prove, on examination, any increase in the cerebro- spinal fluid which, on theoretical grounds, they had expected to find. Symptoms and Course.—The symptoms of anemia of the brain 172 DISEASES OF THE BRAIN. that comes on suddenly, and quickly attains a high grade, differ from those due to one which comes on slowly and is less severe. In the former case the patients become dizzy; every thing appears dark be- fore them; they become insensible to impressions and incapable of movement; their pupils dilate, their respiration becomes sIoav, and they lose consciousness; they sink to the ground, usually with slight spasms. In most cases the patients come out of this fainting-fit in a short time; in other cases, usually termed apoplexia nervosa, con- sciousness does not return, the swoon ends in death. Anemia of the brain artificially induced in animals by free bleeding, or by ligation of all the arteries supplying the brain, has just the same symptoms; only the convulsions are usually more severe and more prominent than in persons Avhose brain has suddenly become anemic. The symptoms of paralysis in sudden, extensive hyperemia of the brain are more easily explained than are the convulsions. The former unmistakably depend on the arrested supply of oxygen to the brain. It is known that liga- tion of the abdominal aorta immediately induces paralysis of the lower half of the body, whose nerves are thus deprived of arterial blood. But how shall we explain the convulsions? Henle thinks that in anemia of the brain the blood from the venous plexuses of the spinal marrow and the cerebro-spinal fluid from the spinal canal press toAvard the brain, and that the medulla oblongata and parts at the base of the brain are thus thrown into a state of excitement. But Kussmaul and Tenner, after ligating the afferent vessels, found not only the greater hemispheres, but also the medulla oblongata, bloodless; hence the convulsions cannot be referred to congestion of the medulla. But it is just as remarkable, and as contrary to all experience, to suppose that there should be increased excitement of the nerve-filaments and ganglion-cells, Avith consequent convulsions, from absolute anemia. Kussmaul and Tenner distinctly state that, on autopsy of animals Avhose cerebral arteries had been ligated, the arteries at the base of the brain contained a " slight amount of blood," while all others were found " entirely empty;" this observation gives a small point on which to hang an explanation. For we might suppose that the liga- tion of those vessels caused absolute anemia in the greater hemi- spheres and their consequent paralysis, but (from the anastomosis of the cerebral and spinal arteries) in the parts at the base of the brain it only induced oligemia and consequent morbid excitement. In anemia of the brain that comes on slowly, just as in hyperemia, at first there are usually symptoms of irritation, subsequently those of paralysis. To explain this correspondence, the hypothesis has been advanced that a certain tension of the molecules of the brain is neces- sary for its normal activity, and that an increase or diminution of this AN.EMIA OF THE BRAIN AND ITS MEMBRANES. 173 tension, by too great or too slight a fulness of the vessels, modifies the excitability of the brain in the same way. I haAe already said that this is a hypothesis, and, I may add, that it is difficult for me to beheve that, in anemia of the brain, the symptoms of irritation depend on an inconsiderable, and those of paralysis on a decided, diminution of the normal pressure of the blood-vessels on the brain. On the other hand, it is a physiological fact that the excitability of a nerve is in- creased a short time before it is entirely lost, and that the greatly- increased excitability of a nerve is not a sign of increased normal nu- trition, but, on the contrary, of its diminution. It is true we do not know why this is, but the knowledge that it is so renders it less strange that, in gradually-developing anemia of the brain, symptoms of irritation should, as a rule, precede those of parah/sis, and that, Avhere the anemia does not attain a high grade, only the symptoms of irritation should be seen. Occasionally the symptoms of anemia consist chiefly or exclusively of disturbances of sensibility. The patients complain of severe head- ache, either in the forehead or occiput; they are sensitive to light and sound, have flashes before the eyes, noises in the ears, dizziness, etc. These symptoms occur most typically after severe metrorrhagia and other extensive losses of blood, and frequently only the consideration of the cause, the pulse, color of the skin and lips, and the symptoms of want of blood in other organs, enable us to decide that there is ane- mia, and not hyperemia, of the brain. In other cases of anemia of the brain, particularly in cliildren, the motor disturbances are more prominent. The symptoms of anemia of the brain in children from exhausting diarrhea and other debilitat- ing causes, so-called hydrocephaloid, often so closely resemble those of acute hydrocephalus, that the distinction of the tAvo states may be very difficult. Marshall Hall divides hydrocephaloid into two stages, one of irritation, one of torpor. In the first stage the children are very restless and capricious, constantly toss about in bed; readily fright- ened, they cry out in their sleep, gnash their teeth; the face is usually flushed, the pulse frequent, and temperature elevated. There is al- most always slight twitching of some limbs, frequently also there are general convulsions. In the second stage the children collapse, be- come entirely apathetic, no longer attend to objects held before them; the eyelids are half closed, the pupils insensible to light; respiration becomes irregular and rattling; finally death occurs Avith symptoms of coma. Since Ave regard the so-called symptoms of pressure in diseases of the brain and its membranes (among which are effusions into the ventricles), wliich encroach on the cranial cavity, as due to compres- sion of the capillaries and obstruction of the supply of arterial blood 174 DISEASES OF THE BRAIN. to the nerve-elements of the brain, we do not consider the great simi- larity of the symptoms of hydrocephalus to those of hydrocephaloid as very strange. Different as are the modes of origin of the two dis- eases, we believe that in both of them there is ultimately the same pathological disturbance, that is, capillary anemia. Lastly, in anemia of the brain, morbid symptoms in the mental functions preponderate; there are sleeplessness, great excitement, deliri- um, etc. In some cases this state increases to paroxysms of frenzy and decided maniacal attacks. The latter are seen in persons Avho have had no food or drink for a long time, but they are also not unfrequently seen in weakly, bloodless patients, if their anemia has been greatly increased by exhausting diseases, and abstractions of blood. Treatment.—If the anemia of the brain be one symptom of gen- eral impoverishment of the blood, this is to be treated by limiting the consumption and increasing the supply of suitable nourishment. A consideration of the etiology and other circumstances of each case gives the indications for treatment. If profound and continued faintness, convulsions, and other signs of excessive hyperemia of the brain come on after extensive loss of blood, even transfusion may be necessary. In treating the exhausting diarrhea of infants, we should think early of the danger of hydrocephaloid, and attempt to prevent it by giving raw flesh, wine, etc. If, nevertheless, the symptoms above described come on, a false interpretation of them is very dangerous. If the practitioner be misled into applying leeches or employing debilitating treatment, the children usually die. But if he sees through the con- dition and, in spite of the restlessness, twitching, and consequent sopor, gives concentrated broths and large doses of stimulants, cam- phor, ether, but especially of strong wine, he often attains the hap- piest and most surprising results. In the form of anemia of the brain Avhich occurs as one symptom of general impoverishment of the blood, it is also very important that, until the normal quantity and quality of the blood is reestablished, Ave see that the heart does not receive too little blood; and it is just as important for us to combat any tempo- rary weakness of the heart, that prevents it driving its blood energet- ically into the arteries. Very many patients, with impoverished blood, and convalescents die, solely because the physician has neglected to give them the strictest orders to maintain a horizontal position. If we permit exhausted patients to rise to stool, or to leave the bed too soon, the feet are readily overloaded with blood, the heart receives too little; consequently a sufficient supply does not go to the brain; the patient swoons, and not unfrequently does not aAvake from the fainting- fit. On this very point I have had an experience in my private prac- tice which will ahvays prove a warning to me, not to permit convales- PARTIAL AN.EMIA OF THE BRAIN. 175 cents to leave their beds too early. To prevent the second danger from temporary lessening of the heart's action in anemic patients, besides the horizontal position, Ave may order irritating remedies both by in- halation and internally. The patients should not use these remedies constantly, but only occasionally when they feel an attack threatening. Indeed, it may be important to have Cologne-water or Hoffman's ano- dyne instantly at hand on such an occasion. Trephining is occasion- ally the only remedy for anemia caused by encroachment on the cra- nial cavity ; however, in recent times this is very properly limited to those contractions of the space caused by depression of the cranial bones. Paradoxical as it may seem on superficial observation, we must, nevertheless, say that a venesection often has the best effect on the course of anemia of the brain due to a contraction of the intracranial cavity. We shall give the reasons for this assertion more fully when speaking of apoplexy, and shall only say here, that a venesection hastens the escape of venous blood from the brain, and thus facilitates the entrance of arterial blood. CHAPTER IV. partial anaemia and partial necrosis of the brain, THROMBOSIS AND EMBOLISM OF THE CEREBRAL ARTERIES—SOFTENING. Etiology.—Partial anemia of the brain occurs—1. When the access of blood to certain sections of that organ is prevented by closure of the afferent a essels. 2. When collateral edema develops in the vicinity of apoplexies, of points of inflammation, and softening, and of tumors, etc. 3. When the capillaries of certain sections of the brain are compressed by extravasation of blood, by tumors, or other diseases contracting the cranial caAity. In regard to the pathogeny of the first form of partial anemia of the brain, Avhich develops in the parts supplied by obstructed arteries, Ave must call attention to the following points: In rabbits, the symptoms of anemia of the brain do not occur till both carotids and both vertebral arteries have been ligated. If all these vessels be not ligated, those that have been left free supply plenty of blood, and the free anastomosis of .the cerebral arteries among themselves prevents anemia even of those parts which draw their blood chiefly from the vessels ligated. In the human being it is someAvhat different; here, after ligation of one carotid, there is occasion- ally a symptom Avhich certainly depends on anemia of one side of the brain, that is, paralysis of the half of the body on the opposite side. In other cases of ligation of the carotid in man, this symptom does not 58 -j^g DISEASES OF THE BRAIN. arise, which proves that in these cases the endangered hemisphere receives a sufficient amount of blood from collateral branches, particu- larly through the circle of Willis. The reason for this difference is not fully known. Hasse thinks that in the former case the continua- tion of the thrombus from the point of ligation beyond the circle of Willis prevents the formation of a collateral circulation. On closure of the internal carotid or of the vertebral artery on one or both sides, partial anemia does not generally occur, since a collateral circulation is usually quickly established through the circle of Willis. On the other hand, closure of an artery originating above the circle of Willis, e. g., the arteria fosse Sylvii, almost always induces anemia of the part'supplied by the obstructed vessel, since here circumstances are much more unfavorable for the formation of a collateral circulation. The pathological processes that chiefly induce closure of the arte- ries of the brain are in some cases compression by tumors, but in most cases obstruction by thrombosis formed at the spot or by emboli from some other part. It is only exceptionally that the blood coagulates in cerebral ar- teries whose walls are healthy (marasmic thrombosis). As a rule, the thromboses form at points where, as a result of chronic endarteritis, or, as is usually said, of atheromatous degeneration, the calibre of one of the vessels of the brain is diminished and its inner wall roughened. The emboli by which cerebral vessels are closed are almost always detached clots of fibrin, that have been deposited, in endocarditis or valvular disease, on rough parts of the valves, or else portions of the valves themselves, that have been Avashed off by the current of the blood. These rarely come from necrotic points in the lungs, or from thromboses of the pulmonary vein. In one very instructive case, pub- lished by Esmarch, an embolus obstructing the internal carotid came from an aneurism of the carotid, having been set free by the manipu- lations during an examination. We have but little to add in regard to the etiology of this form of anemia of the brain. Since the atheromatous affection, which most frequently causes thrombosis of the cerebral vessels, generally occurs in advanced age, the stoppage of the arteries of the brain by thromboses is almost exclusively seen in aged persons, and plays an important part in the diseases of .old age. The case is different with embolism of the cerebral arteries; this is seen in young persons also, since en- docarditis and \Talvular disease of the heart occur at all ages. The pathogeny of the partial necrosis, which results in many cases of thrombosis and embolism of the cerebral arteries, is perfectly evi- dent. This form of softening of the brain is analogous to the gangrene of the extremities induced by closure of the vessels. In both cases PARTIAL AN.EMIA OF THE BRAIN. 177 the death of the tissue is due to abstraction of the supply of nutritive material; but the necrosed parts within the skull, not being exposed to the action of the atmosphere, are rarely decomposed. This only happens when the embolus, that has stopped the vessel, comes from a suppurating spot, and transfers Avith it a tendency to suppuration. Closure of a Aessel induces necrosis more readily the later and more incompletely a collateral circulation is established. If the degenera- tion of the walls of the vessels that has induced a thrombosis of the cerebral arteries be extensive, the collateral branches, the elasticity of Avhose walls is diminished, cannot dilate sufficiently to supply the place of any large arteries that may be closed, hence the partial anae- mia is only partly removed, and the anemic part softens. Whether or not closure of a cerebral artery by an embolus shall induce necrotic softening depends chiefly on the seat of the obstruction, since in such cases the walls of the vessels are usually healthy and distensible. If, as rarely happens, there be anemia in the parts chiefly supplied by a vessel which has been obstructed by an embolus before reaching the circle of Willis, it Avill generally pass off soon, and no necrosis results ; if, on the other hand, a vessel be closed by an embolus beyond the circle of Willis, necrosis is the usual termination of the partial ane- mia. The second form of partial anemia of the brain, due to develop- ment of collateral edema around an apoplexy, or a point of inflam- mation or softening, or a tumor, etc., has already been mentioned as the not unfrequent termination of excessive fluxionary hyperemia. When speaking of the different diseases of the brain, Ave shall fre- quently recur to this form. The third division that Ave have made of partial hyperemia of the brain, resulting from compression of the capillaries in certain sections of the brain by extravasations of blood, tumors, and other diseases contracting the space in the skull, has hitherto been too little appre- ciated. Along Avith the best authorities, I myself denied the occur- rence of " partial cerebral pressure." From the fact that the brain is incompressible and is enclosed by an inelastic capsule, I reasoned that an increased pressure, acting on any part of the brain, Avould spread evenly over the entire organ. In support of this vieAv, I ad- vanced the popular illustration that, if a cork be driven forcibly into a bottle, the latter is not by any means ahvays broken at the neck, but just as often at some distance from the point where the force was ap- plied, perhaps at some particularly weak part. HoAvever, a series of observations where there Avas no doubt that those portions of the brain Avhere the disease was located were far more bloodless than the rest of the brain, and a careful consideration of all circumstances af- 178 DISEASES OF THE BRAIN. fecting the space in the skull, have shown me that, in the above rea soning, I overlooked an important fact and hence came to a false conclu sion. Indeed, in spite of the brain being incompressible, and being surrounded by an unyielding capsule, partial pressure .on it may occur; this is so, because the cranial cavity is divided into three chambers by two tensely-stretched membranes, because the falx and tentorium pro- tect, to some extent at least, parts of the brain lying on one side of them from pressure acting on the other side. The three chambers of the skull communicate with one another, it is true, and, if the cerebral substance Avere liquid, pressure on any part of it Avould affect the whole organ equally, in spite of the tense septa traversing it. But the consistence and tenacity of the cerebral sub- stance, which only permit a slight protrusion of a section of brain pressed from an opposite chamber of the skull toAvard the excavation of the tentorium or the lower border of the falx, cause portions of the brain lying in one chamber to be protected to some extent from pressure on those lying in one of the other chambers, in spite of the openings in the septa, particularly the large opening in the falx. The protection afforded by the tentorium is greater than that given by the falx, and the posterior lobes of the cerebral hemispheres are far better protected against a pressure acting on the opposite hemisphere than the frontal lobes are, because the falx is much broader posteriorly, and hangs much farther down than it does anteriorly. In subsequent chap- ters Ave shall frequently refer to these circumstances also, whose great significance in the explanation of the symptoms of disease encroaching on the cranial cavity I Avas, to the best of my knowledge, the first to point out. Anatomical Appearances.—Partial anemia of the brain cannot by any means always be definitely made out in the dead body. The distribution of blood after death and during life is not the same; places which, during life, were distinguished by their vascularity from other less vascular parts, often become just as bloodless as the latter after death. In the cutis, where we have an opportunity for compari- son, we may see this daily; in the brain the state of affairs is just the same. It is remarkable that emboli are almost ahvays found in the left arteria fosse Sylvii. Perhaps this is partly because the left carotid ar- tery leaves the arch of the aorta almost in the direction of the current of blood, while the innominate forms a considerable angle with it (Buhle). The necrosis resulting from obstruction of the vessels and insuffi- cient development of collateral circulation induces relaxation and soft- ening of the brain-substance; hence necrosis caused by anemia is designated as a peculiar form of softening of the brain, as " simple " or " yelloAv " softening. Corresponding to the most frequent and obsti- PARTIAL AN.EMIA OF THE BRAIN. 179 nate obstructions of the vessels, the softening is usually in the greatei hemispheres and chiefly in their medullary substance. It varies in size from that of a bean to a hen's egg. The grade of the softening differs. In the highest grades the cerebral substance, at the point of necrosis, is found changed to a moist, gelatinous trembhng pulp. The color of the softened point is sometimes white or grayish-white, some- times more yellowish. In the former case there is usually a reddish tint about the periphery, due partly to dilatation, partly to rupture of the capillaries and escape of blood from them. In the first of the three forms of partial anemia Avhich Ave have described, that due to thrombosis or embolism of a cerebral artery, on autopsy we do not find the parts supplied by the plugged artery remarkably pale, but they are not unfrequently studded Avith small capillary hemorrhages, par- ticularly at the periphery. This exactly corresponds Avith Avhat is found in other organs when there is stoppage of the vessels by throm- ses or emboli; but, as Ave said when speaking of hemorrhagic infarc- tions of the lung, it is difficult to explain. On account of the difficulty of deciding whether a portion of brain has been anemic during life, we should make it a rule to seek most carefully for any obstruction of the cerebral arteries, particularly of the arteria fosse Sylvii, in any cases Avhere the patient has died from a chronic brain disease or from an acute one beginning with a sudden occurrence of hemiplegia, unless the autopsy gives some other satisfactory explanation of the symp- toms. Before attention Avas called to the occurrence of this anomaly, autopsy, in cases of severe brain-disease Avith hemiplegia, often fur- nished nothing satisfactory. There was nothing left but to suspect an " intravascular apoplexy," which did not at all explain the occurrence of the hemiplegia. The yelloAV color of the affected part often de- pends on this capillary hemorrhage, and is due to the infiltration of the disintegrated brain-substance Avith escaped and altered coloring matter of the blood. After the disease has existed some time, Ave find the affected part changed to a cellular network filled with a chalky, milky fluid (Durand-FardcPs infiltration celluleuse). On microscopical examination of necrosed portions of brain, Ave usually find only remains of nerve-filaments, -granular cells, which correspond to the ganglion-cells or neuroglia-nuclei that have undergone fatty degeneration, coloring matter, and masses of detritus. Partial anemia of the brain caused by collateral edema, occurring in the vicinity of chcumscribed disease, can occasionally be recognized on autopsy by the affected part having a peculiar moist lustre and di- minished resistance, as Avell as by its becoming very slightly promi- nent on a section through the brain. When the disease is more se- vere, the brain-substance is still more relaxed, and finally a state maj 180 DISEASES OF THE BRAIN. occur Avhich is usually designated as Avhite (hydrocephalic) softening. Small capillary extravasations are often found in the vicinity of tu mors, abscesses, or along with collateral edema. The form of partial anemia of the brain, induced by diseases en- croaching on the cranial cavity, is the variety most readily recognized on autopsy. The pressure exercised by large extravasations of blood and extensive tumors is so great that, not only the capillaries and finer arteries and veins of the brain-substance, but also the larger vessels of the meninges, that are subjected to this pressure, are compressed and bloodless. If the disease be in one of the large hemispheres, this be- comes more prominent after the skull is opened, so that on the affect- ed side the dura mater appears more tense than on the other side. If the dura mater be opened and turned back, we see that the surface of the diseased hemisphere is remarkably even, that there is very little, if any, liquid in the subarachnoid space, that the convolutions are loAver, the furrows shallower, and that the vessels of the pia mater are not so full or are quite empty. Lastly, also, on section through the brain, we cannot fail to see a decided difference in the two hemi- spheres in regard to their color and as to the number of blood-points appearing on the cut surface. In those cases where the falx and tentorium have to a certain extent given way to the pressure propa- gated to them, the falx showing a convexity toward the healthy side, the tentorium being flattened, or, when the disease is in the posterior cranial fossa, being more strongly curved, it is certain that the capil- laries are compressed in those portions of the brain where the disease encroaching on the space is located. But at the same time it is found that the anemia does not remain limited to the part first affected, but extends to other parts subsequently, although to a less extent. Symptoms and Course.—Anemia limited to one portion of the brain induces the so-called " herdsymptome " (page 168) ; if the ane- mia be absolute, these consist of symptoms due to complete loss of excitability in the anemic portions of the brain; if it be not absolute, there may even be signs of increased excitability, or morbid excite- ment of the affected portion of the brain. In the vicinity of the anemia, often even through the entire brain, the circulation is dis- turbed, so that, besides the direct symptoms of partial anemia, we may have those of more or less extensive secondary disturbances of circulation. However, neither the " herdsymptome," nor the symptoms of secondary disturbance of the circulation in the brain, nor a combina- tion of the two, are pathognomonic of partial anemia of the brain; on the contrary, we must distinctly state that each of these also occurs in many other diseases of the brain. Not unfrequently, we can recog- nize one or other form of partial anemia of the brain, and exclude PARTIAL ANJ5MIA OF THE BRAIN. Igl other local diseases there, by basing our diagnosis on the etiological conditions, the sequence of the symptoms, the existence of symptoms corresponding to the peculiar frequence of certain forms of disease in certain sections of the brain, as well as on the course of the disease. We shall first describe the symptoms of the occurrence and course of partial anaemia of the brain due to obstruction of the vessels, and shoAV hoAV it is often possible to diagnose this form of partial anemia Avith probability or with certainty by attending to the inducing causes. However, the etiology of thrombosis of the cerebral vessels differs from that of emlxflism, and the other factors also, which might be of aid in diagnosis, are not exactly the same in thrombosis and embolism of the cerebral arteries; hence Ave shall speak of them separately. Since thrombosis of the cerebral vessels most frequently depends ultimately on atheromatous degeneration of the vascular Avails, and as this occurs chiefly in old age, we are more apt to suspect thrombosis, and consequent softening of the brain, in an old, decrepit person, who has the symptoms of severe brain-trouble, than in a young, vigorous one, having the same symptoms. If the peripheral arteries be rigid and tortuous, there is still greater presumption that the arteries of the brain are also degenerated, and that the brain-symptoms are due to this degeneration. However, the condition of tie peripheral arteries does not furnish any certain proof of that of the cerebral arteries. In many cases the degeneration is confined to the latter; in other, rarer cases, while the peripheral arteries are extensively degenerated, the cerebral arteries remain free. Moreover, partial anemia of the brain, and softening of the brain due to necrosis of the anemic portion, is not the only brain-disease caused by atheromatous degeneration of the cerebral arteries. Experience shows that atheromatous degeneration of the Avails of the vessels usually induces dilatation of the larger arterial trunks, and, on the contrary, contraction of the smaller arteries. The atheromatous arteries of the brain are also usually contracted for a long while before they are closed by thromboses. Hence the symp- toms of thrombosis, or, rather, of the partial anemia and partial ne- crosis of the brain depending on it, are almost always preceded by premonitory symptoms, either of disturbance of circulation, induced by the contraction of certain cerebral vessels, or by symptoms of senile cerebral atrophy, Avhich has been caused and hastened by de- generation of the cerebral vessels. The patients complain of pain in the head, dizziness, ringing of the ears, flashes before the eyes, loss of memory and poAver of thought; they are apathetic and indifferent, and much inclined to sleep, but their sleep is disturbed by uneasy dreams. As a rule, very small arteries are at first obstructed, either by the atheromatous process causing their entire obliteration, or be- 182 DISEASES OF THE BRAIN. cause their calibre is contracted, and then obstructed by a thrombosis. The anemia resulting from closure of these small vessels is limited in extent, and hence may readily be removed by an increased supply of blood through neighboring vessels. We must bear this in mind Avhen, in a marasmic patient, who for some time has had the brain-symp- toms that Ave designated as premonitory, limited regional symptoms (herdsymptome) occur, and, after lasting for a time, disappear again. Among these symptoms are inability to say different words, loss of memory for certain names and numbers, pain, or a feeling of formica- tion, or of certain limbs going to sleep, occasionally only of certain fingers or toes, contractions and paralysis, which are also occasionally limited to certain fingers or toes, etc. Many authorities have explained this variation of symptoms, par- ticularly the occurrence and disappearance of paralysis, as a peculiar symptom of softening of the brain. This is a false view of the matter. In cases where the symptoms have presented this variation, if soften- ing of the brain be found on autopsy, the softening did not occur at the time the symptoms changed, but at a later period, Avhen they were constant. On the other hand, the occurrence and disappearance of circumscribed paralyses are certainly, to some extent, characteristic of partial anemia of the brain resulting from atheromatous degeneration and thrombosis of small cerebral arteries, and are rapidly removed again by the establishment of collateral circulation. (The occurrence and disappearance of circumscribed paralyses do not render it certain that there is thrombosis of small arteries of the brain; the same symptom is also seen from small extravasations. See Chapter V.) If a large artery, or several small ones going to the same part of the brain, be closed by thrombosis, as Ave have already shown, a collateral circula- tion cannot be established, particularly if the degeneration of the walls of the vessels be extensive, and then the affected portion of brain loses its functional power forever. There are some parts of the brain—for instance, the large medullary masses of the hemispheres— that may be destroyed without any apparent loss of function. This fact, which is proved by numerous examples, explains the occurrence of those cases of softening during whose course there have never been any symptoms of paralysis. We must know this in order to under- stand that it is occasionally quite impossible to diagnose softenino- of the brain, and to distinguish it from simple senile atrophy, because the most important point for the differential diagnosis is wanting. But, far more frequently, the results of thrombosis of a large artery, or of numerous small ones, extend to parts of the brain, Avhose loss of function induces paralysis, and even hemiplegia, particularly to the corpus striatum and thalamus. The arteries supplying the great hemi- PARTIAL ANEMIA OF THE BRAIN. 183 spheres, and the above-mentioned large ganglia lying in them, AAith blood, are the ones that are most frequently closed by thromboses; and, even if the anemia directly resulting from the obstruction, and the consequent softening, do not extend to the corpus striatum and optic thalamus, these parts will readily lose their functional power from the collateral edema about the point of softening, or from the capillaries of the entire hemisphere being compressed by it. If a large vessel be closed by a thrombosis originating from the Avails, and groAV- ing slowly, or if numerous smaller arteries be closed one after the other, the paralysis comes on sloAvly, and increases gradually. Cases running this course are the most readily recognized; for, although gradually-forming and sloAvly-progressing paralysis also occurs in many other cerebral diseases, if this symptom arise in an old marasmic pa- tient, who has had the previously-described symptoms, we must first think of thrombosis of the cerebral vessels, and of the form of soften- ing of the brain at present under consideration. While the symptoms of paralysis, which are very often and unaccountably accompanied by contractions of the paralyzed part, gradually increase and extend, the patients become more apathetic, grow imbecile, pass their excrements involuntarily, have bed-sores, and finally die of marasmus and coma. The course is different when a large vessel or numerous small ones are rapidly closed by thrombosis. In such cases hemiplegia occurs sud- denly, and the symptoms may be very similar to or identical with those of cerebral hemorrhage. This correspondence is easily explained. In cerebral hemorrhages, also, most frequently, the corpus striatum and thalamus are either broken up, or their functional activity is ar- rested by the compression that capillaries of the whole hemisphere suffer from large effusions. In cerebral hemorrhages also, hemiplegia usually occurs suddenly. Moreover, ruptures of the cerebral arteries usually occur in old persons, and are most frequently clue to the same disease of the vascular walls that generally induces thrombosis. We shall not enumerate the symptoms given for a differential diagnosis, and shall only refer to an assertion of Bamberger's, for which science is indebted to such an undisputed authority on diagnosis. Bamberger says that, in his notes, he finds seven cases where there was an error of diagnosis, and the real state of affairs was only discovered at the autopsy; he considers it impossible to avoid this error, and says he seldom ventures to make an absolute diagnosis of cerebral hemorrhage from an apoplectic attack. Partial anemia and necrosis of the brain due to embolism are also almost ahvays preceded by characteristic premonitory symp- toms. But these are not brain-symptoms, as they were in the pre- vious form of anemia of the brain; they are those of the diseases which 184 DISEASES OF THE BRAIN. almost exclusively cause embolism of the cerebral arteries, that is, of valvular disease of the heart, of endocarditis, or of severe destructive disease of the lungs. The occurrence of these premonitory symptoms, and the presence or absence of valvular disease, endocarditis, or severe disease of the lung, haAe such an effect on the diagnosis betweem em- bolism of a cerebral artery and other brain-diseases, that Avith the same set of symptoms we may diagnose embolism if we find them, and exclude it with certainty if they are absent. The sudden shutting off of arterial blood from the part of the brain supplied by the obstructed artery, instantly arrests its functional poAver. Experience shows that emboli almost always lodge in the arteria fosse Sylvii, particularly the left one; as the closure of this large artery causes great anemia of the parts supplied by it, we may readily see that sudden hemiple- gia, especially of the right side, is the most important symptom from AAiiich we can diagnose embolus in the cerebral arteries, if it occur in a patient with valvular disease, etc. The entire loss of consciousness, the apoplectic attack, which usually accompanies the commencement of hemiplegia, when the arteria fosse Sylvii is stopped by an embolus, is more difficult to explain. I think that this symptom is most prob- ably due to the diseased hemisphere being decidedly SAvollen by col- lateral edema, and that, as occurs in large extravasations of blood, the opposite hemisphere is not sufficiently protected from the pressure by the falx, Avhich only offers a limited amount of resistance. In embo- lism of peripheral arteries at least, I have ahvays found a very decided and wide-spread edema in the vicinity of the obstructed vessel, and have witnessed considerable enlargement of the spleen from embolism of the splenic artery. It is evident that a hemiplegia occurring sud- denly with an apoplectic attack may readily be mistaken for a cerebral hemorrhage. In some cases, it is true, the age of the patient gives grounds for distinguishing a hemorrhage from an embolism. Hemor- rhages occur chiefly, although not exclusively, in advanced age, embo- lism comes in persons of any age; hence, in young persons, the pre- sumption is in favor of embolism. However, the only way of avoiding error is the careful examination of the heart and lungs. The certainty that the diagnosis receives from the discovery of valvular disease is still more increased if we can also find a coincident embolism of a pe- ripheral artery or of one of the internal organs, such as the spleen or kidney. In most cases death occurs sooner or later after the attack, with the symptoms of general paralysis; in other cases consciousness returns after a time. The symptoms of paralysis rarely disappear; this is sufficiently explained, as we have previously shown, by the difficult establishment of a collateral circulation. Partial anemia of the brain, due to collateral edema in the vicinity PARTIAL ANAEMIA OF THE BRAIN. 135 of abscesses, tumors, and other local diseases, induces symptoms of irritation or paralysis, according to the degree of the anemia; these symptoms complicate those directly depending on the original disease, and are due to functional disturbance of portions of the brain- lying beyond the actual disease. On autopsy, it is usually difficult or even entirely impossible to decide, whether edema and capillary anemia exist in the vicinity of an abscess, tumor, etc., and how far they ex- tend. But we have a right to suppose that the vicinity of these points of disease is in a similar state to that of parts affected in the same way, Avhich are exposed to observation; and we are the more justified in this supposition, because for a long time it has not escaped the more accurate observers that, in many cases of partial disease of the brain, symptoms occur that cannot depend on the coarser structural changes of the brain found on autopsy, but must be referred to an impercep- tible participation of other portions of the brain lying in the vicinity of the affected part. It is most probable that this participation depends on disturbance of the capillary circulation and the occurrence of edema, because in other parts of the body also these anomalies often leave no traces. Occasionally the symptoms observed during life give a better means of judging of the extent of the secondary dis- turbances of circulation, or of the collateral edema, than the autopsy does. For instance, if paralysis and spasm accompany a disease of the cortical and medullary substance of the cerebrum, which does not encroach on the cranial cavity, and whose destruction does not induce paralysis and spasm, there is probably an anemia extending to por- tions of the brain lying far deeper. As numerous examples haAe proved that an entire half of the cerebellum may be destroyed without inducing hemiplegia, Ave cannot refer a hemiplegia, observed along Avith structural changes confined to the cerebellum, directly to that oro-an. but must consider it due to the extension of collateral edema to portions of the brain whose loss of function causes paralysis of half the body. The strange experience, that, in disease of one side of the cerebellum, there is sometimes no hemiplegia, at others there is hemi- plegia of the same side, and in still other cases that it occurs on the opposite side, is doubtless due to the fact that, in the latter cases, a collateral edema extends along the crura cerebelli ad frontem to the lateral regions of the pons; Avhile, in those cases where the same side is affected, the edema extends along the crura cerebelli ad medullam oblongatam to the lateral branches of the medulla oblongata; and where there is no hemiplegia the collateral edema has not advanced in either direction to regions whose loss of function involves that symp- tom. These examples may suffice to show how important a role par- tial anemia of the brain, due to collateral edema, plays in the symp- 186 DISEASES OF THE BRAIN. tomatology of brain-diseases confined to certain points. I have already remarked that the variation of symptoms, the temporary improvement or exacerbation, observed in the course of some brain-diseases, depend greatly on the increase or decrease of the collateral edema about the point of disease. The third form of partial anemia of the brain, the result of com- pression of the capillaries of portions of the brain from diseases caus- ing pressure, induces constant and characteristic symptoms, which of course vary according as the anemia is in one of the greater hemi* spheres or is below the tentorium. If the capillaries of one of the greater hemispheres be compressed by an effusion of blood, by a tumor, or any other local disease contracting the space in the skull, there will be hemiplegia, no matter where the said disease be located. This hemiplegia is limited to the lower half of the face, and to the tAvo extremities of the opposite side. It has often been considered as enigmatical, that in many cases diseases above or below one of the greater hemispheres, as Avell as Avithin it, led to hemiplegia, AAiiile in other cases the same diseases at the base, convexity, or in the medulla of a great hemisphere did not induce hemiplegia; and tables have been made out Avhich show at a glance this want of correspondence. I consider these tables as utterly worthless, unless the variety of the disease be stated in them; and I think it very important to distinguish betAveen two classes of disease, Avhose effect is very different; namely, those which occupy more space than the brain-filaments and ganglion- cells which they supplant, and those which do not. Diseases at the base, convexity, or in the medullary portion of the cerebrum only in- duce hemiplegia Avhen they lessen the space, in other cases they do not cause it (unless collateral edema in their vicinity extend to the thalamus and corpus striatum). There are exceptional cases Avhere hemiplegia does not occur in disease of one of the greater hemispheres whose products certainly contract the space. When tumors grow very slowly the brain usually atrophies, and as much space may be gained in the skull by the disappearance of brain-substance as is lost by the sIoav groAvth of the tumor. In such cases there is no anemia of the affected hemisphere from compression of the capillaries, and consequently, if the tumor be not in the immediate vicinity of the corpus striatum and thalamus, hemiplegia does not occur. We must also remember the extensive communication between the two upper chambers of the skull at their anterior part. It is evident that at this place pressure on one hemisphere may more readily be propagated to the other than at any other part. But, the more pressure is divided up, the weaker its action becomes. In accordance with these consid- erations, diseases of the anterior lobes, which do not encroach too much PARTIAL ANEMIA OF THE BRAIN 1S7 on the space, do not entirely compress the capillaries of the affected hemisphere, so that they do not cause hemiplegia, or at least it is only slight, while the propagation of pressure to the other hemisphere is shown by psychical disturbances, AA'hich are usually absent Avhere the affection is limited to one side of the brain. Perhaps this may partly explain the aphasia, AAinch is found Avith disease of the frontal lobe of one side, particularly (but not constantly) of the left side; since, in the region of the frontal lobes, pressure acting on one side is very readily propagated to the other. As the two sides of the brain are so symmetrical, it is difficult to'believe that there is any organ in one which does not exist in the other. Even more characteristic and more constant is the combination of symptoms accompanying compression of the capillaries of the parts of brain in the posterior cranial fossa. This is apparently because the tentorium can offer greater resistance to pressure acting on it than the falx can; also because the communication from the posterior and lower chamber of the skull, bounded by the tentorium and occipital bone, Avith the upper chambers, is far less free than that AAiiich exists be- tween the two upper chambers. As is well known, Ave may readily err in diagnosis of diseases of the brain, but I do not remember to haAe made a mistake when I have given a diagnosis of disease con- tracting the space in the posterior cranial fossa. Many of my former pupils also have assured me that, from experience in then own practice, they must regard the diagnosis of diseases limiting the space in the posterior cranial fossa as easy, and that they have repeatedly diag- nosed them according to my instructions, and have verified the diag- nosis by autopsy. The combination of symptoms from which we may diagnose compression of the capillaries of the parts lying in the pos- terior cranial fossa is as follows: Pains in the back of the head, sym- pathetic vomiting, a peculiar dizziness, diminution of sensibility and motor poAver, but no complete paralysis and anesthesia regularly spread over the body, and impaired articulation and deglutition. The pains at the back of the head doubtless proceed from the filaments of the trigeminus going to the tentorium. As the sympathetic vomiting occurs in various brain-diseases, it alone has no diagnostic Aralue, but, in combination Avith other symptoms, it greatly aids to render the pic- ture of the disease characteristic. The dizziness accompanying dis- eases contracting the space in the posterior cranial fossa is not a hallu- cination, a subjective sensation of movement of the patient's own body, or of surrounding objects, that does not really take place. Unlike this far more frequent hallucinatory form of dizziness, it does not occur while the patient is quietly lying or sitting down, but results from certain bodily movements. When a patient complains of dizziness, 188 DISEASES OF THE BRAIN. * we should make it a rule to ask at once whether the attacks come on during rest, or only during walking, rising, etc.; if the latter points be ansAvered affirmatively, we haAe obtained an important diagnostic point. The dizziness observed in diseases encroaching on the posterior cranial fossa depend, as Immermann has fully proved, on actual move- ments of the body, which the patient does not perfectly perceive, but Avhich only have a general influence on his feeling of equilibrium. In healthy persons, vibratory movements of the body would also occur in Avalking, rising, etc., if they were not prevented by contraction of the muscles which straighten and curve the spinal column. When a person is Avalking stiffly and uprightly, we may readily see, by the in- creased prominence of the bellies of these muscles, that he is uncon- sciously using them. This facility of hmiting, by muscular action, the movements and vibrations conveyed to the trunk is very much im- paired in persons with disease encroaching on the posterior cranial cavity, a circumstance which is apparently supported by the supposi- tion that the cerebellum chiefly causes innervation of the body, and is the prop of the spinal column ( Griesinger). The diminution of sensi- bility and that of motor power, which render the patient awkward and uncertain, without increasing to complete paralysis and anesthesia, are simply explained by the fact that the nerve-filaments, passing from the cerebrum through the foramen occipitale superius, enter the posterior cranial fossa, again leave it by the interior occipital foramen, and are thus subjected to a compression which impairs the propagation of ex citement from the brain to the motor nerves, and of peripheral excite- ment of the sensory nerves to the brain. In the disturbance of speech it may be readily seen that it does not depend on lack of thoughts, or on the impossibility of finding words for the thoughts, but on the un- certainty and clumsiness in executing the movements necessary for distinct, rapid, and connected articulation. The disturbance of deglu- tition is occasionally designated as difficulty of swalloAving; it usually manifests itself by slight choking while drinking. I shall not attempt to decide whether this disturbance of articulation and deglutition de- pends on disturbance of the function of the hypoglossal and glosso- pharyngeal nerves at their origin, or in the nerves themselves, by dis- eases affecting the space in the posterior cranial fossa. Besides the above-mentioned symptoms, there are usually others depending on the injury of certain nerves, and, if the orifice of the vene Galeni into the straight sinus be compressed, and the escape of blood from the ventri- cle prevented, we have the symptoms of chronic hydrocephalus. We shall hereafter speak of this when treating of tumors and abscesses of the cerebellum, pons, medulla oblongata, and of chronic hydrocepha- lus. Here will be the place to mention those symptoms which are * apoplexy. U9 observed, Avith remarkable regularity, in diseases affecting the space in the posterior cranial cavity, no matter what their nature or location. Among my pupils I have noticed that the interest in brain-diseases rapidly increases Avhen it becomes evident that, in many cases, a sure diagnosis can only be made within certain limits. Not unfrequently we are obliged to stop at the diagnosis of a disease encroaching on one side of the cerebrum, or on the posterior cranial fossa. In the following chapters Ave shall show under what circumstances Ave can go further, and how, in other cases, a certain diagnosis may be made of the nature and exact seat of the disease. Treatment.—As may be readily understood, the treatment of partial anemia and necrosis promises little benefit. In thrombosis and embolism of the cerebral arteries, the obstruction to the supply of blood cannot be removed by therapeutic remedies. Hence the indica- tion Avould be to favor the development of a collateral circulation, Avithout exposing the patient to neAV danger from too great collateral fluxion. It is very difficult to fulfil these indications, and Ave may readily do harm instead of good. The purer the symptoms of partial paralysis, the more obstinate they remain; if no symptoms of irrita- tion accompany them, the more a strengthening and stimulant treat- ment is indicated. Hence we ahvays find the administration of stimu- lants recommended in the treatment of softening of the brain. If, on the other hand, the symptoms of irritation caused by fluxionary hyper- emia, such as severe headache, contractions, etc., are prominent, it is advisable to use cold, and apply leeches behind the ears repeatedly. We should be careful about venesection, as it is readily followed by collapse. From AAThat has been said, it is evident that Ave can give no general rules, but the treatment must be suited to each case. We shall speak of the treatment of partial anemia of the brain, induced by collateral edema and compression of the capillaries, when we treat of the diseases that this form of partial anemia accompanies. CHAPTER V. CEREBRAL HAEMORRHAGE--APOPLECTIC STROKE--APOPLEXIA SAN- GUINEA. By the term stroke, or apoplexy, was originally meant, as the word indicates, the sudden occurrence of complete functional inactivity of the brain. Apoplexy is divided into various forms, according as the paral- ysis is induced by an extravasation of blood or by a serous effusion, or as organic diseases can or cannot be found as the cause: thus we have Apoplexia sanguinea, A. serosa, A. nervosa, etc. In the present 190 DISEASES OF THE BRAIN. - chapter we treat of the lesion of the brain characterized by rupture of the blood-vessels and escape of their contents, whether it induces the symptoms of sudden paralysis of the brain or not. Etiology.—Cerebral hemorrhages almost always occur from the smaller arteries or the capillaries of the brain, and are caused partly by structural disease of the arterial walls, partly by an anomalous con- dition of the part of brain surrounding the vessels, partly by increased pressure of the blood against the wall of the vessel. The bleeding most frequently occurs Avhen several of the factors act together. The structural changes in the walls of the vessels, to which then abnormal fragility is due in most cases, are the results of endarteritis deformans, Avhich Avas treated of in the first volume. This explains the frequency of apoplexy in persons over forty years of age, Avhich Avas noticed even by Hippocrates. Next to this, simple fatty degen- eration of the arterial Avails, not dependent on inflammation, but occur- ring in badly-nourished cachectic and chlorotic persons, also induces greater fragility and ruptures of the cerebral vessels. Still we must say that fatty degeneration of the finer cerebral arteries is found far more frequently than would be expected from the proportionately rare occurrence of apoplexy. Occasionally rupture of the entire arterial wall is preceded by rupture of the inner and middle coats, Aviiile the adven- titia still resists. In such cases the blood escapes betAveen the external and middle coats, and small dissecting aneurisms are formed. Lastly, there are cases Avhere abnormal Aveakness of the cerebral vessels must be supposed, although it cannot be proved. These are the rare cases AAThere cerebral hemorrhages are found in convalescents from typhus and other acute infectious diseases and during scorbutus. We have already mentioned that, in necrotic softening of the brain, capillary hemorrhages not unfrequently occur along the borders of the softened part. Frequently, gradual atrophy of the brain causes dilatation and final rupture of the vessels. While the brain-substance disappears, a vacuum cannot form in the skull; hence increase of the cerebro-spinal fluid and dilatation of the vessels are necessary results of senile or any other form of atrophy of the brain, Avhich is a frequent sequel of the most varied forms of disturbance of nutrition. Perhaps the frequency of apoplexy in advanced age depends at least partly on this circumstance, and there is no doubt that the atrophy of the brain which is in many cases caused by the first apoplectic attack, has some- thing to do with the frequent recurrence of apoplexy. The increased pressure of the blood on the walls of the vessels, by which the latter are ruptured, may depend on any of the causes which Ave indicated in the first and second chapters as causes of hyperemia. The frequent occurrence of apoplexy during long and luxurious meals CEREBRAL APOPLEXY. 191 tends to shoAV that the hyperemia of the brain induced by temporary plethora is one of the most dangerous forms. Hypertrophy of the left ventricle, particularly that form resulting from any extensive en- darteritis deformans, plays an important part in the ruptures of cere- bral vessels. In the latter case two dangerous factors unite—the mor- bid fragility of the vessels and the increased pressure of the blood on them. Moreover, small arteries, in which there is otherwise a regular pressure of the blood, and whose walls also maintain a nearly equal tension during the systole and diastole of the heart, pulsate Avhen there is extensive atheromatous degeneration, and at every systole of the heart the normal medium tension of their Avails is decidedly in- creased. It will be readily understood that this circumstance also in- creases the liability of the vessels to rupture. Cerebral hemorrhages so often depend on the complication in question, that, in doubtful cases, the discovery of hypertrophy of the left a entricle and of an atheromatous degeneration of the arteries may decide the diagnosis. Apoplexies occur at all times of the year ; occasionally, AAithout any knoAvn cause, cases accumulate remarkably. They have also been observed at all times of the day, and statistical tables have been made of their comparative frequency at morning, mid-day, and even- ing. Although advanced age furnishes the largest number of cases, apoplexy does occur even among children. Men are someAvhat oftener attacked than Avomen. There is no such thing as an apoplectic con- stitution, indicated by a short neck and broad shoulders. Anatomical Appearances.—The distinction is made into capil- lary hemorrhage and hemorrhagic clots, according as the bleeding consists of numerous small, closely-packed effusions, or of a larger quantity of blood. In capillary hemorrhages the cerebral substance appears dotted with dark-red punctate extravasations at some point of variable size. The cerebral substance between the small extravasations either re- tains its normal color and consistence, or is colored yelloAV or reddish to a variable extent by imbibition; it is relaxed and moist, or, lastly, it is broken doAvn to a red pulp by the extravasation (red softening). Small hemorrhagic spots sometimes press the brain-filaments apart; but larger ones break up and become mixed with the brain- substance. In the former case the effusion is sometimes elongated in the direction of the filaments; in the latter it is more roundish or irreg- ular. In the former case the walls of the effusion are to some extent smooth; in the latter they oftener appear ragged, and are frequently surrounded, for a space some lines thick, by a broken-doAvn pulpy brain-substance discolored with blood. The size of the clot varies from that of a hemp-seed to that of the fist. If it be in the vicinity 59 192 DISEASES OF THE BRAIN. of a ventricle, it often breaks through the Avail of the latter, and its blood escapes into the ventricle. Hemorrhagic effusions, lying near the surface of the brain, not unfrequently break through the cortical substance and pia mater, so that the blood enters the subarachnoid space. Usually there is only one hemorrhagic effusion in the brain, rarely several. Their most frequent locality is the corpus striatum, the thalamus opticus, and the large medullary masses of the hemi- spheres ; less frequently they occur in the cortical substance of the cerebrum, in the cerebellum and pons. Apoplexies in the corpora quadrigemina and medulla oblongata are rare, and they hardly ever occur in the corpus callosum and fornix. The contents of a recent apoplectic clot consist of blood and broken-down brain-substance. The blood either remains fluid or is partly coagulated, and then the fibrin is occasionally deposited at the periphery, while the middle of the clot consists of fluid blood. Changes of the contents and Avails of the clot soon begin. The fibrin of the blood and the portions of brain mingled with the effusion break down into a detritus, the contents become more fluid, the dark-red color becomes brown, then saffron yellow. Granular pigment and often also hematoidin crystals are formed from the hematin. At the same time, in the immediate vicinity of the clot, there is a new formation of connective tissue starting from the neu- roglia, which develops into a thick, hard layer that encloses the clot. In the same way there is a neAV formation of delicate connective tissue, colored yelloAV by the pigment contents and serous infiltration, Avhich covers the Avails and traverses the clot as a fine network. After the elements of the effusion have broken down, all its remains disappear, while their place is gradually supplied by serum ; and then we find in the brain a cavity filled with clear liquid, surrounded by a callous sub- stance, and covered and traversed by delicate yellow-colored connec- tive tissue—an apoplectic cyst. The cysts usually remain permanently. But occasionally the serum is reabsorbed, the Avails approximate, and finally are only separated by a stratum of pigment. These callous spots, enclosing pigment strie, are called apoplectic cicatrices. The cicatrization of a hemorrhagic effusion in the cortical substance is somewhat different. The effusion of blood under the pia mater, which is usually flat and extended, undergoes the same changes as the contents of central clots. The red pulp gradually becomes a red- dish-brown or saffron-yelloAV crumbly mass, which is bounded below by callous brain-substance, above by the pia mater. Lastly, we find an excavated pigmented plate, above which a serous effusion fills the cavity, resulting from the depression. While the above terminations of cerebral hemorrhages must be regarded as the most favorable, in some cases the reactive inflammation in the vicinity of the broken CEREBRAL APOPLEXY. 193 doAvn portion of brain is not limited to a neAV formation of connective tissue, but there is extensive destruction from inflammatory softening, or the apoplectic clot is even transformed to an abscess of the brain. The parts untouched by the hemorrhage are bloodless if the extrava- sation has been considerable, and the more so the larger the extrava- sation ; small capillary hemorrhages have no influence on the amount of blood in the rest of the brain. In large effusions the hemisphere containing the clot is particularly anemic. The subarachnoid spaces also are empty, the convolutions flattened, and the furrows have dis- appeared. Since the uneven appearance of the surface of the brain is to a great extent due to the presence of cerebro-spinal fluid and of vessels containing blood between the convolutions, the surface of the brain appears Aery smooth and even when there is a large extravasa- tion. The brain rarely endures the injury from an apoplexy Avithout impairment of the general nutrition. The gradual diminution of men- tal power seen in almost all apoplectic cases corresponds to a general atrophy of the brain; which, according to the examinations of Turk, is associated Avith a degeneration, extending into the spinal medulla, of those filaments communicating Avith hemorrhagic effusion. Symptoms and Course.—Sometimes apoplexy occurs unexpect- edly in persons Avho have previously felt quite well; in other cases it is preceded by premonitory symptoms that excite in the physician, and even in the laity, the apprehension that the patient is threatened Avith apoplexy. The patients complain of headache, or of heaAiness and fulness of the head, of noise in the ears, flashes before the eyes, and attacks of dizziness; they sleep badly, are excited and irritable. There are also, as peculiarly ominous symptoms, occasional temporary feel- ings of formication and numbness in certain limbs, momentary loss of memory for some Avords and figures, or temporary paralysis confined to certain groups of muscles. Thus Ave see the premonitory symptoms of apoplexy are those that Ave gave in preceding chapters, as due to general and partial hyperemia of the brain, and to partial anemia of the brain resulting from degeneration of the Avails of the vessels: a condition that entirely corresponds with the frequent dependence of cerebral hemorrhages on increased lateral pressure in the cerebral vessels, and on degeneration of then walls. In general it cannot be determined Avhether the temporary partial paralysis and anesthesie, the " Avarnings" preceding the apoplectic attack, depend on throm- bosis of small vessels, or on small capillary hemorrhages. In the latter case, of course they could not be classed among premonitory symptoms. The destruction of brain-filaments, AA'hether they be broken up by large extravasations or be softened by small capillary hemorrhages, 194 DISEASES OF THE BRAIN. can, as avc have often shoAvn, have no other direct result than partial paralysis. Since the destruction of certain portions of the brain, par- ticularly in the medulla of the cerebrum, does not cause any perceptible disturbance of function, we may readily understand that small hemor rhages, as well as other diseases of those parts, may occasionally es- cape recognition during life. We have designated the corpus striatum and thalamus opticus as the most frequent seat of hemorrhage; a destruction of these parts, or of the pedunculi cerebri, induces paralysis of the opposite half of the body. We may readily determine that the paralysis, resulting from destruction of the above parts, only depends on interruption of the conduction between the organs acting in thought and will and the motor nerves and muscles; the poAver to think and will is unimpaired. After the apoplectic seizure, during which there is complete loss of consciousness, has passed off, if we ask the patients to give us the affected hand, they show their desire to fulfil the request, by taking the paralyzed hand in the other one, Avhose nerves and muscles are under the control of their will, in order to accomplish the act. On the other hand, in recent cases, every motor nerve on the paralyzed side, to Avhich Ave apply the induced current, causes contraction in the muscles sup- plied by it. Hence the only failure is in the communication between the central excitory apparatus and the motor nerves. This interrup- tion has no effect on those movements of the paralyzed side that occur in a reflex manner without the influence of the Avill; for patients, who, as a result of apoplexy on the left side, cannot move the right arm or leg, move the right side of the thorax just as Avell as the left during respiration. And the connection betAveen the motor nerves and those nerve-filaments and ganglion-cells which are excited during certain states and feelings of the mind is not always removed with the inter- ruption of conduction at present under consideration. This is shown by the fact that some patients who cannot make the motions of laugh- ing or crying on the one side of the face, at our request, can do so when they do not will to do it, but when their feelings lead them to do so. In the same way, the interruption of conduction of the impulses of the will, from the central organs to the motor filaments, does not necessarily imply that the communication of the latter Avith sensory and Avith other motor filaments is interrupted. On the contrary, we find that occasional reflex movements sometimes remain undisturbed in the paralyzed parts, or even occur more readily, so that it appears as if, vviien the excitement of the motor filaments is no longer subject to the will, it occurs more readily than it otherwise Avould. Paralysis of half the body, due to destruction of the corpus striatum and thalamus of one hemisphere, is characterized by its limitation to the muscles of CEREBRAL APOPLEXY. 