A TREATISE ON THE DISEASES OF THE NERVOUS SYSTEM BY WILLIAM A. HAMMOND, M. D. #»/ SURGEON-GENERAL U. S. ARMY (RETIRED LIST) J LATE PROFESSOR OF DISEASES OF THE MIND AND NERVOUS SYSTEM IN THE COLLEGE OF PHYSICIANS AND SURGEONS OF NEW YORK, THE BELLEVUE HOSPITAL MEDICAL COLLEGE, THE UNIVERSITY OF THE CITY OF NEW YORK, AND THE NEW YORK POST-GRADUATE MEDICAL SCHOOL AND HOSPITAL, ETC. GEJ1ME M. HAMMOND, M. D. WITH THE COLLABORATION OF PROFESSOR OF DISEASES OF THE MIND AND NERVOUS SYSTEM IN THE NEW YORK POST-GRADUATE MEDICAL, SCHOOL AND HOSPITAL ; FELLOW OF THE NEW YORK ACADEMY OF MEDICINE ; MEMBER OF THE NEW YORK NEUROLOGICAL SOCIETY ; OF THE AMERICAN NEUROLOGICAL ASSOCIATION, ETC. WITH ONE HUNDRED AND EIGHTEEN ILLUSTRATIONS NINTH EDITION, WITH CORRECTIONS AND ADDITIONS “ Est quoddam prodire tenus, si non datur ultra.”—Horace NEW YORK D. APPLETON AND COMPANY 1891 D. APPLETON AND COMPANY. Copyright, 1876, 1881, 1886, 1891, PREFACE. This, the ninth edition of my “ Treatise on Diseases of the Nerv- ous System,” has, with the assistance of my son, Dr. Graeme M. Ham- mond, been thoroughly revised and brought up to the present time. The first edition of the work was published in 1871, and it has, there- fore, been for twenty years before the medical profession. During that time it has continued to receive approval both at home and abroad, and has been translated into the French, the Italian, and the Spanish languages. Several new chapters have been added to the present edi- tion, so that I may, I think, confidently express the opinion that it is more than ever worthy of the confidence which it has hitherto obtained. William A. Hammond. Washington, D. C., March 1, 1891. CONTENTS. PAGE Introduction, 17 The Instruments and Apparatus employed in the Diagnosis and Treatment of Diseases of the Nervous System. Electrical Reactions, Normal and Pathological, . . . .28 SECTION I. DISEASES OF THE BRAIN. CHAP. I.—Cerebral Congestion, 32 Active Cerebral Congestion.—Passive Cerebral Congestion. II.—Cerebral Anaemia, 70 III. —Cerebral Haemorrhage, 80 IV. —Cerebral Meningeal Haemorrhage, 124 Pachymeningitis and Haematoma of the Dura Mater. Y.—Partial Cerebral Anaemia from Obliteration of Cerebral Blood-Vessels, 132 Thrombosis of Cerebral Arteries.—Embolism of Cerebral Arteries.— Thrombosis of Cerebral Veins and Sinuses.—Embolism and Thrombo- sis of the Cerebral Capillaries. VI.—Cerebral Softening, 161 VII.—Aphasia, 182 VIII.—Acute Cerebral Meningitis, 212 IX.—Chronic Cerebral Meningitis, 221 Chronic Verticular Meningitis.—Chronic Basilar Meningitis. X.—Tubercular Cerebral Meningitis, 251 XI.—Suppurative Encephalitis or Cerebritis, .... 259 Cerebria. 10 CONTENTS. CHAP. PAGE XII.—Diffused Cerebral Sclerosis, 271 XIII. —Paralysis Agitans, 282 XIV. —Tumors of the Brain, 296 XV.—Athetosis, 315 XVI.—Cerebral Syphilis, 342 Anatomical Lesions.—Etiology.—General Symptomatology. XVII.—Symptomatology of Cerebral Lesions, 334 Cortical Paralysis.—Paralysis consecutive to Central Lesions of the Hemispheres.—Lesions of the Tubercula Quadrigemina.—Oculo-Pu- pillary Troubles.—Lesions of the Optic Tracts.—Lesions of the Cere- bral and Cerebellar Peduncles. XVIII.—Symptomatology of Cerebellar Diseases, .... 348 Tumors of the Cerebellum.—Haemorrhages of the Cerebellum.—Noth- nagel’s Diagnostic Points. SECTION II. DISEASES OF THE SPINAL CORD. I. —Spinal Congestion, 365 II. —Spinal Anaemia, 373 Anaemia of the Posterior Columns.—Anaemia of the Antero-Lateral Col- umns. III. —Spinal Haemorrhage—Spinal Meningeal Haemorrhage, . 406 IV. —Spinal Meningitis, 413 Acute Spinal Meningitis.—Chronic Spinal Meningitis. V.—The Inflammations of the Spinal Cord, .... 429 Acute Myelitis.—Infantile Spinal Paralysis.—Spinal Paralysis of Adults. —Glosso-Labio-Laryngeal Paralysis.—Progressive Muscular Atrophy. —Progressive Facial Atrophy.—Tetanus.—Sclerosis of the Columns of Tiirck.—Primary Symmetrical Lateral Sclerosis.—Amyotrophic Lateral Spinal Sclerosis.—Progressive Locomotor Ataxia.—Sclerosis of the Columns of Goll.—Disseminated Inflammation of the Spinal Cord.—Secondary Inflammation and Degeneration of the Spinal Cord. VI.—Non-Inflammatory Softening of the Spinal Cord, . . 611 VII. —Tumors of the Spinal Cord, 616 VIII. —Syphilis of the Spinal Cord and its Membranes, . . 623 IX.—Syringomyelia, 626 X.—Pseudo-Hypertrophic Paralysis, 629 CONTENTS. 11 SECTION III. CEREBRO-SPINAL DISEASES. CHAP. PAGE I.—Hydrophobia, 641 II.—Epilepsy, 663 III. —Convulsive Tr#\ior, 698 IV. —Chorea, 710 Y.—Hysteria, 727 VI.—Hysteroid Affections, 742 Catalepsy.—Ecstasy.—Ilystero-Epilepsy. VII.—Multiple Cerebro-Spinal Sclerosis, ..... 770 VIII.—Paretic Tremor, 782 IX. —Anapeiratic Paralysis, 784 X. —Exophthalmic Goitre, 789 SECTION IY. DISEASES OF THE PERIPHERAL NERVOUS SYSTEM. I.—Neural Congestion, 804 II.—Acute Neuritis, 806 III.—Sciatica, 809 IY.—Multiple Neuritis, 815 Y.—Chronic Neuritis—Neural Sclerosis—Neural Atrophy, . 817 YI.—Tumors op Neryes, 820 VII.—Neural Paralysis 821 Facial Paralysis.—Paralysis of Third Nerve. VIII.—Neural Spasm, 831 Facial Spasm.—Torticollis. IX.—Neural Anaesthesia, 834 Anaesthesia of Cutaneous Nerves.—Aaesthesia of the Fifth Pair. X.—Neural Hyperesthesia (Neuralgia), 838 Neuralgia of the Fifth Pair of Nerves.—Cervico-Occipital Neuralgia.— Cervico - Brachial Neuralgia.—Dorso - Intercostal Neuralgia.—Lumbo- Abdominal Neuralgia.—Crural Neuralgia. XI.—Syphilis op the Peripheral Nervous System, . . . 849 12 CONTENTS. SECTION V. DISEASES OF THE SYMPATHETIC NERVOUS SYSTEM. CHAP. PAGE I.—Pathology of the Cervical Sympathetic, 851 II.—Neuroses of the Cervical Sympathetic, 855 Migraine, or Ilemicrania. % III. —Pathology of the Thoracic Sympathetic, 863 IV. —Pathology of the Abdominal Sympathetic, .... 865 SECTION VI. CERTAIN OBSCURE DISEASES OF THE NERVOUS SYSTEM. I.—Acute Ascending Paralysis (Landry’s Paralysis), . . . 868 II.—Myxcedema, 870 III.—Acromegaly, 878 IY.—Thomsen’s Disease (Myotonia Congenita), 880 V.—Raynaud’s Disease (Symmetrical Gangrene of the Extremities), 882 SECTION VII. TOXIC DISEASES OF THE HER VO VS SYSTEM. I.—Plumbism, i . 886 II.—Alcoholism, 896 III.—Bromism, 915 IY. —Hydrargism, 921 Y.—Arsenicism, 923 LIST OF ILLUSTRATIONS. PIG. PAGE 1. Static Electrical Machine, Hammond, . . .20 2. Milliamperemeter, “ ... 21 3. JSsthesiometer, “ ... 23 4. Lombard’s Differential Calorimeter, ... “ ... 25 5. Lombard’s Thermo-Electric Pile, .... “ ... 26 6. Dynamometer, “ ... 27 7. Duchenne’s Trocar, “ ... 28 8. Miliary Aneurism of Brain, ..... Bouchard, . . .107 9. “ “ “ Hammond, . . .107 10. Atheromatous Artery of Brain, .... “ ... 109 11. Diagram explanatory of Paralysis in Cases of Cerebral Haemorrhage, “ . . .113 12. Diagram explanatory of Crossed Paralysis, . “ . . .115 13. Cerebral Arterial Thrombosis, .... Heubner, . . . 140 14. Cerebral Capillary Embolism, .... Virchow, . . . 158 15. “ “ “ ... 158 16. Diagram explanatory of the Cortical Lesions producing Aphasia, ...... Modified from Naunyn, 204 17. Agraphia, Hammond, . . . 208 18. Dynamographic Tracing of Patient affected with Paralysis Agitans, “ ... 286 19. Dynamographic Tracing of Patient affected with Paralysis Agitans, “ ... 287 20. Malignant Tumor of Brain, Otis, .... 301 21. Aneurismal Tumor of Brain, .... Prof. W. R. Smith, . 308 22. Hand of Patient with Athetosis, .... Hammond, . . . 317 23. “ “ after Photograph from Dr. Hub- bard, “ ... 320 24. Vertical Sections of the Brain, showing the Sit- uation of the Lesion in the Original Case of Athetosis, ........ From drawings by Dr. Spitzka, . , . 323 14 LIST OF ILLUSTRATIONS. F,°' 25. Side View of the Human Brain and the Areas of the Cerebral Convolutions, .... Ferrier, . . . 33*7 26. Horizontal Section through the Human Brain, showing the Internal Capsule, . . . Hammond, . . . 339 2'7. Diagram of the Relation of the Fields of Vision, Retina, and Optic Tracts, Gowers, . . . 346 28. Diagram explanatory of the Crura Cerebri, . Modified from Gowers, . 347 29. Patient with Probable Atrophy and Sclerosis of Cerebellum, Hammond, . . .379 30. Diagram explanatory of tiie Medulla Oblongata, Modified from Edinger, 359 31. Morbid Anatomy in Cervical Pachymeningitis, Joffroy, . . . 418 32. Deformity caused by Cervical Pachymeningitis, Charcot, . . .419 33. Deformity caused by Chronic Spinal Menin- gitis, ......... Hammond, . .426 34. Spinal Cord in Infantile Spinal Paralysis, . . Charcot, . . . 447 36. “ “ “ “ “ . . “ ... 447 36. “ “ “ “ “ . . “ ... 448 37. Altered Nerve-Cells of Cord in Infantile Spinal Paralysis, “ ... 450 38. Muscle in Infantile Spinal Paralysis, . . Hammond, . . .451 39. “ “ “ 451 40. “ “ “ 451 41. “ “ “ 452 42. “ “ “ “ “ ... 452 43. “ “ “ 457 44. “ “ “ 457 45. Atrophy of Muscles in Spinal Paralysis of Adults, . “ ... 467 46. Atrophy of Muscles in Spinal Paralysis of Adults, “ ... 477 47. Glosso-Labio-Laryngeal Paralysis, ... “ ... 481 48. Writing of Patient affected with Glosso-Labio- Laryngeal Paralysis, “ ... 483 49. Glosso-Labio-Laryngeal Paralysis, ... “ ... 484 50. “ “ “ “ . . . . “ ... 485 51. Progressive Muscular Atrophy, .... “ ... 496 52. “ “ “..... Duchenne, . . . 498 53. “ “ “..... Friedreich, . . . 499 54. “ “ “..... Duchenne, . . . 501 55. Spinal Cord in Progressive Muscular Atrophy, Charcot, . . . 513 56. Progressive Facial Atrophy, Hammond, . . . 522 57. Progressive Facial Atrophy, Lande, .... 524 58. “ “ “ 524 59. “ “ “ 524 PAGE LIST OF ILLUSTRATIONS. 15 PIG. 60. Muscular Fibre in Progressive Facial Atrophy (Longitudinal Section—normal), .... Hammond, . . . 528 61. Muscular Fibre in Progressive Facial Atrophy (Longitudinal Section—abnormal), ... “ ... 528 62. Muscular Tissue in Progressive Facial Atrophy (Transverse Section—normal), .... “ ... 528 63. Muscular Tissue in Progressive Facial Atrophy (Transverse Section—abnormal), .... “ ... 528 64. Diagram of a Section of the Spinal Cord in the Cervical Region, Gowers, . . . 532 65. Diagram explanatory of Anaesthesia in Lesions of Cord, ........ Hammond, . . . 534 66. Section of Spinal Cord in Sclerosis of Lateral Columns, ........ Charcot, . . . 553 67. Section of Spinal Cord in Lateral Sclerosis, . “ ... 553 68. “ “ “ “ “ . . “ ... 553 69. Section of Medulla Oblongata, .... “ ... 553 70. Diagram representing the connection between the Lateral Pyramidal Tract and the Motor Cells, ......... Modified from Bramicell, 554 71. Deformity in Amyotrophic Lateral Spinal Scle- rosis, Charcot, . . . 558 72. Section through Medulla Oblongata in Amyo- trophic Lateral Spinal Sclerosis, ... “ ... 563 73. Writing of Patient with Locomotor Ataxia, . Hammond, . . i 572 74. Dynamographic Tracing of Patient with Loco- motor Ataxia, “ ... 573 75. Dynamographic Tracing of Patient with Loco- motor Ataxia, “ ... 573 76. Superior Extremity of Healthy Humerus, . . Charcot, . . . 585 77. “ “ Diseased Humerus of Pa- tient with Locomotor Ataxia, .... “ ... 585 78. Diagram explanatory of the Nerve-Fibres enter- ing TnE Cord, ....... Modified from Edinger, 688 79. Diagram explanatory of the Course of the Nerve- Fibres in the Spinal Cord, .... Edinger, . . . 589 80. Section of Spinal Cord in Locomotor Ataxia, . Pierret, . . . 591 81. Suspension Apparatus, Hammond, . . . 596 82. Sclerosis of Columns of Goll, .... Pierret, . . . 598 83. “ “ “....“ ... 598 84. “ “ “....“ ... 598 85. “ “ “....“ ... 598 86. Diagram explanatory of the Connections between the Motor Tracts and the Motor Cells, . . Modified from Bramwell, 607 PAGE 16 LIST OF ILLUSTRATIONS. fig. page 87. Tumor of the Spinal Cord, Charcot, . . .618 88. “ “ “ “ ... 618 89. “ “ “..... Leyden, . . .621 90. Syringomyelia, Van Giesen, . . . 628 91. “ “ ... 628 92. Patient with Pseudo-Hypertrophic Paralysis, . Hammond, ... . 632 93. “ “ “ “ “ 632 94. “ “ “ “ “ 634 95. “ “ “ “ . “ . . . 635 96. “ “ “ “ “ 635 9*7. “ “ “ “ 635 98. Cortical Substance of Brain in Hydrophobia, . “ ... 656 99. Nuclei of Pneumogastric and Hypoglossal Nerves in Hydrophobia, “ ... 657 100. Root of Pneumogastric Nerve in Hydrophobia, . “ . . .657 101. Neuroglia-Cells of Cord in Hydrophobia, . . “ . . 658 102. Contractions in Hysteria, Charcot, . . . 734 103. “ “ “ ... 742 104. Catalepsy (after Photograph from Dr. Early), . Hammond, . . . 747 105. “ “ “ “ « '. “ . . . 747 106. Induced Catalepsy, “ ... 751 107. Ecstasy, Bourneville, . . . 758 108. Hystero-Epilepsy, Hammond, . . . 764 109. “ “ “ ... 765 110. “ “ Charcot, . . .767 111. “ “ “ ... 768 112. “ “ Bourneville, . . . 769 113. Writing of Patient with Multiple Cerebro- Spinal Sclerosis, Hammond, . . .780 114. Writing of Patient with Anapeiratic Paral- ysis, “ ... 786 115. Exophthalmic Goitre (after Photograph from Dr. J. B. Crawford), “ ... 792 116. Hand of Patient with Myxiedema, ... “ ... 875 117. Portrait of Patient with Myxcedema, . . . “ ... 876 118. Diagram showing the Anatomical Divisions of the Spinal Cord, “ ... 640 DISEASES OF THE NERVOUS SYSTEM. INTRODUCTION. THE INSTRUMENTS AND APPARATUS EMPLOYED IN THE DIAGNOSIS AND TREATMENT OF DISEASES OF THE NERVOUS SYSTEM. Diseases of the nervous system, like those of the heart, lungs, and larynx, require special means of investigation and treatment. In no department of medical science has progress been more decided dur- ing the last decade than in that class of affections considered in this treatise, and undoubtedly a great deal of the advancement is due to the instruments and apparatus by which scientific research in this direction has become practicable. In the present chapter I propose to describe thejnstruments and apparatus employed in the diagnosis and treatment of diseases of the nervous system, and to explain the methods by which they are used. THE OPHTHALMOSCOPE. The ophthalmoscope consists essentially of a concave mirror per- forated in the centre, and of a double-convex lens. Several modifi- cations of this arrangement are in use, but the simplest instrument is, in my opinion, the best for ordinary use, and this is Liebreich’s; though, when very great exactness is required, as, for instance, in determining the depth of an atrophic excavation of the optic disk, Dr. Loring’s ophthalmoscope is far preferable to any other. Liebreich’s ophthalmoscope consists of a polished steel mirror about one and three-quarters inch in diameter, concave, and perforated in the centre by a hole about the one-twelfth of an inch in diameter. The edges of this aperture are beveled, so as to afford as little ob- stacle as possible to the passage of the rays of light to the eye of the observer. The mirror is set into a bronze ring with a handle, and there is attached also to this ring a clip for holding a concave ocular lens, which in some conditions of refraction, either in the eye of the pa- 18 DISEASES OF THE NERVOUS SYSTEM. tient or that of the observer, is necessary in order to produce the requisite divergence of the parallel rays emanating from the pa- tient’s eye, and thus render the image of the fundus distinct. A direct image is thus obtained. The lamp, which should furnish a steady flame, is placed on the side of the patient’s head correspond- ing to the eye to be examined, and the eye of the observer very close to that of the patient. This process gives a very satisfactory view of the fundus with the optic disk and retinal vessels, but re- quires care, and is more difficult than that by which the inverted image is obtained. In this case the observer illuminates the fundus with the ophthal- moscopic mirror, and then interposes between the mirror and the eye a double-convex lens which he holds lightly between the thumb and Anger, resting the ring-finger on the forehead of the patient, so as to make the hand steady, the little finger being disengaged so as to be employed in raising the eyelid if necessary. The object-lens should have a focal distance of about two inches, and it should be held so as to bring the focus on the pupil. The lamp is placed behind and a little to one side of the eye to be examined. In order to see the optic disk, the patient is told to look at the ear of the observer on the side opposite to the eye being examined. In this way the axis of vision is directed inward, and the optic disk readily brought into view. These examinations are made in a room lighted only by the lamp used in the processes. It is sometimes necessary to dilate the pupil with atropia, in order to obtain a view of the disk, but experience and tact will generally enable the observer to dispense with this rather dis- agreeable procedure. Ophthalmoscopic examinations require the observer to possess a very thorough acquaintance with the anatomy of the eye, and also with the science of optics. Unless these qualifications are enjoyed, it will be much better to send the patient to a competent ophthalmic surgeon for an examination than to rush to hasty conclusions based on the most thorough ignorance. The real value of ophthalmoscopy in diseases of the nervous system is in danger of being disregarded through the sciolism of pert pretenders, who read papers and write memoirs without ever having seen the optic disk to recognize it. Bouchut1 gives the following list of abnormal conditions which are of importance in the diagnosis of diseases of the nervous system : Papillary congestion ; peri-papillary congestion ; papillary ansemia, partial or general; phlebo-retinal flexuosities ; venous pulsation in the retinal veins ; dilatations of the retinal veins ; retinal varices; phlebo-retinal luemostases ; phlebo-retinal thromboses ; phlebo-retinal 1 “ Du diagnostic de3 maladies du systeme nerveux, par l’ophtlialmoscopie,” Paris, 1866, p. 16. INTRODUCTION. 19 aneurism ; haemorrhages into the retina and choroid. The diseases in which he thinks ophthalmoscopy is valuable as a diagnostic means are: The several varieties of cerebral meningitis; cerebral ha3mor- rhage ; chronic encephalitis ; cerebral softening; meningeal haemor- rhage ; chronic hydrocephalus ; tumors of the brain ; contusion, com- motion, and compression of the brain ; general paralysis ; atrophy of the brain; chronic myelitis ; locomotor ataxia ; tetanus ; epilepsy; essential convulsions ; insanity ; and several others of less importance. To these may be added cerebral congestion, general and partial; cerebral anaemia ; and the various forms of sclerosis affecting the brain and spinal cord. ELECTRICAL APPARATUS. The electrical apparatus required in the diagnosis and treatment of diseases of the nervous system must be of two kinds: one for furnishing the primary or galvanic current, the other for yield- ing the induced or faradaic current. Among the best machines of the first category are those in which the current is derived from the Leclanche, the Grenet, or the chloride-of-silver cells. If the Le- clanche elements are preferred, from forty to one hundred cells are necessary; and as these cells are large, this form of battery can only be used as an office fixture. For a portable battery, those manu- factured by AVaite and Bartlett, Jerome Kidder, the Galvano-Fara- dic Company, and the Barrett Battery Company, will be found to meet every requisite. The Barrett battery is especially adapted for transportation, as it contains no fluid. Portable batteries containing from twenty to thirty cells are strong enough for almost all prac- tical purposes. Of faradaic batteries, those manufactured by the firms previously mentioned leave nothing to be desired. Combination batteries, fur- nishing both galvanic and faradaic currents, can also be obtained from these makers. Lately there has been a revival of statical electricity, and such perfect instruments for its production are being manufactured that this form promises ere long to come into general use again. Fig. 1 gives an excellent representation of the modern statical electric ma- chine. I have witnessed some excellent results of its therapeutical power in cases of neuralgia, paralysis, and rheumatism. Although the applications of electricity in the treatment of dis- eases of the nervous system are not so extensively useful as asserted by some authors, it is nevertheless impossible for the physician to treat several affections of the kind mentioned without using the agent in some form or other. This is especially true of those diseases which are characterized by paralysis, in nearly all of which electricity is use- ful. In atrophic disorders it is also indispensable, and in many hys- 20 DISEASES OF THE NERVOUS SYSTEM. terical conditions it is extremely valuable. If only one battery can be procured, the faradaic instrument will be found more generally useful than any other; but, if possible, the physician who intends to Fig. 1. treat to the utmost advantage diseases of the nervous system, should possess one of all three kinds mentioned. THE MILLIAMPEREHETER. This instrument, a representation of which is given in Fig. 2, is used to determine the rate of the current flow, or the quantity of electricity which passes through that part of the individual which is included in the circuit of the galvanic current. The milliampfere- meter is a galvanometer so constructed that the deflections of the INTRODUCTION. 21 needle have definite meanings. Beneath the needle is a scale whose divisions represent milliamperes, or tenths of milliamperes. By means of resistance- coils, which can at pleasure be included in the circuit of the in- strument, each of the divisions can be made to represent re- spectively ten or onehundredmil- iiamp&res. The ampere is the unit of the cur- rent flow; but as a current flow of one ampere is far too great for diagnostic or therapeutic purposes, and as an individual could not en- dure a current of one amphre unless the elec- trodes were of enormous size, it has been found necessary to so regulate the re- sistance of the galvanometer that when a galvanic current is passed through it it will register thousandths of an ampere, or milliamperes. The milliamphremeter is as necessary to the physician who uses galvanism as the graduated measuring-glass is to the pharmacist. It enables him to measure accurately the quantity of electricity used. He can writh certainty administer, day after day, the same How of current, and by this means can definitely determine whether the same effects are always produced. When a current of a certain number of cells is applied to an indi- vidual, it can give no accurate idea of the flow of current through him. The resistance of individuals varies from day to day ; the re- sistance in the electrodes varies according to their degree of moist- Fig. 2. 22 DISEASES OF THE NERVOUS SYSTEM. ure ; and the current derived from the battery-cells varies according to their condition of freshness. It can therefore be readily under- stood, as these three factors are never constant, how impossible it is to pass the same flow of current through the same tissues at any two consecutive trials. But if the milliamphremeter is included in the circuit, the differences in the resistance of the individual and the elec- trodes and the strength of the cells need not be considered. It is simply necessary to include as many cells in the circuit as may be required to deflect the needle of the meter to a certain point. At future trials, when the indicator reaches the same position, it signifies that the same flow of current is passing through the tissues, no matter whether it takes a greater or less number of cells to produce the desired result. CAUTERIZING APPARATUS. It is often necessary, in the ti*eatment of diseases of the nervous system, to make use of the actual cautery to the spine and other parts of the body. The instruments formerly employed were very clumsy things made of iron, and, when required for use, were heated in a furnace of some kind. Lately the Paquelin cautery, furnished with platinum tips of such shapes as may be required, and the electric cau- tery, have come into general use. OTHER INSTRUMENTS AND APPARATUS. Among the other instruments and apparatus required in the diag- nosis and treatment of diseases of the nervous system are the micro- scope, the sphygmograph, the stethoscope, ear-specula, tuning-forks, urinary test apparatus and chemicals, hypodermic syringes, and a spray apparatus. The latter is useful for refrigerating the skin over the spinal column in cases of chorea and other affections. jESTHESIOMETER. The aesthesiometer is an instrument for the purpose of determining the degree of tactile sensibility possessed by the patient. It was de- vised in 1858 by Dr. Sieveking,1 of London. Its value in cases of aberrations of sensibility depends upon the fact, ascertained by Dr. E. H. Weber, that the capability of distinguishing two impressions, made upon the skin simultaneously, varies in different regions of the body according to the distance they are apart. In sensitive regions, as the end of the finger, the two points of a pair of dividers can be distin- guished at about the twelfth of an inch apart, wdiile in the middle of the back only one point is felt, though they are two inches apart. In accordance with this principle, the sesthesiometer is used to determine the sensibility of the skin in various diseases, it being well known that this is subject to variation. 1 British and Foreign Medico-Chirurgical Review, January, 1858, p. 281. INTRODUCTION. 23 Thus, when the sensibility is intact, two points, touching the back of the hand at the same time, can be distinguished as two ppints when separated an inch. If, in examining a patient, we should find that, when the two points were two inches apart, the patient felt but a single impression, we should know that he had lost sensibility in the cutaneous nerves of that part of the body. Dr. Sieveking’s sesthesiometer is nothing more than a beam-com- pass. It consists of a rod of bell-metal four inches in length, gradu- ated into inches and tenths of an inch. At one end is a fixed steel point ; another steel point is made to slide upon the beam, and can be fixed at any distance from the first by a screw which works at the top of the slide. In 18611 I de- scribed an aesthesi- ometer which I be- lieve was the first used in this country. It consisted of a pair of dividers, to one arm of which the arc of a circle, in brass, w'as affixed. This arc was divided so as to meas- ure tenths of an inch. A short time since, I suggested to Mr. Stohlman, the instrument - maker, a modification of this instru- ment, which for convenience is, I think, superior to all others. This, as closed, for the pocket-case, and open, as in use, is seen in the accompanying woodcut (Fig. 3),2 and need not be further de- scribed. The minimum normal distances at which the two points of the aesthesiometer can be distinguished in different regions of the body are stated in the table on the following page.3 Fig. 3. 1 “A Clinical Lecture on Chronic Myelitis,” delivered in the Baltimore Infirmary, March 16, 1861, American Medical Times, June 15, 1861, p. 379. 2 First described by me in the Journal of Psychological Medicine, October, 1868, p. 830. 3 This table is quoted from Muller’s “ Physiology,” translated by Baly, London, 1840, D. 752. 24 DISEASES OF THE NERVOUS SYSTEM. Point of the tongue £ a line. Palmar surface of the third finger 1 “ Red surface of the lips 2 lines. Palmar surface of second linger 2 “ Dorsal surface of third finger 3 “ Tip of the nose 3 “ The palm over the heads of the metacarpal bones 3 “ Dorsum of tongue, one inch from the tip 4 “ Part of the lips covered by the skin 4 “ Border of the tongue, an inch from the tip 4 “ Metacarpal bone of the thumb 4 “ Extremity of the great-toe 5 “ Dorsal surface of the second finger. 5 “ Palm of the hand 5 “ Skin of the cheek 5 “ External surface of the eyelids 5 “ Mucous membrane of the hard palate 6 “ Skin over the anterior surface of the zygoma 7 “ Plantar surface of the metatarsal surface of great-toe 7 “ Dorsal surface of the first finger 7 “ On the dorsum of the hand over the heads of the metacarpal bones 8 “ Mucous membrane of the gums 9 “ Skin over the posterior part of the zygoma 10 “ Lower part of the forehead 10 “ Lower part of the occiput 12 “ Back of the hand 14 “ Neck under the lower jaw 15 “ Vertex 15 “ Skin over the patella 16 “ “ “ sacrum 18 “ “ “ acromion 18 “ The leg, near the knee and foot 18 “ Dorsum of the foot, near the toes 18 “ The skin over the sternum 20 “ “ “ five upper vertebrae 24 “ “ “ spine near the occiput 24 “ “ in the lumbar region 24 “ “ “ middle of the neck 80 “ “ over the middle of the back 80 “ The middle of the arm 30 “ “ “ thigh 30 “ The thermometer is of use for the purpose of determining varia- tions of temperature in different parts of the body. It should be graduated in tenths of a degree, and be held upon the part subject- ed to examination, so long as the mercury continues to rise or fall. Comparative determinations must be made under precisely similar conditions. THERMOMETER. INTRODUCTION. 25 becquekel’s disks. By means of these little instruments very slight variations of tem- perature can be ascertained. They consist of an extremely thin plate of copper about the size of a half-dime, soldered to a thin rod of bis- muth. This latter is contained in a small tube of hard rubber fur- nished with a handle. The disks are two in number, and by means of delicate silk-covered wires are in communication with the poles of a galvanometer. If a lower extremity, for instance, is subjected to examination, one of the disks is placed upon it and the other upon the corresponding part of the other limb. If the temperature of both limbs be the same, the needle of the galvanom- eter remains quiet; if either be warmer than the other, the needle is deflected to the north or south according as one or the other limb has the higher temperature. By this apparatus very much less than the hun- dredth of a degree of temperature can be de- termined with absolute accuracy.1 Fig. 4. 1 See my “ Memoir on the Pathology and Treatment of Organic Infantile Paralysis,” in Journal of Psychological Medicine, No. 1, July, 1867, p. 53. 26 DISEASES OF THE NERVOUS SYSTEM. dr. lombard’s thermo-electric differential calorimeter. For determining differences of temperature nothing equals this instrument, both for exactness of results and facility of application. It consists, as shown in the accompanying cuts, of a galvanometer (Fig. 4) and two thermo-electric piles (Fig. 5). The needle of the galvanometer is astatic, and is suspended by a deli- cate silk fibre so as just to swing clear of the scale it is to traverse. Above the needle and outside of the glass shade is a magnet by means of which the needle is readily made to point to the zero of the scale. Upon the ebonite plate to the left of the gal- vanometer needle are the bobbins and four little cups of mercury by means of which the connections are made, and the resistance of the thermo-electric cur- rent increased or diminished, according as it is neces- sary to make the needle more or less delicate in its indications. There are two thermo-electric piles, one of which is represented in Fig. 5, and which for convenience of manipulation are furnished with handles. These piles are connected by their positive and negative poles, and the other positive and negative poles are con- nected with the stanchions seen on the ebonite plate of the galvanometer. Having lowered the little metallic fork at the far- ther extremity of the bar over the ebonite plate into the cup of mercury immediately under it, the appa- ratus is ready for use. The delicacy is increased by lowering one or two, or all three of the others, each one being in connection with the bobbin immediately opposite to it, and which, when the fork is out of the mercury, is included in the circuit, and hence has the effect of in- creasing the resistance. In the figure all the forks are represented as down. To make an observation, the thermo-electric piles are placed one on the part the relative temperature of which it is desired to know, and the other on the corresponding sound part. If the pile in con- nection with the stanchion nearer the corner of the ebonite plate is in contact with the hotter part, the needle will be deflected to the north. If the other be the hotter, the needle will be deflected to the south. The extent of the deflection indicates the relative difference in hun- dredths of a degree centigrade. It is to be remembered that the instrument must be placed on a firm table or stand, and must be so Fig. 5. INTRODUCTION. arranged that the end of the scale to the right of the cut points to the north ; the ebonite plate will therefore be at the south end, and the galvanometer needle points to the east.1 With this apparatus of Dr. Lombard’s it is easy to make relative determinations of temperature in a minute or two, and with great exactness and delicacy. Within the past year Waite and Bartlett have manufactured an instrument equally as delicate as Dr. Lombard’s and much less com- plicated. THE DYNAMOMETER, Several forms of an instrument for measuring the strength of pa- tients have been devised. The best and most generally applicable is that of M. Burq, modified by M. Mathieu, an instrument-maker of Paris, and still further modified by me. It is very simple, and for ascertaining the strength of the hands leaves nothing to be desired. It consists, as is shown in the cut (Fig. 6), of an elliptical steel spring, to one end of which is attached a semicircular metallic plate, upon Fie. 6. which a scale is marked. An indicator, terminating at one end in a cog-wheel, is capable of being moved freely around the arc of the cir- cle by a steel arm, on one end of which a segment of a cog-wheel is attached, the cogs fitting into those of the indicator. The other end of the arm is fastened, by a bifurcated extremity, to both sides of the elliptical spring. When the dynamometer is taken into the hand and pressed, the two sides of the spring are approximated, and the steel arm with the cogs, being pushed by both sides of the spring, turns the indicator. When the pressure is relaxed the indicator returns to its oi’iginal posi- tion. A second indicator, only attached to the plate by a spindle, is superimposed upon the first one and is carried around by it. This second indicator, not being connected with the spring, does not return 1 For a fuller description of this instrument and directions for its use, the reader is referred to the British Medical Journal for 1875. 28 DISEASES OF THE NERVOUS SYSTEM. to zero, but remains at the point to which it has been carried by the muscular power of the individual. We are thus enabled to see the extent of his strength, after he has made his effort, and do not have to watch him while he is using the instrument. In detecting the ability of the operator to maintain a steady muscular pressure this in- strument is also of service. Fluctuations of the indicator determine immediately whether the pressure on the spring is constant or not. duciienne’s trocar. This very useful little instrument is shown in Fig. 7. It is intro- duced open as at a. When it has perforated the muscle under exam- ination, the small button at the under part of the handle is pushed forward; this propels a half-cylinder of steel against the shoulder at the end of the trocar, and thus a small piece of muscle is detached Fig. 7. and caught in the cavity. The lower figure (b) represents the in- strument ready to be withdrawn. By drawing the button back, the bit of fibre can be taken out, and is then ready for microscopical examination. ELECTRICAL REACTIONS. NORMAL AND PATHOLOGICAL. In the diagnosis and treatment of diseases of the nervous system both the galvanic and faradaic currents are indispensable. In a normal condition of the muscular and nervous systems the muscles respond readily to moderate currents of both of these forms of electricity. If the faradaic current is used, the muscle or muscles to which the current is applied contract with every vibration of the interrupter. If the latter is so arranged as to make the interruptions slowly, there will be a distinct interval of rest between the contractions of the muscle. The more rapid the interruptions, the less interval there will be between the contractions of the muscle ; and, finally, if the vibrations of the hammer are extremely rapid, there will be no ap- preciable period of rest at all, and the muscle appears then to be in a ELECTRICAL REACTIONS. 29 continuous state of rigid contraction. As the current of a faradaic battery is a “ to-and-fro ” current, running first in one direction and then in the other, it follows that normal muscular tissue must respond instantly to these rapid changes of current in order to continue in a constant state of rigidity. In many forms of paralysis this ability to respond to a rapidly vibrating current is lost. It is therefore advisa- ble, in procuring a faradaic battery, to obtain one which admits of both fine and coarse interruptions. If the galvanic current is used, it w'ill be observed that the muscle to which it is applied only contracts at the “making” and at the “breaking” of the circuit, or when the strength of the current is suddenly changed. While the current is continuous the muscle remains quiescent. The same results are obtained whether the electrical applications are made to the nerves or to the muscles. The two poles of a battery are known as the anode or positive, and the cathode or negative. In testing the electrical reactions of a muscle, one electrode, the sponge surface of which should be at least two inches in diameter, should be placed on some indifferent part of the body, such as, for in- stance, the sternum, or the skin over some portion of the spine. The other electrode should be much smaller and must be provided with an “interrupting handle.” This electrode is to be applied directly to the motor points of the muscles which are to be tested. By means of a “ pole-changer ” attached to the battery either electrode can be made cathode or anode at pleasure. In individuals in a normal state of health muscular contraction, under the stimulation of the galvanic current, follows definite laws. If the weakest current is employed that will cause a muscular con- traction, it is found to take place when the negative pole is applied to the muscle and the circuit is then closed. This is termed the cathodal closure contraction, and is designated by the letters C.C.C. or K.C.C. If the current is increased in strength, the cathodal closure contrac- tion will be stronger, and there will also be a slight contraction if the pole on the muscle is made the anode and the circuit is suddenly closed. This latter is known as the anodal closure contraction, and is represented by the letters A.C.C. With increased strength of current we are enabled to obtain the anodal opening contraction, A.O.C., and the cathodal opening contraction, C.O.C. or K.O.C. It will therefore be observed that in health the cathodal closure contraction is greater than the anodal closure contraction, and the anodal opening contrac- tion is greater than the cathodal opening contraction. The normal reactions, therefore, assuming that a sufficiently pow- erful current is employed, are as follows : 1. C.C.C. 2. A.C.C. 3. A.O.C. 4. C.O.C. When degenerative changes occur in the motor nerves or in the motor cells in the anterior horn of gray matter in the spinal cord, the 30 DISEASES OF TIIE NERVOUS SYSTEM. normal reactions both to faradism and to galvanism change materially. These changes have been termed the “ reactions of degeneration ” by Erb, who first described them. The reactions of the nerves and mus- cles differ, and must therefore be considered separately. When the motor nerves are the seat of a degenerative process the reaction of the nerve to both faradaic and to galvanic currents de- creases proportionately as the degeneration increases, and, if the dis- ease is not arrested, all excitability disappears in about two weeks’ time. This is termed “quantitative degeneration.” The muscular contractility also undergoes quantitative degenera- tion. The rapidly interrupted faradaic current fails to contract the muscles at all, but a slowly interrupted current will for a few days induce slight contractions. The reaction to the galvanic current also gradually decreases. At the end of about the first week “qualitative” degenerations can be obtained. It will then be observed that the cathodal closure contraction has either diminished considerably or else has disappeared altogether, while the anodal closure contraction, wrhich was formerly insignificant, now takes precedence over all others. Frequently the cathodal and ano- dal opening contractions cannot be obtained at all, but if they can be it will be observed that the cathodal opening contraction is the stronger. Comparing the normal polar reactions wdth those obtained where disease of the motor nerve exists, we note the following difference : In health : 1. C.C.C. 2. A.C.C. 3. A.O.C. 4. C.O.C. In disease: 1. A.C.C. 2. C.C.C. 3. C.O.C. 4. A.O.C. Sometimes the polar degenerative reactions are not so well marked. In a few instances it will be observed that the anodal closure contrac- tion equals but does not excel the cathodal closure contraction. In that case the reactions are written as follows : . A.C.C. = C.C.C. and C.O.C. = A.O.C. If the degeneration of the nerve advances till it is completely de- stroyed, the polar degenerative reactions gradually fail quantitatively and eventually disappear in the reverse order to that in which they are obtained. That is, the first to be Lost will be the anodal opening contraction, then the cathodal opening contraction, then the cathodal closure contraction, and finally the anodal closure contraction. If the destruction of the nerve is not completed and if regenera- tion ensues, the electrical reactions gradually return to their normal condition. If a nerve has been so injured that it can not transmit vo- litional motor impulses, and even electrical excitation fails to induce muscular contractions, and then recovery takes place, it will be found that the muscles respond to the wilf some time before they will react to any form of electrical irritation. When the anterior horn of gray matter in the spinal cord is dis- eased so that the motor cells are involved, there is paralysis. ELECTRICAL REACTIONS. 31 Within three days after the paralysis appears it will be found that electrical excitation applied to the motor nerves which spring from the diseased area fails to produce strong muscular contractions, and that, as the disease progresses, the excitability of the nerve gradually diminishes to both forms of current till in about two weeks’ time it is abolished altogether. The degenerative reactions observed in the muscular system must not be confused with those obtained by electrically exciting the nerve. The muscles wdiich receive their motor energy from the diseased segment of the cord soon lose their contractility to the faradaic current. At first a slowly interrupted current will induce contractions, but at the end of two weeks from the beginning of the paralysis the strong- est current that the individual can bear is devoid of any motor effect. The galvanic excitability decreases slowly for a few days and then grad- ually increases until a slight current, wdiich in the normal state would not induce any appreciable muscular movement, is observed to be followed by strong contractions. With this quantitative increase the qualitative polar reactions make their appearance in the same manner as when the nerve w7as the seat of disease. The cathodal closure contraction de- clines, the anodal closure contraction is augmented, and the cathodal opening contraction takes precedence over the anodal opening contrac- tion. As the disease advances and the muscles undergo atrophy there is the same quantitative decline in the contractions that is seen when the nerve is completely degenerated ; and, finally, wdien the contractile ele- ments of the muscles have been entirely absorbed no contractions can be obtained from any strength of current. As in cases of degeneration of the nerve, the anodal closure contraction is the last to disappear. When paralysis follow’s from cerebral disease and there is no de- generation of the muscles, of the motor nerve supplying the muscles, or of that portion of the spinal cord from wdiich the motor nerves arise, the electrical reactions will be found to be normal. SECTION I. DISEASES OF THE BRAIN. CHAPTER I. CEREBRAL CONGESTION. Cerebral congestion is of two kinds, which differ as regards their mode of origin and symptoms. In the active form, there is an increase in the amount of arterial blood circulating in the vessels of the brain ; in the passive, the quantity of venous blood is augmented. Occasion- ally the two conditions coexist. This is much the more common form. Of the cases recorded in my note-book, as "occurring in my private and hospital practice, over five-sixths were of this description. Andral, who, however, failed to distinguish the first or hyperaemic stage, recognized eight varieties, all of which may with advantage be comprehended in six, which are appropriately designated from the chief feature characterizing the attack, namely, the apoplectic, the par- alytic, the convulsive, the soporific, the maniacal, and the aphasic, the latter being a sixth form, which is now for the first time systematic- ally arranged in the present category. It will doubtless be the case that, as our knowledge of the functions of the brain becomes greater, other forms of cerebral congestion, especially those of a partial charac- ter—like the aphasic, for instance—will be recognized. Among these will be*various sensory and motor disturbances, and perhaps also ab errations of mentality. For the present, however, it is perhaps better to defer considering these conditions, as often being instances of local- ized congestion, till the science of brain localization is more completely established. Any of these may occur with scarcely a moment’s warning. Gen- erally, however, there is a premonitory or first stage, the symptoms of ACTIVE CEREBRAL CONGESTION. CEREBRAL COXGESTION. 33 which, though well marked, are not peculiar, exclusively, to any one of the fully established conditions mentioned. It is therefore impossible to predict with accuracy, from the symptoms of this prodromatic stage, whether the apoplectic, the paralytic, the convulsive, the soporific, the maniacal, or the aphasic form, will be developed. An attentive study of this stage should always be made, and active measures taken for the relief of the patient at a time when success can generally be obtained. Symptoms. First Stage (Cerebral Hyperjsmia). Among the earliest symptoms of active cerebral congestion, wake- fulness is especially noticeable, and may be for a time the only evidence of disorder which attracts the attention of the patient. He goes to bed feeling weary, and as if sleep would very quickly overtake him, but he is disappointed, for he obtains but an hour or two of disturbed slumber, which is generally broken by unpleasant dreams. During the remainder of the night he tosses restlessly from side to side of the bed, his mind either occupied by the thoughts which have occurred to him through the day, or else filled with the most preposterous ideas. He consequently rises unrefreshed, feverish, and ill prepared for either mental or physical exertion.1 So far as the mind is concerned, there is an inability to give the attention to any subject requiring much thought, and at times an absolute want of power to get correct ideas of even simple matters. This is especially seen in those who have arith- metical questions to solve, or long columns of figures to add up. In- deed, mental labor of all descriptions is not only difficult, but is irk- some in the extreme. Before long the evidences of intellectual derangement become more evident. The ideas are confused and without logical arrangement; the memory begins to fail, especially in regard to recent occurrences ; and there seems to be a special proclivity to forget words, and to sub- stitute others having a similar sound when pronounced, or appearance when written. The names of persons and places are particularly diffi- cult to recollect. The judgment is weak and vacillating ; the most strongly expressed determination is changed apparently without rea- son, and again there may be an impossibility of arriving at a decision in cases where ordinarily but little reflection would be necessary. Any effort toward continuous or severe thought increases the difficulties of the mind, and augments the pain or uneasiness which generally exists in the head. Illusions, hallucinations, or delusions may be present, but are not usually fixed ; and the patient will often laugh at the absurd images he has seen, or ideas he has entertained, not five min- utes before. Persons thus affected will frequently reason clearly in regard to apparitions or voices, of the unreality of which they are fully sensible. 1 For a more complete account of wakefulness in all its relations, sec the author s treatise on “ Sleep and its Derangements.” J. B. Lippincott & Co., 1 hiladclphia, 18<0. 34 DISEASES OF THE BRAIN'. A condition very often present is a morbid apprehension of im- pending evil, for which there is no assignable cause, and the nature of which the patient can rarely define. He is sure something will happen to him, but what, he does not know ; or, if he does designate the form of trouble to ensue, he changes from one kind to another without any more reason than he had for the erroneous idea in the first place. Again, he is afraid that he may do some injurious act either against himself or others, and is hence fearful of being left alone. One patient was afraid to cross the ferry from Brooklyn lest he might be tempted to throw himself off the boat ; another kept away from railway tracks, fearing that he might be led by the sight of a passing train to put himself in the way of the engine ; another begged his wife to lock up his razors ; and another would not take a warm bath, under the appre- hension that he might neglect to turn off the hot water in time. It would be easy to enumerate very many more like instances. They remind us of “ morbid impulse,” but the subjects, unlike those of this last-named condition, never yield to the excitation. In fact, it is not an impulse, but the fear of an impulse, by which they are influ- enced. The emotional system participates in the general mental disturbance, and indeed is often the part of the mind most prominently deranged. The passions are easily roused into activity by slight exciting causes ; trifling circumstances produce great annoyance, and the little every- day troubles of life appear of vast importance. The disposition accord- ingly becomes suspicious, peevish, and fretful. Persons thus affected are very far, ordinarily, from being pleasant companions. Many of them avoid social intercourse, and shut themselves up in their rooms to brood over their real and imaginary disorders. Others, again, plunge into dissipation and excesses of every kind, in the vain expectation of being able by such means to overcome the disease ; and again others strive, by a constant change of one physician for another, or the substitution of one quack medicine for another equally quackish, to get relief from their mental and physical distress. In some, there are very few de- cided symptoms present, except the inability to sleep, and the inca- pability of concentrating the mind upon an object of study or labor, without inducing pain or discomfort of some kind in the head. In all, however, there is the same mental introspection. Every symptom is exaggerated ; and, if one with which the patient has suf- fered should happen to be absent, he is dissatisfied till it makes its appearance again, or till he has, by concentration of his mind on the subject, brought it back, and with it an aggravation of all the other phenomena. “ Doctor,” said a gentleman to me a few days since, “ I am afraid I am getting worse, for last night I slept several hours, and, if stupor should set in, I suppose it would be bad.” Another, who had for several months suffered from an almost perpetual pain in the CEREBRAL CONGESTION. 35 head, was quite sure sensibility was being destroyed when he found himself a whole day without it. This fixing of the attention upon the body is of course apt to de- velop symptoms which would otherwise, doubtless, never make their appearance ; and scarcely a day passes that instances in point do not come under my observation. The experiments of Mr. Braid in this direction are very instructive, and will bear quotation in the present connection. He requested four gentlemen, whose ages varied from forty to fifty-six years, and who were in good health, to lay their hands, palms upward, on a table, and to look at them fixedly for a few minutes. They were not to speak, but were, as far as possible, to concentrate the attention on the upturned palms, and to await the result. In about five minutes one of these gentlemen, a member of the Royal Academy, said that he felt a sensation of great cold in the hand ; another, an author of distinction, said that at first he thought nothing was going to happen, but at last he felt a darting, pricking sensation, as if electric sparks were being drawn from the hand ; the third, late mayor of a large city, reported that he felt a very uncom- fortable sensation of heat come over the hand ; and the fourth, secre- tary to an important association, had become rigidly cataleptic, the arm being firmly fixed on the table.1 Speaking of this subject, Sir Henry Holland a says : “ One limb, for instance, or even a single finger, or a portion of the sentient surface of the body, may be taken for observation, and the results tested and checked by means wholly independent of the subject of experiment, a point often very important to the truth of the result. “We have here, as in other parts of the inquiry, to look to the respective cases of attention directed by express volition, or suggested by some outward cause acting on the mind. In the former and more simple case, if a limb be taken for experiment, a peculiar sense of weight with a vibratory tingling, or sensations approaching to cramp, are produced by the consciousness concentrated upon it. It is difficult to describe by words feelings of this nature, evanescent or changing at each moment, and different doubtless in different persons ; but probably the closest resemblance is to those produced in ordinary cases by muscular fatigue or stagnant circulation through the limb. There is reason, indeed, to suppose that the muscular structure is actually affected in these cases, and frequently even by particular conditions of movement, though not volitional in kind.” Medical men are said, and doubtless with truth—as many cases will occur to the mind of the professional reader—to be particularly liable 1 For many illustrations of the power of the attention over the body, the reader is referred to the author’s “ Spiritualism, and Allied Causes and Conditions of N ervous De- rangement.” New York : 1876. s “Chapters on Mental Physiology,” p. 24. London: 1852. 36 DISEASES OF TIIE BRAIN. to be affected with the diseases to which they have given special atten- tion ; and every winter, during my course of lectures on the nervous system, I am consulted by medical students, who imagine themselves to be the subjects of the diseases I have brought to their notice ; and in some cases with reason. Under another division of the subject, I shall have occasion to return to this matter for further consideration. It follows from what has been said, that, if well persons are liable to contract diseases through mental concentration, the subjects of cerebral hypersemia must be peculiarly prone to the extension of their morbid symptoms through a like influence, and in fact this is exactly what occurs. A slight accidental sensation in some part of the body engages the attention, and becomes a fixture in the clinical history of the patient. Neuralgic pains, numbness, spasm, and even paralysis, may be thus induced, to say nothing of functional disturbances of the several organs. Under this latter head there is none more frequently met with than what, for a want of a better name, may be called false impotence. To the production of this condition, the erroneous ideas which prevail re- lative to spermatorrhoea, and the fears excited by the advertisements and books of unprincipled quacks, largely contribute. Indeed, it is rarely the case that a male patient affected with cerebral hypenemia does not at some time or other of its course imagine that he is impo- tent, and the only grounds he has for this notion are the facts that he has an occasional nocturnal emission, or the exudation of a little ure- thral mucus under the influence of sexual excitement. Still the fact is not to be overlooked that the predominance of this idea is extremely prejudicial to the patient’s well-being, and it is therefore important that the physician should, by obtaining his confidence and enlightening his ignorance, dispel the delusion at the earliest possible moment. In addition, there are certain physical symptoms of disordered cere- bral action which by their prominence force themselves into notice. Thus there are pain, lieat, a feeling of fullness or of distention in the head, the sensation as if a tight hand encircled it, or the impression of a dragging or clawing character at the vertex. Vertigo is, however, the most prominent of all this category of phenomena in the majority of cases, and may be so severe as to prevent the patient moving about. In one case recently under my charge, the subject, a gentleman of about forty years of age, was often seized with intense vertigo while walking in the street, and was obliged at such times to seize hold of a lamp-post, or, if this was not within reach, to sit down on the nearest door-step, or even the curbstone, till the violence of the attack had in a measure abated. Again, the least movement of the body, the slightest attempt at mental exertion, or the most trifling emotional disturbance, is sufficient to excite it. At times it is clearly aggravated by indiscretions in diet CEREBRAL CONGESTION. 37 or the ingestion of even a small quantity of any stimulating liquor, and at others is present during the whole period of being awake. There are two kinds of this vertigo. In one the patient seems to be in mo- tion ; in the other the objects about him appear to be tumbling topsy- turvy around him. In the latter the ground in front appears to rise up to meet him, and hence he walks as if ascending a hill. In some cases the two conditions coexist or may alternate. Probably no symp- tom is more distressing than this. It almost invariably excites more fear of serious consequences than in reality should attend it, and it prevents the patient taking that bodily exercise so conducive to his restoration to health. In some cases, however, it is entirely absent, though such are, I think, rarely met with, and, no matter how intense it may be, is scarcely ever accompanied by nausea. In other cases headache constitutes the chief physical feature of the disease, and even when not predominant is a more or less constant attendant on the morbid condition. It may be very severe, unfitting the sufferer for the slightest mental or physical exertion, or may con- sist of a dull, aching pain, very wearing, but yet bearable. It is ag- gravated by any effort to use the mind or body, and especially by any cause—such as a dependent position of the head, the use of stimulat- ing ingesta, a constriction about the abdomen, chest, or neck—likely to increase the amount of the intra-cranial blood. In some cases there is no actual pain, except as the immediate con- sequence of some one or other of the existing causes mentioned ; but the patient is always conscious of an uncomfortable sensation in the head, which, if not a pain, is capable of being readily converted into one. This is, as I have said, sometimes a mere feeling of fullness or tightness, or as if the brain—so a patient described it—were “being gathered together into a heap,” or, as another said, were “being scratched with a claw.” Again, there is the impression that the head is exactly balanced on a very sharp point, and that some effort is required to keep it from falling off. Usually the painful sensations in the head disappear toward night, or on the attempt to sleep, but resume their violence as soon as the patient awakes in the morning. The special senses could scarcely be expected to escape giving evidences of derangement, and hence among the chief manifestations of the intra-cranial disorder are those connected with the perceptive organs. Thus there are noises in the ears, such as roaring, rumbling, or sing- ing, and occasionally loud reports, such as might be produced by the discharge of fire-arms. A gentleman, recently under my care for the affection in question, informed me that when he first experienced the sensation mentioned he was sitting in his library, quietly reading, when he suddenly heard a report as if a pistol had been shot off within 38 DISEASES OF THE BRAIN. a foot of his head. He jumped to his feet, expecting to see an assail- ant behind him, but, to his surprise, there was no one to be seen, and it was very evident that no explosion had taken place. He was greatly astonished at this, but attributed the whole matter to an exaggeration, excited by his irritable nervous system, of some street noise. He had no further experience of the kind till the following morning, when, on rising from bed after a wretched night of sleeplessness, he again heard the sound, and this time it was as nearly as possible like the noise produced by striking two stoutly bound books together close to his ears. After this there was scarcely a day that the sound’ was not heard. It was entirely subjective, as persons in close proximity to him at the time heard nothing. Several such cases have come under my observation. It is not in all that the sound appears to be in the ears. In some it has seemed to be located in different parts of the head, generally, however, in the posterior region. In some cases patients have experienced the sensation as if some- thing snapped or gave way within the head, and this has, in a few rare instances, been attended with the sudden disappearance of some of the more striking symptoms. Thus, a young lady, in consequence of an intense emotion, was seized with sudden vertigo and pain in the head, and fell to the floor unconscious. Recovering her senses in a few minutes, she found herself unable to speak a word, though she uttered in an excited way inarticulate sounds having no resemblance to speech. This condition continued for several hours, when she sud- denly felt “something snap” in the head, and she instantly recovered the power of talking. The vertigo, pain in the head, and other symp- toms, persisted for two or three months afterward. In another case the onset of the disease, in a gentleman who had for many years overworked his brain, was extremely sudden, and was attended with facial paralysis. I treated him for this latter condition with electricity, with but little benefit; but one day he struck his head violently against a gas-burner hanging over his desk, and shortly afterward felt something give way within his head with a sharp, snap- ping sound, and the paralysis instantly disappeared, after having lasted some five or six days. Such cases are, in the present state of our knowledge, inexplicable. The ear becomes liypersesthetic, and loud noises are therefore dis- agreeable. At times the sense of hearing is morbidly acute, while at others it is markedly impaired. Sounds are misinterpreted with some persons, and illusions result. This is especially the case at night, when the patient is lying awake, the mind stretched to its utmost tension. A gentleman informed me that a circumstance with which most per- sons are familiar—the conversion of the sound of the ticking of a clock into some phrase or other—was to him a matter of agonizing weari- CEREBRAL CONGESTION. 