195 the extremities, to those muscles of the face going to the angle of the mouth and the nose, and to the muscles that protrude the tongue. The patients can almost always chew normally on the affected side, they can wrinkle the forehead, open and close the eyelids, move the eyes in any direction, etc. On the other hand, the patient frequently cannot lift the paralyzed arm and foot an inch from the bed; the mouth hangs doAvn on the affected side, and the nostril is contracted, occasion- ally the cheek flaps about like a loose sail at every expiration, while, on the sound side, the angle of the mouth is drawn up and the nostril dilated. If the patient protrude the tongue, its point goes toAvard the paralyzed side, because only the muscles of the opposite side push for- ward the root of the tongue and elongate that organ. In most cases, along Avith the hemiplegia, there is also anesthesia of half the body, but after a time this usually passes off partially or entirely. This course of the anesthesia, as well as the experience that animals have no sensa- tion after destruction of their corpus striatum and thalamus, and that, after taking them away, the power of feeling peripheral pain continues, appears to indicate that the temporary anesthesia of the paralyzed half of the body does not depend immediately on destruction of the corpus striatum and thalamus, but on the compression of the capil- laries in the sections of brain lying beloAV them, caused by the effusion of blood. The same symptoms as are caused by effusions of blood into the thalamus and corpus striatum, are induced by effusions at other parts of the cerebrum, provided they are extensive enough to compress the capillaries of the thalamus and corpus striatum. After the discussion in the previous chapter concerning partial anemia of the brain and its influence on the cerebral functions, this similarity cannot appear strange to us, but must rather be regarded as evident and necessary. The only difference is the following: A large apoplectic clot, destroying the corpus striatum or thalamus, leaves a hemiplegia that never dis- appears ; only small clots in these parts, by Avhich the filaments and ganglion-cells are not broken doAvn, but only pressed apart, leave paralysis Avhich is occasionally temporary. Hence we may conclude that the apparatus for exciting the motor nerves, Avhich doubtless exists in the brain, although it may itself be excited by the Avill, is located in the vicinity of the corpus striatum and thalamus. On the other hand, extensive apoplectic clots at other parts of the cerebrum not unfre- quently leave paralysis, which sooner or later disappears again. From this course Ave may suppose that the capillaries of the motor centres, being relieved of the pressure by the partial resorption of the extrav- asation, have again become permeable to the blood; or that the col- lateral edema in the vicinity of the broken-doAvn part of brain, Avhich 196 DISEASES OF THE BRAIN. extended to the motor centres, has disappeared with the cicatrization of the apoplectic clot. Hemiplegia occurs in some, but not in all, of the cases where the effusion is into the cortical substance of the cerebrum; these are gen- erally accompanied by hemorrhage into the tissue of the pia mater. The difference, doubtless, depends on how far the frequently-mentioned results of the hemorrhage, compression of the capillaries, or collateral edema, extend inward; whether they reach the corpus striatum and thalamus or not. When the clot is in this position, general convulsions are often observed, and in most cases there is severe disturbance of the psychical functions. Since experience shows that persons with very advanced and extensive degeneration or atrophy of the cortical sub- stance (if it be only on one side) often have no psychical disturbance, the frequent occurrence of the latter in apoplexy on one side is prob- ably because hemorrhages readily affect the other hemisphere; and particularly because this is likely to occur in the complicating inflam- mation of the pia mater, which has a great tendency to spread. Hemorrhages in the pons, if of any considerable size, and in the medulla oblongata, even if very slight, usually cause death. In small effusions in the lateral portions of the pons, there are anesthesia and paralysis on the opposite side of the body; in small extravasations in the middle of the pons, there is paralysis of both sides. In hemorrhages of the cerebellum we often find paralysis of the opposite side. But this cannot depend on the affection of the cerebel- lum, for there is often no paralysis observed when this is extensively destroyed. We must not think that, because hemorrhages are found at very different parts of the brain, the different cases of paralysis dependent on cerebral hemorrhages will differ widely from each other. On the contrary, the large majority of cases show a great similarity, as they induce the hemiplegia above described. It is, of course, of great prac- tical importance to know this, Avhich is simply explained by the fact that, according to statistics, seven-eighths of all cerebral hemorrhages are located in the cerebrum and particularly in the vicinity of the cor- pus striatum and thalamus. There are some very wonderful excep- tions to the one-sidedness of the paralysis and to its occurrence on the opposite side, in hemorrhage of the cerebrum, which we are at present unable to explain satisfactorily. HoAvever, we must add that, of late, since all anomalies existing with the hemorrhage, particularly plugging of the cerebral arteries, are more carefully attended to, and used in explaining the symptoms, the number of such cases published has greatly decreased. Another series of symptoms in cerebral hemorrhage, which is CEREBRAL APOPLEXY. 197 called a stroke of apoplexy, and is only absent Avhen the hemorrhage is slight, do not depend directly on the local injury of the brain, but on its effect on the rest of the brain. We shall hereafter shoAV that the apoplectic fit usually occurs at the outset, but sometimes does not come on till after the appearance of the paralysis. The stroke of apoplexy rarely develops gradually and probably only does so when the hemorrhage occurs slowly; in most cases it comes on suddenly, and the patient falls to the earth (often with a cry) as if " knocked down." During the attack, consciousness is entirely lost, as Avell as the power of feeling and moving. The sphincters also are generally paralyzed, so that feces and urine are passed involuntarily. Respira- tory movements alone, which depend on the medulla oblongata, are continued; but the inspirations follow at long intervals, and are usually loud and stertorous, since the paralyzed and pendulous soft palate is thrown into vibration by the air. The patient has a peculiar appear- ance, from the relaxed cheeks being puffed out with every expiration. There is often Amounting at the commencement of the attack; the pulse is very sIoav, the pupils contracted. It is usually supposed that the apoplectic fit is a result of the pres- sure or bruising of the nerve-filaments and ganglion-cells of the entire brain by the extravasation. HoAvever, it is evident that this pressure can never exceed that of the blood in the cerebral arteries; for, as soon as the pressure in the parts around the arteries is as great as that of the blood in the vessels, no more blood can escape from the latter. But, from experiments that we can make on peripheral nerves, there is no doubt that such a pressure is entirely insufficient to annul the excitability of the nerve-filaments. The following fact also tends to disprove the current explanation: If the symptoms of paralysis de- pended on the pressure to which the filaments of the brain are sub- jected in apoplexy, bleeding should remove these symptoms not only in some but in all cases, provided enough blood be draAvn to lessen the pressure in the whole vascular system, particularly in the arteries. Hyrtl, who also speaks most decidedly against referring these symp- toms to pressure on the brain, thinks that the accidents generally re- ferred to " pressure on the brain " are due to a slight amount of con- cussion ; but, apart from the fact that there is no such concussion in cases of extravasation which are not of traumatic origin, no anatomi- cal changes referable to such a cause can be found. We refer the apoplectic fit to sudden compression of the capillaries, that is, anemia of the brain-substance. In all large hemorrhages this anemia may not only be recognized with certainty after death, but even during life it shoAVS itself by a very important symptom which is usually falsely interpreted, that is, by a remarkable pulsation of the carotids. This 19S DISEASES OF THE BRAIN. symptom is very generally regarded as a sign of " increased pressure of blood to the head," although it really indicates that the flow of blood into the skull is obstructed; we may at any moment induce the same phenomenon in the artery of the finger by tying a string tightly around the end of the finger. All diseases of the brain and its mem- branes affecting the space in the skull enough to prevent the escape of blood from the afferent vessels, hence not only large effusions of blood, but also abundant exudations and transudations, large tumors, etc., are accompanied by increased pulsation of the carotids. If we find this symptom, when there is no hypertrophy of the left ventricle, nor corresponding pulsation in other arteries, it will, in doubtful cases, be a great aid to the diagnosis of some brain-disease encroach- ing on the cranial cavity. In my clinic my pupils have frequently had an opportunity of satisfying themselves of the correctness of the indi- cation and of the great diagnostic value of this symptom. If Ave re- gard the physical conditions, we see that anemia, at all events arte- rial anemia, of the brain can never result from rupture of the capil- laries ; for the escape of blood from the ruptured capillaries can only last till the tension of the contents of the skull equals that of the blood in the capillaries. In accordance with this we see that the apo- plectic fit does not occur in capillary hemorrhage. If, on the other hand, an artery be ruptured, and the bleeding does not soon cease from some other cause, the tension in the surrounding parts finally becomes as great as it is in the artery; and, as it is greater there than in the capillaries, the latter must be compressed and become impassa- ble for the arterial blood. In accordance with this, apoplectic fits al- most ahvays accompany arterial hemorrhages of any extent. If we analyze the above symptoms of the apoplectic fit, Ave find that, Avhile it lasts, the functions of both sides of the cerebrum are lost. The pa- tients have no feeling, even on the strongest peripheral irritation; they cannot make the slightest motion, and consciousness is entirely lost. On the other hand, those portions of the brain through Avhich acts indispensable to life, especially respiration, are performed, retain their functional power. This is, apparently, because the falx protects the opposite hemisphere less, from the compression of the capillaries by the extravasation, than the tentorium does the medulla oblongata. Effusions of blood beloAV the tentorium, even when slight, are very dangerous, because in them the medulla oblongata is not thus pro- tected, and its functions are readily disturbed by compression of its capillaries. I shall not attempt to decide whether or not the slowness of the pulse, the diminished frequency of respiration, and the contrac- tion of the pupil, observed during apoplectic fits from effusions above the tentorium, are due to increased excitement of the vagus and oculo- APOPLEXY. 199 motor nerves as a result of pressure acting on them, but somewhat modified by the tentorium. If the patient does not die during the apoplectic fit, but recovers consciousness, he shoAvs signs of a more or less severe encephalitis in a few days. This depends on the injury to the brain from the hemor- rhage, hence must be regarded as traumatic. When it does not reach a great height and only leads to neAV formations of connective tissue about the clot, the symptoms are increased frequency of pulse and other signs of fever, headache, sparks before the eyes, delirium, occa- sionally also twitchings and contractions of the paralyzed parts. Af- ter a time these " symptoms of reaction " moderate and finally disap- pear, and the patient is Avell except the remaining paralysis. But, if the inflammation in the vicinity of the clot be of considerable intensity and induce inflammatory softening, the above symptoms are accompa- nied by those of general paralysis, and the patient dies as a result of too great severity of the so-called symptoms of reaction. From the varied size and number of the hemorrhages, their differ- ent seats, the greater or less rapidity of their occurrence, as well as from the more or less severe inflammation of the surrounding brain, Ave have many A^arieties in the course of cerebral hemorrhages, of which Ave shall mention only the more important. A rather frequent appearance of the disease, which corresponds to a rapidly-occurring extensive effusion, or to the coincident occurrence of several hemorrhages, is the folloAving: After some premonitory symptoms, or even without them, an apoplectic fit suddenly occurs; the patient does not again recover consciousness, the paralysis ex- tends to the medulla oblongata, the breathing becomes irregular, the pulse intermittent and sIoav, the pupils dilated, and death occurs in a Icav minutes (apoplexie foudroyante), or after some hours. In a second class, Avhich is most frequently seen, and Avhich is also due to a rapidly-occurring but probably less extensive hemorrhage at the usual places, there is also first an apoplectic fit; even during uncon- sciousness we may see by the distortion of the face, by the peculiar relaxation of the muscles on one side, sometimes also by the dilatation of one pupil, which is the paralyzed side. After a feAV minutes or some hours, or occasionally not till next day, the patient gradually arouses from the stupor; but he speaks indistincth, and hemiplegia, with the peculiarities above described, becomes eAident. On the sec- ond or third day there are fever and the other symptoms of traumatic encephalitis. After these have disappeared, the patient remains for the rest of his life paralyzed on one side of his body, although the part of the paralysis due to edema in the vicinity of the apoplexy disap- pears after a time. 200 DISEASES OF THE BRAIN. In other cases, most probably when the hemorrhage ceases for a time and returns again, and continues moderately, the disease begins Avith an apoplectic fit, from which the patient arouses after a time. We note the hemiplegia, but hope that this time the patient will es- cape with his life. But, after a few hours, consciousness again begins to disappear, and finally is lost entirely, does not return, and the pa- tient dies comatose. A sloAvly-occurring hemorrhage, which finally becomes very abun- dant, appears to induce the cases where an apoplectic fit does not open the scene, but where there is first hemiplegia, and, later, loss of con- sciousness and general paralysis of the brain. It would require too much time to fully describe other appearances, particularly the modifications resulting from the different severity of the reactive inflammation in the vicinity of the clot, and from the varied grades of the consecutive atrophy of the brain. Treatment.—For the prophylaxis of apoplexy, Ave may refer to Chapters I. and IV. of this section, since the prophylaxis of cerebral hemorrhage demands the same general rules that we gave for the treatment of cerebral hyperemia, and for the disturbances of circulation resulting from disease of the arteries. If a patient has had one attack of apoplexy, he must be particularly careful to avoid all causes by which the cerebral vessels may be overfilled and distended; he must especially avoid long, luxurious meals, and must keep his bowels regular. If cerebral hemorrhage has occurred, it becomes our object to pre- vent a continuance of the bleeding, to induce reabsorption of the ex- travasation, and the formation of an apoplectic cicatrix. But we must not deceive ourselves as to our power, and must understand that we have no remedy for arresting the hemorrhage, or for hastening the reabsorption and cicatrization. In the treatment of this disease we are restricted to combating the more dangerous symptoms as well as possible. Not a few patients, in apoplectic fits, recover consciousness during venesection, and it seems as if we could, not unfrequently, pre- vent the extension of the paralysis from the cerebrum to the medulla oblongata, which is indispensable to life, and so save the patient by bleeding. On the other hand, there is no doubt that, in many cases, bleeding during an apoplectic fit hastens a fatal result; collapse occurs immediately after the venesection, and the patient never arouses. We have previously said that bleeding must always prove beneficial, if the symptoms given as signs of pressure on the brain were actually in- duced by the pressure to which the brain is subjected by the extrava- sation ; and we have also said that the want of success in venesection, in many cases, spoke against this explanation. From the explanation APOPLEXY. 201 that we have given of the apoplectic fit, it is evident that, under some circumstances, venesection is a very useful remedy; under others it is very injurious, and the indications for it may be very exactly given. In order that as much arterial blood as possible may enter the brain, we must try to facilitate the escape of the venous blood, Avithout, how- ever, diminishing the propelling power too much. If the impulse of the heart be strong and its sounds loud, if the pulse be regular, and no signs of commencing edema of the lungs exist, avc should bleed Avithout delay. Local bleeding by leeches, behind the ears, or to the temples, or by cups to the back of the neck, cannot replace general bleeding, but may be used as adjuvants. If, on the contrary, the heart's impulse is weak, the pulse irregular, and rattling in the trachea has already begun, we may be almost certain that bleeding would only do harm, since the action of the heart, which is already weakened, would be still more impaired, and the amount of arterial blood going to the brain would thus be still more decreased. When the latter state occurs, the symptomatic indications require just the contrary treatment, in spite of the original disease being the same, and being- due to the same causes. We must strive Avith all our skill, by the use of stimulants, to prevent paralysis of the heart. If we cannot give wine, ether, musk, etc., internally, Ave should apply large sinapisms to the chest and calves of the legs, rub the skin vigorously, sprinkle the breast Avith cold Avater, or drop melted sealing-Avax on it. If the patient has recovered consciousness after the apoplectic fit, we simply prescribe a mild, unirritating diet, keep the boAvels open, and cover the shaved head Avith cold compresses, so as to prevent, if possible, too severe inflammatory reaction. 'According to the severity of the inflammatory symptoms which, nevertheless, occur, Ave may continue this simple treatment, and at most give a purge, or apply leeches behind the ears, and repeat the application if necessary. In this stage venesection is superfluous and dangerous. On the other hand, especially AAiien the fever-symptoms have moderated, good is done by derivatives to the nape of the neck, such as blisters and pus- tulating ointments, which subsequently are no more to be used. If the stage of inflammatory reaction has happily passed, and the patient is pretty well, except the paralysis, we should avoid prescribing strychnia and other remedies, wiiich are neither theoretically nor prac- tically useful, but should regulate the diet and bowels, and place the patient under the best possible hygienic influences. Well-to-do pa- tients may be sent to Wildbad, Gastein, Pfafers, or Ragatz. We must not hope that the destroyed filaments of the brain will be restored by the use of these waters, but experience shoAvs that, at these places, both cerebral and spinal paralysis often improve; probably this im- 202 DISEASES OF THE BRAIN. provement is due to the favorable influence of the baths on the inflam- mation about the clot, and on that portion of the paralysis due to it. Lastly, it cannot be denied that paralyses are generally improved by the employment of the induced current of electricity. This is doubt- less solely because " faradisation localises " is one of the most powerful means of therapeutic gymnastics. After paralysis has lasted some time, its degree almost ahvays depends partly on diminished excita- bility of the nerves, and on commencing atrophy of the muscles from long disuse. For both of these states the methodical excitement of the nerves by the induced current is certainly the best remedy, and, at all events, it deserves the preference to irritating liniments, salves, and tinctures. CHAPTER VI. HAEMORRHAGES OF THE CEREBRAL MEMBRANES--APOPLEXIA MENIN- GEA--HEMATOMA OF THE DURA MATER. Etiology.—Excepting traumatic hemorrhages of the meninges, among Avhich are to be classed those occurring during birth, this is a rare affection. Effusions of blood in the subarachnoid space, or be- tAveen the dura mater and arachnoid, result mostly from the breaking through of a cerebral hemorrhage. Occasionally, ruptures of aneu- risms, or of degenerated arteries, cause the meningeal bleeding; in other cases, the cause cannot be found. The extensive capsulated collections of blood occasionally found, on autopsy, on the under surface of the dura mater, are not, according to Virchow's instructive examinations, as was formerly supposed, simple extravasations of blood, at whose periphery the fibrin has been precipitated and the fluid part capsulated, but they are the remains of chronic inflammations of the dura mater (pachymeningitis), with hemorrhagic exudations. Virchow calls this blood-sac hematoma of the dura mater. The blood filling it comes from the numerous large and thick-walled capillaries that have formed in the pseudo-membrane of the dura mater during this variety of chronic inflammation, and it has been effused between the layers of the pseudo-membrane. The causes of chronic pachymeningitis, Avith hemorrhagic exudation, are not perfectly known. The disease occurs chiefly in old age, and re- markably often in persons with mental disease, and in drunkards. It appears to develop sometimes as an independent, sometimes as a sec- ondary disease, due to injuries of the brow. In the latter case it is said that years may intervene between the injury and the first symp- toms of hematoma (Grfeslnger). Anatomical Appearances.—If the blood be effused in the sub- ILEMATOMA OF THE DURA MATER. 203 erachnoid space, Ave usually find it as a more or less thick layer spread over the surface of the cerebrum and cerebellum. If the arachnoid be not torn, of course Ave cannot Avash off the extravasation by turning a stream of water on it. Usually part of the extravasation reaches the ventricles, and there also Ave find more or less blood. In hemorrhages between the dura mater and arachnoid the extravasation is generally collected, more particularly on the tentorium and at the base of the skull, and thence extends into the vertebral canal. But on the con- vexity of the hemispheres we also find bloody masses, Avhich may be Avashed off by squeezing out the sponge over them. In both forms of haemorrhage there is either simply flattening of the convolutions and anemia of the brain-substance, or else the layers of brain-substance next to the hemorrhage are suffused with blood and softened. Hematoma of the dura mater is usually located near the sagittal suture and has the form of an oval flat sac, which may attain consid- erable size, and may be four or five inches long, two or three broad, and half an inch thick. The Avails of the sac are colored rusty-brown by altered hematin; its contents are partly fresh fluid or coagulated blood, partly dirty reddish-broAvn clots, that are unmistakably older. The corresponding half of the cerebrum is flattened, or even sIioavs a depression. Not unfrequently the hematoma is on both sides. We have the opportunity, rather frequently, of observing the commence- ment of a pachymeningitis hemorrhagica; for, in many autopsies, Ave find a delicate yellow or brown connective tissue, larger on the inner surface of the dura mater and firmly adherent to its surface. Symptoms and Course.—Hemorrhages in the subarachnoid space or on the free surface of the arachnoid, do not belong to the " local" but to the " diffuse " diseases of the brain. Hence, Avhen there is no complication Avith cerebral hemorrhage, they are not accompanied by the regional symptoms characteristic of this, especially hemiplegia; on the other hand, the apoplectic fit is usually uncommonly severe, as the bleeding is generally very abundant, and is spread over both sides. Frequently the apoplectic fit occurs suddenly Avithout any premonitory symptoms, and the patients die Avith the above-described symptoms of apoplexie foudroyante. When this occurs, we can, at most, make only a probable diagnosis, which depends solely on the absence of hemi- plegia, the symptoms of which may, as a rule, be distinguished, even in the severest fits, from cerebral hemorrhage. In other cases the apoplectic stroke is preceded by severe headache, and in some cases by general convulsions. Since these symptoms, particularly the latter, only occur exceptionally in cerebral hemorrhage, and are often seen in extensive disease at the convexity of the hemisphere, they, in con- nection Avith the absence of all signs of hemiplegia, enable us to decide 204 DISEASES OF THE BRAIN. with greater certainty that the case is not one of cerebral but of me- ningeal hemorrhage. Hematoma of the dura mater often runs its course with symptoms from AAiiich the disease cannot be certainly diagnosed, and Avhen it occurs in the course of mental affections, as so often happens, Ave can- not usually make even a probable diagnosis. In other cases, the fol- loAAing factors, to which Griesinger has called attention, enable us, with more or less assurance, to make a diagnosis of hematoma of the dura mater; if circumscribed headaches, gradually increasing to great severity, in the vicinity of the vertex and forehead be the first, and, for a long time, the only trouble of Avhich the patients complain ; and if, between the appearance of these pains and that of other severe brain- symptoms, there be an interval not so short as in acute diseases of the brain and its membranes, but shorter than in most chronic diseases of these parts, particularly in the different cerebral tumors, the first sus- picion falls on inflammation of the meninges, particularly of the dura mater, since inflammation of the other membranes has so great a ten- dency to spread, that it is accompanied by diffuse, not by chcumscribed, headache. We are the more justified in this, as the form of pachy- meningitis in question occurs just at the point where the patients com- plain of pain. If the patient had been mentally diseased before the commencement of the headache, or given to drinking excessively, or it he had had an injury of the head, particularly of the forehead, some time previously, there is still more reason for supposing the case one of pachymeningitis, as is evident from the etiology. But we also know that this form of meningitis usually leads to a large effusion of blood, encroaching on the cerebral cavity, and that then the effusion is cap- sulated on one or both sides of the sagittal suture. Hence, if the headaches be subsequently accompanied by the signs of compression of the capillaries of the cerebrum, by mental disturbances, loss of mem- ory, diminished power of thought, increased inclination to sleep, which finally increases to coma, a sloAvly-developing and usually not pure hemiplegia, after excluding various brain-diseases, we must think of hematoma of the dura mater as being in the first rank of those that may possibly be present. Since, in hematoma of the dura mater, there may be reabsorption of the blood and consequent freedom of the brain from the pressure on it, a favorable course of the disease and recovery of the patient speak for hematoma in doubtful cases. If the effusion of blood does not take place gradually, as in the course of the disease above described, but occurs suddenly; if it is large and limited to one side, the symptoms are those of an abundant hemorrhage in one side of the cerebrum. On superficial examination it may appear remarkable that, even in large hematomata of one side, there is occasionally no INFLAMMATION OF THE DURA MATER. 205 hemiplegia, or else it is very incomplete; but we must bear in mind that hematoma occurs just at the place where the increased pressure on one hemisphere is most readily transferred to the other, through the free communication between the two sides in the anterior portion of the skull, particularly when the hemorrhage comes on sloAvly. Among the symptoms of hematoma, Grleslnger also lays stress on the almost constant contraction of the pupil, and is inclined to regard this as a " symptom of irritation of the surface." In the preAious chapter I attempted to give another explanation of the contraction of the pupil (which was also hypothetical) in diseases encroaching on the space above the tentorium. Treatment.—In the treatment of meningeal hemorrhages, the same rules hold good as were given for that of cerebral hemorrhages, and Ave may the rather refer to the former chapter, as it is impossible to make an exact diagnosis between the tAvo. If Ave consider the diagnosis of a hematoma as certain, Ave may, in recent cases, apply leeches behind the ears, ice-compresses to the head, and give a purge occasionally. In the latter stages, blisters or pustu- lating ointments to the nape of the neck suffice. With this treatment I have had very good results in two cases that I have observed; still, in spite of the very characteristic symptoms in these cases, there may, possibly, have been an error of diagnosis. IXFLA3IMATIONS OF THE BRAIX AND ITS MEMBRAXES. In the following chapters Ave shall speak—1. Of inflammation of the dura mater and its sinus. 2. Of inflammation of the pia mater, with puro-fibrinous exudation. 3. Of tuberculous inflammation of the pia mater, including acute hydrocephalus. 4. Of epidemic cerebro-spi- nal menino-itis ; and 5. Of inflammation of the brain-substance. Since inflammation of the arachnoid cannot be distinguished from that of the pia mater, Ave shall not treat separately of arachnitis. CHAPTER VII. INFLAMMATION OF THE DURA MATER, INFLAMMATION AND THROM- BOSIS OF THE CEREBRAL SINUS. In the previous chapter Ave spoke of one form of pachymeningitis, because, on account of the hemorrhage it causes, and its clinical sourse, it is most suitably classed among meningeal hemorrhages. Now Ave have only to speak of that form Avhich, since Virc/ioio's studies «n hematoma of the dura mater, is called pachymeningitis externa. 206 DISEASES OF THE BRAIN. Etiology.—It is very doubtful whether pachymeningitis occurs, as a primary and independent disease, from cold and other causes. At all events, it is generally secondary, and as such accompanies fissures, fractures, and especially caries of the cranial bones, particularly of the petrous and ethmoid bones, as well as caries of the upper cervical vertebra. In periostitis of the outer surface of the skull also, pachy- meningitis occasionally occurs, without our being able to distinguish any continuity between the two diseases by changes in the cranium. Inflammation of the cerebral sinus, with consequent thrombosis, 01 even thrombosis of the sinus, with subsequent inflammation of its walls, occurs proportionately often, being most frequent in the sinus lying on the petrous bone, the lateral and petrosal. This is evidently because inflammation and thrombosis of the cerebral sinuses are induced, in the great majority of cases, by caries of the petrous bone advancing to the base of the skull. The numerous patients suffering from tedious otorrhea, as a result of otitis interna, are constantly threatened, as with a Damocles' SAvord, by inflammation or thrombosis of these si- nuses. Not unfrequently there are suppuration and breaking down of the thrombus, and then particles of it may enter the efferent veins and lead to embolism and metastatic inflammation. Anatomical Appearances.—The anatomical changes in mild and chronic cases of pachymeningitis externa are limited to a gradual thickening of the dura mater as a result of proliferation of connective tissue on its outer surface; the dura mater thus becomes firmly attached to the cranium, and subsequently the neoplastic tissue partly ossifies. In acute and seAere cases the dura mater is usually reddened by vTascular injection and small ecchymoses, is thickened and infiltrated in circumscribed spots corresponding to the point of injury or caries of the cranial bones. Later, this membrane becomes discolored, its tissue is relaxed and softened; finally, there is suppuration, and, if pus collects betAveen the dura mater and cranium, the inflamed part be- comes detached from the bone. In the latter case the pia mater also is almost ahvays inflamed, and generally to a great extent. Even on autopsy it is often difficult to decide whether the inflammation of the VA^all of the sinus preceded the thrombosis, or the reverse. If the thromboses be not disintegrated, they adhere firmly to the relaxed rough inner surface of the thickened wall of the sinus, and occasionally extend backAvard to the torcular Herophili, and in rare cases down to the internal jugulars; as has been shown by the observations of Lebert, who has very greatly advanced our more accurate knowledge of this disease. More frequently on autopsy we find the thrombus already broken down, and the inflamed sinus filled with a purulent or sanious, occasionally gray-green and stinking fluid, mixed AAith flocculi. Alono- INFLAMMATION OF THE CEREBRAL SINUSES. 207 with these changes we generally find those of otitis interna, and ex- tensive caries of the petrous bone; viz., destruction of the drum, absence of the ossicula, polypoid proliferations of the mucous mem- brane, the tympanum full of pus, which also infiltrates the labyrinth, cochlea, and mastoid cells. Symptoms and Course.—Chronic pachymeningitis, which causes thickening of the dura mater, and its firm adhesion to the cranium and ossification of the thickened layer, may be accompanied by headache and other symptoms; but these are not at all characteristic and do not show us Avhat the disease is. The symptoms and course of acute pachymeningitis externa also are almost always so modified by the symptoms of the original disease, by complications with extensive inflammation of the pia mater, and by extension of the inflammation to the cerebral sinus with its results, that it is impossible to give a pure description of the disease. If an injury of the skull, or, still more, if a caries of the temporal bone, due to otorrhea, be accompanied by unusually severe and extensive pain in the vicinity of the diseased bone, by fever, vomiting, dizziness, noises in the ear, twitching, delir- ium, and other symptoms of irritation of the brain, which are sub- sequently folloAved by those of depression, and finally by general paral- ysis, we may conclude, that the disease of the bone has at first caused inflammation of the dura-mater, and later diffuse inflammation of the pia mater. The first stage is often short and indistinct, and, on the first visit or at their reception into the hospital, we find the patients in deep sopor. But even in such cases the above diagnosis may be made with tolerable certainty, if aa e find an injury of the skull, or particu- larly a chronic otorrhea, and can discover no other causes for the brain- disease. The symptoms induced by inflammation and thrombosis of the cerebral sinuses are always accompanied by those of meningitis as o-iven above; hence it Avill be enough to limit ourselves to pointing out under what circumstances we are to suspect inflammation or thrombo- sis of a cerebral sinus, when we have a meningitis or encephalitis accom- panying caries of the petrous bone. From the great frequency of this complication, I think it is well to keep in view its possibility and even its great probability, although the very doubtful signs of the disease should be absent. The suspicion will acquire more probability, should avc observe a symptom of thrombosis of the transverse sinus, that was o-iven by Gerhardt Avith great acuteness, namely, less fulness of the jugular vein drawing its blood from the obstructed sinus. The same Avould be true if we found a symptom given by Griesinger, AA'hich was only found in one case, it is true, a circumscribed painful edema behind the ear ; although, in caries of the mastoid process, this edema 60 208 DISEASES OF THE BRAIN. (which Griesinger calls a phlegmasia alba dolens en immature) maj arise from other causes than from the extension of the thrombus through the emissaria santorini which pass out in the sigmoid fossa. In most cases it is only from the occurrence of rigors and the signs of metastatic deposits in the lungs that we can conclude that canes of the petrous bone has not only induced meningitis and encephalitis, but has also led to thrombosis in the cerebral sinuses. Treatment.—On the signs, or even suspicion, of inflammation of the dura mater, we should use energetic antiphlogistic treatment by repeated application of leeches behind the ears. At the same time, if there be any otorrhea, we should make Avarm injections into the af- fected ear and cover it with cataplasms. Active purges and large blisters to the back of the neck are also useful. In other respects, the treatment of pachymeningitis corresponds with that of inflammation of the pia mater. CHAPTER VIII. INFLAMMATION OF THE PIA MATER, WITH PURO-FIBRINOUS EXUDA- TION--MENINGITIS OF THE CONVEXITY--MENINGITIS SIMPLEX. Etiology.—In acute meningitis, an exudation containing many pus-cells is effused into the subarachnoid space; in chronic meningitis there are diffuse cloudiness and thickening of the pia mater and arach- noid, from proliferation of the connective tissue. Acute meningitis, with puro-fibrinous exudation, is in many cases a secondary disease, and as such accompanies injuries and diseases of the skull and of the dura mater or other inflammations and other dis- eases of the brain. Except in the epidemic form, of which Ave shall speak in Chapter IX., it rarely occurs as an independent disease in pre- viously healthy persons, but is somewhat more frequent in cachectic indiAiduals or in those exhausted by long illness. Thus it is observed in convalescence from pneumonia and pleurisy, or from acute exanthe- mata and other infectious diseases, and from protracted diarrheas, but especially during Bright's disease, etc. Although in these cases we frequently cannot discover any new source of injury acting on the body, Ave have no right to consider this inflammation of the pia mater as metastatic or even as secondary. The action of the sun's rays or of a very high or even of a very low temperature on the head, chilling the body, or getting Avet, misuse of liquor, etc., are mentioned among the exciting causes of meningitis. But only the last of these causes has been proved to have any influence in exciting this disease. Re- cently Griesinger has called attention to a form of meningitis which MENINGITIS SIMPLEX. 209 appears as one symptom of constitutional syphilis ; and in the Greifs- walder clinic I have seen a case of this kind, AAiiich has been fully de scribed by Professor Zlemssen, at that time my assistant. Anatomical Appearances.—Meningitis, with puro-fibrinous exu- dation, occurs chiefly on the convexity of the cerebrum. In the acute form we there find the small vessels of the pia mater more or less dis- tinctly injected, and in the subarachnoid space, especially between the convolutions and around the large vessels, we find a yellowish, generally firm exudation, consisting of pus-corpuscles and fine granular fibrin. In milder grades of the disease the exudation is chiefly in the perivascular spaces. Occasionally the arachnoid is at the same time covered with a more fibrinous or more purulent coating. The cortical substance of the brain is sometimes of normal consistence, sometimes it is softened by inflammation. The ventricles which, in tubercular basilar meningitis, are almost ahvays filled vvith fluid, are generally found empty in purulent meningitis of the convexity. In chronic me- ningitis we usually find the arachnoid adherent to the dura mater either by a few points or throughout a considerable extent; the pia mater is thickened and cloudy, the subarachnoid spaces filled with turbid fluid; or else we find the pia mater also transformed to a firm, decidedly thickened membrane, which cannot be removed from the brain without tearing. Symptoms and Course.—Acute inflammation of the pia mater is accompanied by symptoms of severe fever, particularly by a very fre- quent pulse, and, like acute and extensive inflammation of other or- gans, occasionally begins with a chill. Fever of similar character and equal severity occurs in scarcely any other disease of the brain, and consequently is very important in the diagnosis of meningitis. If the frequency of the pulse disappear after the disease has lasted some time, if it fall from 120-140 beats per minute to 60-80 beats, while the other symptoms of fever and the functional disturbance of the brain increase, the eAidence is still more in favor of meningitis. The other symptoms of the disease are headache and the repeatedly-men- tioned functional disturbance of the brain, partly with the character of irritation, partly of depression or complete paralysis. In acute me- ningitis, the headache becomes very severe; patients not only com- plain of it while they retain consciousness, but even when this is im- paired they frequently grasp the head and moan slightly, so that we may suppose they still feel pain. In almost all cases there are psychi- cal disturbances even at the outset of the disease, probably from the vicinity of the cortical substance; the patients are very excited and restless, usually quite sleepless, and soon become delirious. In the sensory functions also there is more irritability, so that the patient 210 DISEASES OF THE BRAIN. is very sensitive to light, sound, and even to slight friction on the skin. Finally, there are noise in the ears, sparks before the eyes, restless- ness, gnashing of the teeth, tAvitchings, and often also contraction of the pupil, and vomiting. We had to mention all these symptoms in simple hyperemia of the brain and in hydrocephaloid; indeed, there is no pathognomonic sign of meningitis, Avhich is present in this and ab- sent in other brain-diseases. It is true the etiology, the grade of the fever, especially the height of the pulse and the unusual severity of the headache, occasionally speak, even in this stage, with great proba- bility against simple hyperemia or anemia of the brain; but frequent- ly it is only the subsequent course, the severe accidents that charac- terize it, the want of success in treatment, and the usual fatal result, that render the diagnosis certain. If any of the characteristic symp- toms be absent in the first stage, we must give a guarded diagnosis. Frequently only the effect of a laxative or of local blood-letting verifies the diagnosis betAveen hyperemia of the brain and meningitis. An attack of convulsions, usually preceded by stiffness of the neck, from tonic contraction of the muscles of the nape of the neck, often indi- cates the passage into the second stage. In this the patients fall into a deep sopor, become entirely insensitive to the irritation, cannot move their limbs, although certain muscles, particularly those on the back of the neck, are in a state of tonic contraction, and there are general convulsions from time to time. The pupil, which was previously con- tracted, now often becomes dilated, and the pulse also is usually, but not always, retarded. While the stupor and general paralysis increase, the patients generally die of coma in a few days, more rarely not till the second or third week. These stages in the clinical course, between Avhich there is occasionally a slight improvement, cannot be referred to any perceptible change in the pathologico-anatomical course; as if for instance, the first stage corresponded to the hyperemia of the me- ninges, and the second to the exudation in the subarachnoid space. Nor must we omit to mention that not unfrequently, especially Avhere the meningitis is due to caries of the petrous bone or to disease of the brain, the first stage is very little marked or not at all noticed. In these cases the symptoms begin with an attack of convulsions which is repeated several times, and is folloAved by deep coma and general paralysis, usually accompanied by contraction of certain muscles. The most frequent termination of acute meningitis is death. Ac- counts of successful cases, and especially of rapid cures must excite the suspicion of erroneous diagnosis, which may readily occur from the similarity of the symptoms of meningitis to those of simple cerebral hyperemia, particularly in children. The symptoms of chronic meningitis are not accurately knoAvn, fre- ACUTE HYDROCEPHALUS. 211 quently as its remains are found on autopsy of drunkards and insane patients. This is especially true of the commencement of the disease. It is probable that it is accompanied by headache and functional dis- turbance of the brain of an irritative character; but in drunkards, for instance, it will always be doubtful Avhether these are symptoms of inflammation of the brain or of alcoholic poisoning. The adAranced stages of the disease may be more readily made out. If, in a patient who has been exposed to the above causes, and in whom we can ex- clude other brain-diseases, we find decided impairment of memory, dul- ness of intellect, disjointed frame of mind, if there be also trembling of the limbs, tottering gait, and other symptoms of gradually-progress- ing paralysis, we may diagnose chronic meningitis. Treatment.—There is no doubt that favorable results are some- times attained by active treatment in acute meningitis with puro-fibri- nous exudation. It is not generally proper to bleed from the arm, but we may apply leeches to the broAV and behind the ears, and, if the strength of the patient permit, may repeat the application. We may also cover the shaved head with cold compresses, and give an active purge of calomel and jalap. In the later stages of the disease, if, in spite of the previous treatment, there be coma and other signs of cere- bral palsy, we may apply a large blister to the nape of the neck, and rub pustulating ointment on the head. Still more efficacious than these derivatives are douche baths, pouring cold water over the head from a pitcher held some distance above it. The patients almost al- ways recover consciousness as this is being done; but, it must be re- peated at intervals of a feAV hours, to secure a permanent result; Avith each successive employment of the douche we must increase the num- ber of pitcherfuls. I shall lastly mention that frictions with mercurial ointment, and the continued administration of calomel, are much em- ployed. In chronic meningitis, Kruckenberg also recommended cold douche baths as the most efficacious treatment. He particularly quoted the case of an old official, over whose head he daily poured as much as fifty pitcherfuls of cold water. CHAPTER IX. BASILAR MENINGITIS, TUBERCULOUS INFLAMMATION, AND SIMPLE MIL- IARY TUBERCULOSIS OF THE PIA MATER--ACUTE HYDROCEPHALUS. Etiology.—In basilar meningitis there is a deposit, in the sub- arachnoid space at the base of the brain, of a readily-coagulating exu- dation, containing feAV pus-corpuscles. At the same time, there are almost ahvays tubercular granulations in the meninges, causing a form 212 DISEASES OF THE BRAIN. of disease designated as tuberculous basilar meningitis. This must be distinguished from simple miliary tuberculosis of the meninges, where the development of tubercle is not accompanied by inflammation and exudation, because the symptoms and course of the two diseases differ in some respects. Both basilar meningitis and simple tuberculosis of the meninges almost always cause effusions of fluid in the ventricles, and softening of their walls and the surrounding parts. The latter is the result of maceration, or destruction of the brain-substance by a simple transudation or inflammatory exudation. Tuberculous basilar meningitis, as well as mihary tuberculosis of the meninges, rarely occurs, as a primary and independent disease, in persons previously healthy. We must bear this in mind, as it is very important for the differential diagnosis of the various forms of menin- gitis. These diseases are most frequently parts of a general acute or chronic miliary tuberculosis, or, at least, of one affecting most of the organs of the body. This form of the disease has many victims among those children of whom, when speaking of pulmonary tuberculosis, we said they had a strong predisposition to pulmonary consumption, if they did not die early of croup or hydrocephalus. These are not only children with marked scrofulous diseases, but also the offspring of con- sumptive or otherwise debilitated parents. They are badly nourished, and not well developed physically, but are often very bright men- tally ; have a fine skin, very perceptible veins, long eye-lashes, and a blue sclera. Caseous degeneration of the bronchial and mesenteric glands, caseous deposits in the lungs, and other old disturbances of nutrition, which, along with fresh deposits of tubercle in different organs, are found on autopsy of these children, if they finally die of hydrocephalus, cannot usually be recognized with certainty during life; hence the brain-affection is regarded as a primary disease. The case is different when the tuberculous inflammation or miliary tuberculosis of the meninges attacks adults. For then the symptoms of meningeal tuberculosis have either been preceded, for a short time, by those of acute miliary tuberculosis, or, more frequently, for a long time, by those of chronic consumption of the lungs. In other cases, tuberculous me- ningitis and miliary tuberculosis of the meninges accompany old tuberculous affections, such as chronic pulmonary or cerebral tubercu- losis, and cheesy degeneration of the bronchial and mesenteric glands, but are not accompanied by fresh deposits of miliary tubercle in other organs; they form the only acute complication of these chronic tuber- culous affections. Lastly, although rarely, tuberculous meningitis or miliary tuberculosis of the meninges occurs, without any precedent tuberculosis of other organs, in previously healthy persons, or during convalescence from severe diseases, such as typhus, measles etc. ACUTE HYDROCEPHALUS. 213 During the first year of life, tuberculosis of the meninges is rare; .ater, during childhood, it is proportionately frequent; in adults, only solitary cases occur, except where it complicates chronic pulmonary consumption. Among the exciting causes, premature or excessive mental exertion is blamed most frequently for exciting hydrocephalus in children; this is probably unjust. Children not predisposed to it may be mentally stimulated to any extent without inducing hydro- cephalus ; and the early development of children falling a prey to this disease is due to their predisposition, not to then bringing up; this is not the cause of their hydrocephalus. The same is true of the asser- tion that a blow or fall on the head induces tuberculosis of the menin- ges and acute hydrocephalus. It is almost always easy to make out that the sick child has, some time or other, fallen on its head; but it does not thence folloAV that this fall is to be regarded as the cause of his disease. Anatomical Appearances.—In basilar meningitis we find a yel- loAvish, opaque exudation, Avhich is sometimes very plentiful, in the meshes between the pia mater and arachnoid, especially about the optic chiasm, as Avell as in the portions of the meninges extending toward the pons and medulla oblongata, and thence along the larger cerebral fissures, particularly the fossa of Silvius, toward the convex surface of the brain. At the same time, we almost always find the pia mater covered with A\Thitish granulations, the size of a grain of sand or a hemp-seed, most distinctly so in the vicinity of the blood- vessels. In simple miliary tuberculosis of the meninges the changes are less marked, and it is only on careful examination at the above places that Ave find numerous, usually very small, Avhitish, granular opacities of the pia mater, Avhose significance is often only rendered evident by the coincident occurrence of hydrocephalus and the presence of tubercle granulations in other organs. In both forms, the ventricles, especially the lateral and the third ventricles, are sometimes moderately, sometimes considerably dilated by serous fluid. The latter is occasionally quite clear, but is usually clouded by flocculi. The walls of the ventricle, but especially of the fornix and commissures, are at the same time so softened that they usually break down da the slightest touch. This (hydrocephalic) soft- ening spreads indefinitely, often far beyond the immediate neighbor- hood of the ventricle. The larger the effusion in the ventricles, the more bloodless and pale the brain becomes, and the whiter the soft- ened parts. Symptoms and Course.—There is no symptom pathognomonic of basilar meningitis, and which alone will render a diagnosis possible. 214 DISEASES OF THE BRAIN. Nevertheless, the disease is almost always easy to recognize and to distinguish from other diseases. Characteristic peculiarities in the sequence of the symptoms, distinct signs from which the original seat of the affection and its subsequent extension may be determined, as well as the very regular subacute course of the disease, almost always give sufficient grounds for a certain diagnosis. At the commencement it is a local disease, situated at some point on the base of the brain, where numerous nerves start from that organ and run to the foramina through which they leave the skull. Later, when the disease extends to the ventricles, the local disease at the base becomes complicated, by the excessive effusion in the ventricles and by extensive hydrocephalic softening of the brain-substance, with diffuse disease of the cerebrum. In accordance with this, among the most constant symptoms of basilar meningitis are such as indicate irritation and afterward paralysis in the parts supplied by the nerves of the eye, the vagus and medulla oblongata. Among these are contraction and, later, dilatation of the pupil, ptosis of the upper eyelids, vomiting, slowness and subsequent frequence of the pulse, the peculiar changes of the respiration, and de- pression of the abdomen, according to the results of Budge's observa- tions. In the same way, corresponding to the course of the patho- logico-anatomical changes, the functions of the cerebrum at first shoAV no marked disturbance, except the symptoms of so-called general cere- bral irritation, while, as the disease advances, there is severe disturb- ance, of the character that we have frequently mentioned as due to compression of the capillaries by diseases encroaching on the space; such as loss of consciousness, epileptiform convulsions, paralysis of the extremities, etc. In cases where this second set of symptoms is not very marked, Ave may even conclude that the effusion in the ventricles is not very large. Lastly, when the symptoms of paralysis are limited to one side in certain cases, or are more decided on one side than on the other, it is usually because the hydrocephalic softening is more ad- vanced on one side than on the other. Although basilar meningitis, particularly its tuberculous form, and miliary tuberculosis of the meninges, very rarely occur in persons pre- viously healthy, we must not count among its premonitory symptoms those of the diseases which it usually accompanies. On the other hand, in most cases, especially in children, the violent symptoms char- acteristic of a later stage of the disease are usually preceded for a time by insidious and indefinite symptoms, which may correctly be consid- ered as premonitory. Such children shoAv a change of manner, have no desire to play, like to sit in a corner, rest the head on the hands, are sleepy, and dream a great deal. They do not ahvays complain of severe headache, and when they do it is especially in cases AA'here there TUBERCULOUS MENINGITIS. 215 is not simple mihary tuberculosis, but a tuberculous inflammation of the meninges. During these symptoms, which usually last for several weeks, the children become emaciated because their digestion is im- paired, and probably also because they have fever. Nevertheless, it often happens that the mother overlooks or pays little attention to this period, and subsequently, Avhen severe symptoms appear, assures the physician that the child was suddenly taken sick. We must know Iioav important it is to decide Avhether there is the beginning of a new disease, or the commencement of the final stage of an old one, so as to make a more accurate examination. I have often found that the rela- tives and neighbors had noticed the altered manners of the child, while the mother had entirely overlooked them. If the above symptoms be accompanied by vomiting, which cannot be traced to errors of diet, and does not occur after eating, but when the child is raised up, if the patient at the same time suffer from con- stipation and the abdomen is sunken, the physician must regard the case as very serious, although the parents usually think it free from danger. The little patients soon begin to complain more of their heads; they become sensitive to light and sound, gnash their teeth during sleep, and occasionally give a piercing cry (crie hydrocepha- lique). From time to time we see tAvitchings of certain limbs, or sud- den spasm of the entire body. The patients start from their sleep AAith terror at some dream, and do not find relief from it even in wak- ing. They are very much excited, and often repeat the same Avord or phrase innumerable times. At this time the pupils are usually con- tracted and the pulse is more frequent. When these symptoms succeed the premonitory stage, and when Ave at last see the child bending its head backAvard, boring into the pillows, Avith the muscles of its neck contracted, and the cervical lymphatic glands swollen, we become cer- tain of the sorroAvful fact. After a few days, or eA~en sooner, the scene usually changes Aery suddenly. The passage into the second stage is generally marked by an attack of general convulsions, such as Ave have already described. The vomiting then becomes rarer or ceases entirely, the children no longer complain of pain, but put then hands to their heads in a pecu- liar way; loud noise does not disturb them, and the}- do not turn the face aAvay if a bright light be held before it; the peculiar cry and the o-nashino- of the teeth continue. We often find the muscles of some of the limbs or of one half the body slightly contracted, while those of the other side are relaxed. Noav the preAiously-contracted pupils be- come dilated, occasionally first one, then the other; the cliildren no longer regard objects held before them, and they begin to squint. The previously-frequent pulse becomes sloAver, falling to sixty beats a 216 DISEASES OF THE BRAIN. minute or even less. The respiration generally shows very peculiar changes; for a time the inspirations are very superficial, and it almost looks as if the child forgot to breathe; then there is a deep sighing in- spiration with which it repairs the neglect, as it were. The coma gradually becomes deeper; the lucid intervals that at first interrupted it grow more incomplete and shorter; the eyelids are either not closed, and the eye stares into space, or else the upper lid droops, and the eyeball is rolled up, so that the pupil is half covered by the upper lid. At the same time the color of the face often changes in a short time, and such a child, with its blooming cheeks, widely-open eyes, which have a peculiar dark and brilliant appearance from the dilata- tion of the pupil, has, to an uninitiated person, the appearance of not being very sick. During this stage there usually are attacks of con- vulsions at intervals; these are sometimes on one side of the body, sometimes on both. We must not conclude, from the convulsions on one side the body, that the opposite side of the brain is chiefly affected. The tetanic contractions of the muscles on the back of the neck, and the backward curvature of the neck, usually continue in this stage. The stage of the disease last described occasionally continues a week or more. In spite of the hopelessness of the patient's state, the physician must continue his visits, and at each one he is asked anew if there is no chance of averting the danger; at last the parents are utterly overcome, but even then the disease occasionally continues for days, or a temporary appearance of improvement again excites deceit- ful hopes. These are hard times for the physician, especially as he is almost powerless against the slowly-advancing but inevitable result; and as, for days, he has but little to do except prepare the parents for the child's death. We must note that death is not imminent till some decided changes occur in the symptoms, to which it is well to call the attention of the attendants. Almost always twelve to tAventy-four hours before death the pulse becomes very frequent, the skin is covered with copious perspiration, the previously-sunken belly becomes puffed up; defecation and urination are involuntary, and we may hear exten- sive moist and uneven rales in the chest. Most cases of tuberculous basilar meningitis, and of miliary tuber- sulosis of the meninges in children, run their course in the above man- ner and resemble each other very much. Slight differences result from the predominance of certain symptoms, and from the different dura- tions of certain stages or of the whole disease. But we must add that in some cases the disease runs a much more rapid course, and is accom- panied by symptoms so similar to those of acute meningitis, that it is impossible to distinguish them. On the other hand, we must mention that occasionally, on autopsy of patients Avho have died of consump- TUBERCULOUS MENINGITIS. 217 tion, we find mihary tuberculosis of the meninges, and slight amounts of hydrocephalus, which were not indicated by any prominent symp- toms during life. These cases seem to show that, in the description of the disease first given, the premonitory stage belonged to the com- mencement of the cerebral affection, and not to its complications or to the general tuberculosis. Lastly, Ave must point out that tuberculous basilar meningitis, and mihary tuberculosis of the meninges, develop- ing during advanced pulmonary consumption in adults, have no dis- tinct premonitory symptoms, but are first recognized from the occur- rence of contractions of the muscles of the nape of the neck, coma, sIoav pulse, dilatation of the pupil, and the other symptoms of the fully- formed disease. Death is the most frequent termination. Well- proved cases of recovery are very rare; but, even excepting the cases Avhere the diagnosis was someAvhat uncertain, there is no doubt that it has occurred. Neither the ordinarily variable course of the disease, nor the surprising remissions that usually occur, should induce us to give a more favorable prognosis ; only a continued improvement of all the symp- toms dare excite the hope that the disease Avill take a favorable course. Treatment.