39 ness. Night after night as he lay in bed, the ticking of a large clock in the hall seemed to be the constant repetition of the word “ fare- well.” Not wishing to reveal the matter to others, he endured for many nights the consequent suffering, till finally he made an excuse for leaving the city. But still the wheels of the railway cars seemed to be uttering the word “ farewell,” and it was only after a fatiguing journey to Baltimore and repose in a quiet room that he escaped the infliction. In addition to illusions, hallucinations of hearing are not uncom- mon, and are usually in the form of whispered words, which the patient hears with as much vividness as though they were real utter- ances. Like the misinterpretations of real sensorial impressions, these are usually experienced at night, and may be excited by any circum- stance, mental or physical, which tends to inci-ease the amount of blood circulating in the intra-cranial vessels. Thus, a powerful emotion, an unusually severe mental task, a strong muscular effort, or a dependent position of the head, may induce them. In one case, that of a gentle- man of rather obese development, a whisper of some kind or other was always heard when he stooped to button his gaiter-boots. In another, straining in the water-closet frequently caused a like symp- tom. In one very interesting instance the sounds were like those of musical instruments, and were arranged into familiar tunes, to the no small satisfaction of the subject ; and in another they assumed the similitude of the bark of a dog. Occasionally they are in the form of commands to perpetrate some act of violence, such as suicide. A patient, who came from Brooklyn to consult me, heard a voice whis- pering in his ear, and ordering him to throw himself into the river. “ What is the use of your going to see a physician ? ” it said. “ The best thing you can do is to kill yourself. You are of no service to yourself or any one else. Jump overboard and end the matter at once.” Though these hallucinations never imposed upon the reason of the patient, they were nevertheless sufficiently distressing, giving rise, as they did, to the fear that he might, some day or other, be in- fluenced by them to commit an act which he abhorred. The aural speculum is almost, if not quite, as valuable as the oph- thalmoscope in affording important information relative to the affec- tion under notice ; and I have been in the habit for the last five years of employing it in every case presenting the more obvious features of the disease. I do not mean to be understood as intimating that posi- tively affirmative results are to be obtained in all instances, but neither are they of any other single symptom. That the tympanum does afford an indication of the state of the intra-cranial circulation is sufficiently evident, from a consideration of the expei’iments performed by my friend Prof. Roosa and myself1 relative to the influence of the 1 “ The Influence of the Disulphate of Quinine over the Intra-Cranial Circulation.” Psychological and Medico-Legal Journal, October, 1874, p. 230. 40 DISEASES OF THE BRAIN. sulphate of quinine, the results of which have been amply confirmed by the subsequent investigations of Prof. Roosa, as well as by those of other observers. In the cerebral disorder under notice, evident congestion will almost always be observed of the vessels over the handle of the malleus, and the tympanum will be seen to be of a light pinkish color. In some cases we are prevented making the usual examination owing to the accumulation of cerumen. This must be removed by forceps or by washing, and the inspection deferred till next day. I may add that physicians, wishing to observe the connection be- tween cerebral hyperEemia and tympanic congestion, have a ready method of satisfying themselves on this point by examining the tym- panum before and after the subject has inhaled a few drops of the nitrite of amyl. This was first done, so far as I am aware, by Mr. Galton,1 and detailed in his paper entitled “ Notes on the Condition of the Tympanic Membrane in the Insane.” The faculty of vision is almost invariably more or less disturbed. Sometimes there are bright flashes of light, from over-excitation of the retina, and these, like the other symptoms, are rendered more intense upon mental or physical exertion. At other times dark spots—muscce volitantes—render the vision indistinct; and again there is the appear- ance of an undulatory vapor, such as is seen around a hot stove, or on a plain heated by the sun. The conjunctiva? are suffused ; the pupils contracted. There is intolerance of light, and motion of the eye- balls is painful, and the ophthalmic symptoms are aggravated by the effort to use the eyes. The ocular muscles easily become fatigued, and hence pain is excited by any attempt to read or to adjust the visual foci for near objects. Ophthalmoscopic examination shows the arteries of the retina to be increased in size and tortuosity, and vessels which in health are not visi- ble are now clearly perceived. The optic disk is often more or less congested, exhibiting the appearance to which Allbutt has applied the name “Congestion Papilla,” but which is perhaps more generally known as “ choked disk.” The tint of the choroid is deeper than it is when in a normal condition. The effect of cerebral congestion in giving rise to visual hallucina- tions has long been known, though it often happens that in practice the value of the fact as an indication of the state of the intra-cranial cir- culation is in a great measure disregarded. In another work2 I have considered the subject of hallucinations of sight at some length, and, as showing the influence of undoubted cerebral congestion in producing them, I quote the following case which occurred in my own experience : 1 “West Riding Lunatic Asylum Medical Reports,” vol. iii., 1873, p. 258. 2 “Spiritualism and Allied Causes and Conditions of Nervous Derangement.” New York, 1876, p. 8. CEREBRAL CONGESTION. 41 “A gentleman under the professional charge of the writer can always cause the appearance of images by tying a handkerchief moder- ately tight around his neck, and there is one form which is always the first to come and the last to disappear. It consists of a male figure clothed in the costume worn in England three hundred years ago, and bearing a striking resemblance to the portraits of Sir Walter Raleigh. This figure not only imposes on the sight, but also on the hearing ; for questions put to it are answered promptly.” “ A similar instance is related in ‘ Nicholson’s Journal.’1 ‘ I know a gentleman,’ he states, ‘in the vigor of life, who, in my opinion, is not exceeded by any one in acquired knowledge and originality of deep research, and who for nine months in succession was always visited by a figure of the same man, threatening to destroy him, at the time of his going to rest. It appeared upon his lying down, and instantly disappeared when he resumed the erect position.’ ” A case somewhat like the first of the two foregoing is referred to by De Boismont,* in which an individual was able to obtain hallucina- tions of sight by inclining his head a little forward. By this move- ment, the return of blood from the interior of the cranium was pre- vented, and hence a state of repletion favorable to the production of hallucinations was induced. Now, in the state of cerebral hypereemia which results from exces- sive brain-work or intense emotional disturbance, a condition exists not essentially different from that present in the case referred to, ex- cept in the circumstance that the excess of blood is mainly arterial, instead of venous, and that hence the congestion is more active than passive. But it must be borne in mind that it requires a very great degree of hyperaemia to cause the production of visual hallucinations, and therefore that we are not to expect them to occur in all patients who are its subjects. So far as my own experience extends, only about one in five exhibits the symptom with any degree of distinctness. Double vision is occasionally a phenomenon of the disease in ques- tion, though it is generally transient, and, as Krishaber remarks, ordi- narily only manifested in regard to bright objects. This author also speaks of a peculiarity of sight which has not come under my notice. “ A patient,” he says, “ looks at himself in a glass with astonishment, as if he had forgotten his appearance. * An- other is horrified at his image, which represents a being altogether of different traits from those which he conceived himself to possess. But he is not alarmed, for he knows that it is only his perception which is changed. This aberration exists not only as regards his own person, but other objects as well. The patient finds men and things changed ; 1 Vol. vi., p. 166. 5 “ History of Dreams, Visions, Apparitions, etc.” American edition. Philadelphia, 1835. 42 DISEASES OF THE BRAIN. he is astonished, always astonished, and it seems to him that he is a being transported to another planet.” 1 The sense of smell is very often lost, perverted, or intensely exalted. Perhaps the second named of these changes is the one most frequently met with. I have a patient now under my care, a gentleman, who from over-mental work is suffering from cerebral hyperaemia, and who constantly, while awake, smells the odor of illuminating gas. So strong is this, that he is at times unable to resist the impression that gas is escaping somewhere, and he goes from burner to burner of his resi- dence and office seeking for the imaginary leak. Another is constantly sensible of the smell of turpentine or new paint, and another has the odor of mint constantly present in his nostrils. The taste is also occasionally affected in like manner, usually, so far as my experience goes, in the way of perversion. “ Things don’t taste as they used to,” is a common complaint, and the saliva and buc- cal mucus often give the gustatory impression of other substances. It is not at all unlikely, however, that “ the bad taste in the mouth,” so often mentioned by patients, is due to a real change in the properties of the saliva or mucus. I have observed several cases in which any mental or emotional strain was sufficient to cause a bitter or other un- pleasant taste in the mouth, and the same phenomenon is quite common as a consequence of gastric disturbance. Krishaber cites two cases in which both smell and taste were entirely abolished. Sensation and the poicer of motion are usually affected, and general- ly, though not always, on one side of the body only. Thus, the arm or the leg feels heavy, and a feeling as of ants crawling over it, pins and needles sticking in it, or as if the limb were “ asleep,” is experienced. Sometimes these sensations ai’e confined to the face, the muscles of which feel drawn or tight, and the skin of which has the various indica- tions of anaisthesia mentioned. Most frequently, however, they are, I think, experienced on the scalp, giving rise to the several sensations already mentioned. Again, there is an exaltation of the sensibility of the skin and of the sensory nerves generally, and thus neuralgic pains are felt in vari- ous parts of the body ; or the cutaneous surface is extremely sensitive to the impression made upon it, whether of heat, cold, or slight pres- sure. Slight convulsive actions or twitchings of individual muscles or groups of muscles are generally present. Sometimes a few fibers only are affected. The face, and especially the eye-lids and angles of the mouth, is particularly liable to be thus involved. The muscular strength is usually weakened. The patient tires after slight physical exertion, and occasionally certain muscles, such as the deltoid and tibialis anticus, become distinctly paretic, so that there is an impair-- 1 Op. cit., p. 168. CEREBRAL CONGESTION. 43 ment of the ability to raise the arm from the side or to elevate the foot sufficiently high in walking to clear ordinary inequalities in the pavement, The dynamometer shows the grasp of the hand of one or other side, or of both, to be weakened, and the line made by the dy- namograph is zigzag or uniformly depressed. The appetite is capricious, and the stomach acts imperfectly and sluggishly. The gastric juice is not secreted in sufficient quantity for the purposes of digestion, and, the peristaltic action of the stomach being weakened, the food remains within it a long time undigested and undergoing fermentation. Regurgitations, both of the solid con- tents and of gases, are common, and the patient tastes his meals sev- eral hours after they have been swallowed. Gases accumulate in the stomach, and give rise to the sense of fullness experienced even after a very slight repast has been taken. Such symptoms are usually classed under the name of “ nervous dyspepsia,” a not improper designation, if it does not lead us into the error of regarding them as of primary importance, instead of considering them, as they are, merely consequent on the head trouble. The bowels are ordinarily costive, though at times this condition alternates with diarrhoea. The urine is in some patients scanty and high-colored, in others it is profuse and almost as pale as water. Oxalate of lime is often pres- ent, and an excess of phosphates an invariable condition, so far as my experience extends. I have already spoken of this circumstance. Whether or not the phosphates in the urine are to be regarded as the ashes of the nervous system, and hence a measure of the amount of nerve tissue decomposed, there is no doubt that they are inordinately increased after intense mental or emotional strain. I have spoken of the heat of the head of which the patient gener- ally complains. That there is a real increase of temperature can often be perceived by the hand or by the use of an ordinary thermometer. But in some cases the actual rise of temperature is so slight, notwith- standing the feeling of heat which the patient experiences, that we can- not detect it by either of these means. In such cases resort should be had to the thermo-electric differential calorimeter of Lombard, by which very minute changes of temperature can be detected, and the part of the brain in which the temperature is highest be readily ascer- tained. The experiments of Lombard, performed several years ago, show very beautifully the influence of cerebral action in augmenting the external heat of the head, and it may be remembered that, over two years ago, I detailed to the Neurological Society the results of some experiments of my own in the same direction. For several years past I have never examined a patient presenting the more obvious features of cerebral hyperaemia without carefully determining the sur- face temperature of various parts of the scalp. At times and in some 44 DISEASES OF THE BRAIN. regions the elevation reaches two degrees of centigrade above the normal standard.1 But one of the chief categories of symptoms remains to he consid- ered—chief, at least, so far as the more obvious appearances go, though, like the other visceral derangements, I must regard these as being due to the brain disorder—and that is the group of phenomena connected with the heart. To Krishaber, in the Avork already cited, belongs the credit of being the first to call attention to this remarkable series, for in the publication of my own, to which I have referred, it was in a great measure overlooked. As Krishaber remarks, the troubles of the circu- lation consist especially in an irritability of the vascular system, so that the least movement, such as rising erect from the sitting posture, or to the sitting from the recumbent, leads to an acceleration of the pulse of from 20 to 30 or even 40 beats a minute. Besides this, there are frequent and Ariolent palpitations, either spontaneous, or pnrvoked by the most insignificant causes, either mental or physical. Emotional excitement is, howeA’er, the most prolific cause of cardiac disturbance in patients affected with cerebral hyperaemia, and at times leads to serious results. The pulsations of the heart may be so irregu- lar and the action of the organ so strong as to induce grave inter- ference Avith the respiratory apparatus. Upon one occasion a lady, while in my consulting-room, was seized with a paroxysm of the kind in question, of so severe a character that for a moment or tAVO I thought she was about to die. For several months she had been wakeful, had suffered from vertigo and slight pain in the head, and, Avhile relating to me her symptoms, a blast near by, where a cellar Avas being excavated, exploded, and produced so violent and sudden a shock as to bring on the excessive cardiac action mentioned. The heart throbbed Avith so great a degree of violence that its pulsations could be readily seen through her dress and heard at the distance of two or three feet; her face and neck became livid, and, gasping for breath, she fell to the floor insensible. In a very short time, however, the inordinate movements ceased, and she recovered consciousness. Physical examination of the heart fails in these cases to reveal the existence of any organic lesion. In the intervals between the paroxysms of inordinate cardiac ac- 1 Since the above was written I have become acquainted with some recent experiments of Prof. Broca, of Paris, in the same direction. As he does not refer to either Lom- bard’s or my own experiments, though the former (“ Experiments on the Relation of Heat to Mental Work”) were published in the New York Medical Journal, January, 1867, p. 198, and a synopsis of my own in the Journal of Nervous and Mental Disease, January, 1876, I presume he is unacquainted with cither. Prof. Broca ascertained by means of thermometers, applied to different parts of the scalp, that the external temperature was affected by different internal morbid and physiological conditions, and hence confirmed the previous observations of Lombard and myself. His experiments would have yielded much more delicate and accurate results if he had employed Lombard’s instrument. CEREBRAL CONGESTION. 45 tion, the pulse is small, often slow, soft, compressible, but by no means regular, either in force or frequency. Intermissions of the beats are a common phenomenon, and give rise to anxiety and morbid apprehensions in the patient. Krishaber states that at the very beginning of the disorder there is sometimes present a series of phenomena simulating fever, such as a chill, followed by a distinct period of febrile excitement. Dur- ing this last stage the temperature of the body is elevated almost half a degree centigrade, or nearly a whole degree of our scale, and may even be double this. This accession may be repeated with some degree of periodicity, but it soon ceases, and does not reappear after the full development of the disease. I have observed this condition in about one third of the cases that have come under my observation, though usually close question- ing is necessary to elucidate the fact of its existence, so little im- pression does it make upon the mind of the patient. Sometimes, however, the paroxysms are of such severity as to excite the belief that they are of malarious origin, and, being treated with quinine, they and the other symptoms attendant on the disease are greatly aggravated. During the most intense period of the disease there are occasion- ally paroxysms characterized by entire inability to move a muscle of the body, the consciousness, respiration, and circulation not being ma- terially disturbed. I have never had a case which exhibited these symptoms, though Krishaber appears to regard them as not uncommon. On the other hand, syncope with complete loss of consciousness, which he speaks of as rare, is, according to my experience, by no means uncommon. With both of these conditions, there is an almost con- tinuous prsecordial pain, sometimes severe enough to excite the idea of the existence of angina pectoris, and causing the gravest appre- hensions on the part of the patient and his friends. That one of the primary effects of intellectual exertion or emo- tional disturbance is an increase in the amount of blood circulating through the brain, does not admit of a doubt, except from those who, still refusing to learn, contend that the cerebral circulation is not sub- ject to variation under any circumstances. Experimental physiology has, however, determined this point so positively in the affirmative that it is scarcely necessary to adduce the evidence in its support. It will be sufficient to recall the numerous facts observed by others and myself with reference to the immediate cause of sleep, by which it is shown that during the condition of wakefulness the quantity of blood in the brain is much greater than it is during sleep, the first being a state of intellectual activity, the latter one of almost complete cere- bral rest. Excessive mental exercise inordinately augments the activity of 46 DISEASES OF THE BRAIN. the cerebral circulation. The blood-vessels become over-distended, and, if the brain be kept long in a condition of extraordinary action, they may be rendered incapable of returning spontaneously to their normal dimensions. Like a bladder filled to repletion with urine, they become in a manner paralyzed and unable to contract upon their contents. They lose, to a certain extent, their elasticity, and, like the India-rubber band kept too long around a large bundle of papers, they do not regain their natural size even when the distention is removed. A state of cerebral hyperaemia is thus induced, which gives rise to a set of perfectly characteristic symptoms, and which is fraught with peril to those in whom it occurs. In a monograph published some seven years ago, Dr. M. Krishaber1 described a disorder of the brain and heart which is probably identi- cal with the one under consideration, and to which, under the name of cerebral hyperaemia, or the prodromatic stage of cerebral hyperae- mia, I called attention in the first edition of my “Treatise on Diseases of the Nervous System,” published in 1871. Krishaber’s studies have very considerably advanced our knowledge of the subject, and, as my own more recent investigations and enlarged experience have tended still further to the elucidation of a very interesting and important condition of the nervous system, I have thought it would not be out of place to bring some of the more notable results of our labors to the notice of the Neurological Society. It may be as well, however, to state here, at the outset, that I differ with Krishaber entirely relative to the pathology of the disorder we have both described, and that I am of the opinion that the cardiac symptoms upon which he lays great stress are really of quite secondary importance. In other re- spects there is no essential point of difference between us in the repre- sentations of an affection studied independently of each other, and from altogether different standpoints. The disease is sometimes developed with great suddenness, but ordinarily it advances little by little to completeness. When the former is the case, the patient experiences, under the influence of great mental excitement, pain in the head, vertigo, an inability to speak, or, at least, imperfection of articulation. There are noises in the ears, flashes of light before the eyes, and occasionally for a short time double vision. The heart beats with increased force and rapid- ity, and is more or less irregular in its action ; the face is flushed, and a feeling of suffocation is experienced. If he attempts to walk, his gait is uncertain or staggering, not only in consequence of the vertigo present, but from actual loss of power in the limbs. Numbness is commonly felt in some part of the body, and clonic spasms of the muscles, notably of those of the face, are generally present. With all these physical symptoms, there are others indicating men- 1 “De la nevropathie cerebro-cai’diaque.” Paris, 1873. CEREBRAL CONGESTION. 47 tal disturbance. Chief among these are hallucinations, or illusions of the senses, particularly of sight and hearing. Insomnia is an almost invariable attendant, and what little sleep the patient obtains is inter- rupted by unpleasant or even frightful dreams. Gradually the disor- der becomes established, and then other functions, especially those connected with digestion, are deranged. From the first the urine is loaded with urates and phosphates. As instances of the suddenness with which the disease may make its onset, I cite the following cases from my note-book : F. H., a gentleman engaged in a manufacturing business which re- quired all his attention to make it profitable, was informed one morn- ing by his superintendent that a large lot of material had been spoiled. He at once experienced an intense sensation of vertigo, a sharp pain in the head, palpitation of the heart, and would have fallen, had he not been supported by the bystanders. There were also a roaring sound in the ears and flashes of light before the eyes. On attempting to stand, the vertigo and palpitations were increased. There was at no time loss of consciousness, though the ideas were confused and the speech thick. In the course of a few hours the severity of these symptoms diminished, but that night he was unable to sleep, and in the morning the morbid phenomena reappeared, though with dimin- ished violence. For several months afterward he was troubled with wakefulness, a sense of fullness and tightness in the head, occasional weakness of the limbs, slight numbness, and a total inability to exert his mind in his business affairs without an increase in all the symp- toms. Under appropriate treatment he entirely recovered. S. L., a book-keeper, after a day of unusually arduous work, left his place of business to go home. He had hardly taken half a dozen steps when he was seized with vertigo, and fell unconscious on the side- walk. He almost immediately regained his senses, but, on trying to stand, found that he was paralyzed in both legs, and that the least motion of the body brought on a return of the vertigo, which was now attended with pain in the head, mostly in the frontal region, noises in the ears and indistinctness of vision. On attempting to speak, his articulation was so imperfect that he could scarcely be understood. There wras an uneasy feeling at the pit of the stomach, but neither nausea nor palpitation of the heart, though the action of this organ was irregular. He was taken home in a carriage, and after a sleepless night found himself very little better, except in the fact that, though his legs were still weak, there was no absolute paralysis. Gradually he got somewhat better, though walking always produced vertigo, and his gait was similar to that of a partially drunken man, as he found it impossible to avoid a zigzag course, or a decided tendency to sidle over to the edge of the pavement. Sleep was almost every night im- perfect, being disturbed by dreams of difficulties from which he could 48 DISEASES OF THE BRAIN. not extricate himself, such as the house being on fire, and, on his spring- ing from bed, discovering his door to be locked on the outside ; falling into the water, and being on the point of drowning from inability to divest himself of heavy boots, and so on. Mental application wras im- possible without leading to an aggravation of all his symptoms, and the least emotional excitement was sufficient to augment them to a high degree. He suffered in this manner for nearly a year, before re- lief was obtained, being in that time treated with remedies directed to the removal of cerebral amemia, when, in fact, the intra-cranial condi- tion was directly the opposite. M. S., a young lady, aged nineteen, and without notable predisposi- tion to neurotic disturbances, was deeply chagrined at not being in- vited to a ball at which she had confidently anticipated being present. While talking the matter over with some friends, she suddenly expe- rienced a severe pain in the head, vertigo, noises in the ears, flashes of light alternating with darkness, and violent palpitation of the heart. At the same time a peculiar thrilling sensation was felt throughout the body, especially on the left side. These symptoms continued with great intensity all that day, notwithstanding that stimulants and anti- spasmodics were administered in large quantities by the physicians called to attend her. During the night, every attempt to turn over in bed was attended with vertigo and palpitation of the heart. For over a year there was very little improvement, and the course of the disease was not essentially different from the other cases cited. The most dis- tressing symptom in her case was the persistence of the insomnia, it rarely happening that she obtained over an hour or two of unrefresh- ing slumber. When she came under my care, some thirteen months after the inception of the disease, I found that the affection, though mitigated in the violence of the attendant phenomena, was still suffi- ciently distressing to impair her capacity for enjoyment and her useful- ness to others. Recognizing the existence of congestion of the brain rather than anfemia, for which she had uniformly been treated, I acted accordingly, and had the satisfaction of seeing her gradually improve, till, at the end of less than six weeks, she was as well as she ever had been in her life. These cases are cited, not as exhibiting perfect representations of cerebral hyperaemia, but merely for the purpose of illustrating the suddenness with which the condition may be induced. They are se- lected at random from many others occurring in my hospital and pri- vate practice, and detailed in my note-book. Eventually, no matter how brusque may be the development of the symptoms, the course of the disease is not materially different from that of the more gradually established form next to be described. In- deed, there are no differences except as regards the order of sequence in which the symptoms ensue and in the fact that, in the present form, CEREBRAL CONGESTION. 49 there is, in the beginning, a greater degree of intensity in the abnormal manifestations. In the majority of cases, therefore, the affection is evolved more slowly, and the order of appearances of the phenomena somewhat dif- ferent. The foregoing constitute the ordinary assemblage of symptoms which are first met with in congestion of the brain. Some of them may be absent, others so slightly manifested as to escape ordinary ob- servation, and others, again, so strongly exhibited as to excite the grave apprehensions of the patient and his friends, and to require him to keep his bed. Generally, however, they are not so severe as to prevent him attending in a measure to his ordinary avocations, and they may alto- gether disappear, either spontaneously or in consequence of appropriate medical treatment. A spontaneous cure is, however, rare, and, without proper manage- ment on the part of the patient or his medical attendant, the symptoms pass, sooner or later, into one of the fully developed forms mentioned. Thus, of the cases that have been under my observation, the disease was arrested at the first stage in about ninety-five per cent, by appro- priate treatment, while there was not a single instance of spontaneous cure. The fact that abscesses of the liver may be associated with cere- bral hypera?mia, probably as a direct result, was pointed out by me1 a short time since, and several cases detailed in which aspiration had led to the evacuation of pus from the liver. Since the publication of the original paper on the subject, other similar cases have come under my notice, and like ones have been reported by other observers.2 It is probable, however, that other brain lesions—as is well known of blows upon the head—are capable of inducing the condition in question. The subject will be more appropriately considered in detail in my forthcoming work on mental disorders. Second Stage, a. The Apoplectic Form.—Occasionally this va- riety of cerebral congestion is initial, but ordinarily it is preceded by the group of symptoms just detailed. In either event the onset is gen- erally sudden. The patient is perhaps walking in the street, when he staggers, loses consciousness, and falls. The loss of intelligence and sensibility is, however, rarely complete, and may last but a few minutes or even seconds, though sometimes continuing for several hours. Paralysis, to a greater or less extent, is always present for a time. 1 “ On Obscure Abscesses of the Liver: their Association with Hypochondria and their Treatment.” St. Louis Clinical Record, June, 18*78. 2 “ The Diagnosis of Abscess of the Liver by Symptoms of Cerebral Hyperemia,” etc. By J. Marion Sims, M. D. Virginia Medical Monthly, January, 1880. “ Hyperaemia of the Brain associated with Hepatic Abscess,” by W. H. De Witt, M. D Medical Gazette, April 3, 1880. 50 DISEASES OF TIIE BRAIN. One limb only may be affected, or those of one side, or all four mem- bers. It is never complete, the patient being able to perform some movements, though not to exert his full strength. The face is rarely involved, and the patient, though answering briefly when addressed in a loud voice, speaks indistinctly and with difficulty. The respiration is loud, slow, but rarely stertorous, and it is not often that there is puffing of the lips and cheeks. The pulse is slow, hard, and full. Sometimes the face is flushed, and sometimes it is unusually pale. The sphincters generally retain their power. The senses, though weakened, are often capable of being exercised by tolerably strong excitations. A bright light causes uneasiness and closure of the eye- lids. A loud noise is productive of discomfort, and a limb, when pinched, is withdrawn. The power of the mind is greatly lessened, and some faculties are altogether abolished. Answers, more or less direct, are given to simple questions put in a loud tone, but even moderate intellectual action seems to be impossible. Gradually the attack passes off, leaving the patient in a state of mental and physical depression, which may last for several days. The paralysis usually disappears, but occasionally it does not, one or more limbs or muscles remaining permanently, or for a long time, disabled. It sometimes happens, however, that the termination is not so favor- able. The vessels may remain congested, serum may be effused, and death may result without there being any vascular lesion. Two cases have come under my notice, in which death ensued from this cause in first attacks. A person who has once had a paroxysm, such as has been described, is thereby rendered more liable to subsequent seizures, each one of which still further permanently impairs his mental and physical powers. In one case, occurring in my practice, there have been eleven attacks in five years ; and in another, fourteen in four years. In both of these, and in several similar instances I have witnessed, there was paralysis, which had become more profound with each accession. It is therefore inexact to say, as do some writers, that the paralysis of cerebral con- gestion always disappears in a short time. The apoplectic form of cerebral congestion is more common than any other of the fully developed varieties, about one half of all the cases being of this type. b. The Paralytic Form.—Like the apoplectic variety, this may be unpreceded by the premonitory symptoms constituting the first stage, but usually they have been present. The loss of power or of sensibil- ity, or of both, may be very circumscribed, limited to a single group of muscles in the one case, or a small portion of the cutaneous surface in the other, or one entire side, or both sides of the body, may be in- volved. It differs from the apoplectic form in no essential respect, except that there is no loss of consciousness. Its onset is sudden. CEREBRAL CONGESTION. 51 c. The Convulsive Form.—This, like the variety just described, may come on suddenly, or may be preceded by premonitory symptoms. The phenomena of the attack do not generally differ from those attend- ant on an ordinary epileptic paroxysm, except that there is never an aura, and no peculiar cry, such as is so often met with in pure epilepsy. There is the same tonic spasm, followed by clonic convulsions, which may or may not be confined to one side of the body, and which may or may not be followed by temporary or long-continued paralysis. Stupor likewise supervenes, but is neither of so long a duration nor so pro- found as in true epilepsy. In other cases, and especially in infants or young children, there is no loss of consciousness. The pain in the head is intense, the pupils are contracted and insensible to light; there are vomiting and accelera- tion of the pulse. The convulsive movements, which may be either tonic or clonic, or both alternately, are either quite general or confined to a single limb or even a group of muscles. This form of cerebral congestion is never developed during sleep, for then the brain contains less blood than when the individual is awake. It may occur during stupor induced by certain drugs, constriction of the neck, or a dependent position of the head ; but stupor is not sleep, although the two conditions are frequently confounded. Convulsions occurring during ordinary sleep are never the result of congestion. This point will be more fully considered under the head of epilepsy. After the stupor the patient may feel comparatively well, or there may be delirium, continuing for several hours. As in the apoplectic form, there may be a succession of attacks, and the mind and physical power of the patient are thereby greatly weakened. The variety under consideration is, perhaps, more liable to occiir in individuals past the age of forty, though I have witnessed several cases in quite young persons. It is not often met with in old age, and, when it is, is generally fatal, probably from secondary lesion. A majority of the cases of epileptiform convulsions, occurring for the first time in persons over the age of forty, are instances of the convulsive form of cerebral congestion. cl. The Soporific Form.—This form will be more fully described under the head of passive cerebral congestion, to which condition it is almost entirely restricted. It differs from the apoplectic form in the circumstance that the invasion is gradual; and from this and the para- lytic in the fact that there is no paralysis, although the limbs may be in a state of general resolution. The chief phenomena are pain in the head, dilatation of the pupils, and stupor. e. The Maniacal Form.—This variety, though not so common as either of the others, is yet not infrequent. It is characterized by an accession of mental derangement not materially different from that in- dicative of acute mania. The delirium is of a very active character, the 52 DISEASES OF THE BRAIN. eyes are suffused, the face is red, the head hot, the motility active, and the whole manner, character, disposition, and mental processes are changed. During the paroxysm, the patient may commit some act of violence, and it almost always happens that his combative proclivities are aroused. He may likewise attempt to injure himself. The attack may come on with great suddenness. In the case of a gentleman recently under my charge, it was the result of eating a hearty meal in a great hurry at a railway station. A few minutes after his return to the train, he was attacked with furious delirium, during which he attempted to injure himself and all within his reach. He was seized and held, but continued, as far as he was able, to bite, scratch, and kick at those who were near him. The paroxysm lasted about two hours. He then fell into a heavy stupor, from which he did not arouse for two hours longer. For several days his mind was weak, and there was numbness in various parts of his body. Gradually, however, he regained his former powers, but he suffered from occasional confusion of thought and difficulty of speech, with headache and wakefulness, for several weeks. In another case—that of a boy thirteen years of age—it was charac- terized by paroxysms of maniacal excitement, during which the subject attempted to bite and otherwise to injure those around him, indulging at the same time in the most profane and obscene language. These seizures took place about once a week. There was generally a distinct recollection of all the events which had happened. In several other cases, the seizures were the result of malarial poisoning, and were ex- actly periodical in their occurrence. Paralysis, as in the other forms, may be one of the phenomena of this variety of cerebral congestion. Death may take place during the attack, or from secondary lesions afterward.1 What is called temporary insanity, mania ephemera, or impulsive insanity, generally depends upon cerebral congestion. The subject, therefore, is of vast importance in its medico-legal relations.® f. The Aphasic Form.—The inception of this type is usually very sudden. There may or may not be the accompaniments of pain in the head, vertigo, and confusion of mind. The chief symptom is the im- pairment or abolition of the faculty of speech, and this may be the only phenomenon. A very interesting case is that of Prof. Lordat, which is graphically described by Trousseau.3 The loss of speech was at first complete, but was entirely regained in twelve hours. ' The whole subject of cerebral congestion has been well considered by Calmeil, in his “Trait6 des Maladies Inflammatoires du Cerveau.” Paris, 1859. 2 See a memoir by the author, entitled “ A Medico-Legal Study of the Case of Daniel McFarland,” in the Journal of Psychological Medicine for July, 1870; also published separately by D. Appleton & Co. New York, 1870. Also a paper on “Morbid Impulse,” Psychological and Medico-Legal Journal, August, 1874. 3 “ Lectures on Clinical Medicine,” etc. Translated by P. Victor Bazire, M. D. Lon- don, 1866, p. 219. CEREBRAL CONGESTION-. 53 Several similar instances have come under my observation. In a case at this time under my charge, the patient, a lawyer, was suddenly deprived of all power of speech, after passing several hours in very in- tense study. There was a little confusion of ideas, but neither pain nor vertigo. There was loss both of the memory of words and of the power of so coordinating the muscles of speech as to articulate. There was no paralysis anywhere. Recovery was complete in less than six hours. In two cases occurring in my own practice, the patients were sud- denly rendered aphasic by inhalation of the nitrite of amyl. The effect continued for half an hour in one case, and for nearly an hour in the other, after all the other phenomena from the amyl had entirely disappeared. The subject of aphasia will be more fully considered in a subse- quent part of this work. It is quite probable that certain disturbances of the sensory organs, restricted spasmodic actions, and paralyses, illusions, and hallucina- tions, intellectual, emotional, and volitional impulses of a morbid char- acter, and other abnormal cerebral manifestations, to some of which attention has been directed, are the results of localized and quite lim- ited congestions of the brain. As already said, however, it would be premature to differentiate these with any attempt at exactness till our knowledge of the various sensory, motor, and mental centers of the brain is more exact than it is at present. Third Stage.—This period may be considered as beginning after the immediate effects of the paroxysm, whether it has been of the apo- plectic, paralytic, convulsive, maniacal, or aphasic form, have passed off. It is characterized by feebleness of body and mind, by gastric or intestinal derangement, by pain in the head, with transient attacks of vertigo, and occasionally by numbness and slight paralysis of one or more of the limbs. Many of the symptoms met with in the first stage are again found in this. But the principal phenomena are those connected with secondary lesions, such as inflammation, abscess, softening, and adventitious growths of various kinds. These will be considered under their proper heads. It must not be forgotten that one circumstance al- ways exists, and that is, the proclivity to other paroxysms of some one of the fully-developed forms. This condition is the result of causes which increase the amount of venous blood in the brain. It is more commonly met with in old per- sons and in those of feeble constitution. Women are more frequently affected than men. Symptoms. First Stage.—As in active cerebral congestion, there is a premonitory stage, the symptoms of which are similar to those PASSIVE CEREBRAL CONGESTION. 54 DISEASES OF THE BRAIN. previously described. There is, however, a tendency to stupor, and the other phenomena are, in the main, less strongly marked. Vertigo, pain, illusions, hallucinations, and delusions, are nevertheless generally present at one time or another. But the stupor, or tendency to som- nolence, is the most prominent feature, and the sleep, even when com- paratively natural, is attended with dreams, unpleasant or even fright- ful in character. The degree of congestion may be suddenly increased, or, what is a more probable sequence, there may be effusion of serum, and then in either case the second stage, exhibiting itself as in the apoplectic, the paralytic, the convulsive, the soporific, the maniacal, or the aphasic form, results. The proportion of cases of passive cerebral congestion which pass to the second stage is greater than in the active form of the affection, and it is accordingly a more serious disease. Second Stage, a. The Apoplectic Form.—In this variety the onset of the affection is sudden, like that of active cerebral congestion. The loss of consciousness is generally complete, the face is red, the pupils are dilated and insensible to light, the respiration is stertorous, and the faeces and urine may be passed involuntarily. The action of the heart is slow and feeble, and the pulse corresponds to these facts. Paralysis may be general, or confined to a lateral half of the body. If sensibility returns, there are pain in the head, vertigo, tinnitus aurium, generally some embarrassment in the speech from lingual pa- ralysis, and more or less loss of the power of motion in other parts of the body. There will also be general or partial anaesthesia. As the condition of the patient improves, these symptoms generally disappear. Death', however, is not an infrequent sequence. This form of cerebral congestion is most common with elderly persons, and appears to be particularly apt to attack old women. b. The Paralytic Form.—This does not differ essentially from the apoplectic form, except that there is no loss of consciousness, the pa- ralysis constituting the main symptom. It may be either sudden or gradual in its inception. c. The Convulsive Form.—This may not differ materially from the convulsive form of active congestion, except as regards increased length of the fit and prolonged stupor. Generally, however, there is a repeti- tion of the seizures, and I am led to believe, from my experience, that there is a greater tendency to biting the tongue. Paralysis is a more common sequence, and is of longer duration, and the mind appears to suffer more seriously and at an earlier period. d. The Soporific Form.—The first symptom observed is commonly a general numbness and indisposition to muscular exertion. The drow- siness, which has probably been present to some extent, increases, and CEREBRAL CONGESTION. 55 soon becomes the most notable feature. At first, it is easy to rouse the patient from this stupor, but it gradually becomes more profound and overpowering, until at last a persistent comatose condition is reached. The faculties of the mind may, in the earlier stages, be ex- cited into a moderate degree of activity ; but with the advancing coma they are no longer capable of being manifested. The cutaneous sensi- bility becomes less and less, the urine dribbles, from paralysis of the bladder and its sphincter, and the bowels, if not obstinately constipated, allow their contents to pass involuntarily. With these symptoms, the pupils are dilated, and, as long as sensibility exists, pain in the head is complained of. The faculty of speech is impaired at an early period, but, although the tongue is restrained in its movements, there is no actual paralysis of this or any other muscle. This condition may last for several weeks, and, though recovery occasionally takes place, this is never complete. Death is the more usual termination. e. The Maniacal Form is not often met with in passive cerebral congestion, and, when it is, the delirium, so far from being of a furious type, is low. The patient mutters to himself incoherently, and exhibits great muscular restlessness, but never attempts to do violence to him- self or others. Coma often occurs as a sequence. f. The Aphasic Form.—Aphasia without other complication is not often met with as a consequence of passive cerebral congestion. Two instances only have come under my notice, and in both the development was much slower than is usually the case in the active form of the affec- tion. In both of these there was disease of the right side of the heart, manifested by mitral and tricuspid regurgitation, jugular pulsation, great fullness of the veins of the neck and face, and ascites and general anasarca. The loss of the idea of language was complete in both cases, and persisted for about forty-eight hours. There was no paralysis, stupor, or convulsion, and but slight pain. The ophthalmoscope re- vealed the existence of great turgescence of the retinal veins, with ve- nous pulsation. Causes.—The causes of cerebral congestion are : of the active form, those influences which are capable of increasing the quantity of arterial blood in the brain : of the passive, those which produce a similar effect upon the amount of venous blood circulating in the vessels within the cranium. The causes of the first category induce activity of circulation, those of the second torpidity. The causes of active cerebral congestion may either, by their grad- ual operation, initiate the premonitory stage, or they may suddenly induce the development of this stage into one or other of the varieties already described as constituting the second stage. Among them is temperature either very high or very low. Thus, the disease is more frequent in hot climates than in those of more temperate character, and in the summer months than in the spring or autumn. It is, however, 56 DISEASES OF THE BRAIN. more common in very cold than in warm weather. Thus Andral, of one hundred and fourteen cases, found that twenty-six occurred in sum- mer and fifty in winter. My own experience is to the same effect, as will be seen from the following table, which embraces the cases in my private practice in the city of New York during a period of five years, beginning January, 1865, and ending December, 1870 : January 66 February 64 March 60 April 89 May 42 June 37 July 68 August 74 September 27 October 31 November 62 December. 72 Total 622 An examination of this table shows that one hundred and ten cases occurred in the autumn months, one hundred and thirty-one in the spring, one hundred and seventy-nine in summer, and two hundred and two in winter. All my subsequent experience is to the same effect. Passive cerebral congestion is very much more frequent in cold than in warm weather. The direct rays of the sun are capable of producing sudden attacks (insolatio), of which congestion is a prominent feature, but which re- quire separate consideration ; and it is not uncommon for artisans, whose heads are exposed to heat from furnaces, to suffer in a similar manner. Some authors contend that certain winds increase the liability to cerebral congestion. Leuret, quoted by Mosmant,1 could attribute an epidemic of cerebral congestion, which appeared at Charenton, to noth- ing but a long-continued wind from the northwest. The supposition that atmospheric electricity is a causative influence rests upon nothing but hypothesis. Unhealthy situations, such as those subject to the influence of ma- laria and to noxious emanations of any kind, and which are not well ventilated, also predispose to attacks of cerebral congestion. The ingestion of a large quantity of food into the stomach may occasion passive congestion, by the pressure which the distended organ makes upon the large veins of the abdomen. Rapid eating, even though the quantity of food be moderate, may cause the active form of the affection by some influence exerted through the sympa- thetic system. Sudden and violent physical exertion, especially if made in the stooping posture, is very liable to induce cerebral congestion. Child- birth is an instance in point, and I have known several cases to be' caused by severe straining in the water-closet. The constipation of 1 “ Essai sur la Congestion C6rebrale.” Paris, 1858. CEREBRAL CONGESTION. 57 the bowels rendering such efforts at defecation necessary is itself pro* ductive of the disease. A dependent position of the head and constriction of the neck from the dress are also, by impeding the return of blood from the head, liable to induce congestion of the passive form. Certain articles of food and medicine, such as spices, alcoholic liquors, opium, belladonna, quinine, etc., act either by augmenting the power of the heart, or by their effect on the sympathetic, paralyzing the vaso-motor nerves, and thus increasing the caliber of the cerebral blood-vessels. In this connection, the influence of the nitrite of amyl, when inhaled to increase the quantity of blood in the brain, may be cited as an instance of this latter power. Tumors in the neck, or in other parts of the body where the return of blood from the head may be impeded by their pressure, likewise cause congestion. Other causes are to be found in certain diseases, as fevers of various kinds, erysipelas, disorders of menstruation, the suppression of hemorrhagic or other discharges ; local affections of the brain, as embolus, thrombosis, tubercle or apoplectic clots, and sympathetically by worms in the intestinal canal, or irritation existing in other portions of the system. Hypertrophy of the left side of the heart is a common cause of active cerebral congestion ; and any affec- tion of the right side of this organ, tending to impede the return of the venous blood, is an important factor in giving rise to the passive form of the affection under notice. But the most influential and common causes of cerebral hypersemia, and eventually of congestion, are to be found in long-continued intel- lectual exertion, mental anxiety, or sudden, violent, or prolonged emo- tional disturbance. It is from the action of such factors that the pre- monitory symptoms are generally induced, though they may, especially those embraced in the last-named category, immediately develop a fully formed attack. The fact that cerebral exercise increases the amount of blood in the head is made evident to all of us at times, by the distention of the superficial vessels, the suffusion of the eyes, the heat and pain w'hich we feel when we have overtasked our brains. Cerebral action is always attended with hyperaemia, just as is the activity of the liver, the kidneys, or other organs. Active cerebral congestion is thus induced, and is, within certain limits, perfectly nor- mal. But these limits are liable to be exceeded—and, in this active period of the world’s history, often are—and then the condition de- scribed as the first stage of congestion is established. The vessels, from continued over-distention, lose their contractility, just as I have said does the India-rubber band, used to keep a bundle of letters together, when the package is too large, or it has been kept stretched for a long time. An additional disturbing force, heat, cold, an overloaded stomach, increased mental labor, emotional excitement, or any of 58 DISEASES OF THE BRAIN. the causes mentioned, may suddenly evolve a fully developed par- oxysm. ' Emotion acts in a similar manner, though, as has been said, often with more suddenness. The emotions of shame, of anger, and others cause the face to become red from dilatation of the blood-vessels, and a like effect is produced in the vessels within the cranium. If the emotion is very strong or lasting, a correspondingly increased hyper- semia results. There are certain circumstances which render the action of the causes specified more effectual or powerful. These are inherent in the individual, and may be classed as predisposing causes. Among them are sex, the disease being more common in males ; age, it being more frequently met with in middle-aged or old persons; hereditary influence ; hypertrophy of the left ventricle of the heart, by which the flow of blood to the head is directly increased ; dilatation of the right ventricle, by which its power is diminished, and the return of blood from the head impeded ; insufficiency of the auriculo-ventricular valves, or constriction at the auricular or ventricular orifices on the same side, by which a similar result is produced, and perhaps, though this point is by no means established, shortness of the neck. Diagnosis.—Cerebral congestion may be confounded with cerebral haemorrhage, meningeal haemorrhage, embolism, thrombosis, softening, epilepsy, urinaemia, stomachal vertigo, auditory vertigo, and with the very opposite condition, cerebral anaemia. From each of these affec- tions it is, however, distinguished by well-marked characteristics. The premonitory symptoms are not liable to be mistaken for cere- bral haemorrhage, but this error may be made as regards the second stage. The apoplectic form is, however, distinguished from apoplexy due to extravasation, by the fact that in it the loss of intelligence is rarely complete, and that, when it is so, the mind is dormant but for a few moments ; that sensibility and the power of motion are never alto- gether abolished ; that coma, when present, is rarely profound ; that the paralysis, when it exists, is seldom limited to one side of the body ; by the general absence of stertor, and puffing of the lips and cheeks in breathing ; and by the short duration of the symptoms. From meningeal haemorrhage, it is discriminated by the comparative lightness of the symptoms, and by the fact that they do not progres- sively augment in severity or intermit in violence. Cerebral congestion and embolism present some features in com- mon, and it is therefore occasionally difficult to distinguish them. In the former, however, the pulse is slow and the respiration regular and deep ; in the latter, the pulse is more rapid, is often irregular, as is also the respiration ; in the former, there is increased heat of the head ; in the latter, the temperature of this part of the body is unchanged ; in cerebral congestion the symptoms are transient; in embolism they are CEREBRAL CONGESTION. 59 more lasting ; in the former there is often a distinct premonitory- stage ; in the latter, the attack always takes place without a moment’s warning. In the former, though there may be cardiac difficulties, they are different from those predisposing to embolism, which are consecu- tive to endocarditis—generally rheumatic—and which implicate the semi-lunar or mitral valves, and in the fact that recovery from an at- tack of cerebral congestion is generally complete, which is rarely the case in embolism. From thrombosis, cerebral congestion is diagnosticated by the cir- cumstances that in the former the progress of the disease is slow, that there is usually well-marked paralysis from the beginning ; that the phe- nomena indicating mental disturbance are more strongly pronounced ; that the articulation and memory for words are more permanently af- fected ; and, notwithstanding occasional remissions, by the persistency and gradual advance of the symptoms. In softening there are often a sudden loss of consciousness, persist- ent hemiplegia, and death in a few days. Again, there is delirium -without paralysis or convulsions, and in other cases there is a gradual accession of the symptoms. This latter is the only form liable to be mistaken for cerebral congestion. It is attended with headache, feeble- ness of intellect, and a gradually advancing paralysis generally, begin- ning in one of the lower extremities, and extending to the whole of one side of the body. The speech is always seriously impaired, and the mental disorder is of a far graver character than that due to cere- bral congestion. The gradual advance of the affection to a fatal ter- mination is also a characteristic circumstance. With urhuemia, cerebral congestion may be confounded, if only the more obvious head symptoms be taken into consideration. The his- tory of the case and full inquiry will always, however, enable the proper discrimination to be made. Thus, in urintemia the existence of kidney disease, as evidenced by a chemical and microscopical examination of the urine, the anasarca of the face or limbs, and the repeated attacks of convulsions and coma, will be sufficient diagnostic marks. From epilepsy, cerebral congestion is distinguished by the fact that the former is not preceded by the group of symptoms constituting the first stage of congestion ; that the congestion of the vessels of the face and neck is preceded by a death-like paleness ; that an aura is often present ; that there may be a peculiar cry ; that the patient does not stagger and fall slowly to the ground, but drops as if knocked down by a severe blow ; and that the tongue is frequently bitten. The re- verse is the case as regards all these phenomena in cerebral congestion. Nevertheless, so accurate and experienced an observer as Trousseau, in his clinical lecture on “Apoplectiform Cerebral Congestion in its Re- lations to Epilepsy and Eclampsia,”1 confounds the two conditions. 1 “ Clinique M£dicale,” tome ii., p. 66. Also Bazire’s Translation, London, 1866, p. 19. 