—Until Avithin a short time, the treatment of tuber- culous meningitis and acute hydrocephalus presented no difficulty to the physician. The inflammation of so important an organ naturally required the employment of all kinds of antiphlogistics. At the out- set of the disease, venesections were ordered, calomel and flor. zinci vvere administered, and mercurial ointment was rubbed in the nape of the neck, then the occurrence of calomel stools, or the first signs of salivation, were anxiously awaited, for they were a guaranty for the efficacy of the treatment. In the later stages, absorption of the exuda- tion was to be induced; hence the mercurial frictions Avere continued, and diuretics and active derivatives, even moxa on the shaved scalp, or pustulating ointments to it, Avere prescribed. If, in spite of all this, the paralysis continued to advance, an infusion of arnica and camphor was given. The more this disease was recognized as one symptom of extensive tuberculosis, the more antiphlogistic treatment was aban- doned ; then the opposite error was fallen into, either nothing was done (expectant treatment), or else all the efforts were directed to the cure of the tuberculous dyscrasia. The best mode of treatment of tuberculous meningitis and miliary tuberculosis of the meninges is as follows: At the commencement of the disease, especially Avhen severe headache indicates tuberculous inflammation rather than simple miliary tuberculosis, we should apply leeches behind the ears. This is the more urgently to be advised, as in this stage an exact diagnosis of the different forms of meningitis is scarcely possible, and aw do not certainly know whether the disease 21S DISEASES OF THE BRAIN. is not at first a simple inflammation of the meninges, which is sub- sequently accompanied by the development of the tubercle, after repeated relapse of the inflammation. When the local abstraction of blood proves beneficial, it may be repeated during subsequent relapses. In these cases, at the onset of the disease, laxatives and ice compresses may also be used. Otherwise the treatment is the same as that for meningitis, Avith puro-fibrinous exudation. But the treatment must be entirely different when the inflammatory symptoms are less decided, when the headache is slight, and the disease drags on slowly. Then a single venesection is admissible, it is true, but it rarely has even a temporary effect, and its repetition is almost always injurious. On the strength of tAvo successful cases, opposed, it is true, by a large num- ber of unsuccessful ones, I recommend large doses of iodide of potas- sium, continued for a long time. In the cases above mentioned, Avhere recovery took place under this treatment, there was a very extensive iodine eruption, and an iodine catarrh of the nose. These signs of iodism were absent in the unsuccessful cases. It cannot be denied that cold douches have a palliative effect, but I would advise against their use in marked cases of tuberculous basilar meningitis, and con- sequent acute hydrocephalus. During the affusion, the children almost always recover consciousness, but it is only for a short time. More- over, when not successful, the operation is very painful, not for the children, but for the persons around. The latter feel very much pained that the child was worried at the last, when it could not be assisted. The same is true of the application of moxe, and of frictions to the scalp with tartar-emetic ointment. Hasse recommends very small doses of morphia (-fa of a grain) even in the early stages, as he has seen undoubtedly beneficial effects from it in some cases. CHAPTER X. EPIDEMIC cerebro-spinal meningitis. From the fatal epidemics of this disease which have occurred of late years in Germany, cerebro-spinal meningitis has acquired a great interest for German physicians, to whom it was previously almost ex- clusively known from the accounts of French observers. In 1865 I wrote a treatise on epidemic cerebro-spinal meningitis; this article was well received on many sides, but also caused some opposition, because, in spite of the small number of my observations, I had ventured to make various hypotheses concerning the nature of the disease and the indications of the symptoms. But, on careful examination of the ex- tensive literature on the subject, of late years, I have found nothing EPIDEMIC CEREBRO-SPINAL MENINGITIS. 219 decidedly new, and have satisfied myself that my views had been gen- erally received; so, in the present chapter, I shall chiefly follow my preAious work. Etiology.—We are unacquainted Avith the injurious poAver Avhose action induces this form of meningitis, and whose spread over greater or less extents of country excites more or less extensive epidemics of the disease. But we may regard it as very probable that epidemic cerebro-spinal meningitis does not depend on atmospheric or telluric influences, but is rather due to an infection of the body AAith a specific poison. It is true, the occasional frequent occurrence of a disease in regions generally free from it, and even the affection of several mem- bers of the same family, do not alone justify the conclusion that the disease depends on infection. But the passage of an epidemic from place to place, as is often seen in epidemic cerebro-spinal meningitis, is an important evidence of miasmatic extension. Apparently there is no transfer of the disease by contagion, although solitary instances are brought up to prove the infection of one person from another. But cerebro-spinal meningitis does not, by any means, belong to that class of infectious diseases, of which Ave may take typhus as an example, and of Avhich we shall hereafter speak in a separate section. The consideration of this disease as a peculiar form of typhus, Avhich was formerly so common in France, has been entirely disproved during the late epidemic in Germany. I separate this affection from classes of infectious diseases to Avhich the different forms of typhus belong, on the following grounds: In the latter, the severe con- stitutional symptoms, especially the fever, for the most part, depend immediately on the reception of the infecting material into the blood, and the anatomical changes in the organs, caused by the infection, are very peculiar; they are induced only by infection AAith the specific poison. In epidemic cerebro-spinal meningitis, on the contrary, the fever and all other symptoms depend solely on the local disease in- duced by the infection, and on its injurious effect on the body, just as they do in croupous pneumonia or in erysipelas; and the changes in the meninges of the brain and spine are just the same as those some- times induced in other ways. This circumstance also induces me to treat of cerebro-spinal meningitis amcng the local diseases, in spite of its miasmatic origin. Epidemics of this disease are more frequent in AAinter than in sum- mer, and usually disappear as warm weather begins. But there aret exceptions to this, which contrast very remarkably with most epidemic diseases. Among the different ages, childhood has the greatest quota of cases and deaths. Persons of middle age are often attacked also, while the aged are rarely affected. Unfavorable hygienic influences 220 DISEASES OF THE BRAIN. of all kinds, among which are croAvding of barracks, dwellings, etc., favor the outbreak of the disease. Persons exposed to these influences are in greater danger, at times of epidemics, than those VA-ho live under more favorable circumstances. Anatomical Appearances.—In recent cases, the result of au- topsy is almost always as follows: The subjects show no emaciation, protracted rigor mortis, or extensive hypostasis; there are often groups of dried herpes vesicles on the face and other parts of the body; the muscles are dark; in rare cases they are pale (Zlemssen). The cranium contains much blood; in the longitudinal sinus there is abundant fluid, or softly-coagulated blood; the dura mater is more or less tense, and occasionally covered with small hemorrhagic or pa- chymeningitic deposits. There is usually no effusion betAveen the dura mater and arachnoid; in the subarachnoid space there is an exudation, which, both in extent and character, occupies about a medium position between the pure purulent exudation in meningitis of the convexity and the puro-serous exudation in basilar meningitis. In almost all cases, the convexity of the cerebrum and the base of the brain are affected at the same time, the latter usually the more severely. The exudation appears to be peculiarly plentiful about the chiasm, in the fossa Sylvii, at the base of the cerebellum, and in the fissures of the cerebrum. The nerves, from the base of the brain, are often entirely embedded in it. The brain itself is more or less vascular, almost al- ways less resistant, even becoming pulpy in the vicinity of the ventri- cles; the latter generally contain small amounts of purulent fluid, rarely large quantities of clear serum. The dura mater of the spine is more or less vascular, occasionally very tense, especially at the lower part. Between the dura mater and spinal arachnoid there is rarely a clear or purulent opaque fluid. The arachnoid usually presents no peculiarity except a decided opacity. There is more or less purulent fluid between it and the pia mater. The tissue of the pia mater is infiltrated with sero-purulent exudation. This infiltration extends very irregularly; in most cases the cervical portion is free; the process first begins in the dorsal region, thence extends toward the cauda equina, and is almost exclusively on the pos- terior surface. The purulently-infiltrated spots form irregular humps, broader in the middle, smaller at the ends, which are usually connected together by small strie accompanying the larger vessels. Even where ,the pia mater does not contain this puro-serous infiltration, its tissue appears thickened and cloudy. The spinal medulla itself is more or less vascular, occasionally infiltrated and relaxed. In a case related by Zlemssen, the central canal Avas dilated and filled with purulent fluid. EPIDEMIC CEREBRO-SPINAL MENINGITIS. 221 Except some accidental complications, there are no particular anom- alies of the other organs; we should especially note here that the spleen is almost always normal. The post-mortem appearances, in protracted cases, are known only from a very few observations. In one such case I found the exudation thickened, and partly affected with caseous metamorphosis, as well as considerable fluid in the ventricles. The same appearances have been noted by other authors. Symptoms and Course.—I must again repeat that the symptoms and course of epidemic cerebro-spinal meningitis may be fully explained by the changes in the meninges of the brain and spine, and that, on this account, the malady differs from most other infectious diseases. Every thing that has been advanced in opposition to this view may be refuted by the simple fact that, in genuine croupous pneumonia, which no one classes among the infectious diseases, certain symptoms, such as the frequent herpetic eruptions, albuminuria, etc., are just as diffi- cult to explain, from the inflammatory changes in the lung and the copious exudation in the alveoh, as are some of the occasional symp- toms of epidemic cerebro-spinal meningitis. Only in rare cases is the outbreak of the disease preceded by a premonitory stage, characterized by slight headache and pain in the back. Usually the scene opens Avith an unexpected chill of variable duration, which is soon accompanied by severe headache, and in most cases by vomiting. The headache rapidly becomes very severe, the patient grows very restless, tosses about constantly, the pupils are con- tracted, the intellect remains clear. The pulse is 80-100, the bodily temperature moderate, the inspirations increase to 30-40 per minute. Even at the end of the first or second day, rarely later, Ave notice that the head is drawn backward. At this time there is often a herpetic eruption near the mouth, on the cheeks, eyelids, ears, and oc- casionally on the extremities. The complaints about severe headache continue; the pain extends from the head to the nape of the neck and the back. The restlessness becomes excessive, the ideas confused, the pupils remain contracted, the belly is sunken, and the bowels are con- stipated. The pulse and respiration become more frequent, occasion- ally the pulse is over 120 and the respiration over 40 per minute; the bodily temperature still remains proportionately low, or rises to 103° or over. The third or fourth day of the disease the tetanic con- tractions of the muscles of the neck and back become more evident, and are occasionally accompanied by trismus ; there is excessive opis- thotonus ; consciousness is lost, but the patient still tosses about in bed, the pupils remain contracted, constipation continues, the belly is sunk- en, urine is passed involuntarily, or else the bladder becomes distend- 222 DISEASES OF THE BRAIN. , ed, and must be evacuated Avith the catheter. The now unconscious patient falls into deep stupor, the moaning respiration is accompanied by moist rales, and death occurs with the symptoms of acute edema of the lungs. In some particularly severe cases the above symptoms develop far more rapidly; consciousness is lost even during the first day, while severe tetanic spasms of muscles of the neck and back draw the head far backAvard. Death may occur even on the first or second day, when the disease is very malignant. Lastly, in some few cases (of which there can be no doubt) the dis- ease runs a still more rapid course, and causes death in a few hours, from general paralysis, occasionally even without the appearance of the most characteristic tetanic symptoms (menlnglte foudroyante). But the disease does not by any means ahvays terminate fatally when it has commensed and run its course for the first few days in the manner above described. As favorable signs, we usually first notice that there is less jactitation, and the mind becomes clearer, while the complaints of pain in the head and back and the tetanus of the cervi- cal and dorsal muscles continue, or only slightly decrease. If the im- provement progresses, all symptoms of the disease may disappear in a feAV days, and the patient begin his tedious convalescence. Occasionally improvement begins, but does not continue, and the disease drags on. In such cases convalescence may not occur for weeks. Headache, contraction of the neck or opisthotonus continue. Paralysis of the motor and psychical functions causes a complicated series of symptoms, and the majority of such patients finally die of gradually-increasing marasmus. Lastly, I must mention the occasionally intermittent course of the disease. I have only seen one such case. Hirsch distinguishes three forms of the intermittent course: in the first it only occurs in the first stage; one or more attacks of evident premonitory symptoms pass away, but another follows which is immediately succeeded by the out- break of the disease. In the second form there is a sudden remission of the symptoms; these again groAV worse the next day, and occasion- ally this alternation occurs several times, usually Avith a more or less regular quotidian type. In the third form, which is far the most fre- quent (to Avhich my case belonged), perfect intermissions are seen during convalescence. The symptoms remaining after the disease, particularly headache and stiff neck, regularly increase very consider- ably for some time, usually with a quotidian type, while in the inter- val the patient feels quite comfortable. To the above vieAV of the symptoms and course of cerebro-spinal me- ningitis I Avill noAV add a short description of the individual symptoms, EPIDEMIC CEREBRO-SPINAL MENINGITIS. 223 6oth of those that I have already mentioned, and of others of which I have not yet spoken, as they are less constant. Severe headache occurs even in those cases Avhich, as meningite foudroyante, terminate in death in a few hours. In the cases that run the usual course, as long as the pa- tients retain consciousness they complain of headache, either sponta- neously or on being questioned, and it also seems as if the restless- ness, groaning, and complaints of the patients, after the intellect is clouded, were partly due to the headache. Lastly, during an epidemic of this disease, there are almost always a few cases where, without the disease actually occurring, persons complain of very severe head- ache continuing for several days without any other apparent cause. We may consider such cases as abortive forms. Cervical and dorsal pains usually begin very early either with the headache or very soon after; they are generally increased by pressure on the spinal processes of the vertebre; Avith rare exceptions, this pain is far greater when the patients make voluntary movements of the spine or on passive motion being made. If the disease be pro- tracted, the dorsal pains and their increase by movements of the spine may continue for weeks. Painful sensations in the extremities, unmistakably neuralgic in their nature, and caused by irritation of the posterior roots of the spi- nal column, are not constant symptoms; occasionally they only occur on motion of the spine. Hyperesthesia and Anaesthesia of the Skin.—Usually for the first days of the disease, and in some cases during its whole course, the pa- tients are very sensitive to any rough handling; their restlessness, groaning, and complaints are increased when they are turned over in bed, occasionally even if they be percussed. Later, -Ave often see no reaction even Avhen the skin is greatly irritated; but in such cases, Avhen the patients are in a state of stupor, there is cerebral anesthesia. Far more rarely, there is peripheral anesthesia, during Avhich, Avhile the patient is quite conscious, he feels irritation of the skin very little or not at all. This symptom apparently depends on loss of excitabil- ity of the posterior roots from inflammation. Tetanic spasms of the cervical and dorsal muscles are only absent in some few cases of meningite foudroyante. At first the head is only slightly retracted, later it may form almost a right angle with the body. This position of the head and the addition of opisthotonos in the dorsal and lumbar regions usually render it impossible for the pa- tient to he on the back. If the tetanus attain a high grade, it almost ahvays affects the respiration. Occasionally it disappears shortly be- fore death; more frequently it continues more or less severe till death or convalescence. 61 224 DISEASES OF THE BRAIN. Epileptiform convulsions are rare, which is very remarkable, con sidering the exudation is often widely spread over the convexity of the hemispheres. Paralysis.—Usually there is no actual paralysis till death; but there are a few cases where hemiplegia or paraplegia, and quite a number where paralysis of the facial, oculomotor, or of the abducens, were observed. It is not at all difficult to explain these paralyses; on the contrary, it is almost wonderful they are not more frequent. Psychical Disturbances—At the commencement of the disease, the intellect is almost always unclouded; the patients answer ques- tions correctly. But they soon become ill at ease and Aery restless. Then questions prove annoying, and they will only give short and in- complete answers. The incessant jactitation, which is scarcely inter- rupted by pauses of a few minutes, is very characteristic in the first stage of the disease. Subsequently most patients have delirium of variable intensity, which finally gives place to a soporose condition. Disturbances in the Organs of Special Sense.—Patients not un- frequently become blind from keratitis, which is probably induced by incomplete closure of the eyelids, due to paresis of the orbicularis palpebrarum, or from exudative choroiditis and neuro-retinitis, prob- ably a result of direct propagation of the purulent infiltration along the optic nerve from the cranium to the eye. Deafness is remarkably frequent, so that we are almost obliged to suppose that it has several causes, among which, however, the most important, doubtless, is the propagation of purulent infiltration along the auditory nerve to the in- ternal ear. Among the eruptions, groups of herpes vesicles in large numbers are very often seen, and more rarely erythema, roseola, urticaria, pete- chia, and sudamina. The frequency of the exanthemata, and particularly the occasional symmetry of their occurrence, have led to the supposition that they might depend on irritation of the cutaneous nerves, as Bd- rensprung has shown to be the case in herpes zoster from neuralgia. According to Zlemssen's numerous and accurate observations, the fever has no regular course. Very feAV temperature curves resemble each other; sudden leaps and exacerbations of short duration often occur. But generally a remitting type, with exacerbations of half a degree to a degree, is most frequent. Very high temperatures are al- most exclusively seen in severe cases that terminate fatally. In most cases the temperature does not rise above 103°. The intermittent fever that occasionally accompanies the other symptoms during conva- lescence is regarded by Zlemssen as a reabsorbing fever, while he re- fers that occurring during the first and second weeks to an interrupted progress of the meningitis. The frequency of the pulse does not at INFLAMMATION OF THE BRAIN—ENCEPHALITIS. 225 all accord with the height of the fever; with moderate fever it is oc- casionally very high; slowness of the pulse is only rarely observed at the commencement of the fever. Treatment.—Just as in other malignant and fatal epidemics, in deciding the best means of treatment, we must only consider cases where there is at least a slight hope of recovery. Whoever tries any proposed plan only on the severest cases will attain negative results by any procedure. The customary treatment of sporadic meningitis, consisting of the energetic use of cold as ice-compresses to the head, the application of leeches behind the ears, and the internal adminis- tration of calomel, is also advisable in epidemic cerebro-spinal menin- gitis, as is very evident from its excellent effect in patients attacked by the premonitory symptoms of the disease, severe headache, and pain in the neck, during an epidemic. But, according to most observers, this mode of treatment has pre- served its reputation even in marked cases of the disease; there is but little opposition to it, and even this is based on its want of success in the severest forms. I have no personal knowledge of the success of morphium when given internally or hypodermically. But a number of trustworthy observers, Zlemssen and Mannkopff among others, speak most favorably of it, especially in the form of subcutaneous in- jection. Zlemssen says: " Although we have used morphia frequent- ly, we have never seen any injurious effects from it, but, on the con- trary, such a decidedly palliative action that, along with cold, it seems the most indispensable remedy in the treatment of meningitis." Al- most all observers agree that quinine is entirely useless even in deci- dedly intermittent cases. CHAPTER XI. INFLAMMATION OF THE BRAIN—ENCEPHALITIS. Etiology.—In encephalitis, just as in the inflammation of other organs containing little connectiv e tissue, there is not much interstitial exudation, but there are most important changes in the nerve-filaments and ganglion-cells and then scanty interstitial tissue. These tissue- elements swell from absorption of nutrient fluid and subsequently break doAvn, partly to simple detritus, partly after precedent fatty de- generation ; in the latter case, in the inflamed parts we find quantities of fatty, granular cells (the formerly so-called Gluge's inflammation globules), which avc have a right to suppose come directly from fatty deo-eneration of ganglion-cells and neuroglia nuclei. In the subse- quent course of encephalitis there is often an extensive formation of 226 DISEASES OF THE BRAIN. pus-cells; abscesses are formed, which, besides the usual constituents of pus, often contain some remains of disintegrated brain-substance. Cerebral abscesses are either surrounded by brain-substance softened by extension of inflammation to the surrounding parts, or by newly-formed connective tissue; in the latter case they are said to be capsulated. Encephalitis is a rare disease, and is not induced by the causes which usually excite inflammation in other organs. 1. The most fre- quent form is traumatic encephalitis; it results not only from direct in- juries affecting the brain after the skull is opened, but there are nu- merous cases where the cranium has remained uninjured, and where there was apparently only slight contusion. It is most probable that in such cases the brain has been bruised by the vibrating cranium, and some small vessels have been ruptured and ecchymoses formed. It also appears as if the small extravasations of blood occasionally in- duce no symptoms at first, but excite inflammation in the surround- ing parts, and thus subsequently cause encephahtis. At least, the first signs of the inflammation are occasionally not observed till long after the injury. Among the cases of traumatic origin we must in- clude those where breaking down of the brain by an extensive extrav- asation of blood has caused inflammation in the vicinity. 2. In other cases the encephalitis depends on the irritation of the brain from neo- plasia and necrosed spots. 3. Among the most frequent causes of en- cephalitis are diseases of the cranial bones, especially of the petrous bone. As we shall hereafter show, the presence of an otorrhea may decide the question between an abscess of the brain and a tumor. Cases are also known where caries of a superior maxillary extended to the brain and caused encephahtis. I remember a clergyman in Mag- deburg who died of abscess of the brain a few years after a large por- tion of the upper jaw had been exsected on account of extensive ca- ries. 4. Occasionally the disease occurs in the course of acute and chronic infectious diseases, such as pyemia, glanders, typhus, etc., without our being able to give any plausible explanation for it. 5. Lastly, but rarely, encephalitis occurs without any known cause in persons previously healthy. Anatomical Appearances.—This disease never attacks the entire brain; it is always confined to certain points. The size of these spots varies from that of a bean to that of a fist, or larger. They are usually of an irregular spherical shape. Ordinarily there is only one, but sometimes there are several. They may be located either in the cere- brum or cerebellum; they are most frequently in the gray substance and very near the surface, if they do not quite reach it. In the com- mencement of the disease at the affected parts, we find the brain-sub- stance SAvollen, infiltrated, softened, and pointed with red spots from INFLAMMATION OF THE BRAIN—ENCEPHALITIS. 227 small extravasations of blood. The SAveUing of the inflamed parts may be recognized by the surface of the brain on the affected side appear- ing smooth, just as in apoplectic effusions, and the brain itself being anemic from encroachment on the cranial cavity. On incision also the diseased portion not unfrequently rises above the level of the in- cised surface. After long existence, the relaxation of tissue gets the upper hand, and a red pulp results, which gradually acquires a rusty- brown or yellow color, from change of the hematin, or when there is a slight admixture of blood it becomes grayish. This pulp, Avhich may be vvTashed off by a slight stream of vvater, consists of remains of nerve- filaments, blood-corpuscles, granular cells, and fine granular exudations or masses of detritus. The subsequent changes in the inflamed parts, which are usually called the results of inflammation, vary. Occasion- ally, in the vicinity of the inflammation, there is a new formation of connective tissue, which is also continued through the inflamed spot as a delicate network; the contents of the abscess are absorbed, and there remains a cavity, filled with a chalky milky fluid, the " cellular infiltration" of Durand-Fardel, previously mentioned in apoplexy. In some cases, especially when these cysts lie near the surface of the brain, their walls gradually approach each other, while the contents disappear, and in place of the abscess there is formed a cicatrix, at first pale red and vascular, subsequently Avhite and callous. When ence- phalitis terminates in suppuration, the appearances are different. Re- cent abscesses of the brain form irregular round cavities filled with yellow or gray, occasionally also reddish, thick fluid; then walls con- sist of ragged masses infiltrated Avith pus. In the immediate vicinity of the abscess we usually find inflammatory softening; farther off there is edema of the brain-substance. Such abscesses increase till they break into a ventricle, or reach the meninges; or, if extensive menin- gitis do not occur in the latter case, the ulceration extends to the cere- bral membranes and the skull, and finally the pus may perforate out- wardly or into neighboring cavities, especially into the cavity of the tympanum. If the cerebral abscess be capsulated by new formations of connective tissue in its wall, it has a more regular form and smooth walls. If it has lasted a long time, Ave occasionally find the capsule much denser, and the contents thickened by reabsorption of the fluid part, and changed to a cheesy chalky mass. Symptoms and Course.—Like the symptoms of cerebral hemor- rhage and of partial necrosis, those of encephahtis are partly the im- mediate result of destruction of the portion of brain affected, and partly the result of disturbances of circulation in the brain, especially in the vicinity of the seat of inflammation. Since large portions of the brain may be destroyed without caus- 228 DISEASES OF THE BRAIN. ing perceptible functional disturbances, and since encapsulated ab- scesses frequently do not decidedly affect the circulation in the skull, we may readily understand that we should occasionally find abscesses of the brain on autopsy, which had not been suspected during hfe. With this knowledge we may also understand those cases of cerebral abscess which run then course without any symptoms except the inju- rious influence they exercise on the general nutrition of the brain. It is not at all rare for a patient to have dull headache, increasing apathy, loss of thinking-power, even advancing to idiocy, a blunting of the senses, increasing weakness, and uncertainty of movement- symptoms which indicate the existence of severe brain-disease, it is true, but which do not by any means justify a diagnosis of abscess of the brain. Even the most experienced and accustomed observers occasionally mistake abscesses of the brain. But these and similar mistakes, which unfortunately are made public far less frequently than brilliant diagnoses, can only seem strange to the ignorant, and to those who are not thoroughly acquainted with the physiology and pathology of the brain, and with the diagnosis of brain-diseases. These latent cases of encephalitis are far less frequent than those where the disease may be very strongly suspected or recognized with certainty. If the abscess be located at a point where it destroys the centres of special sense, or interrupts the conduction of the impulse of the will to the motor nerves, or the impressions of special sense to the organs, we have partial anesthesia and partial paralysis, sometimes of the cerebral nerves, again of the cerebro-spinal, at others of both. These anesthesias and paralyses not unfrequently extend to both extremities of one side of the body; in other cases they are confined to the parts supplied by certain cerebral or cerebro-spinal nerves, but in the latter case also they are always on one side. Bilateral anesthesias and paral- yses only occur exceptionally, and in cases where the abscess is in the middle portion of the brain, which is not double, or where different abscesses are in the same parts of the brain on opposite sides. From the occurrence of these symptoms we can only determine that there is some local disease; but we cannot decide on its nature, for they occur in the most varied forms of local disease where nerve-filaments and ganglion-cells are destroyed. To come to a conclusion on this point, we must pay particular attention to the etiology, to the course of the disease, and to those symptoms which show the effect of the local disease on the rest of the brain. If we can make out that the symptoms of a local disease of the brain have begun after an injury of the head, or if the patient has caries of the petrous bone, the case is most probably one of ence- phalitis. If, on the other hand, there has been no injury of the head INFLAMMATION OF THE BRAIN—ENCEPHALITIS. 229 and no caries of the temporal bone can be found, it is almost equally improbable that there is encephahtis. While these points are gen- erally true, they have in some cases led to erroneous diagnosis. Autopsy has revealed abscesses of the brain where there had been no injury of the head or caries of the cranial bones. There have also been cases where patients with cerebral tumors have had a blow on the head, and occasionally the previously latent brain-disease had not become manifest till after this injury. (These cases are analo- gous to those where women first have their attention directed to a carcinomatous mamma by a blow on it, and then consider it beyond a doubt that it is due to the injury they have received.) But, prac- tically, it is best only to think of these exceptional cases Avhere there is sufficient reason. Encephalitis never affects the entire brain, but is always limited to certain points; nevertheless, at the commencement of the disease, there are almost ahvays signs of temporary irritation of the entire brain or meninges, such as increased frequency or great sloAvness of the pulse, increased bodily temperature, headache, dizziness, sleepless- ness or restlessness, exciting dreams, psychical irritation, even mild delirium, great sensitiveness to slight irritation of the organs of special sense, bodily disquiet, and great Aveakness, etc. According to Gries- inger, this violent commencing stage, which may be folloAved by quiet, is almost pathognomonic of encephalitis and abscess of the brain. In the criminal records there are numerous cases where the above symp- toms were considered by the attending surgeon as traumatic fever, be- cause they apparently disappeared without any traces, and the complete recovery of the patient from the injury received was officially certified to, AA'hile, after a time, there were unmistakable signs of a severe brain- disease, and autopsy showed abscess of the brain as the fatal termina- tion of the injury. Even in those cases where an injury of the skull is folloAved at first by the symptoms of general irritation of the brain and meninges, and subsequently by the above-described decrease of all the cerebral functions, we should first think of abscess of the brain, and attribute the absence of local symptoms to the location of the ab- scess at a point where it does not interrupt the conduction of excite- ment, in the centripetal and centrifugal cerebral filaments. The influence that local inflammations in the brain have on the rest of the organ consists partly in their encroachment on the cranial cavity, and chiefly on those chambers of the skull where they are located, partly on the collateral hyperemia and edema in then vicinity, and, lastlv, partly on then injurious effect on the nutrition of the entire brain. On the first of these factors depend the headache, the attacks of dizziness and vomiting, as well as the evanescent occurrence of pain, 230 DISEASES OF THE BRAIN. mdefinite feelings, anesthesia, twitchings, contractions, paralyses in some parts of the body, which, in many cases, accompany the symp- toms previously mentioned, and which we fully described in the second and fourth chapters, as the results of partial hyperemia and partial anemia of the brain. These do not continue unchanged, like the local symptoms, which are the immediate results of partial destruction of the brain from the inflammatory process, but are rather apt to have a variable course; this is partly due to occasional enlargement of the abscess, by which the space is more contracted, partly on the occasional increase and decrease of collateral hyperemia and collateral edema. It is evident that such a variation in the symptoms would occur oftener in encephalitic inflammations than in slow and steadily-growing tumors of the brain. The attacks of epileptiform convulsions, which not unfrequently occur during encephalitis, are more difficult to explain, and we shall not even offer a hypothesis as to the mode of their occurrence. Sta- tistics have been made as to how often headache, contractions, epilep- tiform convulsions, etc., were present or absent in a large number of cases of cerebral abscesses. In individual cases, the results of these statistics are, of course, of but little value in the diagnosis of abscess of the brain, or in its differential diagnosis from tumor of the brain. The injurious influence of the local inflammation on the general nutri- tion of the brain, which may occur earlier or later, but never fails when the disease is protracted, evinces itself by the previously-described symptoms of a general paralysis of all the cerebral functions. I think I have fully shoAvn, by this description, that, in many cases, it is possi- ble to recognize an abscess of the brain, although it has no constant or pathognomonic symptom. The duration of encephalitis varies; some cases terminate in death, after a few days or weeks, Avhile in others this does not occur for years. Occasionally, while the symptoms of cerebral paralysis increase, so that the patient becomes idiotic, Ave find a remarkable development of fat. Death occurs either suddenly and unexpectedly, from the devel- opment of meningitis, from sudden increase of the abscess, and, occa- sionally, without our being able to find, on autopsy, any cause for the sudden catastrophe; or else it occurs with the symptoms of gradually- increasing sleepiness, finally becoming deep coma, or else it is induced by intercurrent diseases. Recovery is very rare. Even in the most favorable cases, where the cellular infiltration forms a cicatrix or en- capsulates the abscess, while its contents calcify, we can only speak of a relative cure, since both the remains of the inflammation and the atrophy of the brain, which usually develops under such circumstances, affect the functions of the brain for the rest of life. PARTIAL SCLEROSIS OF THE BRAIN. 231 Treatment.—The treatment of encephalitis cannot be very suc- cessful, from the simple fact that the disease is not generally recog- nized until it has induced irreparable destruction of the brain. In very recent cases, particularly in those of traumatic origin, Ave should em- ploy local antiphlogistics, leeches, and cold compresses. Later, but little can be expected from this treatment. Moxe and setons, Avhich Avere formerly much used in protracted cases, have been abandoned, and very justly so, as has the administration of mercurials. The prepa- rations of iodine also, which have been recently recommended, promise but little benefit; hence, in most cases, there is little to do but have the patient observe proper regimen, particularly to guard him from every thing that can increase the pressure of blood to the head, and to confine ourselves to combating the most urgent symptoms. Among the latter, the apoplectiform attacks are to be treated according to the rules given for the treatment of cerebral hemorrhage, while any intercurrent meningitis demands the employment of energetic anti- phlogistic remedies. CHAPTER XII. partial sclerosis of the brain. In previous chapters we have repeatedly mentioned the formation of indurations in the brain as the results of cicatrization of apoplectic and inflammatory deposits. Besides these, partial scleroses, Avhich occur as a result of other processes, indurations from neAv formations of connective tissue, and displacement of the normal elements, occur at circumscribed spots in the brain, whose pathogeny is entirely ob- scure, and of AAThich it is even doubtful whether they are of inflamma- tory origin or not. These idiopathic forms of partial sclerosis of the brain have been almost solely observed early in life, and more fre- quently in males than in females, but their causes have never been discovered. On anatomical examination the points of disease are found oftener in the white than in the gray substance; then number varies; some- times they are solitary, occasionally several are present. They form irregular nodules, or rough spots as large as a lentil or an almond, which may be distinguished from the parts around by their hardness and toughness. On the cut surface they appear bloodless, dull, and milk-white; after remaining exposed for a AAiiile, they are covered with a scanty serum, and become somewhat depressed. In the midst of the nodules there are usually small blue or grayish-red spots, which contract strongly and press out a quantity of serum, after being 232 DISEASES OF THE BRAIN. divided. On microscopical examination we find amorphous fine gran- ular masses along with well-preserved nerve-elements in the milk-white indurated spots. In the grayish-red prominences, on the other hand, there are no nerve-elements; they consist of a filamentary mass and the remains of capillary Avails, in which fat granules are embedded (Valentiner). . ■ The symptoms and course of partial sclerosis of the brain are not so characteristic as to render the disease easy of recognition; on the contrary, it must be regarded as a triumph in diagnosis, that this has been done in a feAV cases (Frerichs). Since the sclerosis is limited to scattered and circumscribed points and develops slowly, the paralyses accompanying the disease have the peculiarity that, in the commence' ment at least, they do not extend over one-half the body, but always begin in single groups of muscles, or in a single extremity (always one of the lower extremities), and thence extend gradually to other groups of muscles and other extremities, till finally the central parts governing respiration, deglutition, and the actions of the heart, are affected. This extension is not regular: for example, paralysis of the right hand does not necessarily folloAV that of the right foot, but it is entirely lawless. This fact in itself speaks in any case for the depend- ence of the paralysis on numerous separate points of disease, and not on one gradually-increasing spot. Besides the paralyses, which are the most constant, and, from their peculiar mode of extension, the most characteristic symptoms of partial sclerosis of the brain, there are also disturbances in the other functions, but these are far less distinc- tive and characteristic of the disease. Headache is absent in most cases; but there are often peripheral pains, and a feeling of formica- tion in the extremities which is followed by a diminution of sensation, increasing to perfect anesthesia. The special senses are rarely affected, and among these that of sight almost exclusively. In most cases there are moderate symptoms of irritation in the psychical functions; but these are soon followed by a gradually-increasing deep depression, which in some cases exists from the first. Convulsions only occur exceptionally; but trembling is a very constant symptom. The nutri- tion of the body is not generally affected till late in the disease, and in some patients, just as in encephalitis, there is even a remarkable development of fat. The course of the disease is very tedious; most of the cases observed lasted from five to ten years. During this time the disease occasionally appeared to remain at a stand-still but no existing paralysis was ever observed to disappear. No instances of recovery are known. In the cases that have been described, death resulted partly from the extension of the disease to the medulla ob- longata and consequent disturbance of the respiration, partly from TUMORS OF THE BRAIN AND ITS MEMBRANES. 233 marasmus and hydremia which developed toward the end, partly from intercurrent diseases. Treatment is fruitless against this affection; it can only be of use in combating the more severe symptoms. CHAPTER XIII. TUMORS OF THE BRAIN AND ITS MEMBRANES. Under the head of tumors of the brain are included growths and parasites occurring in the skull, and aneurisms of the cerebral arteries. We shall follow this custom, since it is very convenient on account of the great correspondence of the symptoms due to these otherwise dif- ferent diseases. Etiology.—The pathogeny and etiology of cerebral tumors is very obscure. This is true not only of carcinoma, sarcoma, glioma, and myx- oma, but also of the rarer tumors, cholesteatoma or pearl tumors, lipoma, and cystoid growths. Cancer of the brain occurs chiefly in advanced age; it is sometimes primary, and then usually remains the only carci- nomatous disease in the body; sometimes it is secondary to carcinoma of other organs. The other neoplasia that we mentioned above, also occur chiefly, but not exclusively, in advanced age, and according to statistics are more frequent in males than in females. We know nothing of the morbid predisposition or the exciting causes to which these neoplasia are due. They have been frequently observed after precedent injuries of the head; but in such cases there is no certainty of a genetic connection between the injury and the growth. We must bear in mind hoAV frequently slight injuries of the head occur, and hoAV carefully they are inquired after, in any patient suffering from symp- toms of brain-disease, and, Avhen found, how strong the inclination is at once to refer the disease to them. Tubercles in the brain with rare exceptions occur in children, and chiefly in those over tAvo years old. They are rarely primary; but almost always form complications of the so-called tuberculosis of the lymphatic glands, and of pulmonary tuberculosis. Cysticerci and echinococci of the brain, as of other organs, depend on the emigration of the embryos of these parasites. Aneurisms of the cerebral arteries are usually due to degeneration of the arterial walls from endarteritis deformans. Anatomical Appearances.—Carcinoma of the brain is usually in the form of round or lobulated, generally chcumscribed tumors, with the softness and other peculiarities of medullary cancer; more rarely they have the firm tissue of scirrhus, and then they usually pass into the neighboring cerebral substance Avithout having any distinct bound- 234 DISEASES OF THE BRAIN. aries. They sometimes start from the brain itself, sometimes from the dura mater and cranial bones, or they develop originally from the external soft parts of the skull and neighboring cavities, especially in the orbit, and thence press into the skull. On the other hand, it rarely happens that carcinoma occurring in the brain perforates the meninges and cranial bones. There is usually only one carcinomatous tumor of the brain, and this is generally located in the cerebrum; where there have been several, they have occasionally been found symmetrically located on the two sides of the brain. Cerebral carcinomata, which may attain the size of the fist, never suppurate unless they perforate outwardly; on the other hand, they readily undergo partial retrogres- sive metamorphosis, become yellow and cheesy in the middle, shrink, and thus cause umbilicated depressions on the surface of the brain, if the cancer had advanced so far. Sarcomata occur as often as carcinomata in the brain. They are often attached to the meninges, and the tumors of this variety, at the base of the brain, usually attain greater size than those of the dura mater that covers the convexity. (Just as often sarcomata are em- bedded in the midst of the brain-substance, in the majority of cases in the cerebrum.) They form round or lobulated tumors, from the size of a hazel-nut to that of a good-sized apple ; their cut surface is smooth, dirty white, or grayish red; they are usually soft, even medullary, more rarely hard and fibrous. Occasionally they contain cavities filled with fluid. Sarcomata consist chiefly of spindle-shaped cells, arranged in filamentary strie. They differ from cancer, and especially from glioma, not only in being sharply bounded, but in being often surrounded by a vascular emelope, from AA-hich they can be turned out. Small lumps of carbonate of lime not unfrequently occur in sarcoma of the dura mater ; on rubbing the tumor between the fingers, these lumps cause a sandy feel. Vlrchow has designated tumors, containing numbers of the chalky lumps, as psammonea, or sand-tumors. Then mode of origin is not yet exactly knoAvn. Myxomata consist of mucous tissue—that is, of variously-formed cells, embedded in a homogeneous, mucous, hyaline, intercellular sub- stance. They are not very rare in the' brain. Like sarcomata, they are located most frequently, but not exclusively, in the medullary sub- stance of the cerebrum, where they generally appear as circumscribed tumors, more rarely as infiltrations of soft gelatinous substance. The tissue of myxoma is somewhat translucent, and of a weak yellowish or red color, but may acquire a varied hue from extravasated blood. Myxomata also correspond with sarcomata in regard to the size they may attain; and, between these two forms of tumors, there are all possible grades of transformations (gelatinous sarcoma). TUMORS OF THE BRALN AND ITS MEMBRANES. 235 Gliomata result from a local proliferation of the neurogha, or con- nective tissue of the brain, at the expense of its nervous elements. Microscopically, they consist of roundish nuclei, distributed through a finely-reticulated basement substance. By the naked eye they are distinguishable from not forming chcumscribed tumors, but passing gradually into the healthy brain-tissue; also from the fact that they never pass from the brain to its membranes. Gliomata may attain the size of a fist; they most frequently originate from the medullary sub- stance of the cerebrum. Hemorrhages into or partial retrogression of glioma may take place after precedent fatty degeneration of its ele- ments. The consistence of these tumors varies between that of a me- dullary cancer and of healthy brain. The cut surface varies in color from whitish yellow to bright grayish red, and usually shows a number of cut vessels. Formerly glioma was regarded as infiltrated cancer, and, as it occurs chiefly in young persons, or, at least, in those under forty years of age, we see why it Avas said that cancer of the brain has been observed at all ages. Cholesteatomata, or pearl tumors, are rare. They sometimes start from the cranial bones, at others from the meninges, again they de- velop in the brain itself. They form irregular tumors, of variable size, of a pearly lustre; they are enclosed by a delicate membrane, and con- sist of concentric layers of epidermic cells. Lipornata, as small lobulated tumors, starting from the dura mater, cysts filled with fluid, or fat and hairs, and cystoid neoplasia, with cauliflower excrescences from the walls, belong to the rarities, and have more pathologico-anatomical than clinical interest. Tubercles of the brain are-the most frequent form of cerebral tu- mors. Usually Ave find only one collection of tubercles, occasionally two, more rarely a greater number. The size varies from that of a hemp-seed to that of a cherry, or, in rare cases, to that of a hen's egg. They are located most frequently in the cerebellum or cerebrum, more rarely in the mesencephalon. Tubercles of the brain form irregular, roundish, non-vascular tumors, of a yellow, dry, and cheesy character. They are sometimes surrounded by a layer of loose connective tissue, Avhich separates them from neighboring parts of the brain; sometimes the main portion of the yelloAV nodule gradually passes into the brain- substance as a gray-Avhite, slightly-translucent, narroAV margin, consist- ing of young tubercle elements. In the latter case the tubercle has been groAving till death; in the former, Avhere it can be readily turned out of its capsule, groAvth has ceased long before death. From soft- ening of its centre, the tubercle nodule is occasionally transformed into a vomica, filled with tubercle pus. Syphilomata only rarely occur in the brain in the form of nodules •n 236 DISEASES OF THE BRAIN. (gummata); they are more frequent as diffuse infiltrations. Nodular syphiloma always passes from its edges very gradually into the healthy brain-substance. Since such nodules become changed by atrophy, and fatty metamorphosis of the cells commencing in the centre, to a sub- stance resembling yellow tubercle, syphiloma has probably been occa- sionally mistaken for tubercle. This may be avoided by bearing in mind that, in syphiloma, the passage from the cheesy centre to the broad, grayish-white, peripheral zone, is very gradual, while, in infil- trated, growing tubercle, these zones follow each other more closely, and, in tubercles that can be turned out, they do not exist. In regard to consistence, and the character of the cut surface, syphilitic infiltra- tions greatly resemble old, simply sclerosed parts; indeed, even the microscope cannot always decide between them. Cysticerci are not very rare in the brain, and, when found, they are usually in large numbers; they generally occur in the gray sub- stance. Occasionally some of these parasites are found dead, and changed to a mortar-like concrement, in which some of the hooks from the circle can usually be recognized. Echinococci of the brain are much rarer. They form large vesicles, enclosed by a very delicate adventitia, with the well-known peculiari- ties of which we have often spoken. Aneurisms of the cerebral arteries are not frequent. They chiefly occur in the vessels at the base of the brain, in the arteria basilaris, a. corporis callosi, a. fosse Sylvii, and in the a. communicantes of the circle of Willis. In rare cases, they attain the size of a small hen's egg, while usually they only reach that of a pea or a small hazel-nut. Symptoms and Course.—The symptoms of cerebral tumors have the greatest resemblance with those of the local diseases of the brain previously described. There is no symptom, occurring during the course of a cerebral tumor, that does not sometimes occur from soft- ening of the brain, from abscess, or from some other local disease. This resemblance cannot astonish us; on the contrary, we could not understand how it should be otherwise, since, like other local diseases, a tumor of the brain destroys a circumscribed portion of the organ, encroaches on the intracranial space, and interferes with ih.e circulation in the vicinity of the diseased part. Nevertheless, it is only in rare cases that it is difficult or impossible to recognize a cerebral tumor, and to distinguish it from an abscess, or other local disease of the brain. (According to my experience during the last ten years, I must hesitate about agreeing with the first part, at least, of Bamberger's assertion, AA-hich I have previously quoted, where he says, " With few exceptions, the diagnosis of tumors of the brain is rather a guess than a diagnosis, TUMORS OF THE BRAIN AND ITS MEMBRANES. 237 and the determination of its locality, likewise with certain exceptions, is impossible.") This apparent paradox is due to the fact that, in spite of the absence of constant symptoms pathognomonic of tumors of the brain, in most cases the diagnosis .may be made partly from the eti- ology? partly from the location of the disease at a point where other local diseases are rare and tumors common, and, lastly, partly from the peculiarities of the entire course of the disease. The important evidence furnished by the etiology is chiefly nega- tive. In every case of brain-disease we should make it a rule to seek for the exciting cause by obtaining an exact history of the case. If we thus find that the patient has had no injury of the head, that he has no caries of the petrous bone, no hypertrophy or valvular disease of the heart, and probably also no degeneration of the arteries; in short, if we can find no cause for the disease, our suspicions must first turn to a tumor of the brain. Before speaking of the cases where cerebral tumors can be recognized with facility and certainty, I shall say a few words concerning the rare cases where they induce no symp- toms, or else have those of severe brain-disease, but do not give any means of determining that they are caused by a tumor. The tumors Avith latent course can only be located at parts of the brain Avhere they do not disturb the intercerebral centres of the cranial nerves, or inter- rupt the conduction of excitement in the centripetal and centrifugal brain-filaments, that is, chiefly in the extensive medullary masses of the cerebrum. At this part tumors often attain a large size without in- ducing local symptoms (herdsymptome), Avhile at most parts of the base of the brain, and in the vicinity of the large ganglia, even the smallest tumors are accompanied by these symptoms. But even in the cerebrum only those tumors run a latent course which grow slowly, and are not so vascular as to swell at times from the vessels being overfilled, and at others to decrease in size from containing less blood. To explain the remarkable but very certain fact that the symptoms ac- companying rapidly-groAving tumors are not unfrequently absent in those that grow slowly, a certain " poAver of accommodation " has been ascribed to the brain, Avhich enabled it to accustom itself to gradually- increased pressure. I consider the following explanation more satis- factory : In tumors that grow rapidly there is a compression of the capillaries and a loss of function of those parts of the brain where they are located. On the contrary, in the vicinity of sloAviy-growing tumors there is atrophy of the brain-substance, and its shrinkage sup- plies as much room as is lost by the growth of the tumor. Under these circumstances the capillaries of the affected part of the brain are not compressed, and its function not disturbed. Perhaps the presence or absence of local, symptoms (herdsymptome), in tumors of the cere- 238 DISEASES OF THE BRAIN. brum having the same location and 'equal size, depends partly on Avhether the tumor has displaced the brain-filaments or has developed at their expense and has substituted them. My colleague, Prof. Schuppel, who has given me some other valuable points on the histol- ogy of cerebral tumors, asserts that the different forms of tumors vrary in the above respect. Naturally, tumors, rich in vessels which increase and diminish in size according to then fulness, are not apt to run their course without symptoms; but, as a rule, are at least occasionally ac- companied by symptoms of irritation and paralysis. Lastly, I shall mention that tumors running a perfectly latent course are proportion- ately more frequent than those having the symptoms of a severe in- explicable cerebral disease. In abscesses of the brain, just the opposite is true. This difference is probably due to the entire nutrition of the brain being generally more severely impahed by the presence of an abscess than by a tumor. Even those tumors of the brain where we succeed in making a cer- tain diagnosis during the course of the disease, do not always begin with the symptoms which play the most important part in the diagno- sis, that is, Avith the partial paralysis and anesthesia, which we have designated as local symptoms (herdsymptome), and which we have re- peatedly and fully described. In many cases the first, and often for a long time the only, symptom indicative of brain-disease, is a severe headache. Although this occurs during the most different brain-dis- eases, and although we may even say there is no disease of the brain which is not, under some circumstances, accompanied by it; still there is no cerebral disease Avhere continuous, unusually intense, and severe headache is so prominent a symptom, and there is no other disease where it is so often observed as in tumor of the brain. The cases where patients with cerebral tumors do not complain of headache are such rare exceptions, that its absence in a doubtful case rather speaks against a tumor. The fact that headache occurs even in those tumors of the brain which are located at a distance from the sensitive parts, supports the view we advanced, that in cerebral diseases the pain in the head started from the filaments of the trigeminus supplying the dura mater. We must be very careful about localizing the tumor from the seat of the pain. Only pains constantly confined to the back of the head permit us to conclude that very probably the tentorium is stretched, and that the tumor is probably situated in the posterior cranial fossa. In many patients, attacks of dizziness and vomiting accompany the headache, particularly the severe exacerbations which occur, from time to time, with or without perceptible cause. This may facilitate the correct interpretation of the headache, and show its dependence on TUMORS OF THE BRAIN AND ITS MEMBRANES. 239 disease of the brain, if it should have been doubtful, in spite of the duration, severity, and obstinacy of the pain. Among the local symptoms of tumors of the brain, those of partial irritation (hyperesthesia, neuralgia, indefinite sensations of formica- tion, twitching, etc.) very frequently precede the partial anaesthesias and partial paralyses, and there are cases of cerebral tumors where these symptoms, and not the headache, open the scene. We have seen that partial symptoms of irritation, occurring in seAere structural diseases of the brain, are only to be regarded as secondary effects, and are referable to disturbances of circulation in the vicinity of the affected part. Also that they occur in the most varied diseases, and alone are not pathognomonic of any of them. However, in cerebral tumors, there is one circumstance which is characteristic of the hyperesthesia, neuralgia, and twitchings, and the anesthesia and paralysis which usually follow them, namely, that these local symptoms are observed more frequently, even among the cerebral nerves, than in any of the previously-described forms of brain-disease. But Ave cannot say that symptoms of irritation and paralysis of the cerebro-spinal nerves, such as hemiplegia, etc., are rare, or do not occur;. but only that, apart from other symptoms, the occurrence of neuralgia, hyperesthesia, or anes- thesia, or of spasms and paralysis in the parts supplied by the cerebral nerves, goes to prove, in doubtful cases, that there is a tumor in the brain. The simple explanation of this peculiarity is as follows: In all the local diseases hitherto treated of, in necrotic softening of the brain, in cerebral hemorrhage, in encephalitis, and its results, the mor- bid process is, with rare exceptions, limited to the brain, and does not attack the nerves passing from it. The case is quite different with tumors, v\rhich not only often pass from the brain to the nerves origi- nating from it, but Avhich, in many cases, start from the meninges or skull, and then not unfrequently destroy the cerebral nerves before attacking the brain. Let me call attention to another point, which Avas first published by my friend Zlemssen, at that time assistant in my clinic. Most paralyses of cerebral nerves are peripheral, Avhen due to tumors, whether these have originated in the brain, or have advanced to the brain from the meninges or cranial bones. On the other hand, most of the feAV cases of paralyses of cerebral nerves occurring in the other forms of brain-disease are of central origin. Now, it is well knoAvn that the state of the nerves and muscles, on electrical irritation, is a certain means of distinguishing central and peripheral paralyses. In central paralysis, the muscle contracts normally when an induced current is passed through the nerve; *in peripheral paralysis, on the contrary, the contraction does not take place. Hence we may thus amplify the above proposition: In cases of local disease of the brain, 02 240 DISEASES OF THE BRAIN. paralysis in the parts supplied by the cerebral nerves (especially if the paralyzed muscles do not contract on passing an electric current through their nerve) renders it very probable that there is. tumor of the brain. The assertion that, other things being equal, paralysis of a cerebral nerve favors the idea of a tumor, and that most paralyses of cerebral nerves are of peripheral origin, is not actually true of the facial nerve. Paralysis of the facial, as one symptom of hemiplegia, occurs just as often in other local diseases of the brain as in cases of tumor, and is unmistakably of central origin. What was said above is not true of these cases, but of the other peripheral facial paralyses. Next to the facial, among the motor-cerebral nerves, the oculo-motor and abducens are most frequently attacked. Paralysis of the pars minor trigemini is rare; this is also true of complete paralysis of the hypo- glossal and motor filaments of the glosso-pharyngeal; while incom- plete paralysis of these nerves, as shown by disturbances of articulation and deglutition, is rather common. Peripheral facial paralysis, due to tumors of the brain, is occasionally preceded by twitching of the facial muscles; while twitching of the muscles of the eye precedes paralysis of the oculo-motor, vviiich is characterized by dilatation of the pupil, ptosis, disturbance of mobility of the eye; often, also, by diplopia and strabismus. If the oculo-motor be unaffected, paralysis of the abducens induces diplopia and strabismus conveniens. Before the destruction of the filaments of the trigeminus has caused anes- thesia of the half of the face, of the conjunctiva, mouth, and nose, most patients complain of severe pain in all the parts supplied by the nerve, and not unfrequently these pains continue during the anesthesia (anesthesia dolorosa). Hardness of hearing, or complete deafness, from destruction of the acousticus, is usually preceded, for a time, by troublesome noises in the ears. Disturbances of vision, even to com- plete blindness, are very frequent in tumors of the brain, but they are not, by any means, ahvays due to direct lesions of the optic nerves, chiasm, tractus opticus, or corpora quadrigemina. Not unfrequently, the tumor is at a distance from these parts, as in the cerebrum or cere- bellum. I consider it a mistake to suppose that, in such cases, the pressure has extended, through the intervening substance, to the optic nerve, and, by pressing this against the base of the skull, caused its atrophy. The correctness of this view appears to be opposed, among other things, by the fact that, in blindness from tumors in the cere- brum or cerebellum, the motor nerves of the eye, which are under about the same conditions as the optic nerve, are rarely paralyzed. Many of the cases of amblyopia and amaurosis, caused by cerebral tumors, depend on venous congestions in the eye, and the consequent structural changes in the retina and optic nerve, and are due to com- TUMORS OF THE BRAIN AND ITS MEMBRANES. 