60 DISEASES OF THE BRAIN. Trousseau’s views on this subject do not, however, appear to be accepted by any large number of medical authorities. Epileptic vertigo is, as will be shown at a proper place, a very different affection from any form of cerebral congestion, and is not likely to be confounded with it. Epileptic mania has, likewise, very few points in common with the disease under consideration. In stomachal vertigo the attacks of dizziness are often severe, but they are clearly associated with gastric derangement, and only occur while the stomach is digesting its contents. Other symptoms of dys- pepsia will also be noticed, while the mental and physical disturbances, which constitute so prominent a feature of cerebral congestion, are ab- sent. The distinction, however, is not always made. In auditory vertigo, or Meniere’s disease, the dizziness is accompa- nied with aural troubles, such as deafness and tinnitus ; the face is pale ; and there is almost invariably vomiting, or at least intense nausea. Moreover, when there is loss of consciousness, the premonitory symp- toms are not such as precede the second stage of cerebral congestion, but ai’e connected with the function of audition. From cerebral anaemia, the first stage of congestion is frequently not clearly distinguished, and I have seen several cases in which patients had been treated for the one condition when the other was indubitably present. In both there are headache, sense of constriction, vertigo, noises in the ears, numbness, mental confusion, loss of memory, inapti- tude for labor of any kind, and at times loss of consciousness. But in anaemia the face is not flushed, the carotid and temporal arteries do not throb with violence ; the pulse is quick, feeble, and irregular, the res- piration is hurried, the pupils are dilated, there are bellows murmurs at the base of the heart and in the veins of the neck, and the general aspect of the patient is not of that rugged appearance so generally associated with cerebral congestion. In the syncope of cerebral anae- mia, the paleness of the face, coldness of the skin, and feebleness of the heart’s action, will serve to draw the line between it and the apo- plectic form of congestion. The ophthalmoscope will at all stages prove of great value in the diagnosis. Prognosis.—The prognosis is materially modified, according to the stage of the disease present when the patient is seen, and the form of attack from which he may be suffering. Active cerebral congestion is a more favorable type than the passive. If the affection has not gone beyond the first stage, a fortunate issue may safely be predicted under the use of suitable medical treatment ; but, if, through neglect or im- proper treatment, -or indiscretion on the part of the patient, the disease becomes fully developed, the prognosis is much more grave. I have never known a death to take place in any patient from this disease during the premonitory stage. The apoplectic and soporific forms are the most gx*ave, and the prognosis is rendered more unfavorable with CEREBRAL CONGESTION. 61 each attack. The epileptic form is ordinarily not dangerous to life, nor is the paralytic, maniacal, or the aphasic, except in old persons. Occasionally, however, even in young and robust patients, death en- sues during the paroxysms of these forms. The liability to secondary lesions, such as softening, cerebritis, haem- orrhage, aneurisms, general paralysis, etc., must be taken into account when forming a prognosis. The more frequent the paroxysms of any form, the greater the risk of some such finality. The habits of the patient are also important elements in forming an opinion in regard to the ultimate result. If these are bad, and are persisted in, the probability is that no treatment will be of much avail in preventing a recurrence. Moreover, by such a condition of the brain as the excessive use of alcohol, inordinate mental exertion, or contin- ual emotional excitement induces, the chance of escaping some sec- ondary morbid process is very much lessened. Of the one hundred and seven fully developed cases which have been under my observation during the past eight years, there were eighteen deaths; seven from the apoplectic form, all after repeated attacks ; three from the maniacal, one of which was that of a young man about thirty years of age ; and seven from secondary lesions. Of these latter, four were from softening, one from cerebritis, one from hajmorrhage, and one from general paralysis. Morbid Anatomy.—There are certain appearances seen in the brains of those who have died of cerebral congestion which are characteristic, although it must be confessed that some or all of them are occasionally absent. These are : An increased size of the capillaries and large blood-vessels, both of the brain and the pia mater. It thus happens that, when a section of the brain is made, the red points ordinarily seen are larger and more numerous than usual, and that the pia mater presents in spots, or throughout its extent, a red or rose-colored appearance. The white matter of the brain is increased in consistence and den- sity, and the gray matter is red, or even violet in hue. There is sometimes a large quantity of subarachnoidean effusion ; the ventricles may contain an excessive amount of fluid, and the cho- roid plexuses are often enlarged. If there have been repeated attacks of cerebral congestion, it is not unusual to find, by microscopical examination, little granules of hffimatin in contact with the blood-vessels. The same means of explo- ration shows the minuter capillaries to be more than naturally tortuous, and to have little aneurismal swellings. These may or may not involve the whole circumference of the vessel. Their presence and import were first pointed out by Laborde.1 1 “ La ramollissement et congestion du cerveau principalement consider6a chez de vieillard.” Paris, 1866. 62 DISEASES OF THE BRAIN. On making a transverse section of the hemisphere, a cribriform appearance is seen, if the patient has repeatedly suffered from attacks of cerebral congestion, and especially if he be advanced in years. This is due to the presence of numerous little holes with sharply-defined margins. The brain-tissue bounding these is generally without mate- rial change, either in color or consistence. This condition, called by Durand-Fardel,1 to whom the credit of first describing it is usually given, “ l’etat crible,” is supposed to be due to the fact that the vessels have been so distended during life as to press with increased force upon the perivascular tissue, and that, shrinking after death, they no longer fill their former space, which remains empty. Calmeil2 was the first to notice this condition. He has very often found, in maniacs, the white substance rendered cribriform by vessels distended with blood, sometimes empty, but always greatly dilated. This state, al- though frequently met with in congestion, is not uncommon in other pathological conditions, such as the several forms of softening, of which, however, congestion is often the first stage. Durand-Fardel3 calls attention to the fact that, on making sections of the medullary substance of the cerebrum, it is not uncommon to find in cases of congestion rose-colored patches scattered throughout its substance. On examining these with a lens, they are seen to consist of a large number of delicate vessels partially injected. I have never wit- nessed this appearance, except in one instance, nor is it noticed by au- thors on the subject generally. If the congestion has been severe or long continued, the convolutions may be to a considerable extent obliterated by the compression of the brain against the internal wall of the cranium. At the same time, the membranes of the brain are rendered dry and viscous from the pressure to which they have been subjected. In passive congestion the sinuses of the dura mater are the chief seats of vascular turgescence ; the veins generally are distended, and there is ordinarily a greater amount of serous effusion in the subarach- noid space than in the active variety of the disease. Pathology.—It is almost useless at this day to discuss the question of the possibility of the quantity of blood in the brain being subject to variation. Still, it may be interesting to recall briefly the facts which establish the affirmative in the matter. In the cases of infants, in whom the anterior fontanelle is still open, the scalp is seen to be elevated above the level of the skull when the head is dependent, and depressed when the head is elevated. The same fact is observed in persons who have suffered injury of the 1 “Traite pratique des maladies des vieillards.” Paris, 1854, and deuxi&me Edition, 1873. V * “De la paralysiK,eonsid6r6e chez les alien6s,” etc. Paris, 1826. 3 Op. cit., Paris, p. 21. CEREBRAL CONGESTION. 63 skull, involving the loss of a portion of its substance. During strong emotional excitement, or the action of any cause capable of increasing the force of the circulation, the scalp is elevated. From the action of opposite causes it is depressed. Both in infants and in persons who have received injuries such as those cited, the scalp is seen to be de- pressed during sleep, and to rise as soon as the individual awakes. A dependent position of the head causes a sensation of fullness, or even pain, and blood may flow from the nostrils. The eyes are observed to be “ bloodshot,” and the countenance indicates congestion. A tu- mor, a ligature, or any other cause capable of exerting pressure on the jugular veins, will produce like effects. Ophthalmoscopic examination under such circumstances shows the veins of the retina to be enlarged, indicating that an obstruction exists to the return of blood through the sinuses and veins within the cranium. Post-mortem examination of persons dying, who, during life, have suffered interruption to the per- fect return of blood from the head, reveals the existence of intracranial congestion. Animals, subjected to experiments calculated to act in the manner stated, are after death found to have congested brains. In animals bled to death the brain is found ana3mic to an extreme degree. Direct experiment still more positively establishes the fact under consideration. If a portion of the skull of an animal be removed, and the aperture be then securely closed with a watch-glass, the vessels will be seen to enlarge and contract according to the cause brought into action, and the brain will be correspondingly elevated or depressed. By means of an instrument, devised, independently of each other, by Dr. S. Weir Mitchell and myself, the degree of pressure within the cra- nium can be accurately measured. It is thus seen that the quantity of blood circulating in the brain undergoes material variation.1 The anatomical arrangement of the blood-vessels of the cerebral tis- sue is such as to admit of an enlargement of their calibre without neces- sarily subjecting the perivascular substance to pressure. Robin5 dis- covered the existence of sheaths around these vessels, and his observa- tions were subsequently confirmed by His,3 who ascertained that the same arrangement exists in the spinal cord. According to His, “ Fine transverse sections of a hardened brain, having its vessels injected or otherwise, show that all the blood-vessels, arteries, veins, and even capillaries, are surrounded by a clear space, broadest in the case of the 1 For a more complete argument on the subject, and for a statement in detail of the experiments of Mr. Durham and myself on this point, the reader is referred to the author’s monograph, “Sleep and its Derangements.” Philadelphia: J. B. Lippincott & Co., 1870. The cephalo-haemometer referred to in the text is described in that work (Appendix), and also in the introduction to this treatise. i Journal de la physiologie de Vhomme et des animaux, 1859, p. 527. 3 “Zeitschrift fiir Wissenschaftliche Zoologie,” 1865, B. xv., quoted in the Journal oj Anatomy and Physiology. Translation by Dr. Bastian. 64 DISEASES OF TIIE BRAIN. larger vessels, but in all cases quite sharply defined externally. In transverse sections the vessels are seen to be surrounded by a ring-like space, and in parallel sections the space is seen on each side of the trunk of the vessel, and follows it in all its ramifications.” These perivascular canals are lined by a hyaline membrane, and are capable of being injected, and, in cases of chronic congestion, may be- come permanently enlarged, so as to cause the appearance referred to under the heading of morbid anatomy. The pathology of the subject receives further elucidation from a con- sideration of the causes capable of giving rise to cerebral congestion, and which have been already mentioned in detail. Treatment.—Recollecting the two grand forms of cerebral conges- tion, the principles which should guide us in treatment will be clearly apparent. In the active type of the disease, the force of the cerebral circulation and the quantity of blood in the blood-vessels of the brain are to be lessened ; in the passive variety, the force of the circulation is to be increased, and at the same time the accumulation of blood in the veins to be diminished. In the active form of this alfection, the abstraction of blood from the arm wras formerly very generally practised, but is now rarely perfomed. I have never seen a case in which it wras required. Local bleeding is more generally applicable, and a few cups to the nape of the neck will often afford marked relief. Leeches to the temples are also useful, though they are preferably applied just inside the nostrils. I have many times witnessed the most satisfactory results from a couple of leeches thus used, and from accidental nasal haemor- rhage. The application of the actual cautery to the nape of the neck is also a measure of value, especially in the earlier stages. It is prefer- able, I think, to any other form of counter-irritation, and, when prop- erly done, is not at all painful. It seems to have a positive and, in some cases, an immediate influence in diminishing the calibre of the cerebral arteries. Cold is another very useful agent in the treatment. It may be ap- plied to the nape of the neck, or directly to the cranium, either as very cold water or in the form of ice. The advantages of position should also be brought to bear. The head should be kept elevated, especially during sleep, and no severe muscular exertion should be taken while stooping. The clothing should be kept loose about the neck. As a derivative, a mustard-plaster applied to the epigastrium is often of service ; and the same may be said of warm or even hot water to the feet. Blis- ters I rarely employ, though I have occasionally done so wdth ad- vantage. The constant galvanic current possesses the power of contracting the cerebral blood-vessels, when so used as to stimulate the sympathetic CEREBRAL CONGESTION. 65 nerve. For this purpose, one pole should be placed over this nerve in the neck, and the other on the back of the neck, as low down as the seventh cervical vertebra. The current from about fifteen Smee’s cells is sufficient, and it should not be allowed to act for more than two minutes. If extreme vertigo be produced, the number of cells should be lessened. This property of the primary current was first pointed out by Bernard, Waller, and Budge, but its demonstration by the ophthal- moscope was first made by myself. Observation with this instrument, while the current is acting, shows that the vessels of the retina con- tract, and hence there can be no doubt that the result is produced upon those of the brain. A similar effect is caused by passing the current directly through the brain, the poles being applied to the mastoid processes. A slight feeling of vertigo follows both when the circuit is closed and opened. The good effects of this practice are well marked, a few applications being often sufficient to abolish the vertigo and unpleasant feelings in the head, and to restore mental and physical activity. Of internal remedies the number is not large, and those which it is advisable to employ are generally effectual, with or without the exter- nal measures mentioned, in entirely relieving the patient. First among these must be placed the bromide of potassium. Sev- eral years ago I pointed out the value of this medicine, and explained the rationale of its action. As others have since claimed the discovery as their own, I hope I may be excused for quoting the following pas- eage from a memoir upon an analogous subject,1 in which the action of the bromide is clearly indicated : “ Bromide of potassium can almost always be used with advantage to diminish the amount of blood in the brain, and to allay any excite- ment of the nervous system that may be present in the sthenic form of insomnia. That the first-named of these effects follows its use, I have recently ascertained by experiments upon living animals, the details of which will be given hereafter. Suffice it now to say that I have administered it to dogs whose brains have been exposed to view by trephining the skull, and that I have invariably found it to lessen the quantity of blood circulating within the cranium, and to produce a shrinking of the brain from this cause. Moreover, we have only to observe its effects upon the human subject, to be convinced that this is one of the most important results of its employment. The flushed face, the throbbing of the carotids and temporals, the suffusion of the eyes, the feeling of fullness in the head, all disappear as if by magic under its use. It may be given in doses of from ten to thirty grains, the latter quantity being seldom required, but may be taken with perfect safety in severe cases.” Since then, experiments with the cephalo-luemometer and ophthal- 1 “On Sleep and Insomnia.” New York Medical Journal, June, 1865, p. 203. DISEASES OF THE BRAIN. moscope have abundantly confirmed these views, and more extensive experience in the treatment of cerebral congestion has placed the matter beyond the possibility of a doubt. Other observers have also confirmed the opinions here expressed. The prescription which I often employ consists of bromide of potassium, § j ; water, § iv ; of this a teaspoonful is taken three times a day in a little water. Occasionally the bromide is in- creased to § iss, and sometimes a saturated solution—which contains grs. xxx to 3 j—is used. I continue the medicine till drowsiness, a slight feeling of weakness in the legs, and contraction of the blood- vessels of the retina—detected by the ophthalmoscope—are pro- duced. The more prominent head-symptoms generally disappear in four or five days, and the results above mentioned ensue in about ten days. Latterly I have used the bromide of sodium in corresponding doses instead of the bromide of potassium. It is more pleasant to the taste, and does not cause so much constitutional disturbance as sometimes follows the administration of the bromide of potassium in large doses. The bromide of calcium is also well adapted to the treatment of cases of active cerebral congestion, and has the advantage over the other bromides of acting more promptly. As is well known, ergot possesses the property of constricting the organic muscular fibre. This property has for several years past led to its successful application to the treatment of those diseases of the spinal cord in which it is desirable to lessen the amount of blood in its vessels. It is only lately, however, that this agent has been em- ployed in similar affections of the brain. From my own experience, as well as from a consideration of the investigations of others, I am entirely satisfied that ergot does. contract the cerebral vessels, and hence that it diminishes the quantity of intracranial blood. Among the first, if not the very first, to call attention to this property was Dr. Charles Aldridge,1 who noticed that after the administration of a full dose he found it to cause “ contraction of the arteries of the retina and loss of the capillary tint of the disk.” My own observa- tions are entirely in accord with these results. I have repeatedly found a single dose of two drachms of the fluid extract produce a decided diminution in the calibre of the retinal arteries, and a marked pallor of the disk. In addition, some recent experiments which I have performed upon dogs, in which the ergot was administered hypodermically in doses of from one to three drachms of the fluid extract, after the animals had been trephined and the cephalo-hiemometer inserted into the opening 1 “West Riding Lunatic Asylum Reports,” vol. i., p. 71, London, 1871; also vol. iii., p. 230. CEREBRAL CONGESTION. 67 in the skull, showed from the falling in the tube that the intracranial pressure was notably lessened. Applying these facts clinically, it is found that ergot is of very great value in the treatment of active cerebral congestion in all its forms, but especially in the first or hyperaunic stage. I am in the habit of giving drachm-doses of the fluid extract three times a day, in combination with some one of the bromides. An excellent formula is sodii bromidi, 1 j ; ergotee ext. fluidi, § iv. M. ft. sol. Dose, a teaspoonful three times a day. Or the ergot may be given alone, either in the form of the fluid extract, or of the ergotin of Beaujon, which is simply a solid extract. This latter is made into pills of from three to five, or even ten grains each, one of which should be administered three times a day. In the first or hyperaemic stage, and especially where the pain in the head has been a prominent feature, I have frequently seen prompt relief of the cerebral distress from the administration of ten or fifteen grains of phenacetine. At the end of about ten days it will generally be found that under this treatment all symptoms of congestion—subjective and object- ive—have disappeared, leaving a little debility and mental depres- sion. It then becomes expedient to give tonics and restoratives, and those which have a special action on the nervous system are to be preferred. Among them, strychnia, phosphorus, and cod-liver oil stand first. Strychnia may be advantageously administered in conjunction with iron and quinine dissolved in dilute phosphoric acid, as in the following formula : Strychnise sul., gr. j ; ferri pyrophosphatis, qui- niae sul., aa 3 j ; acid, phosp. dil., zingiberis syrupi, aa § ij. M. ft. mist. Dose, a teaspoonful three times a day in a little water. I pre- fer this extemporaneous prescription to any of the syrups or elixirs with like ingredients. If for any reason the iron and quinine are not indicated, the strychnia can be given alone with the dilute phos- phoric acid. The eucalyptus, in the form of the fluid extract, has certainly in my hands been productive of excellent results in the treatment of the hyperaemic stage of cerebral congestion. This has been espe- cially the case in those instances in which a malarious influence was present, but in which quinia could not have been given without run- ning the risk of still further adding to the quantity of intracra- nial blood. An ounce of the bromide of sodium may be dissolved in four ounces of the fluid extract, and a teaspoonful taken three times a day. Hydrobromic acid is of no service in the treatment of cerebral congestion, except as a solvent for the sulphate of quinia, the injurious effects of which upon the brain it modifies or prevents. A drachm 68 DISEASES OF THE BRAIN. of Fothergill’s solution will counteract the congestive tendency of about two grains of the sulphate of quinia. It may in some cases be advantageously substituted for the dilute phosphoric acid of the for- mula just given. Phosphorus almost always acts well in such cases as those under consideration. It may be given in the form of the phosphorated oil, as in the following formula: I£. Olei phosphorat., § ss ; mucil. aca- ciae, 1 j ; olei bergamii, gtt. xl. M. ft. emulsion. Dose, gtt. xv. three times a day. A very elegant preparation of phosphorus is the phosphide of zinc. The chemical formula of this substance is Zn3 P, and consequently a grain represents a little more than one-seventh of a grain of phos- phorus. The proper dose, therefore, is about the tenth of a grain. I usually prescribe it in cerebral congestion, according to the following prescription : ]J. Zinci phosphidi, grs. iij ; rosar. conserv., q. s. M. ft. in pil. no. xxx. Dose, one three times a day. Instead of the con- serve of roses, grs. x of the extract of nux vomica may be substituted if strychnia is not being administered in some other form. Another very useful form for administering phosphorus is the phosphorated resin, which contains four per cent, of phosphorus, thor- oughly rubbed up with ninety-six per cent, of resin. This is made into pills with conserve of roses, or some other excipient. The dose is about half a grain, containing the one-fiftieth of a grain of phos- phorus. Latterly I have made much use of arsenious acid in cerebral con- gestion, especially in cases which have been the result of mental exer- tion or anxiety. Its action is certainly preferable to that of Fowler’s solution. It should be given in doses of about the fiftieth of a grain, and after eating, and should be continued for several weeks. Lisle1 administers it in the quantity of from a fourth to the third of a grairf daily, and there is no doubt that it may be given to this extent with- out danger. I have never, however, unless there was manifest insan- ity, used it in these doses. In those cases in which there are dyspeptic symptoms—and they constitute the majority—the administration of pepsin and powdered charcoal with each meal will be of decided benefit; and in such cases bismuth is often of great service. Such is the treatment I have found to be most advantageous in active cerebral congestion, and I rarely have occasion to supplement it with other measures, unless some special indication is to be fulfilled. Thus, if the bowels are constipated, a mild purgative may be given, or preferably an enema of warm water or olive-oil ; or, if the urine is scanty and high-colored, saline diuretics are useful. 1 “ Du traitement de la congestion cerebrale et de la folie avec congestion et halluci- nations par l’acide aresenieux.” Paris, 1871. CEREBRAL CONGESTION. 69 In the passive form of the disease it is sometimes advisable to give stimulants, which may be done from the first in conjunction with the bromide of potassium, sodium, or calcium, with ergot. Alcohol in some form is to be preferred when it is well borne, though carbonate of ammonia is sometimes a useful substitute. In several cases of pas- sive cerebral congestion in old people, and in one instance occurring in the person of a very prominent elderly gentleman of this city, I de- rived satisfactory results from sulphuric ether inhaled from a handker- chief to the extent of a teaspoonful several times a day. The pain, constriction, vertigo, numbness, wakefulness, and inability to exert the mind, were lessened with every dose, and finally entirely disappeared. Ether may likewise be given by the stomach—gtt. xv several times daily—in case the inhalation is contra-indicated from any cause. Of course, any influence capable of interfering with the due return of blood from the head should be counteracted at once. In the two cases of aphasic cerebral congestion of the passive form, to which reference has been made, I derived the most signal benefit from the use of infusion of digitalis in tablespoonful-doses adminis- tered every four hours. Hygienic treatment should in both types of the disease be persist- ently carried out. The food should be nutritious, digestible, and ample, though not excessive in quantity. Alcohol and tobacco, if used habit- ually by the patient, should be restricted to moderate limits ; I have never seen the latter do harm unless used to excess. Tea and coffee may safely be left to the patient’s own inclinations and experience. I believe more harm is done by suddenly breaking off a habit, even though it be somewhat injurious, than by tolerating it within due bounds. Exercise in the open air—walking, horseback-riding, or driv- ing—is always beneficial. The same cannot be said of gymnastic con- tortions, which, to make them worse, are usually performed in hot rooms. Bathing daily and subsequent friction with a tape towel are exceedingly useful in determining blood to the surface of the body. The Turkish bath cannot be too highly commended, and douches to the nape of the neck, alternately hot and cold, in which the water is thrown with force and from a distance of ten or fifteen feet, are highly advantageous. But, above all, those persons who have brought on the disorder by inordinate mental exertion or anxiety must consent to use their brains in a rational manner if they wish to recover or to avoid future attacks. They have received a warning, and, if they do not heed it, sooner or later other diseases, more difficult if not impossible of cure, will make their appearance. But it is not always the case that the most positive advice on this point is followed. Men who would readily see the impropriety of walk- ing three or four miles while suffering with an inflamed knee-joint, 70 DISEASES OF THE BRAIN. do not hesitate to exert a disordered brain to the extreme limit of its power. It is impossible that the action of a brain thus affected can be such as to evoke sound and healthy thoughts. It is not to be wondered at, therefore, that the subjects of cerebral congestion who insist upon attending to their vocations, and on concocting schemes for obtaining wealth or fame, should perpetrate acts which result in the loss of for- tune, or the acquisition of a reputation far different from that sought. The cause of cerebral congestion, whatever it be, must, if prac- ticable, be removed, and it must continue removed. CHAPTER II. CEREBRAL ANAEMIA. In cerebral anaemia the quantity of blood in the brain is either reduced below the normal standard, or the quality of the circulating fluid is impoverished. The first-named condition is due either to direct loss of blood, to deficient action of the heart, to impaired nutrition, or to some cause preventing the due access of blood to the brain ; the second to disease of some organ concerned in haematosis or to a gen- eral cachexia. The two states very often coexist, and they may prop- erly be considered together. Symptoms.—In cerebral anaemia suddenly induced from profuse haemorrhage, the most prominent symptom is syncope. Vertigo is generally an attendant, and there are paleness of the features and coldness of the extremities. The pulse is frequent, thread-like, and weak. The respiration is feeble and accelerated. But, when the accession is more gradual, headache is very generally present. It may be, and usually is, confined to a limited portion of the head, sometimes to a spot not larger than the point of the finger. A feeling of constriction, especially across the brows, is complained of, and the vertigo, notably increased on rising from the recumbent post- ure, is as troublesome a feature as in the worst attacks of cerebral con- gestion. There is ringing in the ears, and loud noises are not only painful but are exceedingly irritating to the nervous system. The pupils are largely dilated, and are sluggish, contracting slowly and but little on exposure to a strong light. These phenomena may be restricted to one eye, a circumstance which generally occasions needless alarm on the part of the patient. The retinae are extremely sensitive, and hence ophthalmoscopic examination is painful. When employed, the vessels at the fundus of the eye are seen to be small and straight, and the choroid is paler than is normal. Owing to paresis of the ocular muscles—a very common condition CEREBRAL ANEMIA. 71 in cases of cerebral ansemia—the attempt to use the eyes, as, for in- stance, in reading, produces pain in them and in the head. In many cases the effort of three or four minutes causes very great uneasiness. The complexion is pale, the lips almost colorless, or else redder than in health. The skin is cold and clammy. Nausea and vomiting are present in extreme cases, and convulsions of an epileptic character may occur. In the rapidly-developed form of the disease, caused by sudden and great loss of blood, they are always present, and in the milder and more gradual variety they are occasion- ally seen. Feebleness of muscular power is always met with, and there may be general or partial paralysis, with the usual derangements of sensibility indicative of anaesthesia, such as coldness, formication, and “ pins and needles.” The mind, of course, participates in the general disorder. In ex- treme cases, due to active haemorrhage, the patient is completely insen- sible. In less severe forms there may be all the gradations from low delirium to great mental irritability, or a condition of intellectual lassi- tude approaching dementia. Hallucinations and illusions are common in the slowly-developed forms of cerebral anaemia, and may affect any one or all of the senses. Those of sight and hearing are, however, more prominent. In the case of a young lady under my care, and whose only marked disorder was that under consideration, the hallucination that she saw a black man was almost constantly present. At times she conversed with this im- aginary being, told him not to trouble her, that she no longer feared him, etc. She believed firmly in his presence, and hence had a delu- sion. In all cases of cerebral anaemia there is more or less drowsiness, from the profound syncope of the rapid form to the rather agreeable languor present in slight cases. In instances of medium severity, the patient readily falls asleep in the sitting posture ; but recumbency in- duces wakefulness, from the fact that the quantity of blood in the brain is thereby suddenly increased above the habitual standard, and a state of comparative hypersemia is thus induced. I have, in another place,1 called attention to this form of insomnia, and adduced several cases in illustration. Examination of the heart by auscultation reveals the existence of bellows-murmurs, both systolic and diastolic. They are heard more loudly at the base of the heart. There are also very generally venous murmurs, which are heard most distinctly in the jugular veins, espe- cially when the head is turned toward the opposite side. Arterial murmurs may also occasionally be perceived. These sounds are sometimes heard by the patient, and are then ex- ceedingly annoying. I have had under my charge patients suffering 1 “ Sleep and its Derangements.” 72 DISEASES OF THE BRAIN. from cerebral anaemia, who constantly heard a sound originating ap- parently in the head, and which, as they described it, resembled that caused by a large shell placed in the ear. That these murmurs are anaemic, is shown by the fact that they disappear under appropriate treatment. Cerebral anaemia may be of such intensity and be so suddenly de- veloped as to cause almost instant death. Many cases are on record of patients having died with symptoms of apoplexy, and in whom post- mortem examination has shown the blood-vessels of the brain to be empty, and the brain itself pale and exsanguined. Paralysis of various forms may likewise result from this condition. Sometimes there is hemiplegia, at others paraplegia; again a single muscle or a group of muscles may be affected, and it may even happen that a general state of paralysis may exist. I have frequently seen a single muscle of the eyeball alone involved, and upon one occasion witnessed the loss of muscular power confined to one side of the face in the person of a lady whose brain was evidently very anaemic. Gintrac1 cites the following interesting cases communicated to him by Dr. Ilirigoyen : “ A young girl twenty years old, affected with amenorrhoea, con- sulted a midwife, Avho bled her, attributing her trouble to cerebral plethora. She had hardly lost two hundred grammes of blood when hemiplegia supervened. Iron and tonics entirely dissipated this con- dition. “A young woman, twenty-five years old, was subject to a severe epigastric pain, that had been several times relieved by bloodletting. She was thin, pale, and nervous. Nevertheless, a vein was again opened, but only about one hundred and fifty grammes of blood were taken. Notwithstanding this prudence, a syncope ensued while the arm was being tied up, and there were some convulsive movements. After two or three minutes the patient recovered her senses, but was found to be entirely hemiplegic on the left side, and to have some difficulty of speech. Recourse was had to Hoffman’s anodyne, vale- rian, and appropriate food, and at the end of thirty-six hours she was relieved.” A form of cerebral anaemia met with in young children is of great importance, from the fact of its liability to be confounded with an- other far more dangerous affection, almost its opposite. This was first clearly described by Dr. Gooch,8 although previously noticed by other observers. In children suffering from this affection, the symptoms, so far as they are noticeable, are similar to those present in the anaemia 1 “ Trait6 theorique et pratique des maladies de l’appareil nerveux.” Tome premier, Paris, 1869, p. 648. * “Op Some of the most Important Diseases peculiar to Women; with Other Papers.” New Sydenham Society Publication. London, 1869, p. 179. CEREBRAL ANAEMIA. 73 of adults. The drowsiness is well marked, the head is cool, the pulse is small and weak, the features are pinched, the pupils large and in- sensible to light, and the fontanelle, if still open, has the scalp cover- ing it depressed. After death, the vessels of the brain are found to be almost empty, and the ventricles distended with fluid. From its re- semblance in some respects to hydrocephalus or tubercular meningitis, this affection was called by Dr. Marshall Hall hydrocephaloid. The distinction, however, is so well defined, that none but the most igno- rant or superficial observers would fail to recognize it. In some cases of cerebral anaemia a tendency to melancholia exists, and positive insanity may eventually result. In most instances of the disease there is mental depression, with a strong predisposition to the production of hypochondria. Causes.—Haemorrhage or other exhausting discharge ranks first among the causes of cerebral anaemia. I have known several severe cases induced by epistaxis, and one by the continued loss of blood from leech-bites. Haemorrhoidal bleeding has also caused it in my experience. No influence of the kind is, however, more common than uterine bleeding, such as occurs before, during, or after labor, from miscarriages and abortions, especially if they are frequently repeated, and from excessive menstrual discharge. Chronic dysentery and diarrhoea, malarial and other fevers, the rheumatic, strumous, and cancerous diatheses, diseases of the bones and joints, and long-continued purulent discharges, are likewise causes of cerebral anaemia. I have several times seen the affection apparently caused by con- gestion of internal organs. Niemeyer, referring to this possibility, cites the fact that it may follow the use of Jounod’s boot. At the present time, when this appliance is variously modified and extended beyond its legitimate use by itinerant quacks, it is well to call special attention to this liability. Several cases in point have come under my observation, and in one, a young lady suffering from epilepsy with cerebral anaemia, whom I saw in consultation with my friend Dr. J. Marion Sims, severe paroxysms were induced by each application of the “ exhauster.” In this case the operator placed the whole body, writh the exception of the head, in a vacuum. In another instance, exhaustion from the leg alone caused syncope every time the operation was performed. Pressure upon or obliteration of the arteries supplying the brain is another cause, and may be produced by ligation of the arteries or by tumors of various kinds. Feebleness of the heart’s action, such as results from fatty degeneration, may also occasion cerebral amemia. As we have seen, excessive mental exertion is a common cause of cerebral congestion. Strange as it may appear, I have had several cases of cerebral anaemia under my care, in which the disease was 74 DISEASES OF TI1E BRAIN. clearly the result of a like cause, and these wc-re instances in which the brain had been overtasked to an extreme degree. A little reflec- tion will, I think, show that such cases are strictly in accordance with what takes place in other parts of the body. Thus, we see the moder- ate use of a muscle or set of muscles increase their size and strength. Inordinate exercise induces hypertrophy, but, if the power of the muscles be still more severely tried, atrophy results. One of the worst cases of progressive muscular atrophy I ever saw occurred in the per- son of a ballet-dancer, whose gastrocnemii muscles were the apparent starting-points of the disease. Excessive cerebral action produces exhaustion, and exhaustion causes anaemia, as surely as anaemia causes exhaustion. The action of mental emotions is more obvious. We know that some emotions increase the amount of blood in the brain. Others di- minish it, and sometimes with such suddenness as to cause syncope. Fear is one of these, and we have all seen the face become paler under its influence. Certain medicines are causes of cerebral anaemia, both by their action on the vaso-motor nerves and in diminishing the power of the heart. Tobacco, tartarized antimony, calomel, oxide of zinc, and the bromides of potassium, sodium, calcium, and lithium, are among the chief of these. I was the first to point out this influence of the bro- mides, and, in a recently-published memoir,1 have given several cases in illustration of its action. The drowsiness, vertigo, nausea, faint- ing, weakness of the muscular system, numbness, failure of memory, mental aberration, pallor of the countenance, and anaemia of the reti- na, all go to show that the quantity of blood in the brain is dimin- ished. Recent investigations not yet published have convinced me that the oxide of zinc acts in a similar manner. Insufficient nutrition, either from deficient or improper food or dis- ease of the digestive or assimilative organs, is a very common cause. Through its influence not only is the absolute amount of blood less- ened, but its quality is deteriorated. The quantity sent to the brain is hence diminished, and that which is supplied is lacking in its proper proportion of red corpuscles. Many of the cases of cerebral anaemia occurring in large cities originate from such influences, and likewise from the vitiated air of narrow and crowded streets, from cold, and from deprivation of light. Sudden cerebral anaemia may be produced by the shock caused by physical injuries, or even slight surgical operations unattended by 1 “ On Some of the Effects of the Bromide of Potassium when administered in Large Doses.” Quarterly Journal of Psychological Medicine, January, 1869, p 46. In this paper I stated that one of the most constant phenomena was contraction of the pupils. Very greatly increased experience has convinced me that this is an occasional circum- stance, which occurs during the early period of administration only. CEREBRAL ANiEMIA. 75 effusion of blood. Thus I have several times seen it follow immedi- ately on the passage of a urethral catheter or bougie for the first time. The passage of a galvanic current of too great a degree of intensity through the brain may be productive of alarming symptoms due to sud- denly-induced cerebral anaemia. Upon one occasion I passed a current from ten cells transversely through the brain of a gentleman—the poles being on the mastoid processes—with the effect of causing syncope, extreme nausea, a cold perspiration on the head and face, and such feeble action of the heart as to cause me to apprehend the most serious results. Placing the head in the dependent position, and causing him to inhale the nitrite of amyl, soon restored him to consciousness, and dissipated the other symptoms. In another, somewhat similar though not so violent symptoms were induced by the passage of a current from only six cells. Cologne to the nostrils, and a draught of strong whiskey, afforded prompt relief. These cases, as well as others within my knowledge or experience, show how sensitive some persons are to the primary current, and indi- cate the care necessary in the use of this powerful agent. An instance of extreme cerebral anaemia, produced by excitation of the pneumograstic nerve by a galvanic current of too great a degree of intensity, will presently be cited. Diagnosis.—The principal affection with which cerebral anaemia is liable to be confounded, is cerebral congestion. Indeed, there is no other which can be mistaken for it, if even ordinary perception and judgment be exercised. From this it may be diagnosticated by the history of the case, and a careful inquiry into the etiology, by the facts that drowsiness, not wakefulness, is a prominent symptom ; that the pupils are dilated in- stead of being contracted ; that the pain is more apt to be fixed in a limited part of the head instead of being general; that it and the ver- tigo are increased by the assumption of the erect position, and dimin- ished by lying down ; that the ophthalmoscope shows retinal anaemia ; that the face is pale and the skin cold ; that the pulse is weak and fre- quent ; and that bellows-murmurs are heard at the base of the heart and in the veins of the neck. The effect of stimulants and tonics in mitigating these symptoms, and the fact that they are increased by ex- ertion and debilitating influences, are also important points to be con- sidered in forming a diagnosis. Attentive consideration of these dif- ferential phenomena will prevent a mistake which may be fatal to the patient. Prognosis.—The prospect of recovery in cases of cerebral anaemia depends mainly upon the removal of the cause, and the adoption of suitable treatment. In those cases which are the result of sudden and profuse loss of blood, the prognosis is grave, and this is especially so if the patient is pulseless and convulsions have occurred. In such in- 76 DISEASES OF THE BRAIN. stances, even though the haemorrhage has been arrested, it may be impossible to save the patient. In the gradually-developed form the prognosis is generally favorable. Morbid Anatomy.—The vessels of the brain and its membranes are observed upon post-mortem examination to contain less than the normal amount of blood. The tissue of the brain is pale, and section shows a diminished number of the red points in the white substance. Some- times there is an increased amount of serous effusion in the sub- arachnoid space, but the ventricles are generally empty. Pathology.—The questions to be discussed under this head are similar to those connected with the same point in cerebral congestion. That the quantity of blood within the cranium can be diminished as well as increased admits of no doubt, and the fact that the symptoms grouped together as indicating the existence of cerebral anaemia are really the result of deficient blood-supply to the brain is equally certain. The experiments of Kussmaul and Tenner,1 as well as those of other physiologists, are perfectly convincing. To observe in man the effects of even temporarily cutting off the supply of blood to the brain, it is only necessary to compress the carotid arteries for a few moments. I have repeatedly done this in rab- bits to the extent of producing insensibility and convulsions. Jacobi3 relates the following symptoms as generally observed in the human subject: Dimness of sight, dizziness, stupor, weakness in the legs, stag- gering, swooning, loss of consciousness, and sudden apoplectic falling down. Dr. Alexander Fleming * tried the effect of compressing the carotid arteries. “ There is felt a sort of humming in the ears, a sense of tingling steals over the body, and in a few seconds complete unconsciousness and insensibility supervene, and continue as long as the pressure is maintained. I have recently performed this experiment several times, with the effect of producing similar phenomena, together with pallor of the countenance, dilatation of the pupils, and temporary headache.” In many cases of cerebral anaemia, the cause, as we have seen, resides in the blood-producing functions, and is such as to cause the formation of blood which does not contain its due supply of red cor- puscles. Here, although there may be no diminution in the actual volume of this fluid circulating in the cerebral vessels, the effect is the same so far as the nutrition of the organ is concerned, and hence the symptoms of anaemia are slowly evolved. 1 “ Untersuchungen iiber Ursprung und TVesen der fallsuchtartigen Zuckungen.” Frankfurt, 1857. Also, “On the Nature and Origin of Epileptiform Convulsions, caused by Profuse Bleeding,” etc. New Sydenham Society Translation, 1859. 2 Quoted by Kussmaul and Tenner. 3 British and Foreign Medico-Chirurgical Review, April, 1855, p. 529, in a paper en- titled “ Note on the Induction of Sleep and Anaesthesia by Compression of the Carotids.” CEREBRAL ANAEMIA. Again, it cannot be doubted that spasm of the blood-vessels pro- duced through the sympathetic and vaso-motor nerves explains the origin and continuance of many cases of cerebral antemia. It is in this way that mental emotions act, and sometimes with such rapiditv as to cause instant death. This spasm may be kept up for a very consid- erable period, with the effect of developing the ordinary symptoms of cerebral anaemia, even after the emotion which originated it has long since disappeared. Treatment.—The first indication to be fulfilled in the treatment of cerebral anaemia is to get rid of the cause. It often happens that this is still in active operation when patients come under our care, and there is no hope of permanent success till it is removed. Thus, if there is haemorrhage from a divided vessel, from the uterus, the bow- els, the lungs, or other part of the body, it must be arrested ; if there is exhausting discharge from the air-passages, the intestines, or the genital organs, it must be stopped ; if the digestive or assimilative organs do not perfectly perform their offices, they must be put in good condition ; if a tumor or other obstruction to the due course of the blood to the brain exist, it must be removed ; and if the hygienic conditions surrounding the patient be bad, or the food inadequate in quantity or quality, they must be improved. No medicine exercises so powerful an effect in cerebral anaemia as alcohol in some form or other. Perhaps, all things considered, the spirituous liquors, such as whiskey, brandy, and rum, are more gen- erally applicable ; for the influence is more rapidly felt, and there is not the same risk of exciting or aggravating gastric disorder as when vinous or malt liquors are used. The quantity must be regulated ac- cording to the circumstances of each case, and should always be large enough to materially increase the force of the heart. But if this were the only effect of alcohol, its benefits in cerebral anaemia would be but temporary, and would certainly be followed by a period of depression. Aside, however, from its stimulating action on the heart, its tendency is to improve the appetite and digestive power, and to relax any spasm of the blood-vessels that may be present. Occasionally it happens that alcohol is badly borne by anaemic pa- tients. The brain has for so long a time been deprived of a due amount of its natural stimulus—blood—that time is required to enable it to tolerate, and be improved in tone by, the increased supply. Thus the physician will find that in some cases the patients will be appar- ently rendered worse by the remedy which of all others is calculated to do them most good. The headache and vertigo are increased, the general feeling of debility and malaise greatly augmented, and the complaint is made that the liquor has “ gone to the head.” Now, it must be recollected that the brains of ana3mic persons are 77 78 DISEASES OF THE BRAIN. in very much the same condition as the eyes of those who have for a long time been shut out from their natural stimulus—light. When the full blaze of day is allowed to fall upon their retinae, pain is pro- duced, the pupils are contracted, and the lids close involuntarily. The light must be admitted in a diffused form, and gradually, till the eye becomes accustomed to the excitation. So it is with the use of alcohol in some cases of cerebral anaemia. The quantity must be small at first, and it must be administered in a highly-diluted form, though it may be frequently repeated. Cases in which this intolerance of stimu- lants is exhibited are almost invariably of long duration, and are as those in which from a like cause wakefulness is produced by the re- cumbent posture. The carbonate of ammonia, or the aromatic spirits of ammonia, may be given if there are any special reasons why alcohol should not be used, but they are not to be compared to it in efficacy. In very extreme cases ether is preferable for the time being to any of the foregoing remedies, on account of its diffusive nature ; and transfusion may be necessary to save life. My recent experience disposes me to put a very high value upon the nitrite of amyl in the treatment of cerebral anaemia. Aldridge 1 has shown that it causes, when inhaled, dilatation of the retinal arte- ries ; and the other phenomena of its action, the feeling of fullness in the head and the redness of the face and scalp, unite to prove that it exercises a like effect over the vessels of the brain. In the cerebral anaemia of weak and chlorotic girls it is especially valuable, although there is no form of the affection, whether transitory or permanent, in which it will not prove beneficial. Even a single dose of four drops inhaled from a handkerchief has repeatedly in my hands relieved anaemic headaches, and effectually dissipated syncope, the result of a feeble action of the heart. Upon one occasion I had, rather imprudently, perhaps, acted in a case of goitrous exophthalmia upon the pneumogastric nerve with a galvanic current of too great a degree of intensity. The heart was rendered exceedingly weak and irregular in its pulsations. The patient, a lady, became insensible from syncope, and was unable to swallow the brandy I held to her lips. I poured a few drops of the nitrite of amyl on a handkerchief and held it to her mouth. Immediately the action of the heart be- came stronger, the color began to return to the face, and conscious- ness was at once regained. In chronic cerebral anaemia, the nitrite of amyl should be admin- istered in doses, by inhalation, of from four to eight drops three times a day. This course may be continued as long as may be necessary, without the slightest deleterious result. I have repeatedly persevered with it for a year, in cases of epilepsy, with the happiest effect. It 1 “West Riding Lunatic Asylum Reports,” vol. i., 1871, p. 77. CEREBRAL ANAEMIA. 79 has never in my experience been requisite to use it longer than a few weeks in cases of cerebral anaemia. Among the more efficacious medicines to be employed in cerebral anaemia, opium and its preparations occupy a high place. Several years since I pointed out1 the effects of opium upon the cerebral circu- lation, and, as the result of many experiments, urged that this drug should be used in brain-diseases with due discrimination. It was then shown that small doses of opium increase the supply of arterial blood to the brain. In the treatment of cerebral anemia I have derived the most decided benefit from doses of opium not exceeding half a grain, and preferably a quarter of a grain, given three or four times a day, and continued for several weeks. An equivalent or even smaller pro- portional dose of morphia may be exhibited, instead of the entire drug. It may seem strange, with the cases I have given, and with the knowledge, from experiment and ophthalmoscopic examination, rela- tive to the power of the primary galvanic current applied to the brain or sympathetic nerve to contract the cerebral blood-vessels, that I should recommend the use of galvanism in cases of cerebral anaemia. Clinical experience, however, shows that it is decidedly beneficial, pro- vided the tension be very low. I am satisfied that not more than two or three cells should be brought into action in such cases, and that the current should only be passed for a few seconds at a time. As adjuncts to these means, the bitter tonics, such as quinine, gentian, columbo, and quassia, are useful. Iron is almost always re- quired, though there are patients who do not tolerate it. In such cases manganese may be substituted with advantage. I have frequently used the sulphate, in doses of five grains, with excellent results. When iron is borne, I know of no better combination than that given on page 68. Cod-liver oil is also a valuable agent in the disease under consideration. It must not be forgotten that food is the most important factor in relieving chronic cerebral anaemia. The main permanent influence of stimulants and tonics is exerted upon the appetite and digestion, and the blood and tissue forming functions, mainly as an excitant. The real strength must come from the food. This should, therefore, be of good quality ; animal food, such as milk, eggs, and meats of various kinds, forming its chief portion. The influence of position should always be taken advantage of to facilitate the flow of blood to the head, and the erect posture avoided as far as possible, especially during the early stages of the treatment. Thus the patient should be encouraged to pass a good portion of the day in a recumbent position, and should be instructed to assume it at once on the occurrence of any aggravation of the symptoms. The opposite course is fraught with danger. Physicians are often anxious that their patients should take physical exercise, but it must be 1 “Sleep and its Derangements.” Philadelphia, 1869, p. 26. 80 DISEASES OF THE BRAIN. remembered that those who suffer from cerebral anaemia have very little vital energy, and a diminished amount of blood is circulating through the organ from which the greater part of their nervous power comes. Muscular exercise lessens the energy, and still further reduces the quantity of blood in the brain, for the muscles require an increased supply while in a state of activity. To be sure, after the strength of the system is in a measure improved, the blood increased in quantity and quality, and the brain supplied with something like its proper pro- portion, moderate physical exercise is of the greatest service. I have several times witnessed severe consequences from the as- sumption of the sitting or erect position too soon after a profuse haemorrhage, and in one case death resulted. As regards mental labor, there is not much need of caution, for the reason that it is impossible for the patient to undertake it to any dan- gerous extent. But, as he improves in strength, the desire to make use of his increased power may be manifested. It is, therefore, well at this time to prohibit any such exertion as will probably be followed by marked depression. Moderate mental exercise is, however, far from be- ing prejudicial, for it tends to increase the amount of blood in the brain. Emotional disturbance should also, as a rule, be avoided, although at times it may be productive of great benefit, especially if it be pos- sible to bring into action an emotion contrary to that which may have produced the disease. Thus a lady became subject to cerebral anaunia, directly the result of painful emotions due to domestic trouble. The cause was very suddenly removed, or rather the knowledge of its re- moval was suddenly communicated to her. The reaction was very great; she was thrown into a state of joyous excitement, attended with consid- erable febrile disturbance, and I was apprehensive for a time that her mind might become permanently deranged, for there were hallucinations and delusions of various kinds, and many symptoms of cerebral conges- tion. But in the course of a few days, during which she was kept in entire seclusion, and as far as possible from all mental and physical agitation, she entirely recovered both from the secondary and primary disorders. CHAPTER III. CEREBRAL HAEMORRHAGE. Under the designation of cerebral haemorrhage I propose to con- sider that disease which is often known as apoplexy, hemiplegia, or a paralytic stroke, and which is due to the rupture of a blood-vessel, and the consequent extravasation of blood either into the substance of the brain or into its ventricles. CEREBRAL HEMORRHAGE. 81 Two forms of the affection, differing essentially only in the extent or seat of the lesion, but presenting different symptoms, are to be dis- tinguished ; these are the apoplectic and paralytic. In the first there is loss of consciousness ; in the second the mind, though perhaps im- paired, is not suspended in its action. Symptoms.—Before the full development of the attack there often is, for several days, a group of symptoms present which indicate cere- bral disorder. These are very much of the same character as those denoting the first stage of cerebral congestion, but, though generally not so numerous, are far more striking. Among the more obvious is a sudden difficulty of speech, arising from slight paralysis of the tongue and other muscles concerned in articulation. Words are not pronounced with the usual distinctness ; the tongue seems to occupy more space in the mouth than it should, and is not moved with the requisite degree of promptness and rapidity. The other muscles on one side of the face may be affected, and hence there is a little distortion, lasting, perhaps, but for a few hours. Defects of sight may occur, usually characterized by the presence of dark spots in the axis of vision. Such conditions are due to minute extravasations in the retime, and are always of most serious importance. I have known retinal clots to precede by more than a year the occurrence of a more severe lesion. Bleeding from the nose is a common precursor, and, when occurring without being induced by severe muscular exertion, blows, a dependent position of the head, or other obvious cause in a person over the age of forty, is always to be regarded as a symptom of moment. Numbness limited to one side of the body is of itself sufficient to excite apprehension. I have known several cases in which this symptom was the only premonitory sign. It may be present several days before, or may precede the attack by only a few minutes. In addition, there may be headache, vertigo, slight confusion of mind, a tendency to stupor, and vomiting. None of the premonitory symptoms may be present, and then the attack, if of the apoplectic form, occurs with great suddenness. Even if they have been noticed, there is more or less of abruptness in the onset. Thus the individual is perhaps standing, engaged in conversation, when he is instantaneously struck with unconsciousness, and falls to the ground as if shot; sensibility and the power of motion are abolished, and no signs of vitality are apparent to the ordinary observer, with the exception of the slow and labored action of the heart and respiratory muscles. The breathing is stertorous, the lips and cheeks are puffed out with each expiration, and the pupils are generally largely dilated and insensible to light. Reflex movements are abolished at first, but after a few moments they reappear, and are even more readily excited than in health, owing to the fact that, the controlling influence of the brain is removed. 