241 pression of the cavernous sinus and obstructed escape of blood from the veins of the eye. Tumors in the posterior cranial fossa only have this effect after they have caused abundant effusions in the ventricles, by compression of the openings of the vene Galeni into the straight sinus. Since tumors, Avhich destroy the optic nerve, very rarely spare the oculo-motor, I consider the presence or absence of disturbances of mobility of the eye as an almost certain means of distinguishing Avhether the amaurosis, caused by cerebral tumor, is due to destruction of the tractus opticus, chiasm, optic nerves, or to interference with the intraocular circulation. Ophthalmoscopy also gives important informa- tion on this point. The changes of the optic nerve, in blindness from cerebral tumors, as revealed by the ophthalmoscope, and the conclu- sions that may be deduced from them, are about as folloAvs, according to Graefe: 1. Simple swelling of the optic papilla, with great tortuosity of the vena centralis. It is indicative of obstructed venous circulation, and, in its purer forms, is most frequently seen Avith tumors that encroach on the cavity. 2. Slight inflammatory swelling of the optic papilla, Avith less dis- tinct venous hyperemia and inflammatory participation of the retina. It occurs as a result of an inflammation of the perineurium, and of the optic nerve itself, which extends to the retina (neuritis descendens), and accompanies those intracranial processes, which, from then ana- tomical character or location, are suited to induce irritation in the parts above named. 3. Atrophy of the optic nerve. This may occur primarily, from direct lesion of the optic nerve by a tumor, meningitis, etc., or second- arily, as a final result of either process. The partial disturbances of sensibility and motility in the parts supplied by the cerebro-spinal nerves, that occur in cerebral tumors, do not differ from those accompanying other local affections of the brain. Neuralgic pains, or indefinite sensations of prickling, formication, furri- ness, etc., as well as complete anesthesia, occur, both over large sur- faces and limited to very narrow bounds. The same is true of mus- cular twitchings, of contractions, and paralyses, although, among the latter, hemiplegia far exceeds the other paralyses. If there be morbid symptoms in the parts supplied by the cerebro- spinal and cerebral nerves at the same time, they almost unexception- ally show the peculiarity of being on opposite sides of the body. This " alternation" is simply because the paralysis, anesthesia, etc., of the cerebro-spinal nerves are caused by a lesion of the nerve-fila- ments before they cross, while those of the cerebral nerves depend on destruction of nerve-filaments that have already crossed. 242 DISEASES OF THE BRAIN. In accordance with the slow groAvth of most cerebral tumors, the development and extension of the local symptoms of irritation and paralysis are usually sIoav and gradual. Many patients cannot state exactly when their disease began. In doubtful cases this may de- cidedly aid in the diagnosis, since, from such a course, we may exclude most other local diseases of the brain. But not very rarely these local symptoms come on suddenly; this is chiefly the case where vascular tumors are suddenly increased in size by overfilling of then vessels, or by hemorrhage from them, or where the parts around them are at- tacked by inflammation or softening, or by capillary hemorrhages. If the tumor have previously run a latent course, and these symptoms of paralysis come on suddenly, the case will most probably be mis- taken for one of cerebral hemorrhage, and there are numerous in- stances where the best diagnosticians have made mistakes in such cases. If, on the other hand, there has been a suspicion of tumor of the brain, the frequency of such incidents in the course of this disease should prevent our being deceived. Attacks of epileptiform convulsions occur more frequently from tumors of the brain than from any other local disease of that organ; but it is very remarkable and inexplicable that they occur almost solely when the tumors are in the cerebrum, and especially when they are near the cortical substance. In many cases psychical disturbances do not present themselves throughout the disease. Indeed, it seems that the psychical functions of the brain only suffer when the cortical substance of both hemi- spheres is affected by organic disease, or by disturbance of circulation. The correctness of this vieAV is proved by the peculiarities of those cases where the state of the psychical functions forms an exception to the above. For the general mental ruin that we described when speaking of abscess of the brain also occurs in cerebral tumors, when they are accompanied by extensive chronic meningitis of the convex- ity, or when the cortical substance of both hemispheres is the seat of numerous tumors (cysticerci), or when their capillaries are compressed by encroaching tumors in both hemispheres, or by extensive secondary effusions in the ventricles. In the rare cases where the tumors perforate the skull, the symp- toms above described are accompanied by other symptoms, Avhich are very characteristic. The perforation usually takes place through the parietal or temporal bones, near the root of the nose, more rarely through the occipital bone. At the point of perforation the hair is lost, the skin becomes red, and is traversed by varicose vessels; ulcera- tion of the integument is rare. We may often feel a bony margin at the border of the tumor, which is generally soft and nodular. It is a TUMORS OF THE BRAIN AND ITS MEMBRANES. 243 characteristic but not a constant symptom for the tumor to move with respiration; occasionally it may be replaced. Attempts to do this, Avhich suddenly contract the space in the skull and prevent the en- trance of arterial blood to the brain, usually induce loss of conscious- ness and convulsions. The nutrition, general condition, and the functions of the body in- dependent of the brain, often show no anomaly for a long time. In other cases it seems as if the organic processes went on Avith a certain sluggishness: the heart and pulse beat sloAvly, respirations are rare, the bowels constipated, secretion of urine scanty, and, perhaps as a consequence of this, the body often increases remarkably in size. In other cases, on the contrary, marasmus occurs early, the patients ema- ciate, the skin becomes dry and scaly, the mucous membranes, espe- cially the conjunctiva, are affected with blennorrhea. Lastly, there are bed-sores and dropsy of the feet. The course of cerebral tumors shows many variations which Ave shall not discuss in detail. At first, there are generally exacerbations and remissions of the symptoms, which subsequently become constant and steadily grow worse. In carcinomatous tumors the disease usually lasts only a feAV months, but occasionally a year or more. Non-carcinomatous tumors often run on for several years. The most usual, and perhaps the only, termination is death. If it be not induced early by complications or intercurrent disease, the symptoms of general limitations of the space in the skull become more and more marked. The patients fall into deep coma, followed by death. It is rarely possible to recognize the seat and size of a tumor ex- actly ; but it may often be approximately decided in what part it is located, whether in the cerebrum, medulla oblongata, or in the cerebel- lum, at the base or at the convexity. The "brilliant diagnoses," where the precise localization of a tumor is fully confirmed by autopsy, are not usually due to acumen of the observer, but are cases of lucky diagnosis. If a basilar tumor destroys the function of seAeral cerebral nerves, one after the other and in regular sequence, while it spares neighboring nerves, any one, having a knowledge of only the coarse anatomy of the brain, can decide the seat and extent of the tumor Avith almost absolute certainty. HoAvever, such cases, which are pub- lished with much self-satisfaction, are exceptions, as said before. It would occupy too much time to speak fully of all the factors, be- sides the participation of the different cerebral nerves, which are to be considered when deciding the location of the tumors. We must limit ourselves to the following short hints. The presence of hemiplegia 244 DISEASES OF THE BRAIN. indicates that the tumor is either in one side of the cerebrum (the most frequent seat) or in one crus cerebri, in one side of the pons or in one side of the cerebellum. In tumors of the cerebrum the hemiplegia is usually pure, that is, the other half of the body is entirely free from paralysis. In tumor of one crus cerebri, the paralysis of the opposite side of the body is almost always accompanied by paralysis of the oculo-motor of the same side. In tumors of the lateral portions of the pons, besides the hemiplegia and very common anesthesia of the oppo- site half of the body, there is usually facial paralysis or anesthesia of the side of the face corresponding to the tumor. In tumors of the cerebellum, as we have previously shown, hemiplegia is not constant, and when present is not pure, but extends to the other side of the body to a less extent, especially affecting the muscles of the spinal column. Paresis of the muscles inducing bending, erection, and lateral move- ments of the spinal column, first shoAvs itself by a peculiar form of diz- ziness, which we have already fully described, and referred to vibra- tions of the spine in walking and similar acts; subsequently, it often eA'inces itself by an utter inability of the body to maintain itself, so in the sitting position the patients collapse and cannot move the body, unless held by both shoulders. Paralysis of both sides results from tumors in both sides of the cerebrum, in the middle parts of the pons and in the medulla oblongata. In the above description of the different symptoms it has already been shown that epileptiform convulsions indicate that the tumor is near the cortical substance of the cerebrum; pain in the back of the head shows that it is in the posterior cranial fossa; and severe psychical disturbance either indicates numerous tumors in the cortical substance of both hemi- spheres, or that there is secondary meningitis or hydrocephalus. It appears to me that too little attention has been paid to the fact that the intelligence which is at first intact is very much impaired in the later stages of tumors encroaching on the posterior cranial fossa, which impede the escape of blood from the ventricles and induce ex- tensive transudations into them. Even on most carefully weighing all the symptoms, many errors occur, and it is very desirable that observers, who have access to a large number of cases, should publish their errors of diagnosis, as well as then successes, more than has hitherto been done. The trust- worthiness of the different aids to the diagnosis and locahzation of cerebral tumors cannot become perfectly clear till this is done. The Avide-spread error of designating the various forms of neopla- sia, aneurisms of the brain, and even parasites, by the common name of cerebral tumors, is undoubtedly due to the fact that there are very few cases where the nature of the tumor can be certainly determined TUMORS OF THE BRAIN AND ITS MEMBRANES. 245 during life. If the symptoms of cerebral tumor occur in a person Avho shoAvs signs of carcinoma, tubercle, aneurism, or parasites in some other organ, we are justified in presuming that the cerebral growth is of the same nature as the other tumor, neoplasia, or parasite ; but this aid to diagnosis fails in most cases, except where there are tubercles of the brain in persons Avith tuberculosis of the lungs, and syphilomata of the brain in persons Avith the same affections of other organs. Car- cinoma of the brain is, as a rule, primary and sohtary; aneurism of a cerebral artery is usually the only one in the body, and, Avhen cysti- cerci and echinococci enter the brain, as a rule they also are limited to that organ. . The age of the patient gives some indication as to the nature of the tumor. Most frequently children are affected with tubercle, young adults with benignant tumors, especially sarcoma and glioma, and per- sons of advanced years with carcinoma. In his classical observations on brain-diseases, Griesinger has shoAvn that, under some circum- stances, it is possible to make a diagnosis of cysticerci in the brain, even when there are none in other parts of the body. The large num- ber of these small parasites, and their customary seat in the superficial layers of the cerebrum, explain the severe psychical disturbances and the epileptiform attacks, while the absence of a large compressing body explains the non-occurrence of symptoms of paralysis, on which factors Griesinger founded the diagnosis in his case. On the other hand, I regard Griesinger's experiment, of compressing both carotids firmly against the transverse processes of the cervical vertebre, as entire- ly useless for the diagnosis of basilar aneurism, and he, too, says it is " purely theoretical." The occurrence of convulsions during this act is not at all significant of an aneurism, even of an obliterated one. In many other diseases, also, Avhere there is any thing encroaching on the intracranial space, compression of both carotids causes dizziness and loss of consciousness with or without convulsions. Treatment.—We can do but little to remove carcinoma, sarcoma, and the neoplasia generally, in other organs, by the hunger-treatment, by the administration of iodine, arsenic, etc., and these remedies are of no more benefit in tumors of the brain. They hasten the fatal re- sult instead of retarding it. The treatment can only be palliative and symptomatic. It is useless, and annoys the patient, to apply a seton or issue to the nape of the neck. On the contrary, it is advisable to guard him in every way from hyperemia of the brain, by which acute SAvelling of the tumor and threatening attacks are most fre- quently caused; to regulate the nutrition and mode of life; to attend to the bowels, etc. Apoplectic or inflammatory attacks must be com- bated by venesection, local bleeding, ice-compresses, etc., as before 246 DISEASES OF THE BRAIN. advised. When the pain in the head is unusually severe, we may or- der local abstraction of blood and cold-compresses or derivatives to the nape of the neck. If these fail, we should not be too timid about giving narcotics, and particularly small doses of morphia. When there is the slightest suspicion of syphiloma of the brain, instead of this symptomatic treatment, we should institute an energetic antisyphilitic course. It is unpractical to delay this treatment, or to neglect it al- together, if the syphilitic nature of the disease be not accurately deter- mined. Experience teaches that even very severe structural changes are capable of recovery, and often disappear under proper treatment, and, on the other hand, that treatment is powerless against carcinoma, sarcoma, etc. Hence, we risk little and may gain much, if, on the mere suspicion of syphiloma of the brain, we treat the patient as if there was no doubt about the diagnosis. CHAPTER XIV. SEROUS EFFUSIONS IN THE MATURE SKULL--HYDROCEPHALUS ACQUI- SITUS. We have already spoken of one form of hydrocephalus, that which almost constantly complicates basilar meningitis, and, in the next chapter, when treating of congenital hydrocephalus, we shall also treat of the effusions occurring shortly after birth, before the sutures are closed. In the present chapter we shall only consider those serous effusions into the cranial cavity which occur without basilar menin- gitis and after the skull has closed. Etiology.—Serous effusions into the arachnoid sac (hydrocephalus externus) are rare, and hardly ever become extensive. Effusions into the subarachnoid space and ventricles and edema of the brain are more frequent. Hydrocephalic effusions are due partly to increased lateral pressure in the vessels, partly to an abnormally slight amount of albumen in the blood, partly to disturbances of nutrition, which render the walls of the vessel more permeable. As one symptom of general dropsy, whether dependent on disturbance of circulation or on abnormal quality of the blood (morbus Brightii), the hydrocephalus rarely attains a high grade, although, perhaps, some sudden deaths occurring in the dis- eases inducing the dropsy are to be referred to slight effusions in the ventricle and to a slight edema of the brain. Tumors and other dis- eases in the posterior cranial fossa, by compressing the vene Galeni or straight sinus, and obstructing the escape of blood from the ventricle, sometimes induce high grades of hydrocephalus. Hydrocephalus, de- HYDROCEPHALUS ACQUISITUS. 247 pendent on certain disturbances of nutrition in the capillaries, is more of an independent disease than the other forms ; it closely resembles the inflammatory processes, and may be ranked with the inflammations of the skin that cause serous blebs. This view is supported by an in- teresting observation of Hoppe, who, on examining the fluid from a chronic hydrocephalus, found it differently constituted from the normal cerebro-spinal fluid, particularly that it contained more albumen. This form of hydrocephalus occurs chiefly among children, and, Avhen seen later in life, it almost always dates from childhood. We must mention, as a peculiar variety of the disease, hydrocepha- lus ex vacuo, which develops as a necessary result of diminution of the size of the brain, whether from general, especially senile, involution (hydrocephalus senilis), or from partial atrophy of the brain. Anatomical Appearances.—The amount of fluid effused into the arachnoid sac is difficult to decide, since, on removing the brain from the skull, the fluid from the subarachnoid space is' always mixed with it; but, as we have before said, it never becomes considerable. The fluid effused in the subarachnoid space is sometimes regularly, sometimes irregularly spread over the surface of the brain; in the latter case the arachnoid often forms a vibrating sac filled with serum. When slight, edema of the brain shows itself by the moist lustre of the cut surface; when more decided, the coherence of the brain is decreased, and, if we press on some part, the resulting pit is filled Avith hquid after a time. When of very high grade, the brain-substance is broken down by the edema, and changed to a thin white pulp (hydrocephalic softening). < In acute hydrocephalus internus the fluid effused into the ventricle rarely exceeds half an ounce or an ounce; it is either clear, or, as is usually the case, slightly clouded by a scanty admixture of cast-off epithelium, flocculent clots, and fragments of the surrounding brain- substance. The walls of the ventricle, especially the septum, fornix, and commissures, are in a state of hydrocephalic softening. In chronic hydrocephalus internus we generally find the ventricles considerably dilated: they may contain ten or twelve ounces of fluid, Avhich is usually clear. The ependyma of the cerebral cavities is thick- ened and often streAvn Avith fine granulations. The surrounding brain- substance is also more dense and tough. Symptoms and Course.—Of course, the cavity of the skull is as much encroached on by serous effusions as by extravasations of blood or products of inflammation. As a necessary result of this, we have mentioned obstruction to the entrance of arterial blood, and have given attacks of convulsions and loss of consciousness as the symptoms of complete and sudden arterial anemia; general symptoms of irritation 248 DISEASES OF THE BRAIN. and depression as those of incomplete and gradually-developing anemia. If, at the same time, we remember that those portions of the brain bounding the ventricles are destroyed, in acute hydrocephalus, by soft- ening, in the chronic form by atrophy, and that this may induce partial paralysis, we may construct a picture of the disease, either in the acute or chronic form, exactly corresponding Avith direct observation. Sudden and large effusions of serum into the cerebral substance and ventricles lead to a combination of symptoms which, from its re- semblance to the apoplectic attack induced by extravasation of blood, is usually termed apoplexia serosa. After what was said above, it is hardly werth mentioning that a distinction between serous and sanguineous apoplexy is not by any means possible in all cases, and that, if a diagnosis be made, it is chiefly from the etiology, which indicates one form rather than another. In children, acute hydrocephalus almost always runs its course with the symptoms that we ascribed to high grades of cerebral hyperemia, and to the first stages of acute meningitis. Severe attacks of convul- sions, with loss of consciousness, are the most frequent and character- istic symptoms. If these attacks occur very often, and last unusually long, they should excite the fear that the hyperemia has induced con- siderable transudations in the ventricles, and it is to be feared that the transudation will not be absorbed, or, at least, only partly so, and that chronic hydrocephalus will remain. The symptoms of chronic hydrocephalus either succeed those of the acute form, or they develop insidiously and gradually. They consist of headache, dizziness, weakness of the sjecial senses, particularly of the eyes, very often of a general paresis, preceded by a tottering gait and trembling of the limbs. Among the constant symptoms are dis- turbances of the intellect, especially its gradual loss, even to idiocy. This is sometimes accompanied by convulsions, and occasional vomit- ing. The patients usually have a sIoav pulse, are readily chilled, are occasionally ravenous; they have a puffy look, and varicose vessels on the cheeks. Of course, these symptoms only render the diagnosis of chronic hydrocephalus certain when other cerebral diseases, accompa- nied by similar symptoms, can be excluded, and, consequently, that the diagnosis can rarely be made with absolute certainty. The course of the disease is usually very tedious. If death do not sooner occur from some intercurrent disease, it finally results, sometimes rapidly and unexpectedly, from acute increase of the effusion, sometimes slowly, from its gradual increase, being usually preceded, for some days, by continued deep sopor. Treatment.—The treatment of acute hydrocephalus is the same as that of acute hyperemia of the brain and acute meningitis. In CONGENITAL HYDROCEPHALUS. 249 chronic hydrocephalus, the continued employment of cold douche baths deserves most confidence. CHAPTER XV. SEROUS EFFUSIONS IN THE INCOMPLETE SKULL—HYDROCEPHALUS CONGENITUS. Etiology.—It is most probable that congenital dropsy of the brain is due to inflammation of the ventricular walls that has occurred during foetal life. The etiology of the disease is entirely obscure. Some women have had several hydrocephalic children, without any apparent cause. Anatomical Appearances.—In congenital hydrocephalus the amount of serum, usually clear and limpid, effused into the cerebral cavities, is occasionally very small, Avhile it sometimes amounts to six or ten pounds. In such cases the ventricles are distended to large, thick-walled sacs, the brain-substance around them is thinned, and often atrophied to a layer only a few lines thick; the corpora striata and optic thalami are flattened and pressed apart, the corpora quad- rigemina flattened, the commissures stretched and thinned. The sep- tum is occasionally broken through, and the floor of the third ventricle is often thinned and projecting. The pons and cerebellum appear compressed from above downward. Where the effusion is not large, the skull preserves its normal size; where it is large, on the other hand, it is almost always decidedly dis- tended. Even at birth the head is usually enlarged, but becomes still larger after birth, and may be distended to two feet in circumference. In such cases the cranial bones, especially the frontal and parietal bones, are very large, and are, at the same time, very thin. The mem- branous interstices also, especially the fontanels, are very wide. The forehead is prominent, the roofs of the orbits are depressed, and they are transformed into narrow, transverse slits; the squamous portions of the temporal bones and the occipital bone are more horizontal. The ossification, Avhich is delayed, takes place from formation of points of ossification in the membranous interspaces, or even from the formation of innumerable small bones. The cranium, which, previous to the ossification, was very thin, often becomes thick subsequently, and, in many cases, such a skull retains an asymmetrical or remarkable spheri- cal form. Symptoms and Course.—Many cliildren, born with hydrocephalus, die at birth or shortly after. In others, during the first weeks of life, if the skull be not enlarged, no symptoms of the disease can be observed. This is due partly to the difficulty of judging of the cere- 250 DISEASES OF THE BRAIN. bral functions at this age, partly to the yielding nature and gradual distention of the skull. If an equal amount of transudation occurred in the mature skull, the severest symptoms would arise. Even during the first years of life, the increasing size of the skull and the growing difficulty that the child finds in holding its head up- right are the most prominent and only characteristic symptoms. If the head be not enlarged, or so slightly so as not to be noticed, the disease is generally overlooked in the first year also. It is true the mother wonders that, when the child is nine months old or over, it still remains uncleanly, makes no attempts to walk, and does not even try to speak; she hardly asks the physician's advice, and, when she does finally consult him, he also reassures her. But gradually the child appears more strange. First of all, there is an idiotic manner with outbursts of pleasure or fear, in which the child often shrieks out, dis- torts the face into horrible grimaces, and drums with the extremities. The first year passes, and the child continues to stick all toys, for which other children of the same age seem to understand the use, into its mouth, because it does not know what else to do with them. The eye does not regard any object held in front of, it, but rolls about un- steadily. The face has no expression, but is empty and silly; often saliva flows constantly from the half-open mouth. And gradually comes the sorrowful conclusion that the child does not develop intel- lectually, or even loses ground. Many such children do not learn to walk. If we attempt to teach them to walk, they often cross the legs instead of setting them forward. Others, who do learn to walk, have such an uncertain and helpless gait that they readily fall, and fre- quently cannot step over any elevation. There are usually no anom- alies in the organs of special sense. On more careful observation, apparent deafness generally turns out to be deficient attention. It is difficult to come to any decision regarding the senses of smell and taste; the sense of sight usually remains intact, though there is often strabismus or dilatation of the pupil. In those cases where the head quickly becomes very large, the dis- ease is recognized sooner and more easily, although in them the above symptoms are usually less developed than where the head is mod- erately or not at all enlarged. The little old face, which does not agree with the large skull, and forms with it a triangle pointing toward the chin, the distended veins traversing the skin, especially in the frontal and parietal regions, the thin hair covering the broad skull, the often rachitic bones or a general dwarfy appearance, the vain attempts of the child to hold up the heavy head, which sinks again every time it is raised, give the disease an appearance as melancholy as it is characteristic. HYPERTROPHY OF THE BRAIN. 251 Apart from the intercurrent attacks of convulsions, which are quite frequent, the course of the disease is sometimes regular and steady, so that the symptoms increase gradually till death results from general paralysis, or it is irregular, so that the symptoms are worse at times, while at other times there is a temporary stand-still or even improve- ment. Lastly, it is not rare for the disease, after attaining a certain point, to remain permanent, or even for part of the existing disturbances to disappear. This disappearance probably never goes on to recovery; some intellectual weakness always remains, though it may be only a slight amount. The most frequent termination of the disease is death; this often occurs during the first years of life, partly from the disease itself with convulsions and consequent coma, partly from complications. The increasing encroachment on the cranial cavity shows its effects earlier in the mature skull than in the opposite case, and the life of the child is in greater danger Avhen the skull remains of the normal size than Avhen it is considerably dilated. In rare cases death results from rupture of the distended ventricle and soft parts covering it, either spontaneously or from a fall or blow. Few patients live beyond puberty, and it is very rare for them to attain mature age. Treatment.—In congenital hydrocephalus nothing can be accom- plished by absorbent remedies, diuretics, drastics, preparations of iodine, calomel, or mercurial salve. Compression of the distended skull by strips of adhesive plaster is not free from danger, and in cases hitherto observed has proved of little use. Nor are the results of evacuating the serum by operation very encouraging. Most patients died soon after the first puncture or after its repetition, so that the operation should be limited to those cases where the head has attained a colossal size, and where a steady progress of the enlargement is observed. In the treatment of congenital hydrocephalus as in the acquired form, the treatment is mostly symptomatic, and the patients are to be protected as much as possible from all injurious influences. CHAPTER XVI. HYPERTROPHY OF THE BRAIN. Etiology.—Since, in so-called hypertrophy of the brain, there is not an increase of the true tissue-elements of the brain, the nerve-fil- aments, and ganglion-cells, but only a proliferation of the delicate insterstitial substance which unites the nerve-elements, the name hypertrophy of the brain is not exactly correct. It is sufficient, how- ever, to have noticed this point, and Ave may preserve the old name 252 DISEASES OF THE BRAIN. without fear of being misunderstood. We do not know whether the proliferation of the neuroglia is the result of frequently-recurring hyper- emia, or of some other cause. Hypertrophy of the brain is occasionally congenital, and then often accompanies dwarfishness; more frequently it develops after birth, is chiefly limited to childhood, and becomes rarer with advancing years. Hypertrophy of the brain acquired after birth is usually accompanied by rachitis, deficient involution of the thymus gland, and hypertrophy of the lymphatics (Bokitansky). Mental excitement, abuse of liquor, and lead-poisoning, are mentioned as exciting causes of the disease, but it is very doubtful Avhether they act in this way. Anatomical Appearances.—The brain, almost exclusively the cerebrum, is larger and heavier than normal. On autopsy, if the top of the skull be removed it is difficult to replace it, because the brain bulges out so, and protrudes between the sawed edges of the bone. The cerebral membranes are very thin and bloodless. We often find no trace of liquid in the subarachnoid space. The convolutions on the surface of the cerebrum are flattened and pressed together; the sulci between them are scarcely perceptible. The centrum semiovale is unusually large, the ventricles are small on section; the brain-substance, like the membranes, appears bloodless and dry. Its consistence and elasticity are increased. If hypertrophy of the brain develop before closure of the skull, the latter is distended, just as in congenital hydrocephalus. If, on the other hand, it does not begin till the sutures are closed, the cranial Avail is often thinned by absorption, and the inner lamella loses its smoothness. More rarely, when the disease increases rapidly, the closed sutures are opened and pressed apart. Symptoms and Course.—Of course, hypertrophy of the brain has the same influence on the intracranial circulation as any other increase of the contents of the skull has; hence it is accompanied by extensive symptoms of irritation and of paralysis. And it may readily be un- derstood that these symptoms often do not occur, or only attain a low grade, as long as the sutures of the skull are not closed, and the skull can distend in proportion to the enlargement of the brain. The cir- cumstance that children with hypertrophy of the brain are not always deficient in intellectual development, but are sometimes remarkably sharp and competent in proportion to their physical development, forms a strong point in diagnosis between hydrocephalus and hyper- trophy of the brain in children with very large heads. Among the symptoms most frequently seen, Avhen there is no enlargement of the head, or when it does not correspond to the increase of the brain, the most important are attacks of epileptiform convulsions. These at- ATROPHY OF THE BRAIN. 253 tacks seem to occur principally when the one constantly present cause, arterial anemia, is accompanied by any other, often a very slight one, which suddenly and temporarily greatly increases the anemia. Head- ache, dizziness, photophobia, general hyperesthesia, mental irritability, occasional vomiting, and subsequently anaesthesia, general muscular debility, mental hebetude and droAVsiness, are much less frequent and far less characteristic of the disease. The malady can only be diag- nosed Avith an approach to certainty where the skull is enlarged and hydrocephalus can be excluded, while in most cases only a probable diagnosis can be made. The course of hypertrophy of the brain is al- ways chronic. It is doubtful whether it ever ends in recovery. Death results either from the disease itself, generally not from a gradually increasing paralysis, but during a severe attack of convulsions, or else from complication with hemorrhages and inflammatory exudations; as may readily be understood, even when very slight, these are ex- tremely dangerous for such patients. We cannot speak of treatment of hypertrophy of the brain, for, even where the disease is recognized, we cannot expect any remedy to remove the existing disturbance. CHAPTER XVII. A T.R OPHY OF THE BRAIN. Etiology.—We must not term every diminution of the brain-sub- stance, particularly those due to destruction of its tissue and to develop- ment of shrinking cicatricial tissue in the place of the destroyed por- tion, atrophy of the brain. True atrophy of the brain consists rather in a diminution of the size or number of the elements, without any per- ceptible previous destruction of them. It is convenient to distinguish two forms of atrophy of the brain. In the first, the so-called agenesis, there is incomplete development; in the second there is a retrogression, a disappearance of the previous- ly Avell-developed constituents of the brain. We pass over those forms of agenesis where the brain is so incom- pletely developed that there is either complete idiocy or that life can- not continue, and turn our attention to the interesting and not very rare form of one-sided atrophy of the brain, occurring during fetal life and the first years of childhood, in which not only may life continue, but there may be a certain amount of intellectual development. The etiology of monolateral agenesis is obscure. It is probably due to in- flammation of the brain, meninges, or skull, during fetal life or early childhood. 254 DISEASES OF THE BRAIN. The atrophy occurring after complete development of the brain is sometimes primary, sometimes it accompanies other affections of the brain as a secondary disease. Among the primary atrophies we must first mention that form which occurs as a symptom of senile marasmus. Other senile changes attain unequal grades in different persons, and we also meet very aged individuals who do not shoAV the least sign of cerebral atrophy, while it advances to the highest grade in much younger persons. Next to this comes the atrophy of the brain, AA'hich develops in the course of exhausting and consuming diseases. In many cases which are quoted as examples of great resignation and Avonderful firmness at the approach of death in tedious diseases, the facts Avere really badly interpreted; very often the resignation is cer- tainly due to the dulness and apathy induced by cerebral atrophy. Local diseases of the brain are the chief causes of secondary atrophy. We have already mentioned it as the result of precedent apoplexy, partial necrosis, and partial encephalitis. The paralytic form of idiocy appears to depend on an atrophy of the brain caused by chronic me- ningitis or inflammatory processes in the cortical substance. In other cases the atrophy is the result of continued pressure on the brain. Under this head come the cases where the size of the brain gradually decreases under the pressure of cerebral tumors and hydrocephalic effusions. In meningitis, also, perhaps part of the atrophy is due to the pressure of the inflammatory exudation in the subarachnoid space. Lastly, we must mention that injury and destruction of peripheral nerves occasionally induce secondary atrophy of then centres. Anatomical Appearances.—When cerebral agenesis is limited to one side, the left is the one generally affected; sometimes the Avhole hemisphere is affected, sometimes only parts of it. In high grades of the disease, the cerebral substance between the ventricles and convex surface has become a thin layer only a few lines thick. The convolutions are scarcely perceptible, or else are very small. The large cerebral ganglia are usually atrophied, and the atrophy extends from them through the crura cerebri to the spinal marrow. The consistence of the atrophic brain is usually increased, its color is somewhat dirty. The space created by the atrophy is filled with fluid that has collected partly in the ventricles, partly betAveen the meninges. The skull is often unsymmetrical, and is thickened at the atrophied part. Atrophy of the brain occurring late in life is usually total, but, when it results from partial destruction of the brain, it is generally further advanced on the side corresponding to the disease than on the other. The medulla of the cerebrum is diminished, the convolutions appear thinner, the furrows broader and deeper. The medullary sub- stance is dirty white, more dense and tough, the cortical substance is ATROPHY of the brain. 255 thinner, harder, and of a pale or light-brown color. The ventricles are dilated and filled with serum. There is also a quantity of fluid in the subarachnoid meshes (hydrocephalus ex vacuo). Symptoms and Course.—Although, as Ave have previously men- tioned, agenesis of one side is not always accompanied by psychical disturbances, still it is rare to find cases where we dare assert that one side of the brain fully replaces the other. Far the greater number of patients suffer from Aveakness of intellect, and many from decided idiocy. The organs of special sense, particularly the eye, are usually very insensitive, and the excitability of the sensory nerves of the par- alyzed half of the body is diminished. The most important and ap- parent symptoms are paralysis and a peculiar and excessive atrophy of the side of the body opposite to the atrophied brain. The paralysis is not usually complete, so that the patients can generally perform some imperfect movements. • The paralysis is ordinarily combined with contractions. The atrophy of the paralyzed side affects all the tissues, the bones not excepted, so that the thin and short extremities of a groAvn person appear like those of a child. Most patients suffer from epileptic attacks. As the other functions of the body are usually Avell performed, the disease itself is rarely fatal. But the patients seldom attain old age. Their power of resistance to intercurrent dis- eases is lessened, and they succumb to them more readily than other persons would. The primary atrophy of the brain, which develops chiefly in old persons, and secondary atrophy, which accompanies apoplexies, partial necrosis, and other local brain-diseases, are characterized by gradual weakening of the psychical functions, loss of memory, slowness of thought, absent and childish manners, as Avell as dulness of the senses, and gradual weakening of the motor poAver, unsteadiness of motion, trembhng, incomplete control of the sphincters, etc. The atrophy of the brain found on autopsy of insane patients, who have suffered from paralytic idiocy, belongs to the terminal symp- toms observed in that form of insanity during life, to the symptoms of mental Aveakness and idiocy, but not to the monomania which pre- ceded the mental paralysis, or to the intercurrent maniacal and apo- plectiform attacks. These are rather to be referred to the precedent meningitis, Avhich is rekindled from time to time during the subse- quent course. At the stage of the disease when the psychical exalta- tion of the patient decreases, when the insane ideas and hallucinations lose their richness and reality, when the thoughts are confused, mem- ory defective, symptoms of paralysis also begin to appear in the motor sphere; and the more the signs of psychical weakness increase, the more extensive and marked become the signs of motor paralysis. The 63 256 DISEASES OF THE BRAIN. first symptom of the latter is always impahed articulation, which gradually becomes perfect mumbling. The attitude is negligent, the gait uncertain and tottering, the patients easily fall, then hands trem- ble when held out. Later, they cannot leave the bed, lie motionless, do not react to the strongest irritation, and finally die of marasmus. Treatment.—We cannot expect to treat atrophy of the brain successfully. Treatment must be directed against the original disease, to prevent the progress of the atrophy, if possible. On this occasion Ave shall again call attention to the cold douches which we recom- mended as peculiarly efficacious in chronic meningitis. For the rest, we have to limit ourselves to combating the more threatening symp- toms. In monolateral agenesis we may attempt to arrest the atrophy and fatty degeneration of the muscles by using the induced current of electricity, which, in this case, is of course to be regarded only as a gymnastic remedy. SECTION II. DISEASES OF THE SPINAL 3IABB0W AND ITS MEMBBANES. CHAPTER I. HYPEREMIA OF THE SPINAL MARROW AND ITS MEMBRANES. There is hardly any doubt that the amount of blood contained in the spinal marrow is subject to variation, and that hyperemia and anemia modify its functions just as they do those of the brain. Never- theless, the symptoms wThich we are in the habit of referring to an abnormal amount of blood in the spine are not directly deduced from comparison of the symptoms observed during life with the results of autopsy, but from a priori reasoning. Moreover, in most autopsies no attention is paid to the amount of blood in the spinal marrow, and its estimation offers even more difficulty than is the case in the brain. Remarkable vascularity of the spinal medulla and its membranes is most frequently found on autopsy of new-born children and of per- sons who have died of spasmodic affections or of acute febrile diseases. We also find varicose dilatations of the venous plexus in the lower part of the spinal canal, as one of the symptoms of abdominal plethora accompanying cirrhosis of the liver and other diseases that impair the circulation in the abdomen. Hyperemia of the spinal medulla itself leads to swelling and relax- ation of its substance, and to the formation of small ecchymoses; in higher grades there is softening of the medullary substance. Accord- ing to Hasse, hyperemia of the membranes induces increased transu- dation, as a result of Avhich there "may be overfilling of the subarach- noid space, extending from below upward as far as the skull. As symptoms of hyperemia of the spinal medulla and its mem- branes, the above author mentions a dull pain, mostly hmited to the sacral and lumbar regions, a feeling of numbness and formication in the 258 DISEASES OF THE SPINAL MARROW AND ITS MEMBRANES. lower extremities and their incomplete paralysis. These disturbances of sensation and motility, proceeding from below upward, rarely extend to the upper extremities; when this does occur, the respiration is also said to be occasionally affected, while the bladder and rectum hardly ever participate in the paralysis. From this combination of symptoms we cannot decide on hyperemia of the spinal marrow with any cer- tainty, unless there are other symptoms of it, and the symptoms dis- appear after bleeding from the hemorrhoidal or uterine veins, which anastomose with those of the spinal medulla, or after local abstraction of blood. It is at least doubtful Avhether convulsions result from ex- cessive hyperemia of the spinal marrow, since the hyperemia found on autopsy after severe convulsions may just as well be the result as the cause of the spasm. The same is true of the association between the spinal hyperemia, found after febrile diseases, and the symptoms of the fever. " Spinal irritation," which for a time caused a good deal of talk, is a term used to indicate a condition chiefly characterized by sensitiveness of certain spinal processes to pressure, great inclination to reflex movement, and a general hyperesthesia. We find these symptoms just as frequently as we do headache in many acute and chronic diseases, without its being possible to interpret them. At all events, we are not justified in deciding from their presence, without further proof, that there is hyperemia of the spinal marrow, any more than we are in diagnosing cerebral hyperemia in patients who have only headache. If the causes of the spinal hyperemia be made out, we should, in the first place, attempt to fulfil the causal indications. When the hy- peremia has attained a certain grade and we cannot hope for its sub- sidence without therapeutic aid, we may employ local blood-letting by wet cups and leeches. We should apply the former along the spinal column, the latter about the anus, especially when there is coincident abdominal plethora. The effect of the abstraction of blood is sup- ported by cathartic medicines, particularly the neutral salts. CHAPTER II. HAEMORRHAGE OF THE SPINAL MARROW AND ITS MEMBRANES-- SPINAL APOPLEXY. Except small ecchymoses, which accompany excessive spinal hyper- emia, extravasations between the meninges and into the substance of the spinal marrow are very rare. Degeneration of the walls of the vessels, and increased pressure of blood in the arteries, which are the chief causes of cerebral hemorrhages, appear to have no effect on HYPEREMIA OF THE SPINAL MARROW AND ITS MEMBRANES. 259 spinal hemorrhage. Intermeningeal hemorrhages may almost alwavs be traced to injuries of the spinal meninges from wounds, contusions, or stretching. Their occurrence chiefly among the neAvly-born is due to the severe tension to Avhich the spinal column of the child is so often subjected during severe labor. Extravasations of blood in the medulla spinalis are usually terminal symptoms of chronic destructive processes of the cord, and are only rarely due to injuries of the spinal column. The extravasations of blood from meningeal haemorrhage are usu- ally considerable; they collect chiefly in the lower part of the spinal canal, but often fill large portions of the subarachnoid space. Where the hemorrhage is into the medulla, we find it containing a bloody pulp. The changes undergone by the apoplectic clot, when it has ex- isted a long time, are little known, but seem to resemble those under- gone by the brain under similar circumstances. Apparently intermeningeal hemorrhages only gradually compress the vessels of the spinal cord sufficiently to entirely cut off the supply of arterial blood, and so remove the excitability of the nerve-filaments. In effusions of blood betAveen the meninges, symptoms of severe irrita- tion, pains in the back, and spasms, especially tonic spasms in the parts supplied by the nerves going off below, opisthotonos, rigid con- traction of the extremities, etc., usually precede the paralysis. But where there are large extravasations, there is perfect anaesthesia, and paralysis of the parts receiving nerves from the compressed portion of the spinal cord. If the respiratory muscles be among these parts, death soon occurs; if they remain unaffected, death may be delayed. It is doubtful whether the conduction can be restored and recovery take place after disintegration and reabsorption of the extravasation. From the above symptoms Ave can only make a diagnosis of meningeal spinal apoplexy Avhen they have been preceded by an injury of the spinal canal. If the history be imperfect, and Ave find no causes ren- dering hemorrhage probable, the disease cannot be recognized Avith certainty. Since the substance of the spinal marrow is usually entirely broken doAvn by hemorrhages into it, the conduction from the brain to the peripheral nerves, and from them to the brain, is generally interrupted at the moment of the hemorrhage. The more sudden the symptoms of this interruption—anesthesia, and loss of voluntary motion in the lower half of the body, combined with paralysis of the bladder and rectum—appear, the more probable it is that the communication has been interrupted by a rapid breaking doAvn of the spinal medulla from an extravasation of blood, and not by its gradual destruction from in- flammation, softening, or paralysis. When the apoplexy is high up, so 260 DISEASES OF THE SPINAL MARROW AND ITS MEMBRANES. that respiration is affected, death occurs quickly. If, on the other hand, a part far down be destroyed, death does not result for years, and is generally caused by large bed-sores, or cystitis, induced by paralysis of the bladder. Since we cannot, by therapeutic means, hasten the reabsorption of the effused blood, or aid the regeneration of the broken-down nerve- filaments, the treatment of spinal apoplexy can only be symptomatic. At first, as long as there are severe pains in the back and symptoms of inflammation, the proper treatment is local bleeding, and the applica- tion of an ice-bladder to the part where the hemorrhage is suspected. Subsequently there is usually little to do but to guard the patient against bed-sores, to carefully empty the bladder at regular intervals, and to maintain the strength of the patient. Well-to-do persons, who remain paralyzed from spinal apoplexy, may be sent to Wildbad, Pfafers, or Gastein. But, the more certain the diagnosis, the more improbable it is that these baths will prove beneficial. CHAPTER III. INFLAMMATION OF THE MEMBRANES OF THE SPINAL MARROW— MENINGITIS SPINALIS. Etiology.—Inflammation of the dura mater probably never occurs as an independent disease, but it very frequently follows injuries, and especially inflammations of the spinal column. Acute inflammation of the arachnoid is also almost solely observed as an accompaniment of inflammation of the dura and pia mater; but chronic inflammation of the arachnoid, resulting in partial thickening and ossification, occurs as a primary and independent disease, without perceptible cause. Acute inflammation of the pia mater from epidemic influence has already been described, among the diseases of the brain, as meningitis cerebro- spinalis. Besides this form, there are sporadic cases of inflammation of the pia mater of traumatic origin, or due to inflammation of the dura mater; and, lastly, although rarely, cases that must be referred to catching cold, or some other injurious influence acting on the body Anatomical Appearances.—Inflammation of the dura mater is never spread over large surfaces, but is alwTays more or less circum- scribed. At first the inflamed spot appears injected, infiltrated, and relaxed; later it becomes discolored, friable, and is occasionally cov- ered with purulent exudation. The results of pachymeningitis spinalis are permanent thickening of the dura mater, and its adhesion to the bone; more rarely there is perforation of the dura mater by the pus col- lected between it and the bone, and, as a consequence, diffuse meningitis. MENINGITIS SPINALIS. 261 We must regard as remains of chronic inflammation of the arach- noid, milky opacities of that membrane, and cartilaginous or bony plates, about the size of a millet-seed, which have a rough inner and smooth outer surface, and which are generally very numerous, espe- cially in the lower portion of the spinal cord. Inflammation of the pia mater is usually very extensive. In the acute form we find the pia mater injected, swoUen, and relaxed. In the subarachnoid space there is a copious, purulent, flocculent exuda- tion, or else the pia mater and arachnoid are covered Avith membranous deposits. The spinal medulla is usually pale and bloodless; rarely it is injected, relaxed, or softened. Most cases of so-called hydrorhachis acquisita appear to be due to chronic inflammation of the pia mater. We spoke of opacities and edema of the cerebral membranes as Aery frequent post-mortem appearances in topers, and referred them to a chronic meningitis; it is also probable that inflammatory disturbance of nutrition of the meninges induces the collections of large amounts of fluid in the subarachnoid space of the spine, Avhen they do not de- pend on general dropsy or atrophy of the spinal marrow (in which case they are unimportant, and do not cause any symptoms). More- over, it is difficult to decide, from the tension of the dura mater before it is incised, or by estimating the amount of liquid that escapes after it is incised, whether the amount of subarachnoid fluid is abnormally increased. The more cloudy or bloody the escaping fluid, the more probable it is that the hydrorhachis is due to chronic inflammation of the meninges. Symptoms and Course.—Inflammation of the dura mater is not accompanied by very prominent or characteristic symptoms when it does not lead to perforation, and, by escape of pus into the subarach- noid space of the spine, induce diffuse meningitis. When patients, AATho have had an injury of the back, or have caries of the spine, com- plain of pain in the back, it is difficult to decide whether it is due to inflammation of the dura mater or of the bones and ligaments. The symptoms of chronic inflammation of the arachnoid, and during the formation of the little plates above described, are perfectly ob- scure. Acute inflammation of the pia mater is accompanied by symptoms of severe irritation in the parts supplied by spinal nerves, which are subsequently generally followed by symptoms of paralysis; it is usu- ally distinctly characterized and readily recognized by these symptoms and their sequence. Occasionally after a chill there is fever, and the patients complain of severe pain in the back, which becomes insup- portable on motion, and usually on pressure over the spine. It is ordinarily accompanied by pains in the extremities. Both the pain in H 262 DISEASES OF THE SPINAL MARROW AND ITS MEMBRANES. the back and the peripheral pain are to be referred to the irritation of the sensory nerves within the spinal canal, from the inflammation of their envelopes. Tonic spasms in the muscles of the back and extremi- ties, causing opisthotonos and contraction of the limbs, are just as constant symptoms as the morbid excitement of the sensory spinal nerves. These tonic spasms, Avhich, as is Avell known, we may induce artificially in animals, by hritating the spinal medulla with the in- duced current, usually remit and exacerbate. The exacerbations are not, as in tetanus, induced by irritating any part of the skin, but by movements of the spinal column, a fact which indicates that the tonic spasms in meningitis spinalis are not due to increased reflex excitabil- ity, but are direct results of irritation of the motor nerves from the inflammation of then envelopes. The rigidity and tension of the body, which prevent the patient, Avho is not at first paralyzed, from moving, are from time to time interrupted by convulsive starts. If the respira- tory muscles participate in the tetanic rigidity, breathing becomes im- possible, and the patient soon dies as a consequence. If the res- piratory muscles remain unaffected, there is occasionally a gradual im- provement ; but more frequently paraplegia is developed, or the fever increases, and the patient succumbs to the paralysis, which advances to the medulla oblongata, or to the exhaustion induced by the fever. In the chronic form of inflammation of the pia mater, whose symp- toms we described with those of hydrorhachis acquisita, since Ave con- sider a distinction between them as impracticable, the pain in the back is usually inconsiderable and is easily overlooked. On the other hand, at the onset of the disease, the pain in the extremities is often such a prominent symptom, that the affection is mistaken for peripheral rheu- matism. The most important symptoms are those of paralysis, which, commencing in the lower extremities, extend to the bladder, rectum, and subsequently to the upper extremities. The paralysis is usually incomplete at first, and only gradually increases to complete para- plegia ; along with it there is usually a feeling of formication and fur- riness in the lower extremities, the precursor of anesthesia, which, hoAvever, rarely attains a high grade. In some of these cases the paraplegia develops quickly, occasionally in a few days after being- preceded only for a short time by pain, which is considered as rheu- matic (hydrorhachis rheumatica). The paralysis then often remains stationary at the height it has attained, or may entirely disappear. In other cases the paraplegia develops more slowly and insidiously. In such cases the hope of a permanent decrease of the paralysis is slighter, although the disease almost ahvays shows remarkable varia- tions in its course. Most patients die sooner or later from extension of the paralysis to the medulla oblongata, from bed-sores, or from » MYELITIS. 263 catarrh of the bladder. Paraplegia occurs in some other spinal dis- eases as well as in chronic meningitis. The gait of the patient is not characteristic, and does not differ from the gait in other forms of para- plegia. The old belief that the symptoms of paralysis, due to a col- lection of fluid in the spinal canal, grew worse when the body was upright and less when it was horizontal, from the fluid being dis- tributed more evenly, Avas purely theoretical and not derived from direct observation. The most important points, in distinguishing chronic meningitis and hydrorhachis acquisita from other diseases of the spinal cord, are the symptoms of irritation, particularly the painful sensations which precede the paralysis; also the gradual advance of the paralysis from below upAvard, which does not occur in the disease limited to certain points, and particularly the varying course of the disease, the exacerbations and remissions, which do not occur in dis- eases destroying the spinal medulla. Treatment.—Acute spinal meningitis requires energetic antiphlo- gistic treatment, particularly the application of leeches and wet cups to both sides of the spine. If the disease be of traumatic origin, we should at the same time use cold to the back by means of an ice-bladder, or the frozen compresses before mentioned. In very recent cases, as there is danger in delay, and not much can be lost, Ave may employ the much- lauded frictions with mercurial ointment, and give calomel internally. If the acute stage passes off and the disease is protracted, we may apply flying-blisters to both sides of the spine ; commencing with them at the neck, Ave gradually descend to the sacrum, and then begin again at the neck. In meningitis, flying-blisters appear to be more efficient than moxe and the hot iron, Avhich deserve the preference in diseases of the vertebre, and in inflammations of the spinal medulla limited to certain points. In protracted cases, or at the commencement of those running a chronic course, cold plunge-baths and douches, and particu- larly continued warm baths, are very seniceable. The reputation of these remedies, in paraplegia generally, depends chiefly on their results in chronic meningitis spinalis, which is the most amenable to treat- ment of the diseases of the spinal medulla and membranes. Such patients are also benefited by the bath-treatment at Wildbad and other similar thermal springs. CHAPTER IV. inflammation of the spinal marrow—MYELITIS. In the present chapter we discuss also softening and hardening of the spinal medulla, myelomalacia, and myelosclerosis, since we shall consider these degenerations (except Avhere the softening is due to 264 DISEASES OF THE SPINAL MARROW AND ITS MEMBRANES. hemorrhage and edema, as already described) as results or forms of myelitis until Ave shall have learned some other mode of origin for them, as we have for the analogous changes in the brain. Etiology.—Myelitis induces the same structural changes as en- cephalitis does. In it there is no abundant interstitial exudation, but the nerve-elements undergo inflammatory disturbances of nutrition, and finally break down, just as the ganglion-cells and nerve-filaments of the brain do in encephalitis. Apart from the cases due to propagation of inflammation from the vertebre to the medulla, myelitis must be regarded as a rare disease. But this extension occurs quite frequently. Most paraplegias which come on during vertebral disease are not results of the curvature of the spine, but of inflammation extending from the vertebre to the membranes, and thence to the medulla. This view is supported by the fact that in vertebral disease there is frequently paralysis before the spine is curved, and, on the other hand, great curvature often exists for years without symptoms of paralysis, till these at last accompany the deformity without any increase of the curvature, but usually after pain in the back. More rarely, wounds and contusions of the spinal column, or the development of syphilitic exostoses, induce myelitis. Occasionally the disease develops about neoplasia and extravasations of blood. Lastly, sexual excesses, excessive straining, catching cold, suppression of the perspiration of the feet, etc., are given as causes of myelitis. We do not know whether in such cases the disease is really due to these causes or to other unknown influences. Patients Avith paraplegia, besides their other misfortunes, are usually subjected to the unfounded suspicion that they have brought on their disease by dissolute habits. Anatomical Appearances.—Myelitis is sometimes confined to circumscribed spots, and then, usually starting from the gray sub- stance, it attacks the whole thickness of the medulla; sometimes, as " central softening," it extends widely through the gray substance, and then affects the white substance but little. In the circumscribed spots we find the spinal medulla swollen in recent cases. If Ave cut into it, a more or less consistent red pulp (red softening) rises above the cut surface. In older cases, the color of the pulpy soft spot becomes more brown or yellow (yellow softening), from change of the hematin and fatty degeneration of the broken-doAvn nerve-elements. Far more rarely than in the brain, the inflamed spot in the spinal medulla is converted into an abscess by the extensive formation of pus-cells. The inflammation in the meninges usually ex- tends beyond that of the medulla. From disintegration and reab- sorption of the disintegrated elements in circumscribed myelitis, a MYELITIS. 265 cavity, filled Avith serum and traversed by delicate connective tissue, may be formed in the spinal medulla. In other cases there is in- duration from connective-tissue proliferation. These sclerosed spots, which are usually somewhat retracted and colored yellow by pigment, form analogues to the yellow plates, which we found as remains of peripheral encephalitis. In the second (central) form of myelitis we find the medulla but little swollen at first. On section, the contours of the gray substance appear lost; it is someAvhat darker in color, reddened, and less con- sistent. In older and typical cases the spinal medulla is decidedly swollen, and in its centre we find a thin reddish, rusty, or yellow pulp. In this form, also, the tissue-elements, which have broken doAvn to a fine detritus, are sometimes reabsorbed, and fluid exuded in their place, so that, at last, in the axis of the spinal medulla, there is a cavity filled with serum, and surrounded by delicate connective tissue, or traversed by a framework of the same. Symptoms and Course.—Since acute myelitis is ahvays accom- panied by meningitis, it is also accompanied by the symptoms of spinal meningitis described in the last chapter, and Ave can only decide, from certain modifications of the symptoms there described, that the me- dulla itself, as well as the meninges, is inflamed. In the commence- ment of the disease there is usually severe fever and more or less ex- tensive pain in the back and extremities, tetanic rigidity of the mus- cles of the back and nape of the neck, contractions of the extremities, alternating Avith convulsive attacks, and where the respiratory muscles participate in the tetanic tension there is great dyspnea. The more circumscribed the pain in the back, the more distinctly the peripheral pains and spasms are limited to the parts supplied by nerves from a certain portion of the medulla; but especially the earlier and more completely paraplegia follows these symptoms of irritation, the more probable it becomes that the spinal medulla itself is inflamed. In Aery malignant cases these symptoms may get the upper hand very quick- ly, and, even in the first days of the disease, the patient may die from disturbance of the respiration. In other cases the storm passes over, but a paraplegia remains, which hardly ever recovers. Cases running the above course are rare, and are almost always of traumatic origin, or result from perforation of an abscess into the vertebral canal. Chronic myelitis, also, is generally preceded by symptoms of irrita- tion ; but, as the participation of the meninges in the tedious inflam- mation of the spinal medulla is slighter and less extensive, they are usually limited to vague pains, formication, momentary twitching, or painful contractions of the extremities. At the same time many pa- tients complain of a dull pain in the part of the spine corresponding 266 DISEASES OF THE SPINAL MARROW AND ITS MEMBRANES. to the point of inflammation, which is increased by pressure on the spinous processes, but not by moAements of the spinal column, Avhich is an important point in the diagnosis between myelitis and meningitis spinalis. This pain is sometimes accompanied by the feeling of a cord tied firmly around the Avaist. In other cases there is no spontaneous pain, but the corresponding vertebre are sensitive to pressure. If we pass a sponge, previously dipped in hot water, along the spine, the part at the seat of inflammation is generally more sensitive than else- Avhere. These symptoms, which are usually little thought of, are ac- companied by a heaviness and helplessness in the lower part of the body, which sooner or later become perfect paraplegia. The higher up the seat of the inflammation, the more extensive the paralysis. If the lumbar region be diseased, the lower extremities are paralyzed; if the thoracic region be affected, the sphincters participate in the pa- ralysis .; if the cervical region suffer, the paralysis extends to the upper extremities and corresponding respiratory muscles; with the para- plegia there is generally also anesthesia of the lower part of the body, but this rarely extends to entire loss of sensitiveness to irrita- tion. While the paraplegia and anesthesia, slowly increasing, attain a high grade, the affected muscles are still occasionally attacked by spasmodic tAvitchings, and, if the anesthesia be incomplete, by painful contractions. This symptom is readily explained by the irritation in- duced in the motor nerves of the extremities from the progress of the inflammation, even after their connection with the central filaments is lost. In cases where the connection between the motor nerves and central filaments is completely broken, so that no muscular contrac- tions are induced by the will, it is not at all impossible for an excite- ment to pass from the sensory to the motor filaments, and for reflex movements to occur. On the contrary, Ave often see the reflex excita- bility increased in the parts of the spine below the interruption. This pathological experience exactly corresponds with experiment. It is well known that, in decapitated animals, reflex movements occur more readily than in those whose motor nerves are under the influence of the brain. In Greifswald I saw a young woman, who was paraplegic as a result of vertebral disease, in whom the reflex symptoms in the paralyzed part were so severe that the slightest touch on the skin of the lower extremities caused then muscles on both sides to contract spasmodically. It Avas very interesting to observe that, in this case, when, contrary to all expectation, the paralysis improved, and the pa- tient Avas able to make voluntary movements of her extremities, the inclination to reflex symptoms entirely disappeared. The course and results of chronic myelitis vary. The disease may run on for years; frequently it advances to a certain point, and remains stationary. If GROWTHS IN THE SPINAL CANAL. 267 such patients belong to the educated classes, or to the mechanics proper, they often continue then occupation in spite of then para- plegia. Those cases of paraplegia, Avhere improvement and recovery take place, as I before said, appear to belong to meningitis spinalis, not to myelitis, as it is very improbable that nerve-elements, which have been extensively destroyed, can be regenerated; the favorable course of incised wounds of the nerves does not disprove this assertion. In chronic myelitis, death most frequently results after the patient has been confined to bed a long Aviiile by the increasing paralysis. The consequent bed-sores, or the cystitis caused by stagnation of the urine, generally form the terminal symptoms, if the patient do not sooner die of tuberculosis or intercurrent diseases. Treatment.—The treatment of myelitis promises little. It is to be conducted on the principles laid down for meningitis spinalis. Only, instead of flying blisters, it is well to apply moxe or the hot iron near the supposed seat of inflammation. CHAPTER V. GROWTHS AND PARASITES OF THE SPINAL MEDULLA AND ITS MEMBRANES. Except the cartilaginous and bony plates of the arachnoid, which Ave have already described, growths rarely occur in the spinal canal. Carcinomata, which are usually of the medullary variety, either form primarily in the spinal medulla or dura mater, or extend from the ver- tebre to the meninges and medulla. When they grow considerably, they may at last fill the spinal canal, as the medulla atrophies from pressure, or is transformed into cancer substance. Occasionally, after destruction of the vertebre, they have been seen to spread outAvardly, so as to lie just under the skin. Only a few cases of sarcoma and glioma have been observed in the spinal canal. They almost ahvays started from the inner Avail of the dura mater, and rarely attained any considerable size. Tubercles in the medulla itself only occur Avhen there is advanced tuberculosis of other organs. Just as in the brain, they usually form yellow nodules, the size of a pea or hazel-nut. They are usually in the cervical or lumbar regions. Somewhat more fre- quently we meet tuberculous degeneration of the dura mater, under the form of so-called infiltrated tuberculosis, along .with tuberculous caries of the vertebre. Cysticerci and echinococci have also been very rarely found in the spinal canal. The latter had either devel- oped between the membranes, or an echinococcus sac, near the spinal 268 DISEASES OF THE SPINAL MARROW AND ITS MEMBRANES. canal, had penetrated into the canal, after destroying the vertebre or their processes. Tumors in the spinal canal interrupt the communication between the brain and peripheral nerves; hence they cause paraplegia and anesthesia of the lower part of the body. According as they simply induce atrophy of the spinal medulla by pressure, or cause inflamma- tion of it by the irritation of the parts about them, the paraplegia and anesthesia are preceded by moderate or by very severe symptoms of irritation. Of course, the seat of the growth modifies the extent of the symptoms. The fact that, in tumors, there is usually less pain in the back, but more peripheral neuralgia preceding the paralysis, and that the paralysis often did not begin at the same time on both sides, but gradually extended from one side to the other, is not absolutely decisive in the differential diagnosis between tumors of the spinal me- dulla and chronic myehtis. We can only make an absolute diagnosis in those cases wiiere the cancer extends from the spinal marrow out- ward. The development of carcinoma, tubercles, or parasites in other organs, at least justifies the suspicion of a similar disease in the spinal canal being the cause of a slowly-progressing paraplegia. Treatment is entirely powerless against all tumors of the spinal medulla. CHAPTER VI. HYDRORHACHIS CONGENITA--SPINA BIFIDA. Hydrorhachis congenita is divided into internal and external. The former depends on a collection of serum in the dilated fetal cen- tral canal. It causes atrophy or entire destruction of the spinal me- dulla (amyelia) by pressure, or else splits it more or less completely. Hydrorhachis externa consists in an abnormal collection of water in the subarachnoid space. In both forms the vertebral canal may either remain closed (hydrorhachis incolumis), or there is, at the same time a more or less extensive opening of the canal (hydrorhachis congenita dehiscens). In spina bifida we find a sac filled with serum, and covered by the spinal membranes on the spinal column, which communicates with the spinal canal, as a result of rudimentary formation of one or several vertebral processes. Such tumors are usually located in the sacral or lumbar regions, more rarely in the cervical or dorsal. Their size varies from that of a walnut to a child's head. The skin covering them is sometimes normal, sometimes thinned; occasionally, at the summit, it has entirely disappeared; then the sac is exposed, the place appears excoriated, and is occasionally covered with pus and granulations. HYDRORHACHIS CONGENITA—SPINA BIFIDA. 269 When the spina bifida results from hydrorhachis externa, the wall of the sac consists of the arachnoid and dura mater; the latter is occa- sionally thinned or perforated, and then the Avail consists of the arach- noid alone. If, on the other hand, the spina bifida result from hydro- rhachis interna, the pia mater also assists in the formation of the wall. The contents of the sac are pure serum, of the same constitution as the cerebro-spinal fluid. When the spina bifida has resulted from hy- drorhachis interna, the spinal medulla is either altogether absent, or is undeveloped. On the other hand, if it be due to hydrorhachis ex- terna, the medulla may be perfectly normal; but occasionally, even in such cases, it is defective (Fbrster). The pathogeny and etiology of hydrorhacliis congenita are obscure. The collection of water is probably the primary disease, the incom- plete formation of the spinal canal the secondary. The symptoms of hydrorhachis, complicated with partial spina bifida—of which alone we shall speak, as, in all cases combined with great defect of the spinal medulla and extensive opening of the canal, the children die before birth, or very soon after—consist chiefly of the objective signs due to the above-described tumor. There is usually distinct fluctuation in it. At its base the edges of the bone may be felt. It increases on expiration, still more on crying and straining, and diminishes on inspiration. Occasionally it may be replaced, but attacks of loss of consciousness and general convulsions are readily in- duced by these attempts. In some cases the innervation of the loAver extremities, bladder, and rectum, is normal; in others, especially Avhere the lower part of the medulla is defective, or has disappeared, the lower extremities, bladder, and rectum, are paralyzed. The tumor usu- ally increases rapidly in size and tension soon after birth. If the skin reddens, becomes thin, and finally perforated, death, preceded by con- vulsions and subsequent sopor, generally quickly folloAvs the perfora- tion. But, even Avhere perforation does not take place, most of the children die early of general marasmus, and it is very exceptional for patients with spina bifida to attain or pass the age of puberty. Operative procedures are to be abstained from when complete pa- ralysis and decided emaciation of the loAver extremities indicate that the spinal medulla is incompletely developed. In other cases we may attempt careful compression, and, where this fails, proceed to the opera- tions described for spina bifida in the text-books on surgery. 270 DISEASES OF THE SPINAL MARROW AND ITS MEMBRANES. CHAPTER VII. CONSUMPTION OF THE SPINAL CORD—TABES DORSUALIS—ATAXIE LO- COMOTRICE PROGRESSIVE (Duchenne)—GRAY DEGENERATION OF THE POSTERIOR COLUMNS OF THE SPINAL CORD (Leyden)--LOCO- MOTOR ATAXY. Tabes dorsualis, which was discovered and described by Duchenne as ataxie locomotrice progressive, long after it was generally known in Germany from the classical description of Bomberg, has recently ex- cited much discussion. The views regarding the significance of the symptoms especially vary. According to the plan of my book, I can only criticise the views of others, so far as is necessary to support my oavu. The following description is, in the main, the same as was given in the dissertation of my former assistant, Dr. Ernst Spaeth, which was written under my supervision, and which has not, by any means, received the attention it deserved. (The dissertation of Dr. Spaeth Avas published under the title of " Beitrage Zur Lehre von der Tabes dorsualis," at Tubingen, 1864, by Aug. Ludwig.) Etiology.—In some few cases of decided tabes dorsualis, on autopsy we find no palpable changes in the spinal medulla. This " negative appearance " does not by any means prove that the spinal medulla is normal, but only that its functions may be impaired by molecular changes that escape observation, just as they are by the coarser changes found in other cases. The latter consist in a peculiar degeneration and atrophy affecting particularly the posterior columns and the posterior roots, but occasionally the gray substance also and other columns. In some cases there is no doubt that the degeneration in question is the result of inflammation of the spinal medulla, but in other cases no inflammatory origin can be made out. The predisposition to tabes dorsualis is occasionally hereditary, as is shoAvn by a number of cases, where several brothers and sisters were attacked by the disease. On the other hand, I only know of two cases Avhere it was inherited, that is, where the parents of the patient had tabes dorsualis. Children are not inclined to tabes, persons of mature age are most so, while in the aged the tendency almost disap- pears. Men are far more disposed to it than women. The exciting causes are almost always said to be—1. Venereal excess. The great physiologist Johannes Mtiller, usually very careful and discreet in his assertions, says directly that tabes dorsualis comes only from venereal excess. Besides their other sufferings and mis- fortunes, these poor patients are made to bear the accusation which in many cases at least is unjust, that they have themselves to blame for LOCOMOTOR ATAXY. 271 their disease. There is no doubt that many of the patients attacked have been addicted to excess in venery, but there is just as httle doubt that many patients with tabes dorsualis have led an exemplary life, while others who have been unbounded in their excesses escape the disease. From the great frequency of lewd habits, and from the difficulty of deciding the amount in any given case, I consider the dependence of tabes on venereal excess as not yet proved. 2. On the other hand, there appears to me no doubt of the influence of catching cold and bodily fatigue, especially when they act together, in inducing tabes dorsualis. The disease occurs with remarkable frequency among those Avho, wearied and heated by severe marches or other bodily exertions, have stretched themselves on the damp earth to rest. 3. Many patients ascribe their disease to suppressed perspiration of the feet. We can- not generally lay much Aveight on these accounts, for the laity give suppression of habitual perspiration as a Aery common cause of dis- ease. Doubtless in most cases where the occurrence of a disease is accompanied by the absence of habitual perspiration of the feet, it is because the latter has ceased Avith the appearance of the disease. But I think it is going too far to deny the possibility of a genetic connec- tion between the arrest of perspiration of the feet and tabes dorsualis. At all events, many patients with tabes have previously suffered much from perspiring feet. 4. Lastly, the disease appears occasionally to be of syphilitic origin, a supposition chiefly supported by the fact that some tabes patients who had previously suffered from syphilis Avere benefited by an antisyphilitic treatment. Anatomical Appearances.—The usual appearance of the spinal medulla and its membranes, in decided cases of tabes dorsualis, is as follows: The dura mater is either unchanged or its posterior half is slightly thickened, the arachnoid is moderately opaque, if the medulla be atrophied the fluid in the subarachnoid space is increased; on the posterior surface the pia mater is constantly thickened, clouded, and more or less adherent to the posterior columns. In the early stages, Avhereno decrease of volume of the spinal medulla is as yet observable, there is a peculiar degeneration of the posterior columns; this always begins in the immediate vicinity of the posterior fissure, close under the pia mater, and thence spreads toward the sides and the gray commissure; the diseased part always retains the shape of a wedge, with the base directed toward the pia mater. The degen- eration consists in a transformation of the white substance of the pos- terior columns into a gray or grayish-red, half-translucent, soft mass, On microscopical examination of the latter we only find a few nerve- filaments, partly in various stages of atrophy; most of them have com- pletely disappeared, and between the atrophied cells there is a richly- 64 272 DISEASES OF THE SPINAL MARROW AND ITS MEMBRANES. nucleated connective-tissue substance, corresponding to the ordinary neuroglia and resulting from its proliferation, in which we find only a few granular cells, molecular fatty masses, and numerous corpora amylacea. The vessels passing out from the pia mater have a greatly- thickened adventitia, and thus cause the firm adherence of the pia mater to the surface of the medulla. Corresponding to the extent of the degeneration in the posterior columns, the posterior roots of the spinal nerves are atrophied. They resemble thin, vascular, translucent connective-tissue cords, far more than they do nerves with medulla. This is especially true of the posterior roots of the Cauda equina. The anterior roots of all the nerves, cauda equina included, are normal, cor- responding to the general nutritive condition of the spinal medulla. In the later stages the degenerated gray parts of the medulla shrink greatly. They become a hard tissue, and are less transparent. If the degeneration be limited to the posterior columns, the medulla acquires a cylindrical form. The points of exit of the posterior roots are approximated. If, on the other hand, the degeneration extend to the posterior parts of the lateral columns, the medulla shrinks more in an antero-posterior direction, and we may readily receive the impres- sion that it has become broader. The neuroglia, which in the early stages of the degeneration corresponds exactly with the normal neu- roglia, during the shrinking acquires the appearance of a fine filament- ary substance. A secondary atrophy and induration succeed the growth of the neuroglia. Symptoms and Course.—Although Duchenne is to be reproached for ignorance of Bomberg's works, or else for ignoring them, when he published his first writings on ataxle locomotrice progressive, we cannot deny that he has done much for the correct interpretation of the symp- toms of tabes dorsualis. He originated the doctrine, at present almost generally adopted, that in tabes there is not paralysis, but disturbed coordination of muscular movements. To use our muscles properly, it is not enough that we can contract each muscle, Ave must also be able to cause a harmonious action of all the muscles participating in any motion. Acts apparently the most simple fail or are clumsily performed, if any of the muscles participating in them be contracted too much or too httle, too quickly or too slowly; or if the antagonists be not re- laxed just enough or exactly at the right moment. This poAver of causing the muscles to act properly together, or, as it is usually called, the power of coordination, is much impaired in patients AAith tabes • and the symptoms resulting from this anomaly are peculiarly charac- teristic of the disease. But, along Avith this, there is almost always a decided diminution of the cutaneous and muscular sensibility which Romberg has excellently described: "The floor is no longer distinctly LOCOMOTOR ATAXY. 273 felt; the foot seems to rest on wool, soft sand, or on a bladder filled with water. The horseman no longer feels the resistance of the stir- rup, and has the strap shortened .... If the patient do not see his movements, they will be still more uncertain; if, while erect, he closes his eyes, he immediately begins to SAvay about and totter. If his eyes be closed while in the horizontal position, he cannot tell the location of his limbs; he cannot say whether the right foot be crossed over the left, or the reverse." If, as some celebrated authorities assert, the posterior spinal col- umns have the function of coordinating the movements, the anatomical changes found on autopsy of tabes patients fully explain the symptoms observed during life. We have said that the degeneration and atrophy of the spinal cord constantly start from the posterior columns, and that the posterior sensory roots almost always participate in the de- generation. Ley den, Avho does not believe in a peculiar power gov- erning the coordination of movement and its location in the posterior spinal columns, has advanced a theory for the explanation of the disturb- ances of coordination in tabes dorsualis, which, at first sight, is very enti- cing. He explains the loss of power of coordination as due solely to the diminished cutaneous and muscular sensibility. We must, indeed, admit that Longet is correct in saying that a person, who has lost the perception of his actions, who cannot judge of the position of his limbs, who does not even knoAV Avhether they are present, and, lastly, who does not feel the floor under his feet,' cannot walk erect, preserve his equilibrium, and move his limbs Avith certainty and accordance. Moreover, the peculiarities of the anomalies of movement observed in tabes patients, the energetic lifting of the foot and its passive fall when walking, the spasmodic, uncertain movements, their shooting beyond the mark, all give the impression that the patient is so aAvk- Avard because he does not know what he has done till he has done too much. Lastly, the fact that the helplessness of the patients is greatly increased Avhen they close the eyes, and cannot control their move- ments by the sight, is favorable to the view that the anomalies of movement ia tabes dorsualis result from diminution of the cutaneous and muscular sensibility. Nevertheless, Leyden's theory is false. Its correctness is opposed by the folloAvlng facts : first, that in many pa- tients the disturbances of sensibility are in marked disproportion to the impairment of coordination of movement; second, that in persons Avhose cutaneous and muscular sensibility is far more diminished than is the case in any tabes patients, there is often no indication of dis- turbance of coordination. In Spaeth's Avork there is a full histcry of a peasant, from Wurmlingen, Avho is known to all my students, as I show him in my clinic almost every half year. This interesting pa- 274 DISEASES OF THE SPINAL MARROW AND ITS MEMBRANES. tient has a very marked and extensive anesthesia of the skin and muscles. He is insensible to the severest injuries. He does not know if he bathes in warm or cold water. On loading his extremities Avith a Aveight of twenty-five pounds, he perceives no difference of pressure. On being requested to estimate Aveights, by lifting them, he cannot distinguish between weights of one pound and a hundred pounds. When his eyes are closed, he cannot tell Avhether his limbs are flexed or straightened to the greatest possible extent by strong electric cur- rents. When standing erect or sitting up, if he closes the eyes he immediately falls. He perceives the resistance of his bed so little that, when the light is extinguished at night, he feels as if he were swimming in the air. But this patient has no marked disturbance of coOrdinative poAver; he does not in the least remind us of a tabes pa- tient ; as long as it is light he walks very Avell, although carefully; he travels on foot, without a stick, the mile between Wurmlingen and Tu- bingen. A single such case is enough to prove that the disturbance of coordination qf the tabes patient does not depend, certainly not solely, on the diminished sensibility, but that it exists along with the latter. In many cases the above symptoms are accompanied by disturb- ances of the excretion of urine. Most patients are obliged to attend to the call to urinate as quickly as possible, as they can only stand it a feAV moments, and hence, Avhen their means alloAV it, they buy uri- nals, which they wear in their trousers during the day. I think this symptom arises because the patient does not perceive the fulness of the bladder, and the desire to urinate does not occur till a few drops are pressed out of the bladder into the urethra. Far more rarely than this incomplete enuresis we find retention of urine, and it becomes necessary to draw it off with the catheter. In such cases there is probably paralysis of the bladder, from its having been distended too much or too long. It is asserted that, at the commencement of the disease, sexual de- sire is usually increased but the energy and duration of the erections lessened, as well as that, in the later stages, the virile power is en- tirely lost. The latter assertion alone is certain. > We must also mention the paresis of the oculo-motor and ab- ducens, which occasionally occurs in tabes, which is shown by diplopia, more rarely by strabismus and ptosis of the upper lid; and, lastly, the amaurosis and psychical disturbances which are sometimes met Avith. There is no doubt that these symptoms are due to the disease advan- cing to the cerebral filaments, but hitherto autopsy has failed to show what course this advance takes. Atrophy of the optic nerve was only found in some of the feAV cases where there was disturbance of vision; but even here the atrophy only extended to the corpora quadrigemina, and could not be folloAved further. LOCOMOTOR ATAXY. 275 After having described and analyzed the most important symptoms, t shall attempt to give a general description of tabes dorsuahs, and pic- ture the most frequent course of the disease as briefly as possible. In many patients, the characteristic disturbances of coordination, and the decrease of cutaneous and muscular sensibility are preceded for a long time, even for years, by attacks of severe tearing pain in the lower half of the trunk, and in the lower extremities; these are generally considered as rheumatic. In other patients, on the contrary, the first complaints are that the lower extremities become fatigued very easily and very soon. Persons accustomed to walking notice that they tire sooner and more easily than formerly. These symptoms, which are not usually very suspicious, either to the patient or physi- cian, may precede the decided symptoms of tabes for a long time. But this difference in the initial symptoms is not so marked or decided as it seems to be on superficial examination. The attacks of pain are unmistakably neuralgic, and depend on morbid excitement of the pos- terior roots, while the tendency to fatigue depends on their hyperes- thesia—that is, on their morbidly-increased excitability. Under physi- ological circumstances, the feeling of fatigue depends on the amount of Avork done by the muscles. The state of the muscles resulting from overwork is perceived through the sensory muscular nerves. If the excitability of the posterior roots be increased, slight exertion of the muscles will produce the same effect, which would otherwise only be induced by far greater exertion. Hence the tendency to fatigue in tabes is perfectly analogous to the increased sensitiveness, at the com- mencement of certain brain-diseases, to light, sound, and other irrita- tions, which are not generally unpleasant. The tearing-pain and ten- dency to fatigue in the lower extremities are not recognized to be serious and threatening until they are accompanied by other disturb- ances of sensibility, such as formication, a feeling of furriness, numb- ness, and the sensation of a ligature around the abdomen. Gradually the gait becomes uncertain and awkward; at first this is so only in the dark, so that the patients prefer remaining at home in the evening; afterward it is the same in day-time. The feet are lifted too high, and thrown forward and outward, and then brought heavily doAAm on the floor. If the patient closes his eyes Avhile standing erect, he begins to totter, and, unless supported, falls to the ground. And, even at this time, he must usually be on his guard when the desire to urinate seizes him, so that he may reach a convenient place in season. After a time, walking becomes impossible, even with the aid of a stick or crutches, although, Avhen the body is fixed, the patient can generally make un- complicated movements of the extremities with nearly normal force. The same uncertainty and awkwardness come on in the upper ex- 276 DISEASES OF THE SPINAL MARROW AND ITS MEMBRANES. tremities much later than in the loAver. Then, Avhen eating or drink- ing, the patients shake out the contents of the spoon or glass, they can no longer dress without aid, especially the buttons trouble them; finally, they cannot write, knit, or do any other work. The enuresis now often attains such a grade that the patient voids his urine in bed. If, in consequence of this, a constant moisture of the parts be added to the patient's indistinct perception of the irregularities of the bed and his helplessness in changing his position, we may readily have bed-sores. The course of the disease is always tedious. We see most patients drag on for years in a miserable state, the objects of pity, Avhich is not unfrequently pharisaical. Occasionally the disease remains stationary; in other cases it appears to improve temporarily. Perfect cures are certainly very rare. Nutrition is frequently not impaired till late; the lower extremities, the nates, and muscles of the back emaciate first, so that the spinous processes project. It is not till toAvard the end of the disease that the emaciation extends to the rest of .the body. Death generally results at last from the increase of the bed-sores, from severe cystitis, from pulmonary consumption, or from intercurrent diseases. Treatment.—Bomberg's assertion, that there is no hope of cure for a tabes patient, that they are all doomed, contrasts strongly with the views of Remak, as published by Cyon, according to which the former is said to claim that his treatment Avas successful in the ma- jority of cases, and that, therefore, he cannot be reproached for not having autopsies on his cases. The truth probably lies between the two. Of late, few authorities regard the treatment of tabes so hope- less as Romberg. But very few would agree with Remak, Benedikt, and others, in saying that tabes is a disease where very favorable re- sults can be attained by treatment. We may hope for the best results when there is a suspicion that the disease is of syphilitic origin. In such cases an antisyphilitic treat- ment should be instituted, on the plan to be described hereafter. The more probable it is that the disease has resulted from taking cold, the more acute its occurrence, the more severe the' pains in the lower extremities which preceded the symptoms of disturbance of coor- dination and diminished sensibility, the more probable is it that the disease is of inflammatory or congestive origin, and the stronger the indications to begin the treatment with the local abstraction of blood by leeches, and derivation to the skin by blisters along the spine. Subsequently Ave may order for such patients the waters of Wildbad, Gastein, Ragaz, Pfaffers, TOplitz, etc. There is no doubt that tabes patients have been decidedly benefited by the treatment at these Dlaces. On the other hand, I must warn against the careless employ- LOCOMOTOR ATAXY. 277 ment of the cold-water treatment, which, especially in the form of cold douches to the back, has not come up to the expectations entertained of it at the time it Avas fashionable, and the water-cure establishments are now rarely patronized by tabes patients, who, for a time, all rushed to them for treatment. In very recent cases only, sweating in moist cloths and a subsequent short bath appear to be beneficial. If it be not a favorable time of year to send the patient to Wild- bad, etc., or if these mineral waters do not seem indicated, or if they haAe done no good, we should try the administration of nitrate of silver as recommended by Wunderlich. Nitrate of silver has long held the reputation of being one of the most effective nervines; and it is not at all impossible or improbable that it exercises a modifying influence on the nutrition of the nervous system; it is not these reasons, however, but the fact that reliable observers have found some benefit from the employment of the remedy in tabes dorsualis, that induce me to use it in most cases of the disease. My experience of the efficacy of the remedy, which I have given in a large number of cases, in doses gradually increasing to half a grain daily as advised by Wunderlich, has not been particularly favorable. It is true that most of my patients at the clinic have praised their state a time after using the remedy, but I suspect that many did so to induce me to keep them longer at the hospital. In other cases, the patients actually seemed to move forward more nimbly; but here also it was possible that either greater confidence or increased attention of the patient, with the view of shoAving me improvement, had a favorable effect on the attempts to walk. I shall continue for a time to prescribe nitrate of silver to my tabes patients. My experience of the constant current of electricity is about the same as it is in regard to nitrate of silver. I have no reason to doubt that Bemak, Benedlkt, and others, have had some success vvith the constant current which I consider to be a very active remedy, but thus far I cannot claim any success from its use in tabes, although I have had an excellent apparatus in my clinic these four years, and have treated all my tabes cases Avith it in the manner advised by Remak. This want of success will not prevent my continuing the use of galvan- ism in tabes for a time; and, instead of letting the current act on the spinal column as hitherto, I shall try the current through the spinal nerves, as advised by Benedikt, not because I attach much importance to the theories and the indications he gives for the treatment of dif- ferent diseases, with the current through the roots of the spinal nerves (Ruckenmarks-WurzelstrOmen), through the spinal nerves (Rucken- marks-NervenstrOmen), etc., but simply because I have no reason to doubt what he says on the subject. SECTION III. DISEASES OF THE PEBIPHEBAL NERVES. CHAPTER I. INFLAMMATION OF THE NERA'ES—NEURITIS. Etiology.—Inflammatory disturbances of nutrition rarely occur in the peripheral nerves. They sometimes affect the nerve-filaments, sometimes the neurilemma. The first form ranks among parenchyma- tous inflammations, and ends in the destruction of the nerve-medulla to a fine granular, fatty detritus. In the second form there is an inter- stitial exudation, and a proliferation of connective tissue, by which the neurilemma is decidedly thickened. There is rarely any formation of pus. We shall hereafter speak of the diffuse hyperemia of the neu- rilemma of a wounded nerve, without any perceptible exudation, observed in some cases of tetanus. Among the exciting causes of neuritis, the most important are injuries of the nerves, particularly punctured Avounds, contusions, or lacerations. In other cases neuritis is due to the propagation of in- flammation from neighboring organs. Lastly, some few cases of spon- taneous or so-called rheumatic inflammation are said to have been observed. Anatomical Appearances.—Inflammation of the neurilemma is characterized by a more or less intense redness, which sometimes de- pends on overfulness of the blood-vessels, sometimes on the presence of small extravasations.. The neurilemma also appears relaxed, savoI- len, and infiltrated. If the neuritis has taken on an acute course, and led to suppuration, there is usually more or less pus in the loose con- nective tissue around the nerve. When the disease is chronic, the neurilemma usually appears much thickened, hard, and firmly adherent to the surrounding parts. Inflammation of the nerve-substance is sIioavii by its redness, SAvell- ng, and relaxation; in severe cases it is transformed to a red pulp. INFLAMMATION OF THE NERVES—NEURITIS. 279 The neurilemma is always affected at the same time, and consequently we find the different bundles of nerve-filaments separated by the swell- ing of their envelopes and by interstitial exudation. Occasionally, after reabsorption of the disintegrated medulla of an inflamed nerve, only a simple cord of connective tissue is left. Symptoms and Course.—The symptoms of neuritis cannot be clearly distinguished from those of neuralgia, or rather neuritis is one of the various causes of neuralgia. The most important symptom of neuritis is pain in the course of the inflamed nerve, extending to its peripheral terminations. The pain is increased by pressure on the nerve, and its exacerbations and remissions are usually less distinct, and the paroxysms and intervals particularly are usually less marked than in other forms of neuralgia. While this pain lasts, the sense of touch is usually lost in the parts supplied by the inflamed nerve; and this symptom may be easily explained, although it seems paradoxical on superficial examination. The morbid excitement of the trunk of the nerve, caused by the inflammation in the medulla or neurilemma, is conducted to the brain, and excites the sensation of severe pain; but the inflamed part of the nerve has become a bad conductor; hence irritation of its peripheral termination and the papilla? of touch are conducted to the brain either incompletely or not at all, and cause either no sensation or an indistinct one. At first, at the correspond- ing portion of the periphery, the patient has a feeling of numbness; subsequently, if resolution of the inflammation do not take place, there is complete anesthesia to external injuries, while the pain continues. If the inflamed nerve contain motor fibres, the pain is accompanied by twitching and contraction, while the patient's power of voluntarily contracting the muscles is much affected or entirely lost. This also depends on the morbid excitability of the motor nerves being increased by the inflammation while their conducting power is lost. If the in- flamed nerve lie near the surface, it may occasionally be felt as a hard cord; and we often find the skin covering it slightly reddened and edematous. In most cases there is no fever, unless there be some other inflammation besides the neuritis. The course of neuritis may be either acute or chronic. The more acute it is, the sooner anesthesia and paratysis follow the neuralgia and contractions, and the more probable it is that these symptoms Avere caused by an acute neuritis that has destroyed the nerve. Even after resolution of the inflammation, the nerve usually remains to some extent incapable of function for a long time. When the neuritis runs a chronic course, if the nerve be destroyed, anesthesia and paralysis occur in the same AATay; but, if the nerve be preserved and is only sub- jected to pressure from the SAvollen and thickened neurilemma, the 2S0 DISEASES OF THE PERIPHERAL NERVES. patients suffer for years from neuralgic pain or spasmodic attacks in the parts supplied by the inflamed nerve. Treatment.—In the first place the causal indications must be ful- filled ; with this view foreign bodies driven into the nerve must be re- moved, and inflammations in its vicinity must be carefully treated. Leeches or Avet cups may also be applied along the course of the nerve; cold applications may be made, or, if the disease continue long, mercurial ointment may be rubbed in if the nerve lie near the surface. Chronic neuritis may be treated by derivatives, such as blisters, and, in obstinate cases, moxe, and superficial linear cauterizations of the skin with hot iron. If the disease has run its course, and the nerve has not been destroyed, but its functional activity is affected, we may use electricity to restore its normal excitability, if possible, by methodical excitement of the nerve. CHAPTER II. NEUROMA. Etiology.—Strictly speaking, we can only designate as neuromata those tumors originating from nerves winch are chiefly, or at least to a great extent, made up of nervous elements. The tumors, not unfre- quently occurring on nerves, which have developed without hyperpla- sia of the nerve-elements, and in which consequently the number of nerve-elements has remained the same or even actually diminished, are not neuromata, but, according to their structure, come under the head of carcinoma, fibroma, or glioma, etc. (Virchoxo). Neuromata which consist chiefly of nerve-filaments, or where these exceed the intercellular substance in amount, are termed pure neuromata, in con- tradistinction to those where the intercellular substance is in excess; this division, hoAvever, has more pathological-anatomical than clinical interest. The etiology of neuromata is obscure. Occasionally they may be referred to a congenital or hereditary predisposition. Such cases, as well as the frequent occurrence of numerous neuromata on different nerves, and their repeated recurrence after removal, speak for the con- stitutional orgin of some neuromata. Others unmistakably result from injury of the affected nerve, by a puncture, contusion, etc. In most cases no cause can be discovered. Anatomical Appearances.—Neuromata generally form hard, elas- tic tumors, from the size of a hemp-seed to that of a fist, or larger; they are usually round or oval; in the latter case their long axis lies NEUROMA. 2S1 m the course of the nerve. Virchoio divides them into fibro-, glio. and myxo-neuromata, according as the interstitial tissue between the nerve-filaments resembles fibrous tissue, neuroglia, or mucous tissue. They sometimes contain small cavities filled with fluid. Neuromata are occasionally seated on the nerve; again they originate from its interior, and contain more or less nerve-filaments in proportion to the distance of their origin from the centre of the nerve. The most fre- quent seat of neuromata is the spinal nerves; but there are examples of their occurrence on the sympathetic and cerebral nerves, particularly on the auditory. Usually there is only one neuroma, and its size is not at all in proportion to that of the nerve from Avhich it originates. In other cases there are several neuromata on the same nerve, in still others there are great numbers, originating from the most vTaried nerves. Under the head of neuromata appear also to belong the pain- ful tumors, about the size of a pea or bean, readily moved about under the skin, which are also called tubercula dolorosa, painful tubercle, or neuromantia; although their connection Avith a cutaneous nerve or the presence of nerve-elements in them cannot always be proved. Symptoms and Course.—Peripheral neuromata, which alone can be recognized, show themselves as a more or less elastic tumor, seated in the course of one of the cutaneous nerves, which is only movable laterally, and is covered by the unaltered skin. Large multiple neu- romata occasionally cause neither pain nor other inconvenience, so that their diagnosis can only be made by the apparent connection between the tumors and a cutaneous nerve. The case is different with the customary single small neuroma. It is often accompanied by ex- cruciating pain extending along the course of the nerve and to its peripheral termination. This is not usually continuous, but has par- oxysms with intervals of ease. Slight pressure on the tumor, often even the contact and rubbing of the clothes, increases the pain in the tumor to an unbearable extent. Severe paroxysms of pain are also induced by movement, catching cold, etc. In neuroma, as well as in neuritis, the conducting power of the nerve may be impahed, so that, besides the pain, there may be a feeling of numbness or even of more or less complete anesthesia of the skin supplied by the nerve affected. Rarely, when the motor filaments are affected, there are twitchings and contractions and subsequently paralysis. The extension of the pain from the diseased nerve to other trunks, as well as the increased disturbance of innervation that occasionally complicates the local symptoms, is common to neuroma, neuritis, and to neuralgias of the most varied origin; we shall therefore defer their discussion to the next chapter. Neuromata generally grow slowly, and, after attaining a certain size, often remain stationary. They are among the most 282 DISEASES OF THE PERIPHERAL NERVES. painful of diseases, and may wear the patient out by the loss of sleep and restlessness induced by the pain. Treatment.—We can never cause resolution of neuroma. The only true and trustworthy remedy is removal by the knife. CHAPTER III. NEURALGIA. As we have thus far made use of the anatomical changes lying at the root of the disease as grounds of distinction, it is inconsistent to treat of neuralgia as a disease, and to class it with neuritis and neu- roma. Neuralgia is a combination of symptoms, Avhich does not de- pend on constant anatomical changes. Since no anatomical changes can be discovered in many cases of neuralgia, and since, in many cases, where changes have occurred, they alone are not enough to explain the neuralgia, Ave seem driven to the above-mentioned inconsistency, and Ave shall be unable to escape it in other morbid processes of the nervous system, Avhich are not due to certain anatomical causes. Etiology.—The sensation of pain depends on the conduction to the brain of the excitement of a sensory nerve by an abnormal irrita- tion. Those sensations of pain, also, that arc called neuralgic, depend on a propagation of this excitement to the brain. If neuralgic pains be distinguished from others, it is because they are due to the excite- ment of the sensory nerves by different irritations, or by the action of irritants at different places, from those causing ordinary pain. If a blow, heat, cold, or other cause acting on the termination of the nerves, induce pain, or if this be due to inflammation or other structural change of the skin, mucous membrane, or of the parenchyma of different or- gans, we do not call it neuralgia. But if we can discover no irritation of the peripheral termination of a nerve as the cause of the pain, or if it be probable that the irritation has affected the trunk of the nerve, the pain felt in the distribution of the nerve is called neuralgia. We may mention neuralgia of the supra-orbital branch of the trigeminus, winch is not unfrequently induced by malarial infection, as the type of the form where the pain occurs in the distribution of a nerve, without the perceptible action of an irritant on the nerve itself, or on its termi- nations. As a type of the second form, where the pain in the parts supplied by a nerve is unmistakably due to an irritation of the nerve- trunk, we may mention the very temporary neuralgia induced by bruising the ulnar nerve near the elbow, at the part known as " the crazy-bone." It is most probable that, in those cases, also, where the injurious influence acting on the nerve escapes observation (as in neu- NEURALGIA. 055 ralgia caused by malarial poisoning), the action affects the trunk rathei, than the peripheral termination. This vieAV is favored first by the exact limitation of the neuralgic pain to the peripheral expansions of a single nerve, and the freedom of the parts immediately adjacent, if these are supplied by other sensory nerves. This limitation would be quite inexplicable if the irritation acted on the periphery. How should we explain the constant freedom of the radial side of a finger, or the supra-orbital region of one side, from the injury that so severely af- fected the ulnar side of the same finger or the supra-orbital region of the other side ? The view that neuralgia starts from the nerve-trunk is also supported by the fact that no idea of the variety of the irrita- tion accompanies the pain. It is well known that the cutaneous pa- pille connected Avith the terminations of the nerves are the chief source of the sensation of pressure and temperature. If the neuralgic pain were induced by the action of an imperceptible cause on the skin, the patients would have some impression of the quality of this irrita- tion ; they would complain of burning, piercing, or some other kind of pain. But, on the contrary, if a very cold or very hot body be applied to an exposed nerve-trunk, if we puncture or squeeze it, there is al- ways the same sort of pain, just as in neuralgia; and, from the pain, the patient cannot tell Avhat cause induced it. Finally, the want of benefit, in most cases, from division of nerves, indicates that the seat of the disease is to be sought for in the trunk or branches, not in the peripheral expansions of nerves. We do not know Avhat physical or chemical changes of the nerves cause their morbid excitement in neu- ralgia. We may even suspect that they do not consist in any very evident'deviations from the normal, for these remove the excitabihty, but that injuries only act as causes of neuralgia, when they exercise a comparatively slight irritation on the nerves. If Ave find a nerve, which was affected with neuralgia, much changed at some point, Ave may be sure that this was not the starting-point of the pain, but that it originated from some point higher up, where no changes of structure can be made out with the naked eye or with the microscope. The predisposition to neuralgia varies with the person. A morbid increase of excitability of the entire nervous system, so-called nervous debility, of which we shall speak hereafter, and which is seen more frequently in women than in men, in bloodless and debilitated persons than in the full-blooded and strong, appears to lead to the occurrence of neuralgia in some persons more readily than in others. The exciting causes—that is, the irritations winch, by then action on the nerve-trunk, induce the neuralgia—are partly knoAvn, partly un- knoAvn. We are not justified in distinguishing cases from unknown causes as " genuine " or " pure " neuralgia. The pain caused in the 284 DISEASES OF THE PERIPHERAL NERVES. finger by striking the ulnar nerve near the inner condyle of the hu- merus, or in the toes by a blow on the sciatic nerve where it escapes from the sciatic notch, is also a genuine, pure neuralgia. Practically, it would be better to designate as pure neuralgia those cases that con- tinue after the cause that induced them has ceased to act. Among the injuries that may be regarded as direct causes of neuralgia, the most frequent are: 1. Wounds of the nerves from sharp instruments, such as lancets, needles, etc.; a complete solution of continuity is far less dangerous than these punctured wounds. 2. Irritation from foreign bodies that have entered and become incapsulated near the nerve; ob- stinate neuralgia has very often been observed as a result of the irrita- tion caused by pieces of musket-balls. 3. Compression of the nerves by contracted cicatrices. 4. Pressure on the nerves by aneurisms, ex- ostoses from bones and teeth, and tumors, particularly carcinoma. 5. Neuroma, described in the last chapter. 6. Overfilling of the veins in the vicinity of the nerves where they pass through bony canals. From the predisposition of the left side of the body to intercostal neuralgia, Henle concludes that the latter cause has a material influence on the occurrence of neuralgia. The left side differs from the right in the arrangement of the venous circulation, so that the blood must make a circuit (from the hemiazyos vein into the azyos) to pass from the veins of the spinal cord into the vena cava; if there be any obstacle to the escape of blood from the heart, it must necessarily have a worse effect on the left side than on the right. The theory that neuralgia often depends on dilatation of the venous plexuses surrounding a nerve where it passes through an opening in the bone, is also supported by the fact that the first branch of the trigeminus (whose relation to the venous plexuses in its vicinity resembles that of the intercostal nerves) is far more frequently the seat of neuralgia than the second or third branch, where this is not the case. In the so-called rheumatic neuralgias, caused by catching cold, we can find no material changes in the neu- rilemma to explain the irritation of the nerve; nevertheless, although hypothetical, it is very probable that this rheumatic neuralgia is due to a hyperemia and edematous swelling of the neurilemma, which disappears after death. Lastly, we may mention, as causes of neu- ralgia, poisoning by metallic substances, such as mercury, lead, copper, etc., as Avell as by malarial infection. It is perfectly inexplicable' in these cases, why the irritation from a constitutional disease should only affect a very circumscribed nerve-tract. Symptoms and Course.—In neuralgia we may distinguish two forms of pain: one continuous, increased by pressure, confined to ch- cumscribed points in the course of the nerve (points douloureux, Val- lelx's), not very severe but annoying pain; the second occurs in parox- NEURALGIA. 2S5 ysms, spreading from a point along the course of the nerve; the pain is terrible and almost unbearable. The points douloureux occur par- ticularly where the nerve escapes from a bony canal, or from fascia that it has perforated, and approaches the surface. These spots seem larger to the patient than they prove to be when we mark them out by pressing the finger around. Budge made some very interesting observations on the excitability of the motor nerves of frogs at differ- ent places; he found some spots very excitable while the parts im- mediately next to them were very slightly so; perhaps Vallelx's points douloureux on the sensory nerves correspond to those that Budge found peculiarly excitable in the motor nerves. While Valleix almost ahvays found the points douloureux in neuralgia, other observers have just as constantly failed to find them. The paroxysmal pains some- times pass doAvnward, sometimes pass upAvard along, the course of the nerve, so that there has been a division made into neuralgia descendens and ascendens, the latter being far the more rare. Patients usually say that the pain is not superficial but deep. It is rare for the parox- ysms of pain to be limited to one small twig of a nerve; usually several tAvigs of one branch, but only rarely all the tAAigs of one nerve participate in the affection. It is very remarkable that not unfre- quently the neuralgia extends from one nerve to another that has a different origin. From the laws of conduction Ave should suppose that such a transfer could only occur in the central organs, through the ganglia; but the observation that neuralgia not unfrequently extends from a cerebral nerve, as the trigeminus, to a spinal nerve, as the occipital, renders the transfer in that way very improbable; and Ave must content ourselves with having mentioned the curious fact. Anomalies in the distribution of blood, in the secretion and in the nutrition of the parts supplied by the affected nerve, are not unfre- quently observed without our understanding hoAV the morbid excite- ment of the sensory can cause abnormal excitement of the vasomotor nerves. At the commencement of neuralgic attacks Ave occasionally see the skin become pale, more frequently at the height of the attack that it reddens, that the secretion from the nasal mucous membrane, conjunctiva, and from the lachrymal and salivary glands, is increased. In the same category come the exanthemata that develop in the course of the affected nerve in some neuralgias, particularly in intercostal neuralgia (herpes zoster), and lastly, the atrophy or excessive develop- ment of fat in parts supphed by the affected nerve, when the disease has lasted a long Avhile. The morbid excitement of the sensory nerve is rarely transferred through a gland to a motor nerve. We must beware of carelessly considering the twitchings of patients, during then attacks of pain, as reflex symptoms. 286 DISEASES OF THE PERIPHERAL NERVES. Except in the cases resulting from malaria, the course of the dis- ease is chronic. It is rarely regular, the individual attacks are marked by paroxysms of pain interrupted by free intervals, and in the general course of the disease we are apt to see remissions and exacerbations. At times the attacks of pain are more frequently repeated and are more severe, at others, they return less frequently and are less severe. It is only in the neuralgia caused by malaria, in the so-called febris intermittens larvata, that the paroxysms of pain sIioav a regular type. In other cases the type is irregular, and the attacks not only recur spontaneously, that is without assignable reason, but they are excited by various recognizable causes. Among these are irritation of the skin which the affected nerve supplies, by pressure, friction, cold, heat, etc. Slightly touching the skin often appears to induce attacks of pain more readily, than heavy pressure does. Movements of the parts where the pain is located, i. e., chewing in neuralgia of the trigeminus, walking in neuralgia of the sciatic, coughing and sneezing in that of the intercostals, excite attacks of pain. Mental excitement occasion- ally has the same effect. I treated one old gentleman, with neuralgia of the trigeminus, who had such a severe attack of pain every time I entered his room, that he could not salute me for some time. Each attack of pain usually lasts only a few seconds. But these short at- tacks are often repeated several times in the course of one or a feAV minutes, and then cease for a while, so that in fact we may say that in neuralgia long attacks occur which are composed of a number of short paroxysms. As we are almost compelled to believe that the irritation acting on a nerve, which causes the neuralgia, acts continu- ously, the intervals between the pains appear enigmatical: for their explanation Ave must refer to the physiological fact that the severe irritation of a nerve exhausts its excitability for a time; then in neu- ralgia, states of great excitement would alternate with states of dimin- ished excitability. This hypothesis is to some extent supported by the observation that, after severe attacks of pain, the peripheral ter- minations of the nerve are for a time less sensitive to irritation, as if then excitability were diminished, as well as by the observation that, after inducing a severe neuralgic attack by continued pressure on a painful point, a repetition of the pressure does not induce a second attack. The gentleman above mentioned also had attacks of pain as soon as he began to eat. In order that he might be able to eat at meals, he began them by biting vigorously on some hard bread; this induced a severe attack, but after it passed over he remained free from pain during the remainder of the meal. Neuralgia may continue for many years. Except in the cases caused by malaria or the so-called rheumatic neuralgia, complete cure NEURALGIA. 287 is by no means frequent. Even the termination in permanent anes- thesia is comparatively rare, although we should a priori regard it as the most frequent, since it Avould seem very probable that continued irritation must finally destroy the nerve. In many cases neuralgia, particularly certain forms of it, remains stationary and lasts till death. This is not apt to result from the neuralgia itself, but from accidental complications, or from the disease causing the neuralgia. Treatment.—Where the neuralgia is induced by pressure on, or compression of, the nerves by foreign bodies, tumors, or contracted cicatrices, the causal indications require surgical interference. The circumstance that neuralgia occasionally continues after the removal of foreign bodies and tumors from the vicinity of nerves, should not deter us from operation; since we cannot knoAV beforehand whether the neuralgia has become " habitual," that is, whether the injurious influ- ences that have acted on the nerve have affected it permanently, and have induced a state that will not subside after removal of the cause. The so-called antirheumatica are of little use in rheumatic neuralgias. These would be more successfully treated by the methodical use of artificial or natural warm-baths. Numbers of patients with rheumatic neuralgia seek relief, and some find it, at AVildbad, Baden-Baden, Wiesbaden, and other warm springs. Where the disease is due to malaria and has a regular type quinine, the antidote to malarial poison- ing has a Aery brilliant effect. Sulphur-baths and the internal admin- istration of sulphur have a peculiar reputation in the neuralgias caused by poisoning Avith copper, mercury, and lead. Finally, the causal indications require the treatment of the disposition for neuralgia; and, as we know, to some extent at least, what it depends on, Ave cannot unfrequently fulfil this indication successfully. We cannot regard car- bonate of iron as a specific for neuralgia, but, Avhen poverty of the blood is one of its chief causes (or, as Bademacher has it, " when the neuralgia is an iron affection of the constitution"), the carbonate and other preparations of iron often have a surprising effect. In the same way neuralgia may often be benefited by modes of treatment that greatly modify the change of tissue and the nutrition. Where Ave cannot remove the causes of neuralgia, the indications from the disease require that we should attempt to equalize the disturbances of nutri- tion on Avhich it depends, or to destroy the excitability of the nerves, or finally to prevent the propagation of the morbid excitement to the brain. Among the most effective modes of treatment for this purpose is the use of electricity. Excellent results are not unfrequently attained both by the induced and constant current. Dr. Leube, in his inaugu- ral dissertation in 1862, reported a number of cases of obstinate neu- 65 288 DISEASES OF THE PERIPHERAL NERVES. ralgia that were cured at my clinic by the induced current. Since then, my experience in the result of this treatment has greatly in- creased, and I may combine the results in the folloAving propositions : 1. In treating neuralgia with the induced current, it is best to em- ploy the metallic electrodes known as the electric brush: while one electrode containing a moistened sponge is held in one of the patient's hands or against any part of his body, we stroke the brush along the course of the affected nerve; if there are any points douloureux we allow the brush to remain over them rather longer (electric moxe). 2. Many cases of neuralgia, which had been previously treated with- out benefit by the most varied remedies, were completely and perma- nently cured in from twelve to twenty applications, or even sooner. In other cases no benefit or cure was effected. 3. The first sitting shows whether the neuralgia can be cured by the induced current. We can only expect a cure where the pain is decidedly relieved or entirely disappears immediately after the first electrization, even if it should only be for a short time; if this temporary result do not take place, the continuation of the treatment Avill also prove ineffectual. The application of the induced current as above directed is very pain- ful ; and it is only after the patient has actually experienced benefit that he suffers it with patience, and even then he moans and whimpers during the application. An erythema, that lasts for some time, forms where the current is applied. I shall not attempt to decide whether the induced current acts by derivation to the skin like the linear cau- terizations advised by Vallelx, or as blisters and irritating frictions, or whether it acts in some other way. The constant current is far more effective than the induced in neu- ralgia. Some cases that have been treated without result by the induced current have been cured by the constant, while I have never seen the reverse. I place both poles along the affected nerve, and, without attending to the course of the current, hold the zinc pole on the most painful part, and on those parts Avhere the nerve approaches nearest to the surface, as at the supra or infra-orbital foramen, or at the zygomatico facial foramen, or at the sciatic notch. If it be possible to get the nerve between the poles, as in the cheek or nose, I introduce one pole into the mouth or nose to the point whence the pains radiate, while I place the other at the corresponding point on the skin. At first, the application of the constant current is not particularly painful, • but an unpleasant, burning, piercing pain soon commences and grad- ually increases; where the number of elements is large, it may become unbearable. The changes induced in the skin at the point of applica- tion of the constant current, if the electrodes be applied for a length of time, are far greater than those caused by the induced current. NEURALGIA. 