82 DISEASES OF THE BRAIN. The voluntary power of swallowing is lost, but it is usually not dif- ficult to cause contraction of the muscles of deglutition by excitation of the pharynx. When these cannot be produced, the prognosis is, if possible, increased in gravity, for the reason that the extravasation is probably in the medulla oblongata, or so situated as to compress it. The urine and faeces are often evacuated involuntarily. An apoplectic attack of this character usually terminates in death without the patient recovering his intellect in the slightest degree. If life should be prolonged for thirty-six hours, the probability of a fatal termination is materially lessened. I have never seen a case of cerebral haemorrhage that was instantaneously fatal, and, although from ana- tomical and physiological considerations I admit the possibility of such instances, I am persuaded that they must be rare. Jaccoud1 expresses the opinion that death is immediate in those cases in which the haem- orrhage is in the medulla oblongata, or in those which occur in both hemispheres. Dr. Hughlings Jackson,3 on the contrary, though conced- ing from theoretical grounds that haemorrhage into or near the me- dulla oblongata might cause instant death, has never witnessed such a termination; and Dr. Wilks 8 says that apoplexy is very rarely, if ever, a suddenly fatal disease, no matter what part of the brain may be the seat of the effusion. Among the reports of several thousand post- mortem examinations at Guy’s Hospital, there was but one in which death was asserted to have been instantaneous, and that was a case of meningeal haemorrhage. Even this was doubtful, for the patient had fallen some distance from the hospital, and was brought in dead. I have several times had cases under my observation in which, it was said, death had been as sudden as though the individual had been struck by lightning ; but careful inquiry and post-mortem examination have either shown that the observers were deceived, or that there had been no extravasation at all, death being the result of heart-disease. Nevertheless there are instances on record in which haemorrhage into the medulla oblongata has produced death with as much sudden- ness as any other possible cause. Ollivier4 cites a case which came under his observation at the SalpetriSre: “ Batandier (Jeanne Elisabeth), aged sixty-four, of medium height, and inclined to stoutness, was admitted to the Salpetri&re, for attacks of hysteria, with which she had been affected since her seventeenth year, when her menses appeared. These attacks were very violent, and occurred at each menstrual period. They stopped during a single pregnancy at the age of thirty years, and disappeared altogether at 1 “ Traite de pathologie interne.” Paris, 1870. Tome premier, p. 166. 8 “ On Apoplexy and Cerebral Haemorrhage.” “ Reynolds’s System of Medicine.” Lon* don, 1868. Vol. ii., p. 520. 3 “ Guy’s Hospital Reports,” 1866, p. 178. 4 “ Traite des maladies de la moelle 6pini&re.” TroisiSme Edition, Paris, 1837, tome Ii., p. 140. CEREBRAL HAEMORRHAGE. 83 forty, when her menses ceased. Her intelligence had not become seriously impaired; she had full power of speech, but complete deafness, existing since infancy, rendered this faculty almost useless to her, and she accordingly communicated with others by means of signs. She was very irascible, her gait was irregular, but nevertheless there was no paralysis. In all other respects her health was good. On the 28th of October, at mid-day, while in the midst of a group of women, she be- came very angry, uttered a cry, leaned against the wall, and then fell to the ground. She was raised up, but was dead. “ Autopsy forty hours after death. . . . The sinuses of the dura mater were gorged with blood, the pia mater was strongly injected, and easily detached from the cerebral substance ; the middle lobe of the brain presented a well-marked depression ; the brain was firm, and of good consistence; the hemispheres, carefully examined, presented a de- cided injection of both the white and gray substance, but no haemor- rhagic foyer, old or recent ; the ventricles were empty, the choroid plex- uses thin and granular ; the optic thalami and corpora striata healthy. “ After having divided the spinal cord below the medulla oblongata, and having removed the medulla oblongata with the cerebellum, and the pons Yarolii, a sanguineous clot, irregularly round, and the size of a walnut, was discovered adherent to the posterior part of the medulla oblongata, and extending above as far as the opening into the fourth ventricle, which it entirely closed. The pyramids were not injured, but the olivary bodies were partly destroyed, the right more than the left. The restiform bodies were entirely detached, and were found in frag- ments in the middle of the clot. The clot was removed and the source of the haemorrhage was discovered to be in the central gray substance, four or five lines below the inferior border of the pons Varolii, which was a little softer than normal, but which in other respects appeared to be healthy, as did also the cerebellum. An enormous quantity of san- guinolent serous fluid filled the spinal canal, and flowed out in part from the foramen magnum, and in part from the opening made in the spine for the examination of the cord, which was healthy and non-injected. “ Both lungs were gorged with black blood, but presented no traces of emphysema; the right cavities of the heart were filled with black blood, but the organ was healthy. “ All the abdominal organs were in a normal condition.” Ollivier remarks, in reference to this case, that death was as instan- taneous as though produced by a sudden luxation of the first or second vertebra. Dr. A. Charrier1 has reported the case of a woman who, on the twelfth day after delivery, died instantaneously. At the evening visit, while talking, “ she suddenly uttered a cry, turned over on her pillow, and was dead. Death was as instantaneous as though she had been 1 “ H6morrhagie du bulbe rachidien.” Archives de physiologic, 1869, p. 660. 84 DISEASES OF TEE BRAIN. struck by lightning.” At the autopsy a small clot was found in the centre of the medulla oblongata. The rest of the brain and the heart were perfectly healthy. In the majority of cases attended with complete loss of conscious- ness, the course of the disease is not so rapid or hopeless as in the form just described. The patient falls, is comatose, breathes stertorously, and presents a similar general appearance; but after a time conscious- ness begins to return, and it is possible to partially rouse him from the condition of insensibility. He turns over in the bed, though with diffi- culty, and may attempt to speak. Articulation is, however, indistinct, for the muscles of one side of the face are paralyzed, and the tongue, from a like cause, is restricted in its movements. The paralysis is found to exist in the limbs of the same side, and involves the loss of sensi- bility, as well as of motion, though rarely to the same extent. In some exceedingly rare cases, perhaps not clearly understood, the paralysis of the limbs is on the opposite side to that of the face. A man thus af- fected was present at my clinic, in October, 1870, at the Bellevue Hos- pital Medical College. He was a patient under my charge at the New York State Hospital for Diseases of the Nervous System, and had been attacked several years previously. His history, as elicited with great care by my clinical assistant and resident physician of the hospital, Dr. Cross, was perfectly clear on this point. The facial paralysis presents several points of great interest in a diagnostic point of view. The affected side is incapable of expression, but, so long as the patient does not attempt any facial movements, scarcely any distortion is perceived. Should he endeavor to open his mouth to spit, or to puff out his cheeks, the paralysis is at once noticed. Owing to the fact that the antagonism of the muscles is destroyed, the face is drawn toward the sound side, the angle of the mouth being slightly depressed. It is remarkable, however—and the fact is of im- portance as a diagnostic mark between the facial paralysis of cerebral hasmorrhage with hemiplegia and the simple facial paralysis from injury or disease of the seventh pair—that the patient does not lose the ability to close the eye of the affected side. If the fifth pair of nerves is involved in the lesion, sensibility is im- paired, which is never the case in simple facial paralysis, and the mas- seter and pterygoid muscles, which receive their motor influence from this nerve, will consequently be paralyzed. The ability to masticate on the affected side is therefore lost, and the cheek hangs lower than on the sound side. The tongue is also only paralyzed upon one side. When, therefore, it is protruded from the mouth, the point deviates toward the paralyzed side, owing to the uncompensated action of the sound genio-hyoglossus. All these paralyses occur on that side of the body opposite to the seat of the lesion. In a very few instances the paralysis has existed on CEREBRAL HAEMORRHAGE. 85 the same side with the lesion. This is explained by the fact that it oc* casionally happens, as Longet1 states, that the decussation of the an« terior columns of the cord is imperfect. At times, again, owing to a double extravasation, or to the fact that the lesion is in the mesial line of the pons, or that it forces its way so as to involve both hemispheres, both sides of the body are deprived of motion. Very inexact ideas have prevailed relative to the temperature in cases of cerebral haemorrhage. The researches of Bourneville3 have given us more certain data than we previously possessed, and, aside from their value as contributions to symptomatology and pathology, are of great importance in the matter of prognosis. This observer, as the result of numerous determinations, arrived at the following conclusions: That the animal temperature, in the very inception of the apoplectic attack, undergoes a very considerable reduction, the thermometer in the rectum indicating 36° (=96.8° Fahr.), and even sometimes falling as low as 35.4° (=95.72° F.). This reduction seems to be influenced par- ticularly by the continuance of the haemorrhage and the supervention of additional centres of extravasation. To this period of temperature- depression succeeds another, during which the animal heat remains sta- tionary at its normal point. If the patient is destined to recover, this period is prolonged indefinitely; but, if death is to ensue, a third period, characterized by a remarkable elevation.of temperature, supervenes. During this stage the thermometer indicates 40° (= 104° Fahr.), or may rise to 41.5° (= 106.7° Fahr.). Charcots has called attention to the fact that, in a few cases of cere- bral haemorrhage, an acute bed-sore forms on the buttock of the para- lyzed side. From the second to the fourth day after the occurrence of the attack, an erysipelatous redness of irregular outline occupies the buttock, and frequently extends over the greater part of its surface. Within forty-eight hours a dark-colored spot appears on the central portion, and the epidermis of this is raised by the sanguinolent fluid be- neath it. This vesicle breaks, and a sore is thus formed, which gradu- ally extends. Occasionally but very rarely the sore occurs on the sound buttock. I have only witnessed two cases in which these sores were formed, and both were in persons over seventy years of age. Of course, these eschars are not to be confounded with the bed-sores due to long- continued pressure. It is rarely the case that the third nerve is affected. When it is, there are external strabismus from paralysis of the internal rectus muscle, and ptosis from paralysis of the elevator of the upper eyelid. The pupil is dilated, and is insensible to light. 1 “ Anatomie et physiologie du svsteme nerveux,” tome i., p. 383. * “ Etudes cliniques et thermometriques sur les maladies du svsteme nerveux.” Paris, 1872, p. 116. ’ “ Sur la formation rapide d’une eschare it la fesse du cote paralyse dans I’h6mipl6gie /6ccnte de cause cerebrale.” Archives de physiologie, 1868, p. 308. DISEASES OF TIIE BRAIN. 86 Another phenomenon is sometimes observed, and that is the rota- tion of both eyes toward the sound side. This is accompanied by a like movement in the head, so that, if the patient is paralyzed on the left side, the eyes and head are turned to the right, and conse- quently, as the patient lies in bed, the right side of his face rests on the pillow. I have observed these symptoms in about one-third of the cases of cerebral haemorrhage which have come under my observa- tion. They were present from the very beginning, and disappeared in a few days. Slight convulsive or involuntary movements are occasionally no- ticed. The most frequent of these is yawning, a symptom which Dr. Todd 1 regards as troublesome, and even unfavorable, but which, in my experience, is not very annoying or dangerous. The other convulsive actions may be on the whole of either side of the body, or on both sides, or may be restricted to a single limb or even a group of muscles. Reflex movements are at first sometimes abolished, but subse- quently can generally be excited, especially in the lower extremity, by tickling the sole of the foot. Deglutition, though imperfect, can generally be made to take place by reflex action, unless, as pre- viously stated, the haemorrhage is in, or in the vicinity of, the medulla oblongata. The patellar tendon reflex will be found to be greatly exaggerated on the hemiplegic side, and slightly so on the sound side. This latter is owing to the fact that the motor decussation is seldom, if ever, com- plete, a small proportion of the motor fibres from the injured side of the brain passing into the same side of the spinal cord, where they are continued in what is known as the “uncrossed” or the “anterior” pyramidal tract. The ankle clonus can always be obtained on the paralyzed side if the rigidity and contractures of the leg-muscles are not too great. To produce this symptom, which is an alternating contraction and relaxation of the gastrocnemius, the weight of the leg should be sup- ported by one hand while the other hand grasps the foot near the toes. Sudden and somewhat forcible flexion of the foot should then be made and maintained, when, if the conditions are favorable, the up-and-down movement of the foot will be obtained. Secondary contractures, the exaggeration of the patellar tendon reflex, and the ankle clonus, are all evidences of irritation of the spinal motor tract, and, following a cerebral haemorrhage, indicate a descending degeneration of the motor fibres. Strong tonic contractions of the muscles of the paralyzed limbs are occasionally a prominent phenomenon. The upper extremity is more apt to be their seat than the lower, and the biceps and triceps 1 “Clinical Lectures.” Second edition. London, 1861, p. 708. CEREBRAL ILEMORRIIAGE. 87 muscles are especially liable to be thus affected. This condition may exist at the very beginning of the seizure, or may subsequently supervene. Few systematic authors have noticed the symptom in question—a symptom which is not to be confounded with the secondary contrac- tions coming on several weeks after the attack, and the origin of which is altogether different—attention seems to have been first called to it by Boudet,1 but Durand-Fardel2 studied it more thoroughly, and was the first to determine its connection with a definite lesion. According to this later author, primary contraction is only present in cases of cerebral htemorrhage when the extravasation reaches the ventricles or the subarachnoidal space. So long as the blood remains circumscribed in the cerebral tissue, there are no contrac- tions either in the paralyzed or the non-paralyzed limbs. Of twenty- six cases of cerebral haemorrhage, in which death ensued within one month, and in which the ventricles or the meninges had been invaded, there had been, in nineteen, contractions of the paralyzed members ; in three, contractions of the sound limbs ; and in four, resolution without contraction. Charcot,3 in fourteen cases of ventricular or meningeal invasion, nQticed contractions in eleven, and in two epileptiform convulsions. The contractions take place whether the membranes be distended by the clot, or whether rupture ensues. In the less severe apoplectic form of cerebral haemorrhage now under consideration, the urine and faeces are sometimes passed in- voluntarily from paralysis of the sphincters, and are at times obsti- nately retained from paralysis of the bladder and abdominal mus- cles. The mental symptoms are at first scarcely distinguishable from those which are present in the severest form of the disease. The coma and insensibility are complete, but after a time, which varies in duration with the extent of the lesion, consciousness begins to re- turn. The patient opens his eyes, and gives a little attention when loudly spoken to ; and is perhaps able to express, to some extent, his wishes by signs and gestures. Gradually the mental power in- creases ; he attempts to speak, but his words are misplaced or for- gotten, and his articulation, owing, as already stated, to the paralysis of the face and tongue, is thick and indistinct. Those words which are enunciated by the movements of the lips and tongue are especially 1 “ Memoire sur l’hemorrhagie des meninges.” Journal des connaissances m'edico- chirurgicales, 1839. 2 “ De la contraction dans l’hemorrhagie cerebralc.” Archives generates de medecine, 1843, tome ii., p. 340. Also “ Maladies des vieillards.” Paris, 1873, p. 225. 3 “ Nouvelles recherches sur la pathogenie de 1’hemorrhagie eerebrale.” Archives dc physiologic, 1868, p. 110. 88 DISEASES OF TI1E BRAIN. troublesome, while those formed in the throat are not difficult to pro- nounce. The mental characteristics of’ the patient will be found to have undergone a radical change. He is irritable, unreasonable, and fret- ful. His sense of the proprieties of life, which may in health have been very delicate, becomes obtuse ; his memory is notably impaired, and his reasoning power greatly diminished. The greatest change, however, is perceived in the emotional faculties. He laughs at the veriest trifles, and sheds tears profusely at the least circumstances calculated to annoy him. Even for years afterward this peculiarity is noticed. Such is the first stage of an attack of cerebral haemorrhage marked by apoplexy and paralysis, as ordinarily observed when amendment takes place. It is often the case, however, that this stage is not fully developed, owing to the continuance of the haemorrhage. In such an event the coma becomes more profound, the breathing more irregular and less frequent, the pulse intermits and loses in force, the face becomes purple from imperfect aeration of the blood, and death ensues. In other cases a certain degree of improvement may be attained, and then the haemorrhage may recur, and the patient dies comatose. In a few cases which I have had under my charge, the first symp- tom observed has been intense pain in some part of the head. This has been quickly followed by nausea and the ejection of the contents of the stomach. There have also been slight wandering of the mind and a disposition to stagger in walking These phenomena have per- sisted for from four to six hours, and then the patients have gradu- ally passed into a comatose condition, with general resolution of the limbs. Death has ensued within twelve hours after the beginning of the symptoms. In one of these cases, that of a gentleman of this city, he had re- marked to me, at six o’clock in the evening, that he was feeling remarkably well all day. For several years he had suffered from cere- bral hyperaemia, the result of continued and severe mental applica- tion. At about eight o’clock he was seized with the most agonizing pain in the head, attended with intense nausea. Repeated vomiting took place, and there had been slight delirium and momentary periods of forgetfulness. My friend Dr. Lente, of Cold Spring, who was in my house at the time, went with me to see him, in response to his mes- sage that I would call. We found him as above described ; and, as he was firmly convinced that his stomach was at fault, an emetic of salt water was given him. It acted promptly, but without affording him the least relief. A hypodermic injection of a third of a grain of sul- phate of morphia was next administered, but without benefit; and this was followed by a similar quantity after half an hour. He then CEREBRAL HAEMORRHAGE. 89 thought he might sleep a little, but the pain continued. An hour afterward I left him, being of the opinion, in which Dr. Lente shared, that he was either suffering from a cerebral tumor or an extravasation of blood. Two hours afterward I was again sent for. He was then comatose, the limbs in a state of resolution, the breathing of that loud, rauchous character, and the heart beating with the irregularity so in- dicative of effusion into, or in the neighborhood of, the medulla oblon- gata. Deglutition could not be excited by substances placed in the mouth. The right pupil was strongly dilated, while the left was a mere point. Death ensued within two hours afterward. The post-mortem examination was made the next day by Dr. S. D. Powell, in presence of Drs. Lente, Ripley, Elsberg, and myself. A clot the size of a small orange occupied the posterior part of the middle and central portion of the right lobes. It was entirely con- fined to the white substance. Another, about as large as a hickory- nut, was situated in the right half of the pons Varolii. In all probability the clot in the right hemisphere began to form first, and the second, into the pons Yarolii, which was the immediate cause of death, did not originate till a considerably later period, indi- cated by the disturbances in the respiration and circulation, and the impossibility of exciting deglutition. In those cases in which the improvement has been progressive up to the point of partial resumption of the mental faculties, we find that a second stage characterized by different symptoms often supervenes. This is the period of inflammation. It may begin at a variable time after the occurrence of the extra- vasation, usually not later than the eighth day. It is marked by fe- brile excitement and pain in the head, the latter being often very severe. There is gastric derangement, as evidenced by nausea and vomiting ; and convulsive movements of the limbs, with contractions of the flexors of the paralyzed side, are generally present. Delirium is also a prominent feature. Sometimes there is obstinate wakeful- ness, and at others a strong tendency to coma. This stage may last three or four days, or at most five or six, when it either causes death by extension of the inflammation from the immediate vicinity of the lesion to other parts of the brain, terminates in the formation of an abscess, or gradually ends in resolution, with abatement of the symp- toms. Disregarding for the present the first two of these results, we pro- ceed with the consideration of the phenomena of a case in which reso- lution takes place. With the cessation of the inflammatory action, the improvement of the patient becomes very marked. His speech is every day more distinct, his mind more active, his paralyzed limbs more capable of motion. Usually the leg recovers power with much greater rapidity 90 DISEASES OF THE BRAIN. than the arm, and thus the patient is able to walk tolerably well before he can raise his arm from his side, bend the elbow, or extend the fingers. The paralysis in the leg is most marked in those muscles whose office it is to elevate the foot, and this neces- sitates a peculiar gait in order to avoid dragging the toes along the ground. The abductors are rarely affected to any great ex- tent. The patient in walking, therefore, throws the leg out from the body, and then, swinging it around, clears the ground in this manner. In the upper extremity there is almost invariably a disposition toward contraction of the pectoralis major and minor muscles, by which the arm is drawn across the front of the thorax. At the same time the latissimus dorsi, the trapezius, the rhomboidei, the teres major and minor, are generally in a state of relaxation, and eventu- ally tend to atrophy. The elbow is slightly flexed, the wrist bent upon the forearm, and the fingers drawn in toward the palm of the hand. These actions may, in a great measure, be prevented by appro- priate treatment, and they may vary in extent according to the gravity of the attack. It is a curious fact that the muscles of respiration are never paralyzed in cerebral haemorrhage unless the medulla oblon- gata be involved. Trousseau 1 has insisted with great force on the fact that, when the arm regains power before the leg, the termination is always fatal. There is no foundation for this theory. Whether the arm or leg re- covers first, depends upon the extent and situation of the haemor- rhage. Now, with all these troubles of motility, sensibility may likewise be involved to a greater or less extent. When this is the case, the limbs of the affected side at first feel heavy as if made of lead, and after a while numbness, as exhibited by a feeling as if ants were crawling over the skin, or water trickling over it, as if pins and needles were sticking in it, or as if that part of the body were “asleep,” is noticed. Sometimes the sense of touch is greatly less- ened, while the ability to feel pain is scarcely impaired, and indeed is often considerably increased. Again, there may be hyperaesthesia of the skin of the affected regions, and pain along the course of the nerves. The circulation is inactive in the paralyzed limbs, and this, to- gether with the deficient nervous power, tends to cause a permanent reduction of temperature. The difference may amount to as much as five or six degrees, and, as the ability to resist cold is diminished, the patient is obliged to use additional covering on the paralyzed members. 1 “ Lectures on Clinical Medicine.” Bazire’s Translation. Part I. London, 1866, p. 16. CEREBRAL ILEMORRHAGE. 91 From continued disuse, atrophy of the paralyzed muscles always takes place unless suitable treatment be begun at an early period. Thus far we have only considered those attacks of cerebral haem- orrhage which are accompanied with unconsciousness. One of these forms kills, without the patient so far recovering as to show whether he is paralyzed or not, though of course he is so to a profound degree ; the other allows of more delay ; the brain can still act to some extent, and, if death does not ensue from continuance of the haemorrhage, the patient is found to be paralyzed on the side of the body opposite to the seat of the brain-lesion. One other form requires notice, and it is, perhaps, the one most frequently met with. It differs from the attacks just described in the important fact that it is unattended with unconsciousness. Like the others, this species of cerebral haemorrhage may take place very suddenly, without premonitory symptoms, or it may, like them, happen while the patient is said to be asleep. Generally, how- ever, though there may be no long prodromatic stage, there are symp- toms occurring immediately before the attack which indicate both mental and physical disturbance. These are headache, vertigo, numb- ness, vomiting, irritability of temper, and, perhaps, slight difficulties of speech. When the attack comes, the individual, if standing, falls, from the immediate paralysis of one leg. He is fully sensible of his condi- tion, although there is generally more or less mental change. The arm and face are affected, and the speech is rendered impossible or indistinct. If the patient be sitting or lying, he is aware that something has happened, but does not discover its exact character till he attempts to rise. A distinguished general officer of the army, after a fatiguing day of ceremony, entered his carriage with his wife, to be driven to his hotel. As he passed along Fifth Avenue he felt an indescribable sensation, and immediately afterward noticed that he could only see the half of objects. He made no effort to speak, though he is con- fident he did not for a moment lose his consciousness. When he attempted to get out of the carriage he found, to his surprise, that he was paralyzed on the right side, and that his speech was so much impaired that he could not be understood. Another gentleman was reading an amusing book, at which he laughed heartily. He felt suddenly a feeling of vertigo, and the book dropped from his hand. He attempted to pick it up, but found he had lost power in the arm, and, on trying to call to his wife, who was in the same room, discovered that he could not speak. At this time he could walk, but in a moment or two afterward he fell, from paral- ysis of his leg. So far as the paralysis is concerned, I have rarely seen a more severe case than this. DISEASES OF THE BRAIN. Another went to bed, perfectly well to all appearance, having en- joyed uninterrupted good health for several years. In the morning he arose, but felt a little pain in his head. As he stood before his glass, he thought his face was slightly twisted, and he noticed as he was shaving himself that he did not feel the razor on one side. While he was testing his facial mobility and sensibility, he experienced a trace of numbness in his left hand. This gradually increased, and in addition the limb lost power. In a few minutes he could not move it at all. By the time I saw him—two hours afterward—the paralysis had extended to the leg. At no period was there insensibility or mental confusion. A gentleman retired at night in good health. On attempting to get out of bed he discovered that he was paralyzed in the leg. Nei- ther the arm nor the face was affected. In the case of a gentleman of this city whom I saw in consultation with Dr. W. M. Polk, and who had for several years suffered from frequent severe headaches and other cerebral symptoms, the only phe- nomenon was binocular hemianopsia, with occasional slight delirium. Dr. II. Knapp, who saw the patient before I did, discovered no altera- tions in the functions or structure of the eye, and we all agreed that the case was one of very slight cerebral hfemorrhage. Several cases have been under my care in which only the face or the tongue was paralyzed ; others in which the arm alone was in- volved ; and others, like the one just mentioned, in which the symp- toms were confined entirely to the leg. Sometimes there was a mo- mentary feeling of vertigo, sometimes a vacant stare, something like that of the petit mol of epilepsy, sometimes a slight degree of intel- lectual confusion, sometimes headache, and, again, no head-symp- toms whatever. The subsequent progress of such attacks requires no special consideration beyond that already given to the more severe forms. Now, no matter how light the attack may have been, nor how rapid the improvement, the patient who has had cerebral haemorrhage is never mentally or physically the same as he was before. If the seizure has not been severe, he may advance so far toward a complete cure as to evince very little disorder of his mind or body. But close observation shows that he is not entirely restored, and, though he may do very well for light intellectual and physical exertion, severe labor of either kind is beyond his powers—and no one is more sensible of this fact than himself. Even after years his emotions are abnor- mally excitable. A patient in the New York State Hospital for Dis- eases of the Nervous System informed me that he shed tears every time a funeral passed him, and that even hearing of any one’s death, or reading the obituary column in a newspaper, caused his feelings to get the better of him. In the lightest forms of the attack, this CEREBRAL HAEMORRHAGE. 93 easily-aroused emotional disturbance is a marked feature for years subsequently, if it ever entirely disappears. And as regards the mus- cles which have been paralyzed, it is very certain that, though they may be made strong enough for all practical purposes, they never can be restored to their former sound condition. The character and general mental type of the individual usually undergo some change ; and this may be to the extent of reversing his ordinary traits. Causes.