289 They not only consist in a lively erythema, a decided SAvelling of the skin, and an increase of the subjacent tissue, but papules and blebs arise on the skin, particularly at the positive pole ; if the action con- tinues long, the surface of the elevations sloughs off. These changes take place not only at the point of application, but occur equally or at least similarly in the deeper parts, as is shown not only by the increase in volume of the subcutaneous tissue and muscles, but also by the fol- lowing experiments (Erb), which show a great deal about the mode of action of the constant current in neuralgia and other neuroses, as Avell as in some diseases of the muscles, joints, etc. If Ave cross the forearms, placing the volar surfaces in contact, and apply the electrodes to their dorsal surfaces, there will be reddening not only of the parts to which the electrodes are applied, but of the corresponding points on the anterior surfaces. Generally, relief immediately follows the ap- plication of the constant current just as it does that of the induced current; but occasionally the pain is at first increased, and that should not always induce us to stop the treatment. There seems to me no doubt that the curative action of the constant current, in most cases of neuralgia, is to be explained by the modification of the circulation, endosmosis or change of tissue in the diseased nerve, its neurilemma, or the parts around; this " catalytic action" may result from the chemical disintegration induced through the nerves, or the attraction of the constituents of the nutrient fluids toAvard the pole, or it may occur in some other Avay. The SAvelling of the skin, and the eruption of nodules and blebs on it after the application of the constant current, do not prove its action on the vasomotor nerves any more than the redness of the skin after a mustard plaster shows a similar action in oil of mustard. I consider it perfectly unjustifiable, in most of the recent writers on electrotherapeutics, to make a distinction between the effect of the constant current in neuralgia, paralysis, etc., and its effect in dis- turbances of nutrition. In most cases of neuralgia or other nervous diseases, just as in the affections of the muscles, joints, etc., where galvanism has proved useful, there is no molecular change or any alter- ation in the electrical state of the nerves, but, as Bemak distinctly asserts, there are disturbances of nutrition, anomalies of circulation and structure, exudations, etc. For the sake of the good cause, I can- not help regretting the numerous attempts that have been made to explain the benefits from the constant current in disease of the nerves and muscles, by referring to the laws concerning the contractions at the opening and closing of the current, concerning anelectrotonus and catalectrotonus, or concerning the results of irritation and division of- the sympathetic, instead of resting solely on the evident results of clin- ical observation. These very imperfect doctrines, which are founded 290 DISEASES OF THE PERIPHERAL NERVES. on the results of experiments made on healthy frogs and rabbits, fur- nish no useful data for the explanation of cures induced in diseased hu- man beings by the employment of electricity. Supposing, in a paral- ysis, neuralgia, or anesthesia, Ave can succeed in changing the electro- tonus of the affected nerve, which I do not at all deny, there is not the slightest probabihty that Ave shall thus remove the textural changes which he at the root of the existing paralysis, anesthesia, or neuralgia. On the contrary, if cure results, we may make up our minds that, besides the changes of the electrotonus, some other action has been induced. And supposing we succeed, by a few minutes' irritation of the sympa- thetic, in contracting the vessels supplied with nerves from that part, for the length of the sitting, Avhich I also shall not deny, it is just as improbable that Ave should thus remoAe a disturbance of innervation existing in the parts supplied by the contracted vessels. If application of the constant current to the sympathetic causes a cure, we may sup- pose that the disease depended on some disturbance of nutrition of the sympathetic, that has been removed by the catalytic action of the cur- rent. The marked difference between the constant and induced current in regard to their chemical action on water, solutions of salt, albumen, etc., has long been known, and I am fully convinced that the introduc- tion of the former into practice is one of the most valuable advances of modern times, and that in the constant current toe have a means, more powerful than any other, of modifying the nutritive conditions of parts that are deeply situated. But I fear that the rationalistic and doctrinal teachings about galvanotherapeutics, which are recently so popular, and the attempts to make this so "exact," may interfere with moderate and experimental observation, and injure the popularity of an important remedy. In the same class as electrical treatment come the blisters, moxe, actual cautery, and cutaneous irritants, which are used as derivatives to the skin, and which are being more and more supplanted by elec- tricity. Superficial linear cauterization is considered, particularly in France, as one of the most effective of remedies. Among the means by which the excitability of the nerves is de- stroyed, we shall first mention cold. Besides compresses of cold water and ice, lotions with ether and liquor Hollandicus are used; these in- duce cold by their rapid evaporation. If they are more effective than ice-compresses, it is because they are breathed in at the same time, and to some extent stupefy the patient. Cold is a valuable pallia- tive; Ave cannot .generally continue its use long enough for a radical cure. The narcotics, particularly in the form of hypodermic injections of solutions of morphia, are at present the most common remedies for neuralgia. Formerly, if the local action of morphia was desired, a NEURALGIA. 291 blister Avas applied, the resulting vesicle Avas opened, and the desired dose of morphine was sprinlded on the denuded spot, or else the mor- phine Avas mixed with saliva and inoculated into the skin. The intro- duction of hypodermic injections, instead of these troublesome proce- dures, was a great event, and was regarded as an immense advance in treatment. It Avas thought that the affected nerves might noAV be narcotized with facility. The results Avere perfectly surprising. In numerous cases, instead of Avriting a prescription of doubtful efficacy, the physician could free the patient from his pain in a feAV minutes. Moreover, it soon became evident that, not only in neuralgia, but in many other painful diseases also, this effect folloAved the hypodermic injections of morphine; and, secondly, that it did not make much dif- ference whether the injection was made at the seat of the pain or at some other point. I know many physicians Avho never go out to their practice without a Pravaz's syringe and a solution of morphine in their pocket, and who usually bring the morphine-bottle home empty. It cannot be denied that the hypodermic injection of solution of morphia is sometimes abused. From this abuse we have become acquainted with a form of chronic morphine-poisoning that Avas previously little attended to. If injections of morphia have been made for some time, and the dose has been increased more and more, independent of the return of the pain, the patients begin to feel an absolute need of the injections. They feel dull, and complain of an undefinable weakness, discomfort, trembling, etc. Some describe then state as resembling that after a debauch. Indeed, the condition before and after the injec- tion often reminds us most strikingly of that of a toper, before and after his first glass of spirits in the morning. But these bad results may be avoided by the careful use of hypodermic injections of morphia. It is doubtful whether they have any local action; but it is certain that the general effect of the morphine is much more complete and precise, if it be injected under the skin, than if it be administered internally, and we must regard the hypodermic injection of \ to % of a grain of mor- phine as an invaluable palliative for neuralgia. Next to the employ- ment of cold and narcotics, come frictions of the skin with veratrine ointment (gr. iv—x to fat 3 j), or aconite ointment (gr. j to fat 3 j). After using veratrine ointment, the patients feel a peculiar prickling in the skin, which occasionally benumbs the pain. After using aconite ointment, the part rubbed becomes to some extent insensitive to ex- ternal irritants. We have stated that a third requirement of the indications from the disease is to prevent the conduction of excitement from the irri- tated nerves to the brain. The most effective mode of doing this is oy dividing the nerve between the brain and the affected part, or by 292 DISEASES OF THE PERIPHERAL NERVES. cutting out part of the nerve, since it readily heals up if simply di- vided. The want of success in this operation is chiefly due to a di- vision of the wrong nerve, or to its being divided at the wrong place, that is, to the distal side of the point whence the pain orginates (Bruns). Unfortunately, the division at "the right spot" is in most cases entirely impossible, because the pain originates from a point above which the nerve cannot be reached. Cauterization of the nerve, for the purpose of disconnecting it from the brain, should be given up; compression is only to be used as a palliative. The least benefit is obtained from the specifics recommended in neuralgia, such as arsenic in the shape of Fowler's solution, the preparations of zinc, particularly the valerianate and hydrocyanide, nitrate of silver, and other metallic and vegetable nervines. There are cases recorded where each of these remedies is said to have produced brilliant results, but these examples are few, and are far outweighed in number by those where they have had no effect. Up to the present time it is absolutely impossible to determine exactly in Avhat cases these remedies are useful. CHAPTER IV. NEURALGIA OF THE TRIGEMINUS--PROSOPALGIA--TIC DOULOUREUX-- fothergill's FACEACHE. Etiology.—Next to the sciatic, no nerve is so often the seat of pain as the trigeminus. This is partly because many branches of the trigeminus pass through narroAV canals and openings, where they may readily be compressed, partly from the distribution of the nerves to portions of the skin Avhere they are more exposed to cold than other nerves are. Hyrtl is doubtless correct in supposing that the passage of the branches of the trigeminus through narrow openings of the bones has much to do with the occurrence of facial neuralgia; for see the great immunity to the disease of those branches which pass through the wide sphenopalatine foramen to the nose, compared Avith its frequent occurrence in the infraorbital, zygomaticus male, and su- perior and inferior dental branches. Only in a feAV cases have foreign bodies under the skin (in one celebrated case of Jeffreys there was a piece of porcelain) and tumors pressing on the branches of the trigeminus been found as causes of prosopalgia. Somewhat more frequently changes in the bony canals can be found to explain the morbid excitement of the nerves traversing them; among these are exfoliations of a bony Avail in neuralgia of the infraorbital, exostosis of the root of a tooth in neuralgia of the in- framaxillary, general thickening of the bones of the skull with con- NEURALGIA OF THE TRIGEMINUS. 293 traction of the foramina through which the nerves pass, or even inflam- mation and projections on the bones. Finally, in some cases, aneurisms, tumors, thickening of the dura mater, exostoses within the skull, which pressed on the trigeminus, have been found as eAident cause for ob- stinate and extensive neuralgia of the branches of that nerve. I do not know a single case that shows an unequivocally central origin of facial neuralgia. Among the cases described by Bomberg, in one case of neuralgia of the trigeminus that had lasted for twenty-six years, it is true there was a small diseased spot in the pons, but there Avas at the same time an aneurism of the carotid compressing the tri- geminus, Avhich would fully have accounted for the neuralgia. Far more frequently no material causes can be found for facial neu- ralgia. In such cases it is very probable, but cannot be proved, that the disease is occasionally caused by catching cold, which induces hy- peremia and slight edema of the neurilemma that disappear after death. Cases of hemorrhoidal facial neuralgia and those from sup- pression of persphation and exanthemata are very problematical; arthritic cases are somewhat less so. Neuralgia of the trifacial is the most frequent form when the disease is due to malaria. The rather worthless results of statistics shoAV that facial neural- gia is rare in childhood, most frequent between the thirtieth and fiftieth years, and somewhat more common in women than in men. Symptoms and Course.—Of course, the pain from which patients with neuralgia of the trigeminus suffer is more extensive in proportion as the branch of the nerve affected is larger; and conversely, from the limitation of the pain to a circumscribed spot, we may decide that a very small branch is the seat of the disease. Moreover, as the filaments of a nerve are the more numerous the nearer Ave go to its origin in the brain, and become fewer as it approaches the surface, it follows that, when the pain is very limited, we may consider its origin as peripheral; Avhere it is Aery extensive, we may decide that the injurious influence is in the skull itself. In fact, in neuralgias caused by pressure on the trunk of the fifth pah, pain has been observed in all parts supplied by its sen- sory filaments, in the anterior surface of the ear, in the skin of the forehead, temple, face, in the orbit, nose, palate, body of the tongue, floor of the mouth, teeth, and probably in the dura mater. Valleix mentions numerous points douloureux in facial neuralgia; we shall only call attention to three of them, Avhich lie nearly in a vertical straight line, and correspond to the supraorbital foramen, the anterior opening of the suborbital canal, and the mental foramen. If the neu- ralgia be seated in the first branch of the trigeminus, the pain spreads particularly in the branches of the supraorbital, and affects the forehead, ejebrows, and upper eyelid. In some rare cases the pain is chiefly in 294 DISEASES OF THE PERIPHERAL NERVES. the eye, and, from participation of the infratrochlearis, at the inner canthus and caruncula lachrjmialis. The twigs of the first branch, which go to the lachrymal gland and conjunctiva, explain the increased secretion of tears and redness of the conjunctiva, almost always ob- served in neuralgia of that branch, particularly on remission of the paroxysms. If the second branch of the trigeminus be the seat of the neuralgia, the pain is usually most severe in the parts supplied by the infraorbital, that is, in the lower eyelid, ale nasi, upper lip, and teeth of the upper jaw. The attacks of pain in these cases are sometimes accompanied by Avatery or mucous secretion from the nasal mucous membrane. Neuralgia is rare in the course of the third branch of the nerve: this is particularly true in the course of the auriculo-temporal and lingual branches; it is somewhat more frequent in the inferior alveolar, especially in the mental, after it escapes from the foramen; then the patient has pain in the chin and lower lip. Salivation often accompanies neuralgia of the third branch; this symptom agrees per- fectly with the experiments of Ludwig (see vol. i.). Occasionally the neuralgia chiefly affects those twigs of the second and third branches that accompany the ramifications of the facial nerve. This explains why the facial nerve itself Avas formerly often considered as the seat of the neuralgia. In facial, as in other neuralgias, the patients suffer partly from a permanent dull pain located at different points of the trigeminus; partly from attacks of agonizing pain, Avhich occur suddenly, then cease as suddenly, in half a minute or so, and again return till the attack, composed of these short twinges, "Tics," is over. The face often twitches during these attacks, but does not usually do so invol- untarily. Parson Barth, who has given a very careful account of his OAvn facial neuralgia, Avas even able to continue preaching during the attack. The attacks sometimes occur spontaneously, and, except in the eases due to malaria, they are irregular; sometimes they are in- duced by the causes previously mentioned, such as speaking, sneezing, gaping, blowing the nose, by using too cold or too Avarm food, occa- sionally even by any attempt to chew. During the attack the face is usually reddened, its temperature increased, and there is active pulsa- tion of the arteries. To the cases observed by Brodin and Bomberg, where, after long duration of severe facial neuralgia, the countenance of the patient was greatly disfigured by SAvelling and development of fat, I may add the case of one of my Magdeburg colleagues, in whom there was decided disfigurement, particularly by swelling of the lower lip, from facial neuralgia of one year's duration. In old cases of the disease other disfigurements of the face have also been observed, such as increased thickness and prickliness of the beard, acne pustules, etc. NEURALGIA OF THE TRIGEMINUS. 295 The duration of the disease is rarely short, except in the regular intermittent malarial affection; in almost all other forms it usually lasts a long while, even half a hfetime, or more. Among the termi- nations, besides recovery, severe melancholy occurs, which may drive the patient to suicide. Death also occasionally results from the cause of the disease, but not from the disease itself. Treatment.—For the treatment of facial neuralgia we have little to add to the rules given for the treatment of neuralgia in general. Only in a few cases can we cure prosopalgia quickly, by the removal of foreign bodies, tumors, and contracting cicatrices. Extraction of teeth does not often prove of benefit. Usually the unfortunate patient has one tooth after the other draAvn, Avithout the slightest relief to the pain. In recent cases, caused by catching cold, Valleix urgently recom- mends flying blisters and superficial cauterizations with the hot iron. If the disease be due to malaria, large doses of quinine are almost always of service. The administration of Fowler's solution (four to six drops every three hours) is only indicated AAiien quinine has failed. In de- cided anemia, Ave may give preparations of iron, and, when we con- clude that there is some other constitutional disease, whose nature Ave cannot determine, we may order alterant mineral Avaters and baths. Concerning the employment of electricity, cold, veratrine, and aconite, as Avell as of morphine, particularly in the form of subcutane- ous injection, the same is true in facial as in other forms of neuralgia. I have seen tAvo cases of tic douloureux cured by the constant current; one of them Avas of thirty years' standing, and in the other eleven operations, some of them severe ones, such as the ligation of the carotid, resection of the superior maxilla, etc., had been performed without benefit. In no form of neuralgia is division of the nerve, or excision of part of it, more frequently done. After this operation had for a time almost gone out of use, Brims has shoAvn, by a careful ex-4 animation of the cases where it had been done, that, after excluding the cases where its want of benefit depended on error of diagnosis or operation, and after excluding the cases wiiere the recurrence of the pain was to be regarded as a new attack, not as a relapse, there Avas a considerable number of cases where the neurotomy caused either a complete and permanent benefit, or at least a temporary one, for a feAV months or 3 ears. According to Bruns, the operation (whose per- formance Ave will not describe) is indicated when the pain is very limited, and it is probable that its exciting cause is situated at a point beyond which the nerve is accessible to the knife, when other treat- ment has proved fruitless, and when the pain renders the patient unfit for business. There is also an indication to operate when we cannoi 296 DISEASES OF THE PERIPHERAL NERVES. hope to divide the nerve between the point of disease and the brain, but when the pain never occurs spontaneously, being always the result of some external irritation acting on the peripheral terminations of the nerve. In such cases the operation may, to some extent, protect the patients from the exciting causes of then attacks of pain. The tem- porary compression of the affected nerve and the artery supplying it has also sometimes proved an excellent palliative, and deserves a trial in suitable cases. Among the so-called specifics, Bomberg speaks most highly of arsenic; under its use he saw the most evident and speedy benefit in those cases that occurred in hysterical women, or from disease of the sexual organs. Its effect was the more certain, the more anemic the patient. Bomberg also saw temporary benefit from nitrate of silver in large doses (gr. j). Bell, who, as Watson says, " shot an arrow at random," claims to have had excellent results from the internal administration of croton-oil with compound extract of colocynth. Among the narcotics, besides the preparations of opium and morphine, belladonna, stramonium, conium, and then alkaloids, particularly Meglln's pills (consisting of equal parts of extract of hy- oscyamus and flowers of zinc), have a good reputation; we begin with a two-grain pill, morning and evening, and increase to twenty or thirty of them daily. CHAPTER V. HEMICRANIA--MIGRAINE. The combination of symptoms designated as migraine is difficult to explain. It is even doubtful if we are justified in classing it among the neuralgias, as is almost universally done. The almost constant occurrence on one side, of the headache (to which hemicrania owes its •name), the paroxysms and free intervals observed in the disease, the negative results of anatomical examination, are the chief reasons for this view. On more carefully examining into the general course of the disease, and the course of individual cases, however, this view is not supported. There is no variety of neuralgia which, beginning, like migraine, in childhood, and lasting into advanced age, only attacks the patient a few times a year during this period, and, in these attacks, shows a steady increase and diminution of the pain, but never an in- stantaneous occurrence or disappearance. Still other objections to the consideration of migraine as neuralgia AAill appear from the description of the symptoms and course. Whether migraine be a neuralgia or not, the pain must result from excitement of sensory filaments, but it is doubtful whether this excitement occurs in the filaments from the HERMICRANIA—MIGRAINE. 297 trigeminus to the dura mater, in the sympathetic filaments accompa- nying the vessels, or in the brain itself. According to a fanciful hy- pothesis of Du Bols-Beymond, which Dr. Mbllendorf has carried still further, the attack of migraine depends on a dilatation of the branches of the internal carotid, the result of abnormal innervation of the vessels from the ganglion supremum of the sympathetic. According to this vieAv, the brain would, during an attack, be in the same condition as the ear of a rabbit that has had the cervical portion of the sympathetic divided. Migraine is a very common disease, so that, in a moderately-exten- sive practice, we may usually observe a series of cases for years, and be again and again reminded by them of the impotence of our art. The disease occurs in both sexes, but is far more frequent among women than men. Like gout, migraine is considered a fashionable disease, but it also occurs among the lower classes, and is for them a peculiarly-distressing disease, as they cannot lie by for it. In most cases its commencement dates from the time of going to school, if not from early childhood. Probably in half of the women affected Avith migraine, the attacks occur at the menstrual period, or immediately before it. In other cases the attacks are unmistakably due to mental excitement. I treated one lady, who never had a party without suf- fering from migraine next day; another was affected in the same way after each visit to the theatre. In some cases a severe attack, particu- larly if it end with sick stomach, results in a certain immunity to re- lapses. The first lady above mentioned had her guests invited the day she had migraine, so that she might be certain of being able to receive them the folioAving day. In the cases that I have seen, the attack could rarely be referred to an error of diet; but, on the other hand, the pain and general disturbance were almost always increased if the patient took any food, no matter hoAV digestible, during the attack. After feeling perfectly avcII the day before an attack of migraine, the patients perceive the first symptoms as soon as they aAvake, or im- mediately afterward. They feel heavy and depressed, are uneasy and irritated, complain of slight chilliness, are inclined to gape, usually have no appetite, and have a slimy taste in the mouth. Besides the above, there is headache, which is almost always limited to one side, increases rapidly, and becomes almost unbearable. The relaxation and pain drive the patients to bed; they are very sensitive to light and noise; hence they seek the darkest and most retired chambers. They dislike all visits, even that of the physician, during the attack. The pulse is usually slower. Iu many cases, at the height of the at- tack (in some patients at every attack), there is nausea, and, after great 298 DISEASES OF THE PERIPHERAL NERVES. retelling, vomiting, by Avhich quantities of a very bitter greenish fluid are evacuated. Patients Avho have frequent attacks of migraine, usu- ally long for the commencement of vomiting, and even try to excite it by irritation of the pharynx. Generally, toward evening, rarely earlier, the patient falls asleep, and awakes next morning free from pain, although much depressed. The disease never threatens life; but, although the attacks sometimes occur at shorter or longer inter- vals, patients rarely entirely recover from the disease. In Avomen alone, particularly those who have the migraine at their menstrual pe- riods, the disease occasionally ceases at the change of life. Watson asserts that " four to six drops of liquor arsenicalis, given three or four times daily, with attention to the digestion, effected a cure in ten cases of hemicrania;" but this assertion is a solitary one; most other observers say that the disease generally resists all treat- ment. Nor have I seen any decided benefit from arsenic, Pulsatilla, marsh-trefoil, or from the very expensive citrate of caffein (which is also called a specific), of which we prescribe pills (IJ caffein citr. gr. x, ext. granim \Triticum repens] 3j; ft. pil. 10), and, to cut short the attack, give one or two of these pills every hour on the first symptoms, or from the paulinia sorbilis, Avhich is prescribed in the form of pasta guarana 3ss—3j. One patient prepared for herself an infusion of unroasted coffee, and, as long as she drank this daily, appeared to have the attacks more rarely and less severely. Another patient escaped the attacks as long as she took sea-baths at Haringsdorf; but, when she returned home, they began again. In most cases we can do noth- ing but attend to existing disturbances of the general health and of the digestion, and the chances of benefit from treatment are much greater where we can discover any such disturbances. During the attack we should spare the patients from the use of any remedies, and let them take nothing but water. It is best for the patient not to trv to defy the attacks, but to go to bed early. CHAPTER VI. CERVICO-OCCIPITAL NEURALGIA. Cervico-occipital neuralgia, or neuralgia of the sensory nerves of the occiput, neck, and nape of the neck, which originates from the first four cervical nerves, is far more rare than facial neuralgia. The cases known, up to the present time, are not sufficiently numerous to give us any thing definite concerning the etiology. From the observations of Valleix, according to which the disease often began after prolonged exposure to cold, and from one case Aviiere relapses often occurred, and CERVICO-OCCIPITAL NEURALGIA. 299 same only in Avinter, as well as from the generally favorable course and good result of treatment, it seems probable that this disease most frequently results from catching cold. Diseases of the vertebre also appear to induce this form of neuralgia, in some few cases, by pressing on the veins as they pass out of the vertebral canal; and SAvollen lym- phatic glands, deep in the neck, may cause it by pressing on the cervi- cal plexus and the occipitalis major. In cervico-occipital neuralgia, patients also complain of a continued dull pain, hmited to small spots, which is, from time to time, accompa- nied by attacks of very severe lancinating pain shooting out in various directions. According to Valleix, these isolated painful spots are: 1. An occipital point located below the occipital bone, betAveen the mas- toid process and the first cervical vertebra, corresponding to the point where the nervus occipitalis major [posterior occipital] perforates the complexus muscle and becomes subcutaneous. 2. A superficial cervical point, somewhat above the middle of the neck, between the trapezius and sterno-cleido-mastoid muscles, corresponding to the point of exit of the chief cervical nerves. 3. A mastoid point, lying behind the mastoid process, corresponding to the occipitalis minor and auricularis major nerves. 4. A parietal point near the parietal protuberance. 5. An auricular point in the auricle. In the attacks the pain darts from these points toward the occiput, the posterior, and upper part of the neck, anteriorly to the face, and, occasionally, downward, toward the shoulder. Cervico-occipital neuralgia is not unfrequently comphcated with prosopalgia and neuralgia of the brachial plexus. The attacks sometimes occur at irregular intervals, sometimes from movements of the head, or other slight causes. They are rarely so severe as the at- tacks of tic douloureux. Disturbances of nutrition in the territory of the cervical nerves are exceedingly rare, if they ever occur. Cervico- occipital neuralgia is far less obstinate, and is rarely so permanent as facial neuralgia. In this affection division of the nerves has not been tried. In recent cases blisters are recommended, particularly by Valleix, as well as Meglln's pills and all other remedies that are used in prosopalgia. CHAPTER VII. CERVICO-BRACHIAL NEURALGIA. By cervico-brachial neuralgia we mean a neuralgia located in the sensory twigs of the brachial plexus, which is composed of the lower four cervical and the first dorsal nerves. This form of neuralgia has perceptible causes far more frequently 300 DISEASES OF THE PERIPHERAL NERVES. than other forms. Among these are injuries of the peripheral branches of the brachial plexus in the arm or hand from lancets and other pointed instruments, pressure on the nerves from fragments of bullets, contusions, neuromata, etc. The brachial plexus itself is occasionally compressed in the axilla by swollen lymphatic glands, under the clavi- cle by the callus of a fractured rib, by aneurisms of the subclavian or arch of the aorta. Finally, the nerves forming the brachial plexus may be pressed upon and hritated just at their escape from the spinal canal, by diseases of the vertebre. In other cases the irritation act- ing on the brachial plexus or its branches cannot be perceived, and we have to refer the neuralgia to a rheumatic affection of the neurilemma, or to an imperceptible alteration in the nerves, from over-use of the muscles in knitting, playing the piano, etc. Lastly, we must mention that attacks of angina pectoris are usually complicated AAith pain in the course of the brachial plexus. The transfer of the morbid excitement from the nerves of the heart to those of the arm is best explained, according to my idea, by the intervention of the nervus cardiacus mag- nus and parvus, as they originate from the middle and inferior cervical ganglia which are connected by many twigs with the inferior cervical nerves. In some cases the pains spread over a large part of the sensory filaments of the brachial plexus, in other cases they are limited to the axillary region and the upper part of the arm; occasionally they fol- low exactly the distribution of the ulnar, radial, or musculo-cutaneous nerves. Valleix most frequently found a point douloureux in the axilla, and one for the ulnar nerve, the point between the inner con- dyle and the olecranon, and another near the ulna above the hand where the ulnaris becomes superficial; and for the radial nerve the point in the arm where this nerve winds around the humerus, and a second one at the lower end of the radius just above the hand. The lancinating pains, particularly those extending to the fingers supplied by the affected nerve, are severe and recur very frequently, so that the intervals of perfect freedom from pain are usually shorter than in other neuralgias. The pain is generally accompanied by a sense of formication and numbness in the fingers, which lasts longer than the attack. Disturbances of nutrition in the parts supplied by the mor- bidly-excited nerve occur in some cases of brachial neuralgia in the shape of exanthemata (pemphigus, urticaria), or inflammations of the fingers. There are very often complications with neuralgias of other nerves, particularly with cervical, intercostal, and sciatic neuralgia. The course, duration, and termination of cervico-brachial neuralgia are about the same as in other neuralgias. If injuries of the finger, venesection, or similar injuries have in- INTERCOSTAL NEURALGIA. 30] duced brachial neuralgia, neurotomy proves triumphant, particularly in recent cases, and when the neuralgia has not become " habitual." Besides other remedies that we have already mentioned, the internal administration of oil of turpentine has some reputation ; we shall refer to it again when speaking of sciatica. CHAPTER VIII. INTERCOSTAL NEURALGIA. We designate as intercostal neuralgia the morbid excitement of one or several spinal nerves, particularly of those which as intercostal nerves pass along the upper intercostal spaces to the sternum, and along the lower spaces to the epigastrium. Intercostal neuralgia is among the most frequent forms of neural- gia. It is met more frequently in women than in men, shoAvs a sur- prising predisposition for the sixth, seventh, and eighth intercostal nerves. We have already spoken of the shrewd explanation that Henle gives for this peculiarity. The fact that the inferior intercostal nerves are chiefly affected, that is, the ones that empty then blood into the hemiazygos vein, supports the view that one of the chief causes of inter- costal neuralgia is dilatation of the venous plexus, winch most readily occurs at these places, and exercises pressure on the roots of the spinal nerves. In some cases the dorsal nerves are pressed upon, where they pass through the intervertebral foramina, by inflamed vertebre, or, after they have passed through, by carious ribs and swollen glands. Inter- costal neuralgia not unfrequently occurs after recovery from pleurisy. Within a year I have seen two cases which undoubtedly had this origin. It is doubtful what anatomical changes in the neurilemma or in the parts surrounding the nerves, during a pleuritis or the reabsorp- tion of the pleuritic exudation, have occurred in these cases. The same is true of those cases of intercostal neuralgia that occasionally accompany tuberculosis of the lungs. Lastly, as the disease is par- ticularly liable to occur in hysterical women with chronic uterine dif- ficulty, it has also been referred to a propagation of the morbid excite- ment from the nerves of the uterus through the spinal medulla to the brachial plexus (Bassereau). In intercostal neuralgia, the three painful points mentioned by Valleix are more frequently observed than in most other forms of neuralgia. The first or vertebral point is in the posterior part of the intercostal space, somewhat outward from the spinous process, and about on a level with the point of exit of the nerve from the interver- tebral foramen. The second or lateral point lies in the middle of the 302 DISEASES OF THE PERIPHERAL NERVES. intercostal space; it corresponds to the point of division of the inter- costal nerve; from it the nerves pass toward the surface. The third point is near the sternum between the costal cartilages in the upper intercostal nerves, in the lower ones it is in the epigastric region some- what outward from the median line; it is called either the sternal or epigastric point, and corresponds to the place AA'here the terminal branches of the intercostal nerves approach the skin. These usually very chcumscribed points are generally so sensitive to pressure, that the patient cries out as soon as they are touched. The patients often discover the points themselves, and voluntarily point out their position to the physician, and, as the pain very much resembles that from a contusion, they are sure" they must have struck themselves somehoAV. This constant pain is increased by deep inspiration, cough- ing, sneezing, occasionally also by moving the arms, as well as by touching the points; and attacks of lancinating pain are excited, which generally start from the vertebral point and pass anteriorly along the intercostal space; occasionally they pass forward and backward from the lateral point. Hard pressure often relieves the pain. Bomberg tells of a man whose coat had become threadbare at the point where he was in the habit of pressing his hand. The frequent complication of intercostal neuralgia Avith herpes zoster is very interesting, although just as obscure as the disturbances of nutrition in the parts supplied by other nerves affected with neuralgia. The disease runs a very irregular course; it usually develops slowly and passes off gradually after variable duration. Occasionally it is very obstinate and hangs on for years. For the treatment of intercostal neuralgia we would advise the re- peated application of blisters to the points douloureux, and particular- ly the employment of the induced, or, still better, of the constant, cur- rent of electricity. During the treatment any anomalies of constitution are to be looked after, and, where the pain is very severe, morphia should be used internally or subcutaneously as a palliative. CHAPTER IX. MASTODYNIA--IRRITABLE BREAST (Cooper). It is doubtful Avhether mastodynia be a neuralgic affection of the branches of the intercostal nerves going to the mammary gland, or of the nervi supraclaviculares anteriores. According to Bomberg's excellent description, women, about the period of puberty, or from then to the thirtieth year, Avithout any perceptible cause, become sen- sitive to the slightest touch at one or more points over the mammary LUMBO-ABDOMINAL NEURALGIA. 303 gland. Severe pain, like tic douloureux, occasionally shoots out tow- ard the shoulder, axilla, or hip. Occasionally, at the height of these attacks of pain, vomiting comes on. The patients cannot lie on the affected side ; they are unable to bear the weight of the breast. The pain usually increases shortly before the appearance of the menses. The disease often lasts for months or years without any perceptible change in the mammary gland. In other cases, sharply-bounded, very movable tumors, as large as a pea or a hazel-nut, develop in the mam- ma and form the starting-point for the pain, occasionally they cease to be painful; they consist of connective tissue, not of the substance of the gland; they have been previously mentioned as tubercula dolo- rosa or neuromata. Fur worn on the breast, a plaster of equal parts of emplas. saponat. and extr. belladonna, recommended by Cooper, and pills of ext. conii, ext. papaver (ana gr. ij), ext. stramonii (gr. \—£), are mentioned by Bomberg as the most trustworthy remedies. CHAPTER X. LUMBO-ABDOMINAL NEURALGIA. Neuralgia lumbo-abdominalis is the form that affects the cuta- neous nerves of the lumbar plexus, going to the loAver part of the back, to the nates, anterior abdominal wall, and genitals. In this neuralgia, also, there are constantly pains at circumscribed points, which are occasionally accompanied by lancinating pains. These points are: 1. The lumbar points, somewhat outward from the first lumbar vertebre. 2. The hip point, somewhat above the middle of the crest of the ilium, Avhere the ilio-hypogastric nerve perforates the transversalis muscle. 3. The hypogastric point, someAvhat inward from the anterior-superior spine, where the ilioinguinal nerve per- forates the transversalis muscle; and, lastly, some points on the mons veneris, vulva, or scrotum at the terminations of the cutaneous nerves. Where the posterior branches are affected, the lancinating pains chiefly pass toward the nates; where the anterior are affected, they chiefly pass toward the external genitals. The etiology, course, and treat- ment of lumbo-abdominal neuralgia are exactly the same as in inter- costal neuralgia. CHAPTER XI. NEURALGIA ISCHIADICA—ISCHIAS—ISCHIAS NERVOSA POSTICA COTUN- NII—SCIATICA—HIP-GOUT. By sciatica we mean a neuralgic affection of the sensory nerves of the sciatic plexus, which is formed from the fourth and fifth lumbar and first and second sacral nerves. 60 304 DISEASES OF THE PERIPHERAL NERVES. Etiology.—The nerves forming the sciatic plexus may be pressed upon by carious 01 carcinomatous vertebre, just Avhere they pass through the intervertebral foramen, and may thus be morbidly excited. And sciatica not unfrequently depends on pressure, which acts on the sci- atic plexus in the pelvis. In a patient with lymphatic leuchemia, whom I had the opportunity of observing at Greifswald, a severe in- termittent neuralgia, Avhich was undoubtedly caused by the pressure of the immensely-swollen retroperitoneal glands on the sciatic plexus, was for years the most prominent symptom. Tumors in the pelvis occasionally act in the same way, by pressure on the-sciatic plexus, particularly ovarian cysts, collections of hard feces, or, as in a very instructive case of Bamberger's, collections of cherry-pits in the sig- moid flexure, also the gravid uterus, particularly if the child's head remain long impacted. Cases of sciatica that are very obstinate, but usually terminate in cure, result from the pressure of exudations of parametritis and perimetritis in the subperitoneal tissue or in capsu- lated intraperitoneal spaces on the sciatic nerve. Lastly, irritation of the peripheral branches of the sciatic may sometimes be found as a cause of the sciatica. In this class belong the cases due to pressure from tight boots, from phlebotomy, an- eurisms of the arteries of the lower extremity, tumors near the nerve, etc. Among the causes of sciatica that leave no perceptible anatomical changes are excessive straining, suppression of habitual perspiration and exanthemata, and catching cold. It is quite natural that the lat- ter should occur. Indeed, the majority of cases of sciatica are of rheu- matic origin, as they result from exposure to cold of the skin coverincr the sciatic nerve, as occurs particularly in windy privies. It is not at all astonishing that, among the cutaneous nerves, the trigeminus and sciatic should be affected most frequently; the former being all day exposed to the danger of catching cold, and the latter being exposed for a short time once or twice daily. Statistics show that sciatica is one of the most frequent forms of neuralgia, that it rarely occurs among children, is most frequent be- tween the ages of twenty and sixty years, and that it occurs more fre- quently in males and the lower classes than in females and the higher classes. Symptoms and Course.—Most cases of sciatica support Bom- berg's assertion that there is no cutaneous nerve of the lumbar and sacral plexus, from the hip-joint to the* ends of the toes, which may not be affected with neuralgia, and that it is only tradition that locates the pain in the trunk of the nerve. The most frequent seats of the neuralgic pain are the nervus cutaneus femoris posterior, in which SCIATICA. 305 case the posterior and outer part of the thigh becomes painful; the su- perficial branch of the peroneal nerve, where the pain is in the outer and anterior surface of the leg and dorsum of the foot; the sural nerve (communicans tibialis), where the pain is in the outer side of the ankle and foot. The sensory filaments going to the sole of the foot are rarely the chief seat of pain. In the heel and back part of the sole of the foot severe neuralgia, proceeding from the terminal branches of the tibial nerve, is sometimes seen. Valleix gives, as the most frequent points douloureux, some points behind the trochanter, about three points in the thigh corresponding to the course of the chief trunks, some points on the knee, one below the head of the fibula, one above the outer ankle, and a few points on the ankle and dorsum of the foot. Sciatica rarely begins with great severity; it usually develops grad- ually and slowly attains its height. The patients are never free from pain, but complain of its constant presence deep in, particularly near the tuberosity of the ischium, at the point where the sciatic nerve passes out, and of pains in the small of the back. As the latter do not come from the branches of the sciatic, but from the posterior sacral nerves, Bomberg calls them sympathetic. Besides these con- stant pains, there are convulsive pains, particularly in the course of the above-named nerves. A division into ascending and descending sciatica is made, from the direction of these pains being from below upAvard or the reAerse. The pains sometimes begin spontaneously, especially after going to bed, so that they not unfrequently drive the patient out of bed; sometimes they are caused by outward pressure and movements of the legs. Even moderate tension of the fascia may have this effect; consequently the patient usually lies with his legs slightly flexed. Greater tension of the fascia in coughing, sneezing, or straining, is often accompanied by severe pain. In walking, the patient places the foot of the affected side very carefully, because any quick motion or mis- step usually causes severe pain. Participation of the motor filaments in the disease, or a transfer of the irritation from the sensory to the motor filaments through the spinal marrow, not unfrequently causes cramps in the calf or other muscular contractions. Disturbances of nutrition in the parts supplied by the affected nerve are not found in sciatica as they are in other neuralgias. If the disease prove chronic, the limb Avhich the patient favors not unfrequently emaciates decidedly. Occasionally the excitability of the sciatic is gradually impaired, and we have anesthesia and partial paralysis. Sciatica is a very obstinate affection. Even in favorable cases several weeks usually elapse before the disease disappears, and it generally subsides as gradually as it developed. In less favorable 306 DISEASES OF THE PERIPHERAL NERVES. cases it often lasts for months or years. Even after the disease haa disappeared, relapses very readily occur. Treatment.—The causal indications can rarely be fulfilled. If disease of the vertebre be the cause of the sciatica, we may use moxa, the hot hon, etc., to the back. Of the injurious influences that act on the sciatic plexus in the pelvis, overfilling of the sigmoid flexure is almost the only one that is accessible. Although rarely the sole cause of sciatica, this is a frequent complication, hence the old habit of be- ginning the treatment with a laxative is quite proper. If sciatica remain after difficult delivery, and if we have reason to refer it to a para or perimetritis, we may employ frequent abstractions of blood, and use cataplasms for a long while. In rheumatic sciatica warm- baths are useful, particularly the systematic treatment with baths at Teplitz, Warmbrunn, Wiesbaden, or Wildbad. Among the antirheu- matics administered, iodide of potassium in large doses appears to do most good. I saAV relief of the pain occur particularly in those cases Avhere the running from the nose, and the eruption caused by the iodine, came on early. In recent cases, the indications from the disease are best answered by the local abstraction of blood, and wet cups are preferable to leeches. The almost universal mention in text-books of one or more venesections, in the treatment of sciatica, appears to be merely out of respect to old medical authorities, particularly Cotugno, for at present no one ever bleeds for sciatica. In cases not very recent we should use derivatives to the skin, particularly blisters. We apply the first blister to the small of the back near the vertebre, on a level with the points of exit of the nerves forming the sciatic plexus; the second behind the trochanter, and so gradually pass down to the foot, applying blisters to the places where the nerve lies close under the skin. Be- sides blisters, superficial linear cauterizations of the skin in the course of the nerve, the energetic application of the hot iron and of moxe to certain points in the course of the nerve, as well as the actual cautery to the dorsum of the foot and between the outer toes, and finally, even the cauterization of the ear, particularly of the helix, have often been tried. After the use of the last-mentioned remedy there is almost always temporary benefit, which it is difficult to explain. Even in the most obstinate cases of sciatica, the induced, or still more the constant, current of electricity rarely fails. Among specific remedies, oil of turpentine as an electuary (ol. terebinth. 3 i, mell. § i, a table- spoonful twice daily), plays a very important part in the treatment of sciatica. Among others, Romberg speaks very highly of it. Neurot- omy should only be performed on small branches, in wiiose peripheral terminations we can clearly locate the starting-point of the morbid CRURAL NEURALGIA—ISCHIAS ANTICA COTUNNII. 307 excitement. Regarding the use of veratrine, aconite, and morphine as palliatives, we may refer to what we said in the treatment of neural- gias in general. CHAPTER XII. CRURAL NEURALGIA--ISCHIAS ANTICA COTUNNII. Besides the branches of the lumbar plexus whose neuralgic affec- tions we have described as lumbo-abdominal neuralgia, the sensory filaments going to the thigh and leg are occasionally affected by neu- ralgia. This affection has received the peculiar name of ischias antica, because in it the pain is along the anterior and inner surface of the thigh, leg, ankle, and dorsum of the foot, and in the great and second toes, instead of being along the outer and posterior surface as in sci- atica. Ischias antica, or crural neuralgia, is far more rare than ischias postica. Like the latter, it may be caused by pressure on the nerves at their point of escape from the spinal canal, or by injuries to the sacral plexus in the pelvis, or to its peripheral branches. Irreducible inguinal hernia, sprains of the thigh, hip-joint disease, not unfrequently induce morbid excitement of the cutaneous branches by pressure on or tension of the crural nerve. The course and results of crural neu- ralgia are analogous to those of sciatica, and the treatment must be according to the same general laws. In very rare cases the obturator nerve is also affected Avith neural- gia. This is characterized by the extension of the pain to the inner surface of the thigh, and, as the motor filaments of the obturator sup- plying the adductor muscles usually participate in the morbid excite- ment, the function of these muscles is frequently disturbed. The sudden occurrence of these symptoms, together with those of acute obstruction of the intestines, with ileus and peritonitis, are the only means of diagnosticating strangulated hernia through the obturator foramen. CHAPTER XIII. ANAESTHESIA OF THE CUTANEOUS NERVES. Anaesthesia—that is to say, lack of sensitiveness to external im- pressions—arises: 1. When the portion of the brain by which the excitement of sen- sory nerves is recognized has been destroyed or incapacitated. In such a case, notwithstanding that the patient is entirely insensible to external impressions, the excitability of the sensory nerves may still oe normal. For the present, we shall, Avithout notice, pass over this 308 DISEASES OF THE PERIPHERAL NERVES. form of anesthesia, Avhich we have mentioned as one of the symptoms of many of the diseases of the brain, as this section of the work is to be devoted to a study of diseases of the peripheral nerves. 2. Anesthesia may occur when, owing to destruction of the con- ducting fibres of the spinal cord, transmission of the impressions from the peripheral nerves to the brain is interrupted. In this form, like- wise, the excitability of the peripheral nerves may be normal. In treating of myelitis, we have already mentioned that, while the stronger stimulants, acting upon the periphery, fail to call forth any excitement at the centre, even a very feeble stimulus is frequently transmitted from the sensory to the motor fibres, and gives rise to reflex symptoms. Such phenomena as these prove that the excitability, both of the motor and sensory nerves, still remains unimpaired below the point at which the conducting power is interrupted. This form of anesthesia, also, is not the subject of the present section. 3. Anesthesia occurs when theve is nutritive disorder capable of destroying the irritability of the peripheral nerves, as well as when their connection Avith the brain and spinal cord has been interrupted mechanically. It is with this form alone that we are at present con- cerned. We shall here observe that we consider all sensory and motor nerves as peripheral as soon as they leave the brain, no matter whether they continue to lie within the skull or spinal canal, or whether then track be outside of the same. This is by no means an arbitrary dis- tinction. It depends chiefly upon the fact that the portion of nerve lying within the skull or spinal canal is in just the same state as the peripheral portions, as regards extinction of its frritability upon interruption of its connection with the central organs. In the motor nerves this can be proved with ease. In a patient Avho is unable to move the right side of his face at will, owing to an apo- plexy of the left corpus striatum, the nerves of the palsied side retain their irritability for weeks, and all the muscles of that side may be made to contract under the influence of the induced electric current. On the other hand, if the facial be destroyed within the skull after its departure from the brain, its irritability soon becomes extinct, just as though its peripheral branches had been divided, and it is impossible to make the muscles of the palsied side contract by the influence of the induced current. With regard to the sensitive nerves, the proof cannot be made so plain, yet we are warranted in inferring that the conditions are very similar. At all events, in central anesthesia, the trigeminus long remains sensitive, as is proved by the continuance of the power of reflex action, for instance, as is shown in winking wiien the conjunctiva is touched. Etiology.—The nutritive disorder, whereby a nerve is deprived of ANAESTHESIA OF THE CUTANEOUS NERVES. 309 its irritability, is often so subtle in character as to escape our dhect observation. The moment a nerve loses its supply of arterial oxy- genated blood, it loses its functional power. There is no doubt but that this loss of irritability is due to physical or to chemical changes within the nerve. Not unfrequently, in the region of an artery oc- cluded by an embolus or thrombosis, Ave find anesthesia to exist until the collateral circulation has been established. The action of continued cold induces anesthesia of the skin. Part of this is undoubtedly due to the contractile poAver of cold upon the skin, and to the anemia of the cutaneous nerves thus produced. Of the anesthesie of peripheral origin—that is, depending upon extinguished irritability of periph- % eral nerves, Avithout appreciable alteration of then structure—there is the so-called rheumatic anesthesia, which not unfrequently takes place after exposure to cold, as well as a form which Romberg has noticed in the hands and forearms of Avasherwomen. It is doubtful whether the anesthesia arising from lead-poisoning be due to impalpable nutri- tive lesion of the peripheral nerves, or to a morbid state of the central organs. This is also true of the locally anesthetic action imputed to ether and chloroform. It does not seem to me to be proved that the action of these substances is purely local, when locally applied; and I think it more likely that their influence is more or less centric at such times, if not entirely so. Can Ave expect to find a perfect anesthetic action from such agents, the cerebral function remaining intact mean- time ? It bears a peculiar relation to hysterical anesthesia, of Avhich we shall treat in our chapter upon hysteria. Anesthesia due to permanent and uniform pressure of an over- tight bandage or piece of clothing, constitutes a connecting link with those forms of anesthesia where structural lesion of the peripheral nerves is not merely a matter of supposition, but can be absolutely demonstrated. In such cases we find all the tissues, subjected to pres- sure, to be in a state of atrophy and fatty degeneration, and, of course, the peripheral nerves are by no means exempt. The irritability of a nerve is not unfrequently suspended, and its continuity is finally inter- rupted by the pressure of a tumor, an exudation, or extravasation. In other cases of anesthesia, portions of the nerve are destroyed by in- flammation. It would be. superfluous further to continue the enumera- tion of the structural alterations capable of producing anesthesia, as it would be but a repetition of what Ave have already stated in treat- ing of the etiology of neuralgia. The very causes which, excited mildly, or for a short time, serve to exalt the excitability of a nerve, have a more pernicious effect should then action be prolonged or intensified, as the nervous excitability is then arrested, or even the nerve itself may be destroyed. 310 DISEASES OF THE PERIPHERAL NERVES. Symptoms and Course.—Anesthesia is either complete or in- complete. In the first case, irritants acting from without, especially pressure and change of temperature, produce no sensation Avhatever. In the second case, though an impression is produced, it is indistinct and inaccurate. Where the anesthesia is incomplete, there is often a numb or muffled sensation. The patient feels as though a foreign body lay betAveen his skin and the object Avhich he actually touches. Henle believes that this state of affairs is due to an extinction of sensibility of the peripheral terminations of the nerves, and a retrocession of the sensibility in the direction of the centre, so that there actually is a layer of passive substance betAveen the nerve and the object touched. Upon this hypothesis, it is very easy to explain Avhy cold, whose im- mediate action is upon the tips of the sensory nerves, should make the skin feel numb and muffled. There is a peculiar form of anesthesia called analgesia. In these cases there is no pain, even under the most intense irritation of the nerve, although the sense of touch is not. im- paired. We have no satisfactory means of accounting for analgesia. With Henle, Ave might suppose it to be a Ioav grade of anesthesia, and might assume that excessive irritation, instead of producing the usual amount of perception, namely pain, merely gives rise to that normally induced by moderate stimulation of the nerve, Avere it not that, under such a condition, moderate irritation should be impercepti- ble, which is not the case in analgesia. The modifications of anes- thesia, knoAvn as partial losses of sensation, are still more obscure. Here the effect of certain irritants is extinguished, Avhile that of other irritants of no greater poAver continues. For instance, there may be a loss of the sense of touch, Avith unimpaired sense of temperature, or conversely. The so-called " law of excentric impression," according to Avhich the excitement of a sensory nerve, even though produced by irritation of its trunk, always produces the impression of an excitement of its peripheral extremity, fully explains why patients often suffer pain in regions which are entirely insensible to external irritation, a phenome- non to which the name of anaesthesia dolorosa has been applied. Anesthesia dolorosa arises, first, in all cases in which a nerve has lost its sensitiveness throughout a certain portion of its length, while, at the same time, a severe irritation is made to act, above this point, upon that portion of the nerve which still remains in connection with the brain. It is easy to see that both of these factors often coexist, as when a tumor presses upon a nerve. Here the tract of nerve, lying between the compressing groAvth and the brain, remains excitable and receptive of lasting impressions, while from the tumor to the periphery ';he nerve has lost its irritability. ANAESTHESIA OF THE CUTANEOUS NERVES. 3H In anesthesia of the muscular nerves, perception of the degree of contraction or relaxation of the muscles is diminished or destroyed. Sometimes such patients are capable of making every motion required of them, but are unable to tell, without the help of Aision, to Avhat ex- tent they have moved. They can hold fast to an object as long as their eyes serve them as "check-lines of motion" (Romberg), but let it fall as soon as their eyes are closed. If anesthesia of the muscular nerves affect the loAver extremities, the patient is often able to move about tolerably well during the day, but in the dark he will stagger about, and is quite unable to walk even a step or tAvo (see chapter on tabes, page 273). Very often anesthesia is complicated Avith derangement of circu- lation and nutrition in the insensible region. The temperature of the part is often depressed several degrees, its function is impahed, and its secretions are diminished. Besides this, there is an increased vul- nerability of the region. A comparatively trifling degree of heat or cold suffices to burn or freeze the part. Wounds and ulcers heal more slowly, or not at all; bed-sores are very apt to form. The epidermis and nails become fissured and liable to scale off; the skin becomes livid, and edema develops in the subcutaneous areolar tissue. This peculiar state of the insensible region is in some degree attributable to the retardation of the circulation, but the cause of this retardation is obscure. From experiments made by Axmann, it seems probable that it is due to an implication of the sympathetic fibres which accompany the spinal nerves. In frogs, whose spinal nerves had been divided be- tween the spinal marrow and the spinal ganglion, Axmann only found anesthesia and pals}r, but no nutritive disorder of the palsied part. If, however, the nerves Avere divided at a point beyond that at which they are joined by the communicating branches of the sympathetic, in addition to tie anesthesia and palsy, there was desquamation of the epidermis, obstruction of the capillary circulation, and edema. If the nerve, Aviiich has been cut off from its central organ, or Avhich has lost its irritability from any other cause, contain both motor and sensory fibres, partial anesthesia and partial palsy are combined. It would almost seem as if a nerve Avhich had lost its irritability could transmit this passive condition through its ganglion to other nerves, just as an excited nerve can communicate its excitement by means of its ganglion-cells to other nerves. It is in this way that we account for the impairment of the sense of taste and smell in anesthesia of the trigeminus, and for the anesthesia of the auditory organs in cases of nervous deafness, as well as for the partial paralysis which sometimes supervenes upon long-continued anesthesia. It is not always easy to distinguish peripheral from central anes- 312 DISEASES OF THE PERIPHERAL NERVES. thesia. We may rely for a diagnosis, in some degree, upon the fol- lowing points: 1. Upon the extension of the anesthesia and its com- plication or non-complication Avith motor palsy. If the anesthesia be confined to one side, and be combined with hemiplegia, it is probably of the cerebral form. If, hoAvever, it extend over the lower half of the body, and be combined with paraplegia, the case is almost always one of disease of the spinal marrow. The coexistence of palsy of the face with facial anesthesia indicates a central cause of disease, while anes- thesia, with normal motion, indicates its peripheral origin. 2. The character of the reflex symptoms are of great importance as a means of distinguishing between the two forms. When the anesthesia is peripheral, the nerve being either separated from the brain, or having lost its power of excitability, no stimulus can be transmitted from it to the motor nerves, and there can be no reflex symptoms; but if the anesthesia be central, that is, if the region of the brain in which we become conscious of impressions be disabled, the route by which the excitement is transmitted from sensory to motor fibres may still re- main quite perfect, and reflex symptoms may readily appear. It is just the same, in cases of circumscribed disease of the spinal mar- roAV, as in spondylarthrocasis, and partial myelitis. On the other hand, in diffuse inflammation, as in tabes dorsualis, reflex symptoms are not apt to be seen. The following is a striking example of the difference of these two conditions. When anesthesia of the conjunc- tiva occurs from apoplexy, the eye may be touched without the pa- tient's perceiving it, and yet he involuntarily closes the eye because a stimulus is transmitted from the sensory fibres of the trigeminus to the motor ones of the facial. But if the anesthesia be dependent upon loss of the ganglion of Gasser, or of the ramus-ophthalmicus, the pa- tient neither feels the touch, nor does he involuntarily close his eye, since transmission of the excitement to the facial has then become im- possible. The course of an anesthesia depends upon the main disease. If a nerve be divided by an incision, sensation is sometimes restored after a while. If, however, a large portion of a nerve have been destroyed, the anesthesia will remain during life. Rheumatic anesthesia, as well as that occasioned by a moderate and uniform pressure over the course of the entire nerve, warrants a better prognosis than the other forms. Treatment.—The treatment of anesthesia is never satisfactory, excepting when it is possible to remove the cause. Sometimes a sur- gical operation is indicated, sometimes a course of antirheumatic treatment. It does not always immediately happen that cessation of the cause is followed by removal of the effect. In such cases sphituous and ethereal embrocations may be used, as well as elec- ANAESTHESIA OF THE TRIGEMINUS. 313 tricity, cold douches, the baths of Gastein, Wildbad, or Pfaffers, and even the disgusting so-called Thierbader. The reestablishment of ex- tinguished sensibility of sensory nerves by such means, however, is a very uncertain matter. CHAPTER XIV. anaesthesia of the trigeminus. Etiology.—According to an explanation given in a previous chap- ter, the same pernicious agents which we have found to be the causes of prosopalgia, when of greater severity or of longer duration, may give rise to anesthesia over the region of the trigeminus. In anaes- thesia of one-half of the face, the Gasserian ganglion of that side has been found compressed, degenerate, or destroyed by a tumor or in- flammatory process. In other cases but one of the three branches has suffered permanent pressure or other injury within the skull, or else in the passage through the sphenoid bone. In still others, Avhich indeed are the most common of all, a few twigs only of the trigeminus have been cut through, or have been destroyed by the pressure or suppura- tion of glands or tumors, or torn during the extraction of teeth (espe- cially the inferior alveolar branch). The favorable course taken by some cases shows that anesthesia of the trigeminus may also proceed from transitory affections of the neurilemma, or of the nerve itself, which probably are due to cold. Symptoms and Course.—When all the fibres of the trigeminus have lost then irritability, it may be assumed that its main trunk or the ganglion of Gasser is degenerated or destroyed. In such cases the face is divided into halves, standing in abrupt contrast Avith one another, the one being sensitive, the other insensible. The various cavities of the face, AAiiose supply of nerves comes from the trigeminal, are in similar condition. Upon the affected side the eye may be touched, the bulb pinched or pricked, the nose irritated with a sharp instrument, with snuff, or with acrid vapors, without the patient's feel- in«- it. If the patient put a glass to his lips, he feels but one side of it, and receives the impression that it is broken. Half of the tongue also is insensible. The sahva Aoavs from the mouth at the affected side, and the remains of food hang to the lips without the patient's being aAvare of it. Upon irritating the conjunctiva, there are none of the reflex movements referred to in the previous chapter. If, how- ever, the eye be exposed to a strong light, reflex action occurs, as irri- tation of the optic nerve transmits its impression to the facial nerve. Not only do the patients fail to wink Avhen the conjunctiva is touched 314 DISEASES OF THE PERIPHERAL NERVES. but they do not sneeze when the nasal mucous membrane of the af- fected side is irritated, since no reflex action upon the respiratory ap- paratus can be set up in this region. Nutritive disorders of the affect- ed side are associated with these symptoms, similar to those which may be provoked artificially in the loAver animals by extirpation of the ganglion of Gasser, such as varicosities of the eye, with ulceration and atrophy, fungous flabbiness of the gums, bleeding from the mouth and nasal cavities, blueness and edema of the cheeks. In contrast to the observed cases of " ageustia," there are a good many others in which the sense of taste remained normal. The sense of smell and of vision often suffers; but hi such cases it is difficult to say what part the disorders of the nasal mucous membrane and bulb above referred to play in producing such impairment of function. If both portio major and portio minor of the trigeminus be destroyed, in addition to the palsy of sensation of one side of the face, there will be palsy of the muscles of mastication upon that side. If the destruction of the gan- glion be caused by the presence of a large tumor or other extensive disease affecting the base of the skull, the function of other cerebral nerves is likewise usually disturbed, especially that of the oculomoto- rius, the facial, the acoustic, and there are ptosis, dilatation of the pupil, palsy of the corresponding side of the face, and deafness of the ear of that side. If but one branch of the trigeminus, instead of the whole nerve, be diseased, the anesthesia is limited to the region of the face which is supplied by that branch; if it be the first branch, to the socket of the eye, the second to the nose, the third to the cavity of the mouth. If the affection be confined to a few tAvigs alone, the insensible parts of the face are still smaller, and the cavities may be normal. An isolated central anesthesia of the trigeminus without, simultane- ous anesthesia of the corresponding half of the body, is one of the greatest of rarities. In a previous chapter Ave have stated the chief means of distinguishing such a case from a peripheral anesthesia. With regard to treatment, we must also refer to what has already been said of the treatment of anesthesia in general. SPASM INVOLVING PARTICULAR PERIPHERAL NERVES. In the folloAving chapter Ave shall treat of the morbid conditions of excitement to which the various motor nerves are subject. Just as ex- citement of a nerve of sensation is evinced by a feeling of pain and by reflex symptoms, so that of a motor nerve is indicated by contraction of the muscle which it supplies. If the motor nerve be acted upon by SPASM OF PERIPHERAL NERVES. 315 a series of morbid impressions in quick succession, the muscular con- traction resulting from the first impression will continue until the second one succeed it. In this way permanent muscular contractions occur which are called tonic spasms. If the nerve be irritated at someAvhat longer intervals, so that the muscle relaxes ere another impression make it contract again, thus causing alternate spasm and relaxation, we speak of clonic spasms. In the healthy subject the motor nerves receive a portion of then stimulus from the grand centre of the will, thus producing the voluntary movements; another portion of it is obtained from parts of the brain, AA'hich, Avhen thrown into excitement, are independent of the action of the will. To this class belong the movements which occur during the painful emotions, and in anger, and Avhich we call outbursts of pain and anger. It is not through our will that Ave contort the face in Aveeping, Avhen we are in grief; we do not voluntarily clinch the fists when angry; these events occur in spite of our will. Finally, in the healthy subject, there is another series of motions Avhich are likeAvise brought about without the action of the will, and even against the will, by the transmission of a centripetal impression to a centrifugal channel. These are called normal reflex movements; and a distinction is made between those induced by a regularly recurring stimulus of moderate intensity, such as the respiratory movement which is called forth by the collection of carbonic acid in the blood, and the act of deglutition which follows upon the introduction of a bolus into the esophagus (these being called automatic movements), and those in- duced by stronger but less frequent impressions, such as sneezing, winking, and the like. The terms cramp, spasm, and hypercinesis, are applied to certain morbid conditions in which excitement of the motor nerves is produced by an irritant of unusual and generally speaking of unknown origin, and entirely independently of the volition, or else to a condition in which the action of an ordinary stimulus calls forth an excitement of extraor- dinary extent and violence in the motor tract. It is impossible in the present state of science to classify spasms according to the kind of irritant which gives rise to the nervous ex- citement, or according to the region in which the irritant operates. Spasms of which we are about to treat are the result of a variety of causes, and often of unknown causes; and although in some instances the affection is confined to the province of a single motor nerve, yet we are not at all certain that it proceeds from dhect irritation of the fibres of that nerve. 316 DISEASES OF THE PERIPHERAL NERVES. CHAPTER XV. SPASM OF THE FACIAL NERVE--MIMIC SPASM OF THE FACE--TIC CONVULSIF. Etiology.—A morbid irritability involving the twigs of the facial nerve which go to the muscles of the face, but which does not involve the fibres running to the stylohyoid and digastric muscles, is called tic convulslf Whenever it is not combined with general convulsions. The cause of this affection of the facial is obscure. Probably the cases of isolated irritation to which alone AAe refer at present are never de- pendent upon lesions of the brain. Nor does the cause of tic convul- sif seem ever to be an irritation of the facial within the skull, or during its passage through the canal of Fallopius. Whenever the morbid excitement of this nerve is due to the action of some noxious influence upon the face itself, such as cold, a contusion, or the pressure of a tumor, it becomes a matter of doubt whether these influences act directly upon the fibres of the facial nerve, or whether their immediate effect is not upon the filaments of the trigeminus, the facial merely becoming irritated by reflex action. Sometimes, too, tic convulsif has been viewed as a reflex neurosis, arising from the irritation of remote organs, such as the rectum in helminthiasis, or the uterus in hysteria. Finally, mental emotion and the imitative instinct are set down among the causes of tic convulsif. The affection seems to be someAvhat more common among men than among women. Symptoms and Course.—In almost all cases of tic convmlsif, but one side of the face is affected; sometimes the spasm is clonic, some- times tonic. Romberg, in a few brief but graphic lines, gives the fol- loAving description of the mimic spasm: " Grimaces occur, either inter- mittent or constant, involving one side of the face, and, more rarely, both sides. In the former case they consist chiefly of elevation or de- pression of the occipito-frontal muscle, corrugation of the eyebroAvs, blinking and closure of the eyelids, tAvitching and snuffling of the ale nasi, and drawing up and down of the corners of the mouth. These attacks set in suddenly, and as suddenly subside, to recur, with equal suddenness, at short intervals. In permanent tonic contraction of the facial muscles, the furrows and hollows in the affected side of the face are deeper; the tip of the nose, the commissure of the lips, and the chin are drawn toward the convulsed side. The muscles feel hard and tense, and so impede motion that the one eye cannot be as completely closed as the other." The patient is unable to prevent or to control these motions at will. As a rule, any individual motion, made volun- tarily, is accompanied by involuntary contractions of other muscles. SPASM OF THE FACIAL NERVE. 317 In the beginning of the disease the affected side of the face is often somewhat painful. Afterward the pain abates, and, as a great rarity, it is followed by incomplete anesthesia. In some cases, instead of all the nerve-fibres of the facial, a few only are involved in the morbid irritability, as the palpebral branch, the malar, or the labial, or, as in a case reported by Romberg, the auricular branch. The affection of the rami palpebrales causes a series of rapid openings and shuttings of the eye—nlctltatlo, or a rigid, violent closure of the lids—blepharospas- mus. The derangement of the buccal and labial branches gives rise to a movement of the lips, upon one or both sides, as if from laughter, the so-called rlsus caninus, or sardonicus. In the case of tic convulsif of the auricular branches, described by Romberg, repeated fits of twitching of the ear set in daily, during which the ears were drawn up and down for fifteen minutes at a time. Sometimes the tic con- vulsif spreads to other nervous trunks, as does the tic douloureux; so that movement is excited in the muscles of mastication, or those in the region of the hypoglossal nerve, and of the accessory of Willis, or of some of the spinal nerves. The course of the disease is usually chronic, and of uncertain dura- tion. Commencing suddenly (or gradually, Avhich is rather more com- mon), it generally continues during the remainder of life. In order not to mistake the tonic form of mimic facial spasm for the distortion of the face arising from hemiplegia, we must observe the unimpaired muscular power of the undistorted side, and the normal behavior of its muscles under the induced current. Moreover, according to Brims, in hemiplegic palsy, upon handling the healthy side of the face, we do not find the smallest trace of permanent contraction of the muscles, and, by stroking and drawing upon the skin of the face, the mouth may be brought into proper position. Treatment.—In recent cases of tic convulsif, a diaphoretic and de- rivative procedure ahArays seems to do good, Avhile, according to my experience, an old case resists all treatment, even the application of electricity. Where the morbid irritation of the facial manifestly is of reflex origin, and if we can tell from which filaments of the trigeminus the disturbance proceeds, division of those tAvigs from the brain by neurotomy is indicated. In two cases reported by Romberg, where the supra-orbital nerve was divided, great benefit was obtained. On the other hand, division of branches of the facial nerve is not advisable, as that procedure gives rise to another deformity scarcely less un- pleasant than the former one, namely, mimic facial palsy. In one ob- stinate case of tic convulsif, subcutaneous incision of the facial muscles has been practised by Dieffenbach, with good result. 318 DISEASES OF THE PERIPHERAL NERVES. CHAPTER XVI. SPASM IN THE REGION OF THE SPINAL ACCESSORY NERVE OF WILLIS. Etiology.—Like the facial, the accessory nerve of Willis is some- times the seat of morbid irritability. The pathogeny and etiology of this condition are as obscure as are those of tic convulsif. Violent twisting of the neck, cold, disease of the cervical vertebre, have been the assigned causes. The nodding spasm, or salaam convulsions, seen in children, particularly at the period of dentition, does not seem to be a genuine affection of the spinal accessory nerve and the cervical nerves. Indeed, from its complications and course, it seems probable that it is symptomatic of cerebral disease, or of an eclampsia. Symptoms and Course.—Morbid excitement of the spinal acces- sory nerve is manifested by spasm, either of a tonic or clonic character, in the muscles supplied by that nerve, the trapezius, and the sterno- cleido-mastoideus. In the former case, in each paroxysm, the head is drawn obliquely downward several times in succession, the occiput approaching the shoulder, and the ear the clavicle. The direction assumed by the head is more forward or backAvard, according as the contractions are greater in the trapezius or sterno-cleido-mastoideus. In the same Avay the shoulder-blades and shoulders are drawn up during the contractions of the trapezius. If the irritation spread to the facial, the face twitches also; if it involve the portio minor of the trigeminus, the jaws are convulsively set. If the cervical nerves be also implicated, the head is twisted, and the arms are thrown into convulsive agitation. Such paroxysms, which are usually accompanied by pain in the muscles or their attachments, usually last but for a second or two. At the outset of the disease the attacks are less frequent; as it advances, they recur oftener; so that as many paroxysms as thirty may occur in a minute, driving the patient almost to desperation (Hasse). They do not come on during sleep. These clonic spasms of the region of the accessory nerve generally develop in a very slow and gradual manner. They rarely cease, but, as a rule, endure through life, without endangering it. The term " salaam convulsion" of children is applied to solitary or periodically-recurring paroxysms of clonic spasm of both sterno- mastoid muscles, whereby the child is made to nod its head incessantly, like a Chinese image. The nodding is very rapid, and sometimes in- creases in rapidity as the attack goes on, making occasionally eighty to a hundred nods a minute. Generally speaking, the muscles of the face, especially the orbicularis palpebrarum, sympathize in the movement. Epilepsy and idiocy develop in some children affected SPASM OF THE SPINAL ACCESSORY NERVE. 319 in this way, while in others it is said to disappear when dentition is complete. Tonic spasm of the accessory nerve of Willis is the cause of the spastic form of torticollis or caput obstipum. The spasm is usually confined to the sterno-cleido-mastoideus, so that the head is inclined forAvard and doAvmvard. The affection occurs more frequently in chil- dren than in adults, and perhaps, too, it sometimes affects the fetus if congenital torticollis be attributable to an intra-uterine fetal tonic spasm of this muscle. Sometimes the tonic spasm is preceded by a brief attack of clonic convulsions; more generally, however, the muscu- lar contraction is of a tonic character from the first. At the com- mencement the disease is apt to be considered of little moment, and, as it is usually attended by pain, is looked upon as of rheumatic char- acter. An embrocation of opodeldoc is ordered for the " stiff neck," or else some other equally harmless prescription. Finally, however, the obstinacy of the attack and its gradual aggravation furnish evi- dence of its more serious nature. The head is drawn more and more to one side, the sterno-mastoid muscle of that side, particularly its sternal portion, stands out like a hard cord, while upon the up- turned side of the neck the skin is stretched and the muscles are not prominent at all. If the disease last long, the face becomes distorted, the hypertrophied muscles drawing their corresponding half of the face downward. In the same way the permanent obliquity of the attitude often leads to curvature of the spine, and to sinking of the thorax of the affected side. Treatment.—Treatment of clonic spasm of the spinal accessory nerve is seldom very successful. It is true that Moritz Meyer, in five sittings, completely cured a soldier affected with tic convulsif and clonic spasm of the neck, by faradizing each one of the contracted mus- cles. The negative results, however, which I myself as well as others have witnessed in the treatment of tic convulsif, by faradization and gahanism, Avould imply that such brilliant cures were exceptional. So, too, the internal use of sulphate of zinc, and of carbonate of iron, and the application of moxas to the back of the neck, Avould seem to have sometimes been of service. Section of nerves has not succeeded, although, in two cases, division of the muscles was successful. In a third case, in Avhich the division of the muscles was practised more than once, no benefit was derived. We can give no rules for the treatment of the salaam convulsion, since the nature of this affection, and especially its etiology, is entirely unknown. The treatment of tonic spasm, which belongs to the prov- ince of orthopedic surgery, can boast of some success in cases which were not of too long standing. 67 320 DISEASES OF THE PERIPHERAL NERVES. CHAPTER XVII. SCRIVENERS' SPASM—MOGIGRAPHIA. Etiology.—The term scriveners' spasm is employed to denote a mor- bid excitement of the motor fibres of the nerves which supply the muscles of the figers, and which renders further writing impossible, by inducing spasmodic contraction of the muscles to which they belong. If such spasms are provoked by other kinds of manipulation, and not by writing, for instance, by shoemaking or by milking, they receive other names, such as " cobblers' " or " milkers' spasm." Numerous as are the hypotheses as to its origin, Ave knoAV nothing positive as to the pathogeny of this disease, Avhich is not at all uncommon, and which often deprives the individual afflicted of his means of subsistence. The theory of Fritz is in some respects satisfactory. He regards it as a reflex neurosis, in which, however, excitement of the motor nerves is not derived from the cutaneous nerves, as in most reflex neuroses, but proceeds from the muscular nerves. The observation that the touch of a feather or paper is not of itself sufficient to excite the cramp, although holding the hand in the attitude of writing, even though it touch neither pen nor paper, will do so, argues in favor of this view. The theory is equally- probable, however, that the morbid irritation is not reflected from the sensory to the motor nerves, but proceeds from transmission of the im- pression of the nerves excited by the will to other motor nerves. Scriveners' cramp would then resemble the convulsive movements of chorea, and stammering, and the movements VArhich disturb the writer Avould have to be regarded as sympathetic movements. With regard to its etiology, it is to be observed that the affection is much more common among men than among women, in whom it has only been observed occasionally. Will it not turn out upon ex- amination that, just as in many other diseases (although perhaps less strikingly so), the apparent difference of tendency to the disease in the two sexes is really due to a difference of habit and occupation ? Wri- ters' cramp is most liable to occur between the ages of thirty and fifty years, that is, during the time of life when occupation is most intense. Professional penmen, clerks, teachers, and merchants are most subject to the affection. Narrow coat-sleeves, which compress the muscles of the arm during writing, an inconvenient attitude, but, above all (since scriveners' spasm has only come into notice since the introduction of steel pens), the use of a hard steel pen seems to favor the devel- opment of the affection. Why the disease should develop under these causes alone is unknown. Symptoms and Course.—The usual precursory signs of writers' SCRIVENERS' SPASM.—MOGIGRAPHIA. 30J_ cramp are a feeling of slight fatigue of the hand, and a sense of inse- curity as if the Avriter must grasp his pen more firmly. Sometimes the affection does not advance beyond this stage. When the disease is fully developed, the muscles of the first three fingers become convulsed during writing, and, in bad cases, upon every attempt to write, some- times the flexor muscles, sometimes the extensors, are the most con- tracted. Various forms of this spasm have been recognized according to the predominance of one or other convulsive movement, such as convulsive flexion of the thumb, jerking of the index-finger, loss of control of the hand, and a form made up from the last tAvo of these varieties. During these spasms the pen is rapidly tAvitchecl up and doAvn, but, instead of regular, distinct letters, it forms grotesque inter- rupted scribbling. The occurrence of the paroxysm is favored by ap- prehensive attention to the subject and fear of its arising. The harder the patient tries to continue his writing, so much the stronger is the spasm, as so much the more is it apt to extend up the forearm and arm. It is usually painless, although sometimes it is attended by a feeling of tension in the arm. The moment the patient suspends his attempt to Avrite, the cramp ceases, and he can execute all other move- ments undisturbed. In a case of this kind, described by Romberg, a nailsmith, as soon as he grasped his hammer and prepared to strike, was seized by painful spasm of the forearm. He was obliged to give up his trade, and afterward become a useful and skilled painter. Wri- ters' spasm is a very obstinate and tedious disorder. Recovery is very rare, and its uniform persistence is hardly ever broken even by a temporary improvement of the symptoms. Some patients, who are ready for any sacrifice in order to be rid of their burdensome disease, and from their anxiety for this means of subsistence, learn to write Avith the left hand. Unfortunately, however, sometimes in such cases the left hand is also attacked by the disease. Treatment.—The treatment of scriveners' spasm is as a rule unsuc- cessful. Experience has shown that very little benefit is to be derived from the long-continued prohibition of writing, and by only alloAving the patient to resume the practice cautiously, and only permitting him to use goose-quills, or by the use of cold douches, sea-baths, and stim- ulating friction. Division of the nerves is of no benefit to the patient, as it causes paralysis of the finger. In one case only has section of the muscles been followed by benefit. In all other instances there was either no improvement at all, or it Avas a merely transient one. In one case of scriveners' spasm, when, without hoping for success, I applied the constant galvanic current in a manner almost rude, I have succeeded in curing the disease, so that the patient, who for years had written Avith the left hand, noAV uses his right once more. The 322 DISEASES OF THE PERIPHERAL NERVES. treatment proposed by Benedikt, by Avhich he has obtained some suc- cess, and which consists in the apphcation of " spinal-root, and spinal nerve-streams," has utterly failed in my hands; and in one or two cases it has aggravated the disease. If the pathogeny of scriveners' spasm be really as I have suggested above, my treatment of it was an entirely rational one, although I myself was not aware of it at the time. I applied the current to the muscle of the thumb and index- finger, and hence to the sensory muscular nerves running into them: thus if the explanation be correct, the cure would be accounted for by an abatement of the morbid nutritive state, and of the morbid exci- tability of the sensory nerves of the muscles, from whose reflex action the cramp proceeds, by the catalytic action of the constant current. Sometimes apparatus, by means of which the patient Avrites Avithout the aid of his fingers, also are of service for a Avhile. CHAPTER XVIII. IDIOPATHIC CRAMP OF THE MUSCLES OF THE EXTREMITIES-- ARTHROGRYPOSIS. Etiology.—According to the example of the French authors, the term idiopathic spasm (spasmes musculaires idiopathiques) is applied to tonic contractions Avhich sometimes attack the muscles of the ex- tremities, Avithout being attributable to disease of the brain or spinal marroAV. They are analogous to the neuralgias, but we are still less able to point out the anatomical cause of this morbid condition of the motor nerve, causing idiopathic muscular spasm, than to discover that winch acts upon the sensory nerves in neuralgia. The harmless course usually taken by the disease makes it probable that idiopathic cramps of the extremities are due to trifling and transient lesions of the nerves and their sheaths. By many observers, these affections are regarded as a form of rheumatism, and are attributed to hyperemia and edema of the neurilemma. In some cases, this may be the truth, especially in such as occur in children previously healthy. However, the occurrence of idiopathic muscular spasm during the course of and convalescence from acute and chronic disorders, which have an exceed- ingly pernicious effect upon the assimilation and nutrition of the body, and which often lead to great functional disturbance, such as typhus, intermittent, Bright's disease, and epidemic diphtheritis, makes it quite probable that in other instances idiopathic muscular cramps are the result of derangement of the tissues, the character of Avhich is almost unknown, and which develops during the diseases above men- tioned, giving rise to a great variety of functional disturbance. The muscular spasms which arise during pregnancy, during laboi IDIOPATHIC CRAMP. 323 and after it, must be regarded as of this character. The affection is most common during childhood, especially the primitive form in- duced by cold. The statement of Valleix, that the disease is so rare, that few physicians ever see it, strikes me as strange, as not only have I myself observed a great number of such cases, but I Avell remember that Krukenberg used to describe it as a by no means uncommon form of rheumatism among children. Symptoms and Course.—Sometimes the disease is preceded by a feeling of illness, languor, and depression of several days' duration. The actual commencement of the disease is marked by pain, which apparently shoots along the courses of the nerves, sometimes involving the upper and lower extremities simultaneously, sometimes only the hands and forearms, sometimes the feet and legs. In addition to this, there is a sense of formication, and of stiffness and sluggishness in the suffering members. These symptoms having lasted for a variable period of time, fugitive cramps, in the calves of the legs and other muscles, set in, which soon are converted into continued tonic contrac- tions. The upper extremities are usually brought into a state of per- manent flexion, the lower into permanent extension. If we are unac- quainted with the malady, and see a child thus affected for the first time, we shall be deeply impressed by the aspect of the rigid immov- able limbs, the extended knees, the heels drawn up, the thumbs forced into the palms of the hands, and shall be inclined to ascribe it to some serious lesion of a central organ. The attempt to extend the upper extremity or to flex the lower is extremely painful to the patient. The contracted muscles are hard and prominent. Generally the joints seem somewhat swollen by a slight edema of the skin. Sometimes the tonic contractions extend to the muscles of the back and belly, and even to those of mastication and to those of the face. The affec- tion is either enthely free from fever or else the fever is of but little intensity. In some patients the commencement of the contraction is accompanied by a sensation of oppression and of rush of blood to the head. In many instances the course of the disease is brief; the con- tractions ceasing after a lapse of a few days, and free mobility becom- ing reestablished. In other instances it is more protracted. Some- times, too, relapses occur after some days or even some Aveeks have passed. Certain observers, as Delpeche and Hasse, state that the dis- ease consists of a series of spasmodic attacks, that these paroxysms last for some minutes, some hours, or a day or more, and that in the inter- vening period there is merely a certain degree of stiffness and swelling of the limbs, accompanied, perhaps, by anesthesia of the skin and mus- cles. In the cases which I have had opportunity to observe, no such paroxysms and intervals Avere discoverable. 324 DISEASES OF THE PERIPHERAL NERVES. Treatment.—The course of the disease, which usually is favorable, renders active therapeutic interference superfluous. Krukenberg used to recommend fumigation with juniper-berries. The pain in the limbs and the contractions of the muscles certainly subside quite as soon under this simple treatment as under the use of other stimulating and antispasmodic embrocations, and by the internal use of remedies for convulsions, such as flores zinci, henbane, opium, and the like. If the idiopathic muscular spasm be the effect of some grave general disease, the case is different. The spasms do not then cease until the normal assimilation and nutrition have once more become reestablished; and treatment must be regulated accordingly. CHAPTER XIX. PERIPHERAL PALSY. The term palsy—acinesis—of the province of the cerebro-spinal nerves is applied to a morbid condition, in which the motor fibres are no longer acted upon by volition, so that the muscles cannot be made to contract at will. Derangements of the voluntary motion having another origin, especially those caused by disease of the bones and joints, are not counted as palsy. Myopathic palsy shall be treated of hereafter. In treating of disease of the brain, we have already described that class of paralysis proceeding from destruction or derangement of the grand centre of volition, whereby the motor impulse to the peripheral nerves is arrested. Under the same heading, also, we have treated of those palsies due to general derangement of the cerebral circulation and nutrition, in Avhich, the entire mental function having become arrest- ed, no impression is made, and no voluntary motion can take place. Besides this, in a previous chapter, we have already considered the subject of paralysis arising from destruction of the fibres of the spinal marroAV, through which the impulse from the seat of volition is con- veyed to the motor nerves. The present section is exclusively devoted to the variety of palsy arising either from separation of the peripheral nerves from the brain or spinal marrow, or from a loss of irritabihty on the part of these nerves owing to alteration in their structure. Etiology.—Separation of motor nerves from the central organs is not unfrequently the result of injury, and in this class belong the cases of section of nerves by a surgical operation, and by wounds of other kinds. In other instances the disturbance of continuity depends upon the extension of an ulceration or other destructive process to a neigh- boring nerve. The destruction of the facial nerve, during its course PERIPHERAL PALSY. 325 througn the canal of Fallopius in caries of the petrous bone, may be regarded as a prototype of this variety. A peripheral end of a nerve may also be separated from its central organ by the continued pressure of a tumor, an aneurism, or an exostosis which gradually consumes it. Sometimes even a temporary pressure upon a nerve has the same ef- fect, Avhich is probably owing to the continuity of the nerve's having become broken at the compressed point. Thus Hasse has seen a mo- tor palsy of the arm Avhich proved refractory to all treatment, in a per- son who had slept some time with his arm resting over the back of a chair. In very rare cases the disturbance of continuity of the nerve is due to a primary partial neuritis. The structural changes whereby the motor nerves lose then excita- bility, without undergoing solution of continuity, are as unknown as are those which destroy the function of the sensory nerves. Thus cutting off the supply of arterial blood Avill arrest the hritability of the motor nerves without producing in them any structural alteration. It is probable, although not proved, that rheumatic palsy is due to hyper- emia and edema of the neurilemma, causing compression of the nerve- fibres. Physiological experiment Avarrants the supposition that the paralysis, Avhich sometimes arises after violent attacks of cramp, is the result of over-exertion ; but a nerve which has lost its excitability through undue exertion does not differ appreciably from an excitable nerve. It is the same in case of a paralysis arising in consequence of a moderate pressure or strain. Here, from its favorable course, Ave must attribute the palsy to a diminution of the irritability of the nerve, and not to its destruction. Finally, the structural changes of the nerves are unknown, which give rise to the paralysis of lead-poison- ing and of miasmatic poisoning, as well as in the so-called essential palsies. (See Chapter XXI.) Although hysterical palsy has not been counted either among the cerebral diseases or among those of the spinal marrow, it probably does not belong to the class of peripheral paralyses, but rather de- pends upon some impalpable anatomical abnormity of the centre of volition, as we shall explain more in detail Avhen treating of hysteria. Symptoms and Course.—Complete separation of a nerve from its central organ renders the muscles which it supplies incapable of motion, producing complete palsy or paralysis. Textural changes, which absolutely destroy the hritability of the nerve, have the same effect. When the nervous irritability is merely diminished, but not annihilated, feeble contractions still remain possible. This condition is called incomplete palsy or paresis. A paralysis or paresis of peripheral origin is usually distinguishable from a central palsy: 1. By its extent. As we have seen, the charac- 326 DISEASES OF THE PERIPHERAL NERVES. teristic forms of cerebral and spinal palsy are hemiplegia and paraple- gia, Avhile a palsy limited to the range of influence of some particular nerve is an almost pathognomonic symptom of peripheral paralysis. It is only as a symptom of incipient sclerosis, and in rare instances, that the power of volition is suspended in single nerves owing to dis- ease of the brain, or that the connection between the spinal marrow and any particular nerve is broken. The converse of this proposition is not true, hoAvever, as there are many peripheral palsies which in- volve large numbers of nerves. Even in such cases, however, the mode of extension of the malady often reveals its source. When a tumor of the brain causes palsy of the region supplied by the various cerebral nerves, the palsy does not arise in all of the nerves simulta- neously, but extends gradually from one to another as the tumor grows. I shall mention one case observed in the GreifsAvalder clinic, as a striking example of hoAV extension of the palsy may be of great importance as a means of distinction between spinal and peripheral paralysis due to caries of the vertebre. The patient suffered from caries of the vertebre, and his upper extremities were in a state of al- most complete paralysis Avith anesthesia, while the mobility and sen- sation of the loAver limbs was quite normal. From the manner in which this palsy had developed, it could be decidedly inferred that it was the nervous trunks of the brachial plexus which Avere affected by the vertebral disease, and not the spinal marrow. Rheumatic palsy, which likewise not unfrequently affects a large number of nerves, does not present any peculiarity with regard to its manner of extension, and for a differential diagnosis we can only avail ourselves of the fact that it is not apt to assume the form of hemiplegia or paraplegia. On the other hand, the mode of development of lead-palsy is very charac- teristic, so that from it alone the real nature of the disease may be de- termined, and other forms of peripheral palsy, as well as the central palsies, may be excluded from the diagnosis. Lead-poisoning always affects the upper extremities first, attacking the extensors of the fin- gers, hands, and arms in succession, while the flexors remain quite free from disease. 2. If, from the outset of an attack of palsy, there have never been any derangements of the cerebral function, the origin of the disease is, in all probability, peripheral. The converse of this proposition also does not hold good; for a paralysis may be combined Avith serious cerebral disorder, and the paralysis may still be a peripheral one. Ample proof of this condition is given in cases of tumors at the base of the brain. 3. When the affected nerve is a nerve of mixed function, the com- plication of palsy with anesthesia of the region known to be supphed PERIPHERAL PALSY. 327 by its sensory fibres, is an important criterion of the peripheral origin of the disease. 4. The absence of reflex and sympathetic movements in the region of the palsied nerve is of similar import. If the continuance of the normal sensibility informs us that the function of the sensory nerves of a part is still preserved, and that its connection Avith the brain re- mains intact; and if, nevertheless, no reflex signs arise Avhen the sen- sory nerves are irritated, there can remain no doubt that an interrup- tion exists in the motor nerves, and hence that the palsy is peripheral. For instance, if a patient be unable to close his eye at will, and do not even wink when the bulb is touched, although the sensibility of the conjunctiva be normal, the palsy is certainly peripheral. The re- verse of this condition is a still better proof of the central origin of a palsy. If a patient be unable voluntarily to bring a certain nerve into excitement, and, hence, unable to contract the muscles supplied by that nerve (for instance, if he cannot close the eye when told to do so; and, on the other hand, if the nerve be excited, and all its muscles made to contract if a sensory nerve be irritated, as when Ave touch the conjunctiva with the finger), Ave have to do with a central palsy. In such a case the irritability of the motor and sensory fibres is perfect, as is also the path by which the impression is conveyed from the cen- tripetal to the centrifugal nerves; but the centre of A*olition in the brain, or the channel through which the influence of the Avill is im- parted to motor nerves, is destroyed. 5. Finally, the early extinction of electric contractility in a nerve— that is, the absence of contractility of its muscles upon application of the induced current—is an important sign that the paralysis is of peripheral origin. The induction apparatus, the exaggerated and in- discriminate employment of Avhich, for therapeutic purposes, should be discouraged, deserves a much greater employment as a means of diag- nosis, especially in private practice, than it has obtained hitherto. In recent cases of peripheral palsy, Avhich come under our notice tolerably often in private practice, and where, owing to the greater prospect of successful treatment, it is of peculiar importance to know whether the disease be of peripheral or central origin, examination with the induced current will decide the matter almost with certainty. In many cases of peripheral palsy, the electric contractility of the mus- cles sinks to a minimum, even within a few days after the occurrence of the palsy, and soon afterward ceases entirely. In cerebral paralysis it is quite otherwise. There the electric contractility often continues unimpaired for months. Hemiplegic patients, indeed, are apt to be much impressed when the faradizer, by application of the electrodes, readily causes contraction of muscles, which for months have been be 328 DISEASES OF THE PERIPHERAL NERVES. yond the poAver of then will, and they spare neither time nor money in order to subject themselves to a treatment in winch—ineffectual though it be—they place the utmost confidence. The degeneration of peripheral nerves, Avhich soon follows upon then separation from the central organs, and which we are able to demonstrate anatomically, accounts, in some measure, for the early extinction of electric contrac- tility in peripheral palsy. Nor, for the same reason, should we Avonder that it soon ceases in rheumatic palsy, and in cases of lead-poisoning. No matter how slight the disease from which the nerve suffers in such a case, it Avill always suffice to bring about in it such a change that neither the will nor the application of the induced current is capable of producing excitement in it. In cerebral palsy, also, a degeneration of the peripheral nerve finally sets in, as well as an atrophy and fatty- degeneration of the unemployed muscles. Hence, in very old cases, loss of electric contractility can no longer be made use of as a means of distinction between central and peripheral palsy. In spinal palsy the electric contractility is sometimes long retained, Avhile at other times it speedily ceases. Hence, it is of little worth in a diagnostic point of view. I believe that these differences may be accounted for, in some degree, from the results of the investigations of the structure of the spinal marrow by Schroeder van der Kolk. Where centrifugal fibres exist in the spinal marrow, which, instead of passing to the pe- ripheral nerves, first go to the ganglion-cells from which the peripheral nerves spring, it would seem (arguing from analogy) that, upon de- struction of this first set of fibres, a similar condition, as regards the electric contractility, exists, as obtains in cerebral palsy, Avhile, upon destruction of the fibres proceeding from the ganglion-cells, the condi- tion is analogous to that of a peripheral paralysis. It is remarkable that, in many cases of peripheral palsy, the muscles can be made to contract, by means of the constant current, while the induced current will fail of effect, and, still more strange, that streams so feeble as to excite no contraction upon the unaffected side will induce it upon the paralyzed side. We have no satisfactory explanation of this circum- stance, which I have met with in two cases of rheumatic palsy in the course of a single semester. One thing, however, may be deduced from our previous remarks: that the character of the hritation pro- duced in a nerve by the constant current, Avith its catalytic action, is essentially different from that caused by the induced current. Separation of a motor nerve from the central organs and the ex- tinction of its irritability induce the same derangements of circulation and of nutrition Avhich we have described while treating of the pe- ripheral anesthesias, and such derangements are particularly severe in cases Avhere anesthesia and acinesis exist together. Lowering of the PERIPHERAL PALSY. 329 temperature in paralyzed regions depends upon a retardation of the circulation. The quicker neAV blood reaches the peripheral region. which is constantly giving off heat, so much the less readily does it become cooled. On the other hand, the slower new warm blood enters the part, so much the sooner will its temperature assimilate itself to that of the surrounding region. Retardation of the circulation seems to me to be dependent upon a contraction of the arteries; at all events, the pulse is often smaller upon the palsied side than upon the sound one. We are as yet unable to account for this narroAving of the artery upon the paralyzed side. When a palsied part becomes inflamed, an elevation of its temperature is observed in it, instead of a depression. We do not attempt to decide whether the incomplete anesthesia, which usually develops by degrees in palsied parts (even where origi- nally the disease has been a motor paralysis), depends upon retarda- tion of the circulation, or Avhether it is to be ascribed to a transmission of the passive condition, through the ganglion-cells, from the motor to the sensory fibres. The course of peripheral palsy exhibits great variety, according to the cause which produces it. Where a nerve has been cut through, the interrupted connection not unfrequently becomes restored, and the palsy gradually and completely disappears. If, hoAvever, a large por- tion of a nerve be destroyed, the palsy remains stationary throughout life. The progress of rheumatic palsy usually is favorable, and it gen- erally terminates in complete recovery. This is also the case with the exhaustion of irritability resulting from convulsions, and from the in- complete traumatic palsy caused by slight injuries. The paralysis winch sometimes remains after recovery from typhus also admits of faverable prognosis, while that arising from lead-poisoning is exceed- ingly intractable, and often proves incurable. Treatment.—The fulfilment of the causal indication in peripheral palsy is but rarely possible, and even then is seldom folloAved by bene- ficial results. Thus the extirpation of a tumor, Avhich has caused pa- ralysis by pressure upon a nerve, scarcely eAer restores normal motion of the part. Rheumatic paralysis forms an exception to this rule, when not of too long standing, as a proper treatment of the primitive disease in such cases often furnishes the best results. HoAvever, this is not to be anticipated from the use of those very uncertain remedies, colchi- cum, quina, and aconite, but rather from the methodical employment of Avarm baths. Every year troops of paralytic patients, curable and incurable, croAvd to Toplitz, Wiesbaden, Wildbad, or Pfaffers. The reputation which these Avatering-places enjoy, especially in the treat- ment of palsy, is mainly due to their really surprising efficacy in rheu- 330 DISEASES OF THE PERIPHERAL NERVES. matic paralysis. As corroborants of the bath-treatment, but only in cases Avhere, OAving to unfavorable circumstances, bathing is impracti- cable Ave recommend the apphcation of stimulants to the skin, apphed along the course of the affected nerve. The usual prescription of an embrocation of aromatic tinctures, which irritate the nose more than the skin, should be set aside in favor of rubefacients and issues. Of the remedies called for by the indication from the disease itself, the application of the constant electric current is that winch deserves our greatest reliance. We have already expressed our opinion that cures effected by the constant current probably depended solely upon its catalytic action, and that, by means of the galvanic treatment, it is in our power greatly to modify the circulation, the process of endos- mosis, and nutrition itself, even in tissues lying deep beneath the skin. The induced current does not have this effect, and we have seen many cases of peripheral palsy, which had been treated unsuccessfully by the induced current, healed when the constant stream Avas apphed. This is especially the case with the rheumatic and traumatic palsies, and those induced by lead and other poisons. The symptomatic indication demands: 1. That we should preserve what remains of irritability in a partially paralyzed nerve, and avert, if possible, its complete extinction. 2. That we should prevent atrophy and fatty degeneration of the palsied muscles, or check them where they have already begun. Both complete extinction of the already reduced irritability, and the atrophy and degeneration of the palsied muscles, are mainly due to continued rest, and to lack of excitement, which thus constitute a new factor, whereby a palsy, dependent upon other causes, is rendered more severe and intractable. It may even furnish the sole reason why a paralysis merely improves sometimes, without disappear- hio- entirely. For the prevention of such a mishap, localized faradiza- tion is an invaluable remedy. It is an important rule, in its employ- ment, not to protract the sittings too much, and not to employ too strong a current. Since we know that the excitabihty of a nerve is quite as liable to impairment or destruction from too much exertion as from too much rest, this rule needs no comment. It is equally evident that, in traumatic, rheumatic, and toxic palsy, the induced current is not to be employed before the disturbance of continuity has been al- layed, and the excitabihty of the affected nerve has begun to return; or, in other words, that the current is not to be applied until we find that the muscles begin to contract under its influence. It is very de- sirable that every physician should make himself so familiar with fara- dization localizee that he need not leave its employment to some one else. The labors of Zlemssen have rendered this task quite an easy one. A few days of practice upon the healthy subject, under the in- BELL'S PALSY OF THE FACIAL NERVE. 331 structive guidance of this book, suffices to impart the degree of skill requisite to impress the uninitiated. The curative effect of strychnine upon peripheral palsy may be placed by the side of that of the induced current. Nor does strych- nine at all tend to promote the union of divided nerves, nor repah the structural changes wiiich have caused the palsy. On the other hand, it is probable that this drug, by exciting reflex action in the spinal column, and through the augmented reflex excitement thereby induced in the motor nerves, may stimulate the hritability of the latter, where it is not already completely extinguished. In order to obtain results from strychnine, doses must be given of sufficient size, and must be kept up long enough to produce visible effect upon the reflex action of the spinal marroAV—that is, until slight twitching is induced. We prescribe either the alcoholic extract of nux vomica, one-third of a grain, gradually increasing up to two grains, or the nitrate of strych- nine, in dose from the twelfth to the fourth of a grain. Other medica- ments, such as arnica and rhus toxicodendri, scarcely have any effect upon peripheral palsy. CHAPTER XX. PALSY OF THE FACIAL NERVE--MIMIC FACIAL PALSY--BELL'S PALSY. Etiology.—In the coming chapter we leaAe unnoticed the variety of facial palsy arising from suspended volition, Avhich is almost ahvays accompanied by hemiplegia, and constitutes a common symptom of apoplexy, and of other diseases of the brain. The irritability of the facial, or of its attachment to the brain, may be impaired: 1. By causes which act upon it prior to its entrance into the internal auditory meatus. 2. By such as affect it during its course through the petrous bone. 3. By agents Avhich involve the peripheral ramifications upon the face. Within the cranium the facial nerve is most frequently compressed or destrojed by cerebral tumors springing from the base of the skull, or which have advanced toward its base. More rarely it proceeds from exudation, from thickening of the dura mater, or from exostoses. In the canal of Fallopius the nerve is more fre- quently destroyed by caries of the petrous bone, although one or two cases have been observed in which fractures and gunshot weunds have caused injury of the facial within the petrous bone. The peripheral branch es are sometimes cut, either by accident or intentionally, during surgical operations. Thus it was with the coachman Avho Avas so thankful to Bell for the successful extirpation of a tumor about his ear, but who complained that since the operation he could no longer whistle to his horses. The continuous pressure which the ramifications 332 DISEASES OF THE PERIPHERAL NERVES. sometimes are subjected to by enlarged lymphatic glands, or other tumors, as well as contusions and concussions, resulting from blows upon the ear, may give rise to facial palsy. It is not unfrequently ob- served in newly-born children, when branches of the nerve have been bruised by the forceps during labor. Sudden chilling of a warm face, however, is a much more common source of facial palsy than any other agent. Many patients acquire it by looking out of the window imme- diately after rising in the morning. Halla attributes the increasing frequence of facial paralysis to the railroads. People hurry to the station, arrive there warm, enter the carriage, and expose their face to the draught of the window. The result is a palsy of the face. The affection is a someAvhat common one, so that J. Frank has seen twenty-two cases of it in the course of fifteen years. Statistics as to its frequence at various ages, and in different sexes, and different sides of the face, have not led to any important conclusions. If it be true that the affection is more common upon the left side of the face, it is not on account of any predisposition of the left facial nerve, but because of the greater exposure of the left cheek to blows on the ear, and to other injuries. Symptoms and Course.—The symptoms of facial palsy consist in an immobility and relaxation of the facial muscles, which are supplied by the affected nerve-fibres. Palsy of the frontal muscle, and of the eorrugator supercilii, makes it impossible to wrinkle the forehead. Bomberg says: " The old man's forehead becomes as smooth as that of a child, and there is no better cosmetic for old women." Palsy of the orbicularis palpebrarum prevents the patients from shutting the eye completely. If told to do so, they loAver the lid a little, by relaxing the levator palpebre superioris, over which they still have control, and roll the bulb upward, so as to hide the cornea. The tears are no longer conducted to the lachrymal puncta, but flow down over the cheek. The eye, being imperfectly closed, and exposed to all manner of inju- ries, readily inflames. The levator labii superioris, aleque nasi, the levator anguli oris, and the zygomaticus, are unable to draAv up the upper lip, nose, or commissure of the mouth, and to dilate the nostril. The buccinator being disabled, the cheek puffs out during expiration, like a loose sail. Some of the purposes for which the facial muscles are employed, the pronunciation of the labial letters, Avhistling, blow- ing, and expectorating, now fail. Even in chewing, which process, being independent of the facial, goes on undisturbed, the morsel, when on the affected side of the mouth, often falls between the teeth and the cheek, and has to be disengaged thence by the fingers. When the paralysis involves the whole of one side, there is a remarkable dis- tortion of the countenance with every play of expression. This arises BELL'S PALSY OF THE FACIAL NERVE. 333 partly from the fact that muscular contractions only occur on the sound side, while the other remains motionless, and partly because the con- tracting muscles upon the sound half of the face are not counterbal- anced by the palsied half, so that the countenance is drawn to one side. Even during rest the face remains more or less distorted and unsym- metrical. The palsied angle of the mouth is lower than the healthy one, the nostril is narroAver, and all the pits and depressions are ef- faced. The point of the nose and the mouth are drawn over toward the sound half of the face. All this deformity is due to the Avant of balance betAveen the healthy muscles of one half the face and their palsied antagonists. In the same way there is lagophthalmos of the affected side, from a preponderance of the unpalsied levator palpebre superioris over its palsied antagonist, the orbicularis palpebrarum. When paralysis of the facial is bilateral, the face becomes void of all expression, and the patient laughs and weeps Avithout exhibiting any play of countenance. I have never seen such a case myself, but can easily beheve that the aspect of a person whose face remains motion- less, even while he is laughing loudly, Avill present the hideous appear- ance of a mask. The impairment of the sense of taste, the distortion of the uvula, and deviation of the tongue, though less obvious symp- toms, are equally constant. It is uncertain whether the obtuseness of the sense of taste depends upon diminution of the secretion of sahva, and consequent dryness of the mouth, or whether the chorda tympani nerve, by erecting the papilla of the tongue, aids the gustatory sense. Displacement of the uvula to the sound side is accounted for by the fact that the motor nerve-fibres, passing through the nervus petrosus superficialis major to the sphenopalatine ganglion, from which the de- scending palatine branches proceed, only contract the muscles of the uvula upon the side which is not palsied. This explanation, however, is not absolutely satisfactory. Regarding the deviation of the tongue, avc refer to Avhat Ave have already said while treating of apoplexy, as this symptom is of more common occurrence in cerebral than in peripheral paralysis. In a pre- vious chapter Ave have given a detailed explanation of why the reflex motion should be impossible in complete peripheral palsy of the facial, and why the electric contractility of the muscles of the face soon be- comes extinct. In recent and uncomplicated cases, the sensibility of the paralyzed half of the face is normal. When of longer standing, it generally becomes somewhat blunted, probably in consequence of nutritive disorder of the region supplied by the affected nerve. This shows itself chiefly through emaciation and flabbiness of the palsied part of the face, by the disappearance of the fat, and by the shrivelled condition of the skin. 334 DISEASES OF THE PERIPHERAL NERVES. According to Bomberg, the following are the signs whereby we may recognize Avhether the source of the paralysis is to be sought Avithin the cranium, in the petrous bone, or upon the face itself: 1. We may infer that the affection originates in disease at the base of the skull, when there is participation of other cerebral nerves in the palsy, as shown by squinting, deafness, anesthesia, etc., as well as by the simultaneous occurrence of palsy of the extremities of the other side of the body. 2. Evidence that the palsy originates in a disease or destruction of the facial nerve within the canal of Fallopius con- sists in long-standing otorrhea, hardness of hearing or complete deaf- ness, obliquity of the uvula, dryness of the mouth, perversion of the sense of taste, which depends upon implication of the nervus petrosus superficialis minor and chorda tympani, which are never affected except in this form of the disease. 3. We know that the palsy proceeds from the peripheral ramifications, when the disease is plainly dependent upon exposure to cold, or upon some violence done to the face, or upon the pressure of a tumor upon the facial nerve, especially in the region of the stylo-mastoid foramen, the ear itself meantime being sound, the taste normal, and the uvula straight. The course of facial palsy varies greatly, according to the seat and nature of its cause. Where the nerve has been destroyed by a tumor at the base of the skull, or by caries of the petrous bone, the palsy is, of course, incurable, as is also the case when a tumor has broken the continuity of the nerve by continued pressure upon its peripheral branches. When the affection proceeds from exposure to cold, or from slight injuries, the prognosis is better. This is especially true of the congenital palsy induced by pressure of the obstetric forceps. But, even in adults, it by no means invariably happens that traumatic or rheumatic paralysis disappears in the course of a few weeks or months. Treatment.—From what has been stated regarding the prognosis of facial palsy, the rheumatic and traumatic forms of the complaint are the only ones susceptible of treatment. Although they usually recover without interference, it is better, in recent cases of traumatic origin, to employ local antiphlogistics. Whenever an adult has a palsy of one side of the face, caused by a blow or shock, we should prescribe leeches and cold compresses, and should rub the part with mercurial ointment. Congenital paralysis, also, when of traumatic origin, may be left alone. When the disease arises from cold, and is recent, the affected side of the face is to be covered with well-Avruno- cold compresses, covered Avith oil-silk or india-rubber cloth, which are not to be changed until after the lapse of several hours. The face may also be enveloped in cotton wool, and a vapor-bath may be taken. At a later period stronger irritants may be used: lotions of essence of PALSY OF THE SERRATUS MUSCLE. 335 mustard, mustard-plasters, embrocations of croton-oil, blisters, etc. A great number of cases are on record in which rheumatic facial palsy has been cured by the application of the constant galvanic current. In two cases, I myself have succeeded in effecting a cure, although but a gradual one, by employment of galvanism. In each of these cases, treatment by the induced current remained without effect. Where the electric contractility can be reestablished by localized faradization, the cure will be promoted and hastened by the methodical use of the induced current. CHAPTER XXI. PALSY OF THE SERRATUS MUSCLE. Etiology.—In rare instances, two of which have come under my personal observation, palsy of the serratus has formed part of a myo- pathic paralysis, involving many of the muscles, the result of the so- called progressive muscular atrophy (see appropriate chapter). The affection is much more commonly confined to the serratus alone. This fact, and the circumstance that the long thoracic nerve is not distrib- uted to any other muscle except to the serratus anticus magnus, would imply that most cases of palsy of the serratus are neither of cerebral nor of myopathic Origin. We have laid it down as an important sign. of the peripheral nature of a palsy, that the affection involves the re- gion supplied by some particular nerve, and while neighboring muscles supplied by other nerves remain sound. Besides this is the well-known fact that peripheral palsy and peripheral neuroses by preference affect the region supplied by nerves Avhich pass through long, narrow chan- nels and holes, like the long thoracic, which runs through the scalenus medius. This very important point in the pathogeny of palsy of the serratus, and the proof of the fact that, in most of such cases, Ave have to deal with a peripheral neuropathic affection, have not hitherto ob- tained the notice which they deserve. The exciting causes of palsy of the serratus are usually obscure. It is plain that the long thoracic nerve, in its passage through the scalenus medius, may suffer injuries which escape our attention. In some instances, over-exertion of the upper extremities, or cold, has been the assigned cause. In one observation, reported by Neuschler, the palsy of the serratus was preceded by a fall, and a tumor afterward formed in the neck, which the physician in charge proposed to open by incision. In one very interesting case, which came under my own ob- servation, a carpenter, Avho used to carry the heavy beams for build- ings upon his right shoulder, had to employ the left shoulder instead, G8 336 DISEASES OF THE PERIPHERAL NERVES. on account of the development of a palsy of the right serratus muscle. Some time afterward, palsy of the left serratus also began to appear. Symptoms and Course.—Palsy of the serratus muscle is easy of recognition, as the absence of its function and the undue action of its antagonistic muscles occasion characteristic deformities and disorders of motion. The function of the serratus is to press the scapula against the thoracic Avail, and to draw its lower angle downward and outward. The serratus is especially required in the act of elevating the arms above a horizontal line, as it then draws the lower angle of the scapula outward, and turns the glenoid cavity of the joint upward. It is by this act alone, and not by the contraction of the deltoid, that we are enabled to lift the arm above the shoulder. When the serratus is paralyzed, the inner border of the scapula, and particularly its lower angle, instead of lying against the chest, stands up like a wing, draw- ing up a three-cornered fold of skin before it, and admitting of our reaching deeply into the subscapular fossa. At the same time, the lower edge of the scapula stands up too high, and too far inward. The antagonistic muscles, the trapezius and the levator scapule, haAe drawn the superior angle upward, and the weight of the arm and the pectoralis minor have depressed the external angle, and thrown it for- ward. The patient is unable to lift his arm above a horizontal line, and is thus rendered extremely awkward. Any one, who has often watched a patient with this affection put on or take off his coat or shirt, will be able to make a diagnosis in the next case he meets with, from these acts alone. If we press the inferior angle of the scapula against the chest, and, at the same time, push it in, the patient is once more enabled to lift his arm above his shoulder without difficulty. Palsy of the serratus is an obstinate complaint. In none of the cases which I have seen was a complete cure effected. In many in- stances, however, the patients so far improved as to be able to do easy work. Treatment.—The most commendable remedy, in recent palsy of the serratus, is local blood-letting and derivation to the skin, applied over the point where the long thoracic nerve passes through the sca- lenus medius. In chronic cases, according to our present experience, faradization does not promise much benefit. On the other hand, the constant current is strongly to be recommended. Unfortunately, how- ever, hitherto I have had but one opportunity of applying it. The cures obtained by means of the constant current, in cases of peripheral facial palsy, which I consider to be quite analogous with palsy of the serratus, urgently demand the treatment of the latter by galvanism. CHAPTER XXII. PROGRESSIVE PALSY OF THE CEREBRAL NERVES--PROGRESSIVE PALSY OF THE TONGUE, VELUM-PALATI, AND LIPS--GLOSS OLARYNGEAL PALSY. A series of observations have recently been made, particularly by French writers, of a paralysis, which, commencing at the hps, extends successively to the tongue, palate, pharynx, and sometimes to the muscles of the glottis, more rarely to those of the eyes. In all cases hitherto observed no coexistent derangement has been perceptible in the sensory nerves, nor in those of special sense. The pathogeny of this peculiar disease is obscure. The only lesion constantly found post mortem is an intense fatty atrophy of the pal- sied nerves, especially the hypoglossal nerve. In some cases a diffuse sclerosis of the medulla oblongata has also been found. According to an hypothesis which is as yet unproved, advanced by Wachsmuth, Avho proposes to call the malady in question " bulbar palsy," the disease consists in a " central affection of the medulla oblongata, having its seat in the olivary bodies, and in the gray matter lying far back be- tween the diverging lateral and posterior columns, and which forms the floor of the fourth ventricle. According to Wachsmuth, the atro- phy of the nerves is secondary, and a consequence of the degeneration suffered by the nuclei at the points above named. In some cases the palsy of the region supplied by the cerebral nerves Avas preceded by the symptoms of an incipient, progressive muscular atrophy, and the majority of French authorities regard the two diseases as closely related, although, in the progresshe palsy of the cerebral nerves, no diminution in size is observable in the affected muscles. At the out- set the patient makes but little complaint. He cannot pucker up his mouth, and hence cannot blow, whistle, nor spit. The saliva Avhich collects in the mouth runs from it involuntarily. The expression of the countenance becomes blank and strange, as the muscles of the lips cannot take part in the play of expression. Pronunciation of the labial letters is difficult, and gradually becomes impossible. If the malady extend to the tongue, not only does articulation become still more embarrassed, but the acts of chewing and swallowing become impeded; and afterward, Avhen the tongue has become still more help- less—lying quite motionless in the mouth—these acts are no longer practicable. Palsy of the palate shoAvs itself from the nasal tone of the voice, and, as long as the pharyngeal muscles remain sound, by the regurgitation, through the nose and mouth, of food and liquids which enter the pharynx. If the pharynx also become palsied, the patient, 338 DISEASES OF THE PERIPHERAL NERVES. when offered to drink, rejects a large portion of the liquid Avith violent expiratory motions, so that at last it often becomes necessary to feed him by means of the esophagus tube. The choking-fits thus pro- voked by attempting to drink, and the rejection of the liquid amid spasmodic coughing, might awraken the suspicion that a communication exists between the larynx and pharynx, or esophagus. In one case of this kind, my colleague Bruns demonstrated, by means of the la- ryngoscope, that, " if the patient merely Avas fed Avith small spoonfuls of milk or porridge, the swallowed portion only passed as far as the pouch which lies behind the larynx. If, by further SAvalloAving, the level of the liquid rises so as to pass the bottom of the notch between the arytenoid cartilages, the so-called rima glottidis posterior, the soft liquid mass immediately flows forward through this opening into the larynx, and instantly gives rise to a fit of coughing." This disease is generally a tedious one. Death is the usual result, either from impairment of the general nutrition of the patient, owing to the difficulty with which he obtains nourishment, or else from vio- lent bronchitis, or pneumonia, in consequence of the repeated intru- sion of liquid into the air-passages. Hitherto no authentic case of im- proAement or cure has been reported. Benedikt is the only one Avho claims that, by galvanization of the sympathetic, and at the mastoid process, he has obtained important success and even a cure, and in advanced cases has relieved dangerous symptoms, such as difficulty in swalloAving. For this purpose he applied the copper-pole to the spinal column, and strokes with the zinc-pole upon the pomum adami and neighboring parts, so that in each sitting he is able to induce some twenty or thirty acts of deglutition. May there not have been some confusion Avith hysterical dysphagia in these almost miraculous cures ? I have cured a hysterical patient by a treatment almost purely psychi- cal, who for months previously had been fed through a tube, and had carried a canula in her trachea for an equally long period of time. CHAPTER XXIII. ESSENTIAL PALSY OF CHILDREN—SPINAL INFANTILE PALSY (Heine). Etiology.—Whether the essential palsy of children be a disease of the brain, of the spinal marrow7, or of the peripheral nerves, or whether it proceed from all or any of them in turn, as Vogt supposes, *s a matter which, in our present ignorance of its post mortem lesions, cannot be positively decided. The name " essential palsy " I hold to be a most appropriate one. Although the paralysis originally may have been due to an inflammation or effusion in the spinal marroAV, INFANTILE PALSY. 339 yet, at the time AA-hen the palsy is called an essential palsy, all such processes have long since subsided, and it is not the primitive disease, but the paralysis and its consequences, that Ave have to treat. Essen- tial palsy as a rule is the permanent product of a very acute process; for all observers agree that the affection develops within a few hours, and that it never extends from the limb first attacked to the other limbs. The causes of the disease are as obscure as is its pathogeny. It occurs almost exclusively among children during the period of denti- tion, and for a short time afterward; that is, from the sixth month to the third year of life. Girls and boys are equally liable, as are also scrofulous and cachectic subjects, and those previously robust. The assigned causes have been the acute exanthemata, and cold, especially allowing children to sit upon cold stones. The latter idea is unAvorthy of attention, as innumerable children sit daily upon the stones, Avhile essential palsy is not at all a common disease. Symptoms and Course.—In many instances the attack commences with febrile symptoms, and signs of cerebral hyperemia or meningitis. Mental excitement, convulsions, loss of consciousness, gnashing of the teeth, are common to this, as Avell as to the other tAvo maladies above mentioned; and as in such cases it often happens that it is only by the course of the disease that Ave can decide Avhether we have a me- ningitis or a cerebral hyperemia to deal with, so here, too, Ave have no means of distinguishing the primary stage of an essential paralysis from that of hyperemia of the brain, save that, after subsidence of the convulsions and return of consciousness, a total paralysis of one or more extremities remains. Sometimes one foot, sometimes one hand is affected, sometimes both lower extremities; but it never happens that both extremities of the same half of the body are paralyzed, a fact which very plainly implies the independence of the disease from cere- bral apoplexy or encephahtis. The bladder and rectum never take part in the palsy. A mode of commencement of the malady, which is scarcely less common than that by violent cerebral symptoms, consists in an undefined attack of feverish symptoms, during which, without precursory convulsions or stupor, an arm, or leg, or both legs, suddenly hang useless, and are enthely incapable of voluntary motion. The subsequent course of the disease may vary. Sometimes the palsy disappears in a day or two, and the disease ends in complete recovery. Heine, who indisputably has seen the largest number of cases, doubts whether such examples (to which the name " temporary infantile palsy " has been given) proceed from the same causes which give rise to the stationary, permanent essential paralysis. Duchenne noticed that, in recent cases of the temporary form, the electric con- 340 DISEASES OF THE PERIPHERAL NERVES. tractility of the muscles was retained; whereas, in recent cases of the permanent form, a few only of the muscles of the paralyzed limb maintained their electric contractility, while in the others it was lost. These observations may be summed up as follows: that the prognosis of an essential palsy is favorable, and that a cure is to be hoped for, when the affected muscles preserve their contractility; but that it is unfavorable, and that degeneration and atrophy ensue, when the elec- tric contractility is extinct. When the disease passes into the so-called second stage, the re- laxed flexible, soft limbs, which may readily be placed in any required position, gradually lose their original plumpness. They suffer an atrophy which involves the skin, fat, muscles, and even the bones. In the course of a year the circumference of the limb, and even its length, is far smaller upon the crippled than upon the sound side. The pulse is small, corresponding to the deficient nutritive condition and marked depression of temperature of the paralyzed limb. It has a livid hue, and is liable to bed-sores, chilblains, and ulceration. As the disease progresses, deformity and contractions of the crippled limb are added to the atrophy. The Avasted deltoid muscle is often no longer able to hold the head of the arm-bone in its socket on the shoulder-blade ; so that the arm sinks, stretching the capsule of the joint by its weight. We then find a depression immediately beneath the acromion, the head of the bone lying farther downward and backward. It is easy to replace the bone; but, as soon as the arm is permitted to hang down, it is immediately redislocated by its own weight. When the lower extremities are attacked, particularly if it be at the period when children try to move themselves about by shuffling, permanent short- ening takes place in the muscles which still retain some degree of con- tractile poAver and encounter no resistance from their antagonists. This is the mode of origin of a variety of forms of clubfoot, flexions of the hip, and the deformities of the knee-joint known as genu valgus. In advanced periods of the disease, the electrical contractility of the degenerated and Avasted muscles is extinct. No conclusion as to the origin of the affection can be drawn from this condition, as it occurs in all forms of paralysis (even in the cerebral form) after it has lasted long enough for the nerves and muscles to degenerate. The general health usually remains unimpaired in essential paraly- sis. Many patients attain a great age, and, Avhen they belong to the lower classes of society, are often seen as mendicant cripples on the high-roads. Treatment.—It is only in very recent cases of essential palsy that any benefit is to be expected from local blood-letting, or from deriva- tives by the side of the spine. In old cases we have as little reason INFANTILE PALSY. 341 to expect the resolution of the remains of a process Avhich has long since subsided, as to restore the apoplectic cicatrix of the brain after an attack of apoplexy, and thus to cure the hemiplegia. Indeed, where the electric contractility is extinct, and the nerves and muscles have degenerated, the restitution of the spinal marroAV to a state of health would be of no benefit to the palsy. Although Ave scarcely ever are able to fulfil the causal indications, or the indications from the disease, yet a treatment of the symptoms of the disease has been folloAved by comparative success. As long as any of the muscles maintain the slightest trace of then contractility, the systematic and active application of the induced current is indicated as being the best and surest means of preserving and increasing what remains of the irritability, and of arresting the atrophy and degenera- tion of the muscles. It is proved, moreover, by the results which Heine has obtained at his institution, that, even in cases apparently of the most desperate nature, the lot of the unfortunate patient may be materially alleviated by means of tenotomy and other expedients of rational orthopedic surgery. SECTION IV. GENERAL NEUROSES, OF UNKNOWN AN ATOM- ICAL ORIGIN. CHAPTER I. CHOREA—CHOREA ST. VITI--ST. VITUS'S DANCE. Etiology.—St. Vitus's dance may be called a purely motor neu- rosis, all of its symptoms being attributable to a morbid irritability of the motor nerves, while no derangement, or, at least, no constant de- rangement of the sensory or intellectual function can be detected. The pathogeny of chorea is obscure. None of the anatomical re- searches hitherto made upon the subject, nor any study of its symp- toms, give us any positive information as to the real point whence the morbid irritation of the motor nerves proceeds. The results of the somewhat rare autopsies which have been made upon subjects who have died of chorea have been either negative, or else so discordant that any lesion discovered in the central organs of the nervous system cannot be referred to the chorea, but rather to some accidental com- plication, or to the disease of which the patient died. The general implication of nearly all the cerebro-spinal motor nerves altogether contradicts the supposition that the origin of the disease lies in the peripheral nerves. The complete integrity of the other cerebral functions makes it improbable that the movements of chorea originate in the brain. On the other hand, certain pauses in the muscular rest- lessness which occur, particularly during sleep and during the action of chloroform, would seem to imply that the motor influence is derived from the brain rather than from the spinal marrow. There is no good ground for the hypothesis that chorea is dependent upon a dispropor- tion in size between the spinal canal and the spinal marroAV, or upon inflammation of the vertebre, or upon spinal irritation, for we do not even know that the seat of the malady really lies in the spinal marrow. CHOREA. 343 In considering its etiology, in the first place, we are struck by the prevalence of the disease at the time of the second dentition and at the period of puberty. It often happens that an individual suffers from the disease at both these periods, and remains free from it during the interval. This accounts for the belief of the laity, that the com- plaint returns every seven years. Before the sixth year of life the disease is rare; and it is equally uncommon after the age of fifteen. Even the most advanced old age, however, is not entirely secure from it, and in such cases the affection exhibits a peculiar intractability. The predisposition to the disease is far greater in the female sex than in the male; and in certain cases an almost unmistakable hereditary tendency to St. Vitus's dance has been observed. Moreover, hydremia, anemia, and rheumatism seem to augment the tendency to this affection. It undoubtedly is going too far to regard the connection between chorea and rheumatism as constant; but it cannot be denied that a remarkable number of chorea patients have already suffered from acute or chronic rheumatism, or else, during the disease or after it has sub- sided, a rheumatic attack sets in. In like manner, inasmuch as false heart-murmurs are very often heard in the hearts of chorea patients (and although many of them may be considered as blood-murmurs, and due to anemia and to nervous derangement), yet the number which are certainly dependent upon valvular disease is large enough to enable us to judge how many of the patients have already suffered from rheumatic pericarditis and endocarditis. One of the most severe cases of chorea which I have ever witnessed was in a girl fifteen years of age, each one of whose joints successively became SAvollen; and another Avas in a girl, tAventy years old, who had bad disease of the heart. Besides the mimic instinct, various mental emotions, especially fear, have been assigned as causes of chorea, as have also the irritation of worms in the intestines, onanism, pregnane}', and other agents. In particular instances it of course is very difficult to determine the causal connection between chorea and such influences, Avhich so often exist without perceptible effect upon the health. The effect of exam- ple, which plays the principal role in the chorea major as Avell as in chorea minor, is instanced in the epidemic appearance of the disease sometimes observed in boarding-schools. The influence of pregnancy Is inferred from the fact that, among adult patients, very many of them are pregnant Avomen. Chorea rarely appears before the end of the second month of pregnancy, and its appearance is equally rare in the later half of the term. Once established, it usually lasts until after delivery. Symptoms and Course.—St. Vitus's dance is characterized by movements of the voluntary muscles, which, however, are not excited 344 GENERAL NEUROSES, OF UNKNOWN ANATOMICAL ORIGIN. by volition, but take place against the will of the patient, his con- sciousness meantime being perfectly unclouded. These movements go on not only at times when the patient does not intend to move, but also Avhen he moves voluntarily. In the latter case, as the voluntary motion is complicated by the involuntary, the proposed action of the patient either is frustrated or carried out imperfectly or aAvkwardly. The involuntary movements of chorea are distinguished from the more simple and monotonous jerking muscular contractions of epileptic or hysterical attacks, by a great degree of variety, and by a sort of com- bination Avhich imparts the aspect of design to the motions. A cursory and superficial observer would be much more apt to overlook and mis- take the former than the latter. In most instances the disease begins very gradually, and is not recognized for some time. It may be noticed, perhaps, that the sick child drops and breaks things a good deal; that it does not sit still; that it writes badly, or makes more mistakes than usual in playing on the piano, and it is accordingly scolded or punished that it may be more careful and correct its awkwardness. The poor child often does not know what it has done, and, in consequence of the unjust re- proaches, becomes either depressed and sad, or else grows irritated and perverse. The restlessness of the muscles, meantime, becomes more and more apparent. The acts of awkwardness become more frequent, and are grosser than ever. The child misses in reaching for its tum- bler, pricks itself with its fork, or makes extraordinary grimaces. The morbid character of this condition often becomes apparent to the minds of its relatives quite suddenly, and without the occurrence of any special change in the symptoms. It is much more unusual for the dis- ease to develop suddenly, and from the outset to present the remark- able symptoms which characterize St. Vitus's dance in its later stages. In pronounced chorea, the utmost variety of motions folloAV each other, in a manner so manifold and grotesque that the term " insanity of the muscles," Avhich has been applied to it, seems quite appropriate. In the face, the eyebrows are alternately contracted and separated, the forehead Avrinkled and smoothed, the eyelids rapidly winked, and noAV and then are fast closed for a moment. The eyes roll hither and thither, the mouth is successively pursed up, closed, then suddenly opened and shut, now spreading into a smile, now draAvn down as if to weep, while the tongue is often and suddenly thrust forAvard. The head itself is turned, now forward, now backward, now sideways; the shoulders are raised and sunken. The upper extremities are flourished about. In the elbows, hands, and finger-joints, flexion and extension, pronation and supination, abduction and adduction, alternate with one another. Similar movements, which, however, usually are of less CHOREA. 345 active character, are observed in the loAver extremities. The muscles of the trunk also take part in the general restlessness, so that the spi- nal column is inclined either forward, backAvard, or sideways ; some- times in one dhection, sometimes in another. If the patient be lying in bed, he often is tossed upAvard, or toward the foot of the bed, or is even pitched out of it. In the worst forms of chorea, the patients are quite unable to sit upon a chair, but immediately slide off from it to the ground. This morbid restlessness grows all the more intense and general, if the patients pay attention to it, especially if they know that they are being watched. Sometimes it is stronger upon one side than upon the other, or is chiefly confined to one or more limbs. The mus- cles of the larynx and those of respiration but seldom take part in the disease, and the sphincters and the muscles of the pharynx probably never do so. Owing to the constant motion, it is difficult for the pa- tients to go to sleep; when once asleep, hoAvever, the muscular twitch- ing ceases. Occasional exceptions to these rules are now universally ascribed to dreams of movement, ever since Marshall Hall originally suggested the idea. Nearly all the motions of the body, with exception of those of respiration and deglutition, are seriously embarrassed by this restless- ness of the muscles. The articulation becomes indistinct, as the inten- tional movements of the mouth and tongue are accompanied by others Avhich are unintentional. In eating, the fork misses the lips; in drink- ing, the beverage is spilt, so that a patient often has to be fed. Some of them have great difficulty in offering then hand, others are unable to dress and undress themselves. Even in slight cases all occupations requiring delicacy of manipulation become impossible, as, even in walking, the feet only touch the ground by a chcuitous route, and, as the entire body is constantly making superfluous and irregular move- ments, there is something very remarkable and characteristic in the gait of the patient. The other functions and the general health suffer comparatively little. It is easy to comprehend wiiy the patient should be dispirited, sensitive, and wilful, Avhen we consider that for weeks he has not been master of his motions, and that he has been constantly taunted about the mistakes he makes. Not unfrequently the grimaces of the pa- tient are so at variance with his actual humor, or so unsuitable to the subject of conversation, as to give him a foolish, imbecile look, although his mind is quite sound. When of long duration, however, the accu- racy of judgment seems really to be impaired, and other intellectual disorder arises. Sometimes, but not always, there is complaint made of headache and pain in the back. Although, strange to say, there is no especial fatigue of the muscles, the joints of the limbs are some- 346 GENERAL NEUROSES, 01 UNKNOWN ANATOMICAL ORIGIN. times swollen and painful from the constant strain and motion. Un less there be some complication, there is no fever, although the pulse usually is accelerated. The appetite, digestion, secretion, and excre- tion do not present any constant pecuharity. When the disease has been of long duration, the nutrition of the patient suffers in conse- quence of the loss of rest, and he becomes anemic and thin. The course of chorea is chronic. It rarely terminates before the end of six or eight weeks, and it often continues for three or four months. In rare instances it becomes habitual, and lasts throughout life. Its course either is marked by remissions and exacerbations, or else the malady increases constantly to .its acme; then remains stationary for a Avhile, after which it gradually abates. Recovery is the most usual termination of the complaint. The cases are exceptional in which chorea becomes habitual; but it often happens that, in certain of the patient's motions, a trace of the former disease remains for years, as well as a tendency to relapse. Permanent mental derangement is also rare. Death scarcely ever occurs, unless through complications. There are, however, a feAV instances on record Avhere it has been the result of the disease itself. In these cases the muscular contractions rapidly become extremely violent and general. This was folloAved by collapse and coma, in Avhich the patient perished. Treatment.—Our scant knowledge as to the causes of chorea puts a fulfilment of the causal indication almost out of the question. When the disease has been preceded by symptoms of anemia and hydremia, the ferruginous preparations are to be selected from the long list of reputed remedies against chorea. We do not attempt to say Avhether carbonates of iron (gr. v—gr. x pro. dosi), or ferr. hydro- cyanic (gr. ij—gr. iij pro. dosi), which are the favorites, possess any- real advantage over the other preparations. When the patient has suffered from rheumatism, the sulphur-baths (as recommended by Baudeloque), an ounce of sulphuret of potassium to twelve gallons of water, in Avhich the patient is to spend an hour at a time, are as much to be recommended as are the chalybeates, Avhen there is anemia. Where worms are knoAvn to exist in the intestine, the treatment may be commenced by a dose of santonin or other anthelmintic. The number of remedies proposed for the cure of the disease itself is very large. As, however, the disease usually subsides spontaneous- ly, in the course of six or eight weeks, and as it very rarely is possible to cut the malady short in a less period of time, we are very apt, if quite candid and chcumspect in measuring our success in special in- stances, to be in doubt as to whether the chorea abated in consequence of a six weeks' administration of the medicine prescribed, or whether it "got well of itself." Fortunately, most of these remedies, if cau- CHOREA. 347 tiously given, can do no harm. This is especially true of the prepara- tions of zinc, particularly of the oxide. The sulphate, the valerianate, and the hydrocyanate of zinc, are less innocent, but not more to be relied upon, nor are the ammonio-sulphate of copper and nitrate of silver. Romberg's valuable opinion is in favor of arsenic; and, indeed, Avhere we have determined to employ the metallic nervines, Folder's solution (gtt. iij—gtt. v t. d.) is to be preferred to all others. The narcotics may be dispensed Avith, as a rule, in treatment of chorea, and, moreover, are apt to be so ill-borne that Ave often have regretted the administration of an evening dose of Dover's powder or morphine to insure the rest of the patient. My experience as to the action of opiates is, however, in opposition to that of one of our great authori- ties. Trousseau urgently recommends the administration of large doses of morphine, and claims, too, that they are remarkably well borne. Strychnine, another medicine for chorea, strongly recommended by Trousseau, and Avhich has been given, as directed by him, at first in very small doses, afterward in larger ones, until slight signs of poisoning set in, has met with little approval in Germany. Their in- troducer's own experience, which by no means resulted in sudden or even in rapid cures, offers no encouragement to make use of these noxious remedies. This is also true of the proposed hypodermic in- jection of curare. With this article the certainty of benefit is by no means proportionate to the dangers incidental to an overdose. When- ever the v ertebre are sensitive to pressure, a few leeches or cups may be applied by the side of the spine, to be followed by counter-irritants to the skin. Care should be taken, however, not unnecessarily to dis- figure the necks of young girls by scars; hence we should avoid the use of tartar-emetic ointment. Cold affusion upon the back, which is probably the best method of producing determination to the skin, seems to be of decided benefit in some cases, especially in cases of long standing, although it sometimes aggravates the disease. The in- halation of chloroform is an excellent palliative for the severer forms of the chorea; but further experience only can determine whether the repeated and long-continued exhibition of this article, pushed to the point of complete narcotism, has the effect of abbreviating it. A more careful trial will be requisite ere the general adoption can be sanctioned of the practice of forcibly holding or tying patients, a practice Avhich has been proposed by several authorities. Benedlkt declares that, " out of more than twenty cases of chorea, treated by him by the con- stant galvanic current, not one has failed to recover." The current which he employs is just strong enough for the patient to feel it dis- tinctly, and he applies it along the spine, the patient standing erect. Painful currents aggravate the symptoms. During convalescence we 348 GENERAL NEUROSES, OF UNKNOWN ANATOMICAL ORIGIN. should endeavor to teach the patient, by a systematic and humane system of discipline, to resist the involuntary motions by the force of his will. CHAPTER II. LOCKJAW—TRISMUS—TETANUS. Etiology.—Like chorea, lockjaw is a derangement of the motor function. The symptoms of this disease are ascribable to a morbid excitement of the motor nerves, the participation of the sensory nerves in the disease being but slight, and, for the most part, of a secondary character. In this malady, however, we know, with much greater cer- tainty than we do in chorea, that the morbid irritation of the motor nerves proceeds from the spinal marroAV. This hypothesis is supported rather than contradicted by the fact that the results of post-mortem examination of the spinal marrow usually are negative in cases of tetanus, and that real tetanic spasms are seldom observed in cases of grave organic disease of the spinal cord. It weuld be quite impossible for motor impulses to originate from a spinal marrow reduced to a mass of debris, or whose elements were otherwise degenerate or destroyed, Avhile experience teaches that the lesion from which abnormally-active impulses proceed are insusceptible of anatomical demonstration. At the outset of the disease, tetanic spasms are generally produced by the action of trifling but still appreciable irritants, which, acting upon the extremities of the peripheral nerves, throw the spinal marrow into a state of excitement, so that, at this period, the spasms, although dis- tinguishable from other reflex symptoms by their greater violence and longer duration, may be called reflex spasms. As the malady advances, however, such causes are not required in order to give rise to the cramps. The spinal marrow then remains permanently in the condi- tion of intense excitement into which it is thrown by the motor nerves. With regard to the etiology of the disease, a number of noxious agents may be enumerated, which can be proved capable of inducing the morbid state of the spinal marrow to which tetanus is due. First among these are wounds, especially lacerated, punctured, and gunshot wounds, and wounds in which foreign bodies remain lodged. Injuries of this kind are more dangerous upon the extremities than upon other parts of the body; but they never give rise to tetanus except under certain conditions, of which, sudden change of temperature (such as hot days followed by cold nights) is knoAvn to be one, while others are unknoAvn. Bardeleben aptly sums up this condition as follows: that the Avound is the predisposing agent, and the chilling the exciting cause. We do not know, however, Avhat the changes in the nerve- TETANUS. 349 tissues are which induce tetanus, nor how they affect the spinal marroAV. The injection and swelling in the course of the nerve, between the wound and the spinal marrow, which have sometimes been observed, are by no means constant. In other cases, lockjaw occurs from the effect of cold, AAithout any previous wound, as Avhen a man has slept upon the moist earth, or been wet while his body is heated. This form of rheumatic tetanus is much more rare than the traumatic form. Here, too, we are completely in the dark as to the ways and means by which the lesion, suffered by the cutaneous nerves in rheumatic tetanus, is transmitted to the spinal marrow. The tetanus observed sometimes in newly-born infants (tetanus neonatorum) is usually regarded as a third form of the disease, although it should properly be reckoned as belonging to the traumatic variety. Tetanus neonatorum never occurs excepting between the first and the fifth day after the fall of the navel- string. Hence it has always been immediately preceded by a wound (ligation and binding of the cord). The objection that, in some cases, there is inflammation of the umbilicus, while in others there is none, is not valid; for, even in the wounds of adults which have caused lock- jaAv, although, in most cases, they are violently inflamed, and other- wise affected, yet there have been instances in which the wound Avas doing perfectly well, and Avas healing, or even was completely cica- trized. Besides, in infantile tetanus, the ligation and division of the umbilical cord can only be considered as the remote cause, while the chilling of the skin, or other unknown agent, AAiiich sometimes seems to be of an epidemic nature, must be regarded as the immediate cause. Finally, a morbid condition of the spinal cord is induced by poisoning with strychnine, which exhibits precisely the same symptoms as those of lockjaAV, so that the toxic signs induced by strychnine and brucine have been called tetanus toxicus. Traumatic and rheumatic tetanus is of far more frequent occurrence in men than in women. Vigorous constitutions are more liable to it than feeble ones. In the tropics the disease is more common than with us; and certain races, especially negroes, seem to be more prone to the disease than Europeans. Symptoms and Course.—Tetanus is characterized by continuous tonic spasms, which principally involve the muscles of the trunk and those of mastication, and which are marked by paroxysmal periods of aggravation of extreme intensity. The malady is usually preceded by signs consisting of a febrile condition of no great severity, and pain, and stiffness in the back of the neck, which may readily be mistaken, for a trifling fit of rheuma- tism. If such symptoms make their appearance after receipt of a wound of the character above given, and if at the same time the 350 GENERAL NEUROSES, OF UNKNOWN ANATOMICAL ORIGIN. aspect of the Avound change, and should it become dry and pain- ful, we may already fear great danger to the patient. When the disease has fairly set in, the head at first is almost always fixed and drawn backAvard, by rigid contractions of the muscles of the neck. Tonic spasms of the muscles of mastication press the jaAvs firmly together (lockjaw, trismus), and at the same time deglutition is im- peded or prevented by spasm of the pharynx. From the nape of the neck the disease extends over the muscles of the back. Thus the entire body is bent backward in the shape of a bow. The abdominal and thoracic muscles, however, are also involved in the spasm. Hence the belly is tense, contracted, and hard as a board, and there is a sense of constriction at the pit of the stomach, which is very painful to the patient. More rarely the muscles of the extremities, particularly those of the forearms, legs, hands, and feet, are attacked by cramps. The terms opisthotonos, emprosthotonos, andpleurosthotonos, are severally applied to the disease, according as the contractions preponderate in the poste- rior muscles of the neck and back, in the anterior muscles of the neck and trunk, or in those of the side, and according as the body is drawn forward, backward, or sidewise. When there is no such preponderance, so that the body lies rigid as a statue, the condition is called orthoto- nus. Opisthotonos is by far the most common form of the malady; the other varieties are rare. The contracted muscles remain upon the stretch throughout the whole disease. From time to time, however, paroxysms occur, in which the cramps are so severe that the muscles sometimes are torn asunder. At such times the middle of the body is suddenly jerked into the air, so that no part of it touches the bed ex- cept the head and heels. The muscles are hard as stone, and are the seat of frightful pain, which can generally be compared to that of a severe cramp of the leg. The contours of the temporal and masseter muscles stand out in bold relief, imparting a peculiar expression of countenance. This is still further increased by contractions of the mimic muscles of the face. The forehead is wrinkled, the brows knit, the eyes rigidly fixed, and sunken deep into then sockets. The angles of the mouth are drawn outAvard, and the lips are drawn apart, expos- ing the clinched teeth. The aspect of a patient in this condition awakens feehngs of deep compassion mingled with horror. At the outset of the disease the paroxysms do not occur spontaneously, but are provoked by the most trifling causes. Just as in a frog poisoned by strychnine, in which tetanic spasms may be induced by merely tap- ping upon the table upon which he lies, so the slightest touch upon the skin or breath of air upon it, a faint jolt of the bed, the sound of shutting a door, every movement which a patient desires to make, the acts of chewing or swallowing, or even the suggestion of the idea, suf- TETANUS. 351 fice to bring on a new attack. The inability to swallow, and the spas- modic seizures induced by every effort to drink, create a certain resem- blance betAveen tetanus and hydrophobia. The paroxysms are of variable duration. At first they are brief, but at the height of the disease they may continue for a quarter of an hour, or even an hour, ere the remission set it. Consciousness and the intellect generally remain unimpaired until the last in this frightful malady, nor are many of the other functions materially deranged. The unhappy patient suffers from hunger and thirst, which he is unable to relieve. As in all other violent muscular exertion, the skin is bedeAved with sweat, and the pulse is frequent and small. The enormous elevation of the tem- perature, first pointed out by Wunderlich, is a matter of great interest. Now and then it has been observed as high as 110° F., and immedi- ately after death a further rise has been observed almost up to 112° F. It would be rational to attribute this phenomenon to excessively active calorification consequent upon the greatly-increased destructive assimilation which is going on in the muscles, which are in a state of tetanic spasm. This hypothesis has been fully confirmed by the experiments of Leyden and others, who have witnessed the same elevation of the bodily temperature in dogs, in whom tetanus had been produced artificially. The bowels are usually someAvhat constipated, and sleep, though ardently longed for, is impossible. Another source of anguish, as Avell as of the greatest danger, consists in the derange- ment of the respiration. There is no obstacle to the entrance of the air, but, as Watson aptly remarks, the chest is compressed as in a Aice, and respiration is made extremely difficult by reason of the rigidity of the muscles. There are instances where the victim perishes only a few hours after the outbreak of the disease. In such cases, the spas- modic contraction of the diaphragm and other respiratory muscles so increases as to completely arrest respiration and cause suffocation. The majority of patients are not relieved from their sufferings so soon. For three or four days, the cramps, and the frightful pain and dread of suffocation Avhich accompany them, continue to increase in duration and frequence, the remissions becoming more and more imperfect; until the sufferer expires, either poisoned by carbonic acid resulting from the imperfect manner in which respiration is carried on, and from the augmentation in the consumption of the oxygen, or else dying during some very severe paroxysm, through sudden and absolute inter- ruption to the respiration. Sometimes the breathing is not so much interfered with as to cause death from lack of oxygen. The disease may then go on for weeks ere the patient, in a state of extreme emacia- tion, and exhausted by privation of nourishment, succumbs to starvation. Recovery is extremely rare. Transitory remissions, in which the 69 352 GENERAL NEUROSES, OF UNKNOWN ANATOMICAL ORIGIN. patient may even enjoy a brief refreshing slumber, should not be alloAved to deceive us. After such pauses the malady generally breaks out with all its former severity, or even with increased violence. We must not indulge in the hope of recovery unless the seizures continue to diminish in length and frequence, distinct relaxation of the con- tracted muscles occurring during the intervals, and unless the patient become able to take food and nourishment. Even in the most fortu- nate cases this takes place Avith extreme sloAvness; and it is not until after the lapse of weeks that the muscles entirely lose their tension, and the patient is completely well. The symptoms of tetanus neonatorum.are but little modified by the peculiarities of the infantile organism. Here, too, the outbreak of the disease usually is heralded by indistinct prodromata. The child cries out frequently during sleep; has blue rings around the eyes and lips; and lets go the breast winch it has just seized with avidity. The mother first becomes aware of the onset of the disease itself when she finds that neither the nipple nor the finger can be inserted into the mouth. The jaws stand several lines apart, but it is impossible to separate them further. The malady increases rapidly. The muscles of the face are also contracted spasmodically. The forehead is wrin- kled, the eyelids firmly shut, and surrounded by converging wrinkles. The ale nasi are dilated, the lips compressed and puckered, while the tongue usually is fixed between the jaws. Besides this, there is opis- thotonos, the head is drawn backward, and the spine arched like a bow. A touch, or an attempt to move or swallow, provokes a violent spasm; but the remissions usually are more complete than they are in the tetanus of adults. Respiration is impeded, during the seizures by the rigidity of the thorax and the tension of the abdominal mus- cles. Attacks of suffocation arise, of Avhich the child often dies in from twelve to twenty-four hours. In other cases the breathing grad- ually becomes insufficient, and the child succumbs to overcharge of the blood with carbonic acid. Death then takes place more slowly, but still within a few days, during which the child loses flesh rapidly. Recovery from tetanus neonatorum is likewise extremely rare. Treatment.—For the fulfilment of the causal indication, a series of surgical operations—even amputation of the wounded member__ have been proposed and practised. The success of these operations, however, was by no means what had been anticipated of them, and more recently they have been abandoned. From the prominent part which is unmistakably played by exposure to cold, both in rheumatic and in traumatic tetanus, warm and stimulating baths, as well as Russian vapor-baths, Avould seem to be indicated. The objection, that the manipulation necessary in giving such baths tends to aggravate the TETANUS. 353 symptoms, only held good in two of Hasse's cases, and that only at the very commencement, and not after the manipulation had been con- tinued. This circumstance and the rehef which the baths afford to the patients imperatively demand their employment. Upon the supposition that tetanus was an inflammatory affection of the spinal marrow, the attempt Avas formerly made to fulfil the indi- cation of the disease itself by blood-letting, local and general, and by the exhibition of calomel to the point of salivation. Such procedures, however, have been abandoned more and more in later times. Unfor- tunately Ave do not possess any remedy capable of bringing back the irritable state of the spinal cord to its normal condition. Even the narcotics do not have this effect, although they are indispensable for the purpose of alleviating the sufferings of the patient. To accomplish this, large doses must be given ; so that, unless the approach of narco- tism be vigilantly watched, there is danger of hastening the fatal termination. If the patient cannot swallow, morphia should be given hypodermically, or else clysters, containing twenty or thirty drops of laudanum. Injections of tobacco are not of much greater service than opium-clysters, and, unless the dose be regulated with extreme caution, they are much more liable to give rise to a fatal collapse than the lat- ter. The anesthetics, if possible, are of still greater importance than the narcotics ; but, unfortunately, their effects hkewise are merely pal- liative. Too free use of them must be avoided, and the patient must not be kept in a state of permanent insensibility from chloroform. The English recommend the stimulants, especially carbonate of ammo- nia, brandy, and Avine, to Avhich they give much greater credit than to blood-letting and the narcotics. TrustAvorthy observers have obtained very great benefit from the hypodermic injection of a solution of curare in tetanus. This treatment certainly deserves further trial. HoAvever, OAving to the very variable character of the curare, it will be necessary, prior to the exhibition of the preparation to be used, to ascertain, by experiment upon animals or upon the healthy human being, how large a dose may safely be administered. When this precaution has not been taken, we must commence with very small doses (gr. -J to gr. £), and gradually increase them to gr. ^ to gr. 1^. Demme advises that a solution of one or two grains in one hundred drops of water be em- ployed, ten drops of this to be injected as a dose. According to Demme, the action of curare lasts four or five hours, and then begins to abate; and upon this fact the repetition of the dose may be reg- ulated. It is most important that the patient should be kept in a quiet chamber, Avith a uniform temperature, and that his eyes should be screened from too bright a light. For the tetanus neonatorum Ave may prescribe camomile-baths, 354 GENERAL NEUROSES, OF UNKNOWN ANATOMICAL ORIGIN. clysters containing a drop of laudanum, and, if the spasms be very severe, chloroform may be administered, but with great caution. CHAPTER III. EPILEPSY—FALLING SICKNESS—MORBUS SACER—HAUT-MAL. Etiology.—Unlike chorea and tetanus, epilepsy cannot be called a purely motor neurosis; since the interruption which takes place, both in consciousness and insensibility, is quite as essential an element of an epileptic fit as the convulsions. The absence of one or other of these symptoms renders the seizure imperfect. We may assume that the excitement of the motor nerves, of which the convulsions are the exponent, proceeds from the medulla oblongata and the portion of the brain lying upon the base of the skull. This is shown. 1. By the interruption of the functions of the hemispheres, which accompanies the convulsions. It is not probable that motor impulses proceed from the hemispheres at a time when the irritability of the other ganglion-cells and nerve-fibres is extinguished. 2. Because convulsions, similar to epileptic convulsions, can be ex- cited by continuous excitement of the basilar portion of the brain by means of the induction apparatus, while no such result is obtained by a hke irritation of the various parts of the hemispheres. 3. Because Kussmaul and Tenner, in their experiments upon ani- mals, could still produce convulsions of a decidedly epileptiform char- acter after extirpation of both hemispheres. 4. Schroeder van der Kolk has found that, in all bodies of epilep- tics Avhere the disease had been of long standing, besides numerous inconstant lesions, there was alway a dilatation of the arterioles and capillaries of the medulla, with thickening of their wralls. The influences which tend to produce this condition of the medulla oblongata, Avhere- by it throws the nerve-fibres passing through it or originating from it into such intense excitement, and which, for brevity's sake, Ave call a state of irritation, are probably of a manifold character. It is true that the experiments of Kussmaul and Tenner have proved that epileptiform convulsions may be induced by cutting off the supply of arterial blood from the brain; but they do not prove that arterial anemia of the brain is the sole cause of epileptic fits. Schroeder van der Kolk believes that epileptic convulsions depend mainly upon an increased afflux of arterial blood to the medulla oblongata. There is no doubt, moreover, that the morbid irritability of the medulla which occasions epilepsy may arise without any increase or diminution of its EPILEPSY. 355 supply of blood, merely from the improper character of its nutriment and from the admixture of certain materials in the blood. It must also be admitted that the medulla may be thrown into an irritated condition by the transmission of a morbid impression from remote re- gions of the nervous system, whether central or peripheral. It is well known that neuromata and cicatrices, or tumors pressing upon periph- eral nerves, have sometimes occasioned epilepsy (although, indeed, such instances are not common), and that the epilepsy has ceased after section of the affected nerve or after removal of the cause. Per- haps, also, cerebral tumors and other diseases of the brain and spinal marrow may induce epilepsy in a similar manner by gradual transmis- sion of a morbid irritability to the medulla oblongata. This supposi- tion has received strong support from the result of recent experiments by Brown-Sequard, in which dogs, whose spinal marrows had been injured, suffered from convulsions, although not immediately, but some time after the receipt of the injury. It is difficult to say why the morbid irritability of the motor nerves is not continuous, but mere- ly occurs in paroxysms, with intervals which frequently are of very long duration. Are we at liberty to suppose that it is only noAV and then that the medulla oblongata falls into this morbid state? Is there really ground for the hypothesis that the cause of epilepsy is a tran- sitory spasm of the muscular fibres of the arteries, with consequent ar- terial anemia? Is it true that poisons, or the irritation of remote tumors, or other agents which give rise to epilepsy, act by the occa- sional provocation of the spasm of the muscles of the blood-vessels ? May we, with Schroeder van der Kolk, compare the ganglia of the medulla oblongata to a Leyden jar, or to the electric organ of certain fishes ? May an epileptic fit be likened to the spark from the Leyden jar, or to the discharge of the electric organ of the electric fish ? and do the ganglia reload themselves, as it Avere, for a fresh explosion during the intervals ? Or, finally, is the morbid state of the medulla constant, but requiring the additional stimulus of some new transitory irritant transmitted to it from some remote point in the brain, the spi- nal cord, the peripheral nerves, or the intestines, in order that the fit may occur ? Of all these conditions Ave as yet have no accurate knowledge, and it were idle to advance other hypotheses in explana- tion of the foregoing ones. Equally inexplicable is the constant coexistence of irritability of the spinal marrow with palsy of the cerebral hemispheres. The arrest of sensation and consciousness has sometimes been regarded as a sec- ondary condition, resulting from the convulsions. It has been attrib- uted in part to venous engorgement of the brain, arising from com- pression of the cervical veins by the contraction of the cervical mus 356 GENERAL NEUROSES, OF UNKNOWN ANATOMICAL ORIGIN. cles, and in part to surcharge of the blood with carbonic acid, in con- sequence of spasmodic closure of the glottis. The fact that the loss of consciousness and sensation and the occurrence of the convulsions are almost always simultaneous ; and that the former sometimes pre- cedes the latter; and that in many cases of incomplete epilepsy it is the sole symptom of the seizure, is a sufficient refutation of both hypoth- eses. In like manner it must be declared that there is no proof as to the truth of the theory of Schroeder van der Kolk, that, in an epi leptic fit, the ganglion-cells of the medulla excite a spasm of the vaso- motor nerves of the brain, simultaneously with that which they induce in the cerebro-spinal nerves, and thus cause cerebral anemia and palsy. So, too, with Henle's theory, Avhich supposes the existence of a plethoric and an anemic form of epilepsy. He suggests that, in the former, besides the more intense hyperemia of the hemispheres which induces the palsy, a lesser degree of hyperemia, capable of in- ducing symptoms of mere irritation, arises in the medulla oblongata ; while, in the anemic form, he imagines that the lack of blood in the cerebral vessels occasions an increased blood-pressure upon the me- dulla oblongata, inducing in it a degree of engorgement sufficient to cause signs of irritation. Here, too, we shall refrain from further theorizing, preferring to admit that to us the antagonism existing in epilepsy, between the condition of the hemispheres and that of the basilar portion of the brain, is entirely inexplicable. Owing to the scantiness of our knowledge as to the pathogeny of epilepsy, the statistics regarding its predisposing and exciting causes are of but secondary importance. We do not know of one single agent of which we can certainly predict that it will produce epilepsy ; yet, besides this, we must admit that all the assigned causes of this disease by themselves are incapable of inducing it, and that the co- operation of a second and unknowm factor is always requisite. Statis- tics show epilepsy to be a very common disease, about six epilep- tics being found in every thousand individuals. Females suffer from it somewhat more frequently than males. There is no age which is completely exempt from it; but the majority of cases occur between the tenth and twentieth years of life; next to this, between the sec- ond and the tenth year, and between the tAventieth and thirtieth year. It seldom commences during old age, and its congenital occurrence as well as its appearance in the first months of life, is equally rare. Hereditary predisposition plays an unmistakable part in its produc- tion ; its existence is demonstrable in nearly a third of all cases. It is especially apparent in persons descended from epileptic parents, par- ticularly from epileptic mothers, as well as in individuals Avhose par- ents or ancestors have been insane or intemperate. In some families EPILEPSY. 357 epilepsy afflicts many of its members throughout several generations. Sometimes the disease skips a generation, and the grandchildren are attacked, but not the children. Cachectic subjects, drunkards, and onanists, are more liable to it than healthy, vigorous persons, although the latter are by no means exempt. The chief of its exciting causes are violent mental emotions, sudden fear, terror, and the sight of an epileptic fit. In more than a third of all cases the first attack has fol- lowed upon some violent fright. The most common structural altera- tions found in the skull and brain, which, however, like the mental emotions, are not constant, and only give rise to epilepsy under cer- tain unknown conditions, are asymetry, imperfect development of the skull, diffuse thickening or exostosis of the skull, thickening, adhesion and ossification of the dura mater, tumors and deposits in the brain, chronic hydrocephalus, and cerebral hypertrophy. Alteration in the appendages of the brain, Avhich Wenzel mentions as a constant lesion in epilepsy, is absent in the majority of cases. Changes of structure in the spinal marroAV are not so frequently found in epilepsy as similar changes in the brain; but perhaps this is because the former have been less diligently examined than the latter. We have already alluded to the neuromata, tumors, and scars, which sometimes give rise to the disease by the pressure which they exert upon peripheral nerves. In a similar manner, epilepsy may arise from an abnormal irritability of the sensory nerves, induced by some severe irritation at their peripheral extremities. Thence, according as the irritation in- volves the nerve-tips of the thoracic organs, those of the organs of digestion, or those of the urinary or sexual apparatus, the epilepsy is classified into epilepsia cardiaca, pulmonalis, abdominalis, nephritica, uterina, etc. It is manifest that we may easily err in attributing the disease to irritability of one or other of these organs. Uterine epi- lepsy is perhaps the least ambiguous of all, as a gradual transition from hysteria to epilepsy may sometimes be observed, and as some women become epileptic upon then first coitus. The presence of Avorms in the intestines also is sometimes an unmistakable cause of the disease. Symptoms and Course.—Epilepsy is a chronic disease, character- ized by convulsive attacks, accompanied by loss of consciousness, Avith intervening periods of exemption of variable and sometimes of very eng duration. Loss of consciousness during an epileptic fit necessa- rily involves loss of sensation and incapacity for voluntary motion. In incomplete epilepsy, the " petit mal" of the French, there usually are no convulsions during the seizure, or else merely a few twitchings. Such rudimentary attacks, of course, are not to be called incomplete epilepsy unless they alternate with Avell-pronounced seizures, or arise 358 GENERAL NEUROSES, OF UNKNOWN ANATOMICAL ORIGIN. from them, or unless, in the further course of the case, the rudimen- tary fits gradually developed into perfect ones. In some patients an epileptic fit is regularly, or at all events gen- erally, ushered in by an aura. This aura receives its name from a sensation as of a vapor which rises from the extremities toward the head, and terminates in the fit. This prodromic feeling, however, is only described by a few patients. Far more frequently there are other sensations, such as a sense of creeping, of warmth, or numbness, or a peculiar pain in some part of the body darting thence to the brain, which herald the attack, and Avhich are called the " aura epileptica." Instead of this sensible signal, the fit is preceded in other instances by twitching or palsy of some part of the body. This is called the motor aura, in contradistinction to the sensory aura above described. In other cases, again, the seizure is ushered in by abnormal phenomena in the organs of sense, hallucinations, visions of sparks or of colors, buzz- ing in the ears, the report of a loud crack or other sound, dizziness, and sometimes by the regular recurrence of phantasmagoria of more or less grotesque character. This latter form of sensorial or mental aura by no means proves that the epilepsy is of central origin, in the sense, at least, that the malady is the result of appreciable lesion of the brain; nor is the occurrence of an aura arising from the extremities to be regarded as a proof of the peripheral origin of a case of epilepsy. It is an extraordinary fact that an epileptic fit may sometimes be averted by binding a ligature firmly above the starting-point of the aura, and thus, as it were, isolating it. That even such a phenomena as this is no proof of the peripheral origin of an epilepsy is in some degree manifested by the experiments above mentioned of Brown- Sequard. Here it was demonstrated that, in the dogs made epileptic artificially by wounding of the spinal marrow, a fit occurred wherever the skin was irritated within the province of a particular branch of the trifacial nerve. We cannot tell whether the fit was preceded by an aura in these dogs, but we may positively conclude from these experiments that, even when the individual epileptic attacks are induced by periph- eral irritation, the real cause of the disease may consist in palpable structural disease of central organs. Whether preceded by an aura or not, the outbreak of the paroxysm is usually announced by a shrill cry, whereupon the patient loses all sense and falls to the ground, usually backward or sideways. He scarcely ever has time to seek a convenient place, but falls, regardless of place, often in the most perilous situations, striking, perhaps, against a hot stove, a sharp corner, or down the stairs. There are but few epileptics, Avhose disease is of long standing, who do not carry with them the marks of more or less severe injury. The fall is usually fol- EPILEPSY. 359 .OAved at first by tonic contractions, in which the body and extremities are extended, the head drawn backward or to one side, the mouth firmly closed, the eyes wide open, and rolled upAvard or in Avar d, the thorax fixed, and the respiratory movements arrested. After a few moments, during which the jugular veins become distended and the face purple, the tonic spasms are converted into clonic ones, which soon convulse the wiiole body. The countenance, hitherto immovable, is now thrown into active agitation; the angles of the mouth are drawn hither and thither, the forehead and eyebroAvs tAvitch, the eyes open and shut, the jaAvs are forcibly pressed together, and are worked back- ward and forward, so that the teeth grate audibly. The teeth are not unfrequently broken off, the tongue bitten through, and even the lower jaw may be luxated. Upon the lips there appears a saliva, rendered frothy by the constant movements of the mouth, and which, too, is often bloody from wounds of the tongue or cheeks. The head is jerked forward and backward, and from side to side; while the convulsive twitchings of the muscle of the trunk pitch the body hither and thither. In the extremities, and especially in the upper extremities, quick kicking, striking, twisting, and twitching motions occur in turn, and with such violence as sometimes to result in luxation or fracture. The fingers usually are flexed, the thumb being pressed into the palm of the hand, a sign Avhich tfee laity erroneously believe to be pathog- nomonic. Sometimes it seems a if the violence of the convulsions Avere remitting, and as though the fit Avere about to abate; but the lull is soon followed by a fresh outbreak, and the convulsions become more violent than ever. Sometimes the twitching is superseded, for a feAV moments, by a tetanic condition like that by Avhich the paroxysm commenced. Throughout the whole fit the respiration is much em- barrassed, OAving to the impediment offered by the tonic or clonic spasms of the respiratory