—Advanced age is one of the most influential circumstances which predispose to an attack of cerebral hcemorrbage, and this fact has long been known. Thus Hippocrates1 states that apoplexy is most common between the ages of forty and sixty, and modern inves- tigation establishes the truth of the proposition as regards the actual number of cases. It is probable, however, that the liability increases, as Dr. Flint8 says, from the age of twenty upward, and that there are not so many cases occurring in persons over sixty as below, for the reason that the number of individuals alive of that age is less. Of three hundred and eighty-three cases of cerebral haemorrhage which have been under my professional care, at some time or other after the occurrence of the extravasation, in my private and hospital practice, and in which the age of the patient is noted, three hundred and forty-one occurred in persons over forty years of age. Of these, three hundred and eleven were between forty and sixty, thirty-three between sixty and seventy, five between seventy and eighty, and three over eighty. Of the thirty-one cases in persons under forty, twenty were be- tween forty and thirty, ten between thirty and twenty, and one un- der twenty. This latter was a boy of seventeen, whom I exhibited at my clinic at the Bellevue Hospital Medical College in the autumn of 1870. The disease is certainly more common among men than women, though some authors have asserted the contrary. Falret ascertained that, of tw'enty-two hundred and ninety-seven cases, sixteen hundred and sixty occurred in males and only six hundred and thirty-seven,in females. In my own experience, of three hundred and eighty-three cases, two hundred and fifty-nine were in males and one hundred and twenty-four in females. Temperament and organization are supposed to have an influence in predisposing to cerebral hfemorrhage. It was formerly thought that those of sanguine temperament and plethoric habit who had stout bodies, large heads, florid complexions, and short, thick necks, were especially liable ; but more exact and thorough investigation would 1 “ Aphorisms,” chapter vi., aphorism 57. s “ A Treatise on the Principles and Practice of Medicine.” Third edition, Philadel- phia, 1868, p. 582. 94 DISEASES OF TIIE BRAIN. appear to show that such is not the case, and that thin and pale indi- viduals show fully as great a proclivity. Dr. Flint1 expresses the opinion that there is no special apoplectic constitution, and my own experience is decidedly to the same effect. That the tendency to cerebral haemorrhage is often hereditary appears to he very certainly established. Within my own knowledge, I am aware of several striking instances which support this opinion. A gentleman consulted me for hemiplegia, the result of cerebral haemorrhage, whose grandfather, father, two uncles, two brothers, and one sister had died of this disease, and whose son, thirty-six years of age, had been attacked. In another case a lady had her father, two brothers, and one sister die of the disease ; and, in a third very remarkable case, the great-grandfather, grandmother, father, four uncles and aunts, and two brothers, all in a direct line, died of cere- bral haemorrhage. Piorry2 cites the case of a woman, herself paralytic, whose three children had died of convulsions, and whose mother, uncle, and broth- ers and sisters, to the number of twelve, had died of cerebral haemor- rhage or convulsions. It has very often happened in my experience that the father or mother of a hemiplegic patient, whose condition resulted from cerebral haemorrhage, had been affected in a similar manner. As regards the influence of diseases of the heart, Legallois, Briche- toau, Rostan, Andral, and Bouillaud3 adduce instances in support of the existence of a definite relation. While others, among whom Ro- choux, Walshe, and Flint are to be placed, deny the existence of any such causative influence. As tending to produce active or passive cerebral congestion, disease of the left or right side of the heart would reasonably seem to be conducive to the occurrence of cerebral haemor- rhage. The tension of the blood in the vessels of the brain is in- creased thereby, and the liability to the rupture of a diseased vessel rendered greater. The condition of life has also been supposed to exert an effect in pre- disposing to cerebral haemorrhage, it being asserted by some authors that the affection is much more common wTith the rich, and those living in ease, luxury, and refinement, than in the poor and laboring classes. It is difficult to arrive at any very definite conclusion on this point, owing to very obvious reasons, but I am inclined to think the theory to be not well founded. It is only necessary to visit our large hos- pitals, to see how many of the inmates, drawn as they generally are from the laboring classes, are suffering from cerebral haemorrhage or its effects. Thus far we have only considered the more important, intrinsic, 1 Op. cif., p. 683. 2 “ Dc l'heredit6 dans les maladies,” p. 107. 3 “ Traite de clinique des maladies du coeur,” second edition, tome ii., p. 680. CEREBRAL HAEMORRHAGE. 95 predisposing causes ; there are, however, others which may be called extrinsic. Season is one of the chief of these. The disease is much more common in winter than in the other seasons, although some statistics would seem to show more cases during summer. A careful examination of such, however, shows that under the head of apoplexy is included not only cerebral haemorrhage, but congestion, sunstroke, embplus, and in fact nearly every other affection attended with sudden loss of con- sciousness. My own researches have been very exact on this point, and as their results I find that, of the three hundred and eighty-three cases of which I have notes, one hundred and forty cases occurred in winter, eighty-one in spring, ninety-seven in summer, and fifty-eight in autumn. It has been noticed, too, that sudden variations of temperature, especially from mild to cold weather, increase the number of cases of cerebral hiemorrhage. Of the exciting causes, a long list can readily be made. Among them are the excessive use of alcoholic liquors and other stimulating substances; the use of opium in excess ; the ingestion of large quantities of food, especially such as is stimulating and indigestible ; excessive physical or mental exertion, strong emotional disturbance, such as anx- iety, extreme joy, anger, or terror ; the act of coition, especially in old people; straining at stool; enlarged prostate, or paralysis of the bladder, requiring strong muscular efforts for the evacuation of the urine ; childbirth ; tight clothing about the neck, chest, or abdomen ; certain occupations which require the head to be depressed ; vomiting, sneezing, coughing, and laughing ; exposure to the direct rays of the sun or other sources of great heat ; the sudden arrest of a custom- ary flux, such as haemorrhoidal bleeding; the sudden application of cold water to the body ; long-continued bathing in very warm water ; the circumstance that the patient has had a previous attack, and certain diseases, as gout and syphilis. In regard to some of these causes, I may state that several very in- teresting cases have occurred in my own practice. In one, a lady was attacked on hearing that her cook had left her; in another the emotion excited by the fall of a picture from the wall caused a seizure. Four cases produced by straining at stool have come under my observation. In one of them a gentleman well known in public life retained sufficient consciousness and intelligence to take a large key out of his pocket with the non-paralyzed hand, and to rap on the floor for assistance. Two cases occurred during sexual intercourse, one in a man, the other in a woman. In one of these there was, subsequently, a great increase of venereal desire. In one case, the seizure was induced by stooping over to tie the shoe. This was in the boy, seventeen years of age, already mentioned. It must be confessed, however, that very fre- quently, perhaps in the majority of cases, no immediate cause can be DISEASES OF THE BRAIN. reasonably alleged. Of the three hundred and eighty-three cases noted by myself, no cause was noted in two hundred and ten. Relative to the influence of sleep, I am by no means in accord with those authors who regard it as a powerful exciting cause. Inuring sleep the quantity of blood circulating in the cerebral blood-vessels is dimin- ished, and hence there is less tension upon their walls than during wake- fulness.. I doubt very much whether cerebral haemorrhage ever occurs during healthy, undisturbed sleep. But there is a condition which supervenes upon sleep, and which, to ordinary observers, presents the usual phenomena of sleep, but which is really a very different state, both as regards the brain and the symp- toms—and that is stupor due to venous congestion. In this affection there is an increase of the pressure upon the brain, produced by the over- distended vessels; and hence coma, to some extent, ensues. This state is characterized by difficulty of awaking the individual, by turgescence of the larger veins of the neck, by a more or less purple hue of the face, by snoring, and by the puffing out of the lips and cheeks in breathing. Both of these latter phenomena are due to paralysis. In this condition it is not unusual for cerebral haemorrhage to occur, but the existing state is not sleep. So far as my own experience extends, I have not found a majority of the cases, where I have examined into this point, to have taken place either during sleep or the stupor to which I have referred. I have made it a rule, not only in those cases of cerebral haemorrhage which have been under my own care, but all others, in which I could do so, to inquire particularly with reference to the matter in question, and have found that, in three hundred and eighty-five out of four hundred and sixty- seven cases, the individuals were awake at.the time of the attack. Doubtless much of the confusion has arisen, not only from the non- discrimination of sleep from stupor, but also from treating of apoplexy as a disease instead of regarding it as a symptom due to several very different pathological conditions of which cerebral haemorrhage is only one, and of which embolism, thrombosis, congestion, meningeal haem- orrhage, and epilepsy, are others. Finally, it may be said of the etiology, that whatever tends to in- crease the flow of blood to the head, or to retard its exit, is capable of acting as an immediate cause of cerebral haemorrhage. Diagnosis.—The diagnosis of cerebral haemorrhage is ordinarily not difficult, but it must be confessed that one or two affections are very liable to be confounded with it, and the attendant circumstances sur- rounding a patient in a condition of insensibility may be such as to materially increase the obstacles to the formation of a correct opinion. Thus, supposing an individual to be found in a state of profound in- sensibility, the condition may be due to compression from injury of the skull, to concussion from a fall or blow, to congestion, to asphyxia, to CEREBRAL ILEMORRHAGE. syncope, to a recent epileptic fit, to uraemic intoxication, to hysteria, to narcotism, or to drunkenness. A mistake of either of these states for cerebral haemorrhage would be, in the end, embarrassing to the physician, and perhaps injurious to the patient. The coma might also be the result of embolism, of thrombosis, of tumor, of abscess, or of meningeal haemorrhage ; but, as regards these conditions, no opprobrium could be attached to the physician, or harm come to the patient, by any error of diagnosis, although a regard for scientific exactness should always prompt us to be as specific as possible in our inquiries and examinations. From asphyxia, cerebral haemorrhage is distinguished by the fact that in the former the respiration is suspended. The cause is often apparent. A careful examination of the cranium, and a survey of the surrounding circumstances, will enable the physician to ascertain the existence or non-existence of compression from traumatic cause. This cause may either be depression of bone, the rupture of an internal blood-vessel, or the entrance of some foreign body, as a bullet, into the interior of the skull. So far as symptoms are concerned, there might be considerable difficulty in diagnosticating either of these accidents from cerebral haemorrhage, but the history would render a mistake im- possible. Concussion presents more difficulties, because the comatose person may be found in such a situation as to warrant the opinion that he has fallen from a height, or otherwise received a blow on the head, when in fact he is suffering from cerebral haemorrhage. But if he has fallen from a height or been struck, there will probably be more severe bruises about his person than if he is affected with cerebral haemorrhage, and there may be bleeding from the ears or nose—symptoms of cranial injury not met with in the latter condition. If, however, the individual has fallen from a height, he may have done so in consequence of an extravasation of blood in his brain, and ae may present all the marks of suffering simply from the concussion, or he may have fractured skull with compression. It is, therefore, im- possible to make a correct diagnosis in all cases, or to lay down any certain rules which will constitute infallible guides. It is perfectly possible to meet with cases such as those referred to, in regard to which no human judgment can be certainly correct. Such instances are of course rare, and accordingly, in the great majority, the circumstances and the presumption will generally lead to a correct opinion. From congestion of the apoplectiform variety cerebral haemorrhage can generally be distinguished without much difficulty. The absence of stertorous breathing, the short duration of the coma, the transient character of the paralysis, the contraction of the pupils, the fact that the loss of sensibility and the power of motion are not generally confined 98 DISEASES OF THE BRAIN. co one side of the body, and the longer continuance of premonitory symptoms, will be sufficient indications of the existence of congestion. Syncope is distinguished by the circumstances that the respiration and circulation are both diminished in power if not suspended, that there is no hemiplegia, that the face is pale, the skin cold, and that these phe- nomena are all transitory in character. The history of the case will also assist us in arriving at a correct judgment. Epilepsy, if seen from the beginning of the paroxysm, cannot be mistaken for cerebral haemorrhage, nor this latter for epilepsy, if the onset of the attack has been witnessed. Even if there are convulsions present in the apoplectic seizure, the error could not readily be com- mitted if attention be paid to the attendant phenomena. For there is no biting of the tongue, the convulsions are persistent, and the animal heat is lowered, whereas in epilepsy the temperature rises at once and remains high—105° Fahr. or thereabouts, during the convulsive stage. But the person found in a comatose condition, with no previous history to guide us, may be supposed to be either in the comatose stage of an epileptic paroxysm, or to be laboring under a seizure due to extravasa- tion of blood. In such a case, if the fit has been epileptic, foam will be found around the mouth, and perhaps blood from injury of the tongue or cheek. Moreover; the stupor of epilepsy is not usually of long duration, and is not generally characterized by stertorous breathing. In unemia, the coma of which is very similar to that resulting from cerebral hasmorrhage, the history of the case is our chief reliance for a correct diagnosis, though the absence of hemiplegia and the general presence of anasarca are of course of great value. Moreover, in very doubtful cases the urine may be drawn off by the catheter, and exam- ined for albumen and tube-casts. If these are present, the probability of the stupor being due to Bright’s disease and uraemic intoxication is very much increased. The fact, also, that in uraemia there is a pro- gressive fall of the animal temperature—as low as 91.5° Fahr. being reached — and that there is no subsequent elevation, are important points in this connection. Coma is sometimes a manifestation of hysteria, but a very little acquaintance with the phenomena of this condition will suffice to pre- vent mistakes. In some cases of hysterical coma there is well-marked hemiplegia; but even when this complication is present, the facts that the hysterical diathesis exists, that there have probably been other mani- festations of hysteria, that the pulse is small, weak, and frequent, and that the breathing is free from stertor, will enable a correct diagnosis to be formed. In narcotism the condition often bears a close resemblance to that due to cerebral hremorrhage. But in the former there is no hemiplegia, the pupils are generally contracted, the respiration is not stertorous, and the coma comes on graduall}r. CEREBRAL HAEMORRHAGE. 99 Drunkenness and cerebral haemorrhage are often confounded. I have known some sad mistakes of the kind to be made, both by professional and non-professional persons, many of which were unavoidable, for it must be confessed that there are great difficulties connected with the subject. The habit of drinking alcoholic liquors is so general that no reliance can be placed upon the test of smelling the breath. A person may have just taken a glass of wine or of brandy, and be seized with extravasation of blood in his brain immediately afterward, and when not in the least intoxicated. And, even if dead-drunk, he may at the same time have cerebral haemorrhage. In such a case as the latter, discrimi- nation would be impossible. In ordinary cases of alcoholic intoxication the patient can generally be roused to some extent; the pupils are dilated, but this latter is often the case in haemorrhage; the breathing is usually free from stertor, but some drunkards always snore; the pulse is small and weak, and there is no hemiplegia. When all these symptoms are in accord, there will be little difficulty; when they are not, the physician must be guarded in his expressions of opinion, and diligently inquire into the personal characteristics of the patient and all matters bearing on the history of the case. From the centric diseases previously mentioned, the diagnosis of cerebral haemorrhage is easy as regards some, and difficult as to others: Thus, from embolism it cannot in many cases be distinguished in the first stage. But when all the phenomena are taken into consideration the chance of error is very much diminished. Embolism is generally accompanied with disease of the left side of the heart, and there is often a history of rheumatism ; there are never any premonitory head-symp- toms ; it occurs in young persons as well as old ; for reasons which will be explained when the subject of partial cerebral anaemia from embolism is considered, the resulting hemiplegia is generally on the right side ; the paralysis usually disappears in a few hours after the attack ; if it does not, there is no gradual improvement, as in cerebral haemorrhage ; there are no contractions or partial convulsions1; there are slight or no changes of temperature ; and there is more frequently delirium. The gradual development of the symptoms in thrombosis, tumor or abscess, and the frequency with which convulsions ensue in the latter diseases, together with the associated symptoms, will prevent the coma which sometimes exists being mistaken for the stupor of cerebral haem- orrhage. During the subsequent stages of cerebral haemorrhage, when the mental condition and the hemiplegia are the most prominent features, inquiry into the antecedent history will bring out the foregoing points, and assist us in arriving at a correct idea of the cause. Even, however, 1 Jaccoud (op. cit., p. 141) so asserts, though I have seen one case in which post- mortem examination revealed the presence of an embolus in the middle cerebral artery, and in which there had been convulsions. 100 DISEASES OF TIIE DRAIN. should we be baffled in this respect, no great inconvenience could result either to the patient or physician. Prognosis.—The prognosis depends upon the extent or situation of the haamorrhage, and refers to the probability of saving life during the period of attack and immediately afterward, and of curing or mitigating the subsequent paralysis. In the severe apoplectic form, death is almost inevitable; so far as my experience goes, it is the invariable result. It generally takes place within a few hours. If, however, life be prolonged till the fourth day, there is some hope. Irregularity of pulse, or one very rapid, impossi- bility of swallowing, involuntary evacuation of the faeces, and cold sweats, render, if possible, the prognosis still more unfavorable. In the apoplectic form attended with paralysis, the gradual increase of the coma and hemiplegia indicate the continuance of the haemor- rhage, and are consequently of grave importance. About one-third of those attacked with this form die. The prognosis is bad in proportion to the debility and age of the patient, and the circumstances under which the attack has occurred. Thus, if it has supervened in a person who has had no obvious exciting cause, the probability is that there is serious disease of the blood-vessels, whereas, coming on in a young per- son as the result of severe muscular exercise, or mental strain, the prog- nosis is more favorable. A second attack is more apt to prove fatal than a first, and a third than a second, and so on. In the mild form characterized by paralysis, but no loss of conscious- ness, the prognosis is generally favorable. It must be recollected, how- ever, that the risk of inflammation is quite great, both in this and the apoplectic form with paralysis, and that the patient is not safe from it till after the eighth day. And in both forms, if the temperature rise above 100° Fahr.; if the respiration be chiefly abdominal; if the patient is unable to swallow; and rattling of mucus is heard in the throat, the prospect of recovery is bad. The same may be said of pain in the head and contractions of the paralyzed muscles. If, further, as Bourneville has shown, the tempera- ture reaches 104° Fahr., death is inevitable. As regards the probability of recovery from the paralysis, much de- pends upon the opportunities the patient may have for receiving proper medical treatment. The tendency is generally toward amendment even in the worst cases. Gradually the speech improves, the breathing be- comes better, and the arm acquires more strength; but the improve- ment often stops here, and never goes on unaided to complete recovery. The longer the paralysis has lasted, the less prospect there is of great progress under any treatment; and, if strong contractions producing distortions have taken place, the prognosis is unfavorable. Certain muscles over better than others. The extensors of the CEREBRAL HAEMORRHAGE. 101 foot and hand are especially intractable, but, as a rule, those of the lower extremity improve more rapidly than those of the upper. The mind ordinarily improves, pari passu with the physical symp- toms, though not always. I have witnessed several exceptions to the rule. Even in slight cases the intellect may suffer to a great extent, and in no case is it ever in all respects as good as before the attack. Among the unfavorable signs are, persistent irritability of temper, fail- ure of memory, and the existence of delusions. Difficulties of speech, whether as regards the memory of words, or the ability to coordinate the muscles of speech, so as to pronounce them properly, are often very persistent. I have now under my care a gentleman who was attacked with cerebral haemorrhage two years ago, whose physical powers are quite good, and whose mind is not seriously impaired, but who cannot yet remember sufficient words to carry on an ordinary conversation. When the difficulty is simply due to paralysis of the tongue and facial muscles, the prognosis is more favorable. Morbid Anatomy.—The seat of the extravasation from cerebral haem- orrhage may be in the substance of the cerebral tissue, or in the ven- tricles. The former is much the more common. Now, the blood, which is poured out from a ruptured vessel into the substance of the brain must, of course, occupy its place by separating or lacerating the fibres. It thus forms for itself a cavity, which en- larges as the haemorrhage goes on, until at last the resistance to further separation or laceration may be so great as to overcome the tension of the blood, and thus put a stop to the bleeding. The shape of the cavity varies according to the manner by which it has been produced. When it is formed by the separation of the cere- bral fibres, it is generally elongated; whereas, when produced by lacera- tion, it is oval, round, or irregular in form. The situation of the haem- orrhage modifies the form of the cavity. In the hemisphere it is usually round; in the motor tract, irregular or oval. The variations as regards size are great. I have seen clots no larger than a pea, and again as large as an orange. When haemorrhage occurs in the motor tract, the clot is almost invariably small; whereas, in the hemispheres, in the cere- bellum, or in the ventricles, it is large. A clot does not always consist of blood alone. Brain-tissue is very often mixed with it, and this is especially the case when the extravasa- tion has been into the white substance of the hemispheres. Gintrac1 has collected the data of five hundred and sixty cases of cerebral haemorrhage, in which there was a single clot, and in these the seat of the extravasation is shown in the following table : 1 “Traite theorique et pratique des maladies de l’appareil nerveux ’’ Tome deuxi&me Paris, 1869. Art “ Hemorrhagies du cerveau.” 102 DISEASES OF TIIE BRAIN, Corpora striata 72 Optic tlialami 38 Corpora striata and optic thalami simultaneously 48 Middle lobes of the brain 127 Fons Varolii and crura cerebri 78 Cerebellum 36 Ventricles 46 Posterior lobes of the brain 33 Anterior lobes of the brain 17 Medulla oblongata 2 Corpus callosum 1 Cortical substance of the brain 45 Total 560 The ordinary seat of cerebral haemorrhage is thus seen to be in the vicinity of the motor tract, for in nearly one-half of the total number of cases the lesion was situated either in the corpora striata, the optic thalami, the pons Yarolii, the crura cerebri, or the medulla oblongata. And of these parts the corpora striata and optic thalami are preemi- nently liable. As the lesion is seldom confined to these organs, the in- ternal capsule rarely escapes injury. Next in order of frequency come the middle lobes. In the great majority of the cases of cerebral haemorrhage the lesion is situated primarily in the gray substance. This is probably due to the fact of the greater vascularity which this tissue possesses. It would appear, too, that even when the extravasation is not into the corpus striatum or optic thalamus, it is very apt to be in the immediate vicinity of these organs. M. Duret1 has given an anatomical expla- nation of this fact, which appears to be satisfactory. According to this observer, the arteries of the corpus striatum, which are given off gen- erally from the middle cerebral artery, though sometimes from the anterior cerebral, enter the brain through the anterior perforated space. A few delicate branches go to the caudate nucleus of the corpus stri- atum, but the larger ramifications are distributed sometimes to the lenticular nucleus, but more generally they wind around this organ, and give origin to branches which are widely distributed, reaching even as far as the island of Reil. Thus the largest intra-cerebral arteries are situated in the external portion of the corpus striatum. And this is the exact place wThere, according to Charcot, cerebral haemorrhage is most apt to occur. Gendrin2 had previously remarked that the extravasation in cases of cerebral haemorrhage almost always comes from the branches of the middle cerebral artery. The middle lobe, the island of Reil, the corpus striatum, and the optic thalamus are nourished through this vessel, and 1 “ Note sur la distribution des arthres nourrieiures du cerveau.” Mouvement me- dical, 1873, p. 27. Also, “Reclierches anatomiques sur la circulation de l’encepliale.” Archives de physiologic, 1874, p. 316. 2 “ Traite philosophique de medecine pratique.’’ Paris, 1838, tome i., p. 448. CEREBRAL HAEMORRHAGE. 103 lienee the great preponderance of extravasation in these portions of the encephalic mass. It has also been observed—and Durand-Fardel1 calls special atten- tion to the circumstance—that cerebral haemorrhage has a manifest ten* dency to be developed and directed, rather toward the central than the peripheral parts of the brain. It is thus, to say, centripetal in its course, in which respect it differs from cerebral softening, which is not less evidently centrifugal—the peripheral regions showing a greater ten- dency than the central to be affected by this morbid process. The right side of the brain appears to be more frequently the seat of cerebral haemorrhage than the left. Thus, on consulting Gintrac,2 we find that in three hundred and sixty-nine cases in which the side on which the lesion was situated was noted, the parts were affected in the order of frequency shown in the following table: Eight. Left. Corpus striatum, optic thalamus, and these bodies simultaneously 73 63 Middle lobes 63 52 Pons Yarolii 10 10 Cerebellum 14 12 Cortical substance 15 8 Posterior lobes 18 15 Anterior lobes 6 10 Total 199 170 The right side had thus a numerical superiority of twenty-nine over the left. It will be observed, also, that in no one part did the left side predominate except in the case of the anterior lobe. On the other hand, Durand-Fardel,3 from an examination of one hundred and seventeen cases of haemorrhage into the hemispheres, found that the right side was the seat in forty-nine, the left in fifty-seven, and both sides in eleven in- stances. Of eleven cases of cerebellar haemorrhage, the right lobe was affected six, the left five times, and the middle lobe twice. Generally there is but one recent extravasation, but occasionally two or more occur simultaneously, or at least so near to each other in point of time as to be essentially contemporaneous acts of one morbid pro- cess. Of one hundred and thirty-nine cases cited by Durand-Fardel,4 twenty-one were multiple ; eighteen of these were double, and three triple. In my own experience two cases of triple lesions have occurred, and two of double lesions. Of the triple cases the right corpus stria- tum, right middle lobe, and left middle lobe, were the seats in one, and the right and left corpora striata, and left anterior lobe, in the other. Of the double cases the seats in one were the right corpus striatum, and right middle lobe, and in the other the right middle and posterior lobe and right half of the pons Varolii. 1 “Traite pratique des maladies des vieillards.” Paris, 1873, p. 181. 2 Op. et loc. tit. 3 Op. cit., p. 185. 4 Op. tit., p. 186. 104 DISEASES OF TIIE BRAIN. It sometimes happens that the mass of extravasated blood breaks through the cortical substance of the brain, and appears immediately under the pia mater and arachnoid; or these membranes may give way, and the blood be effused into the space between them and the dura mater. In a very few of these cases the blood comes primarily from the cortical substance of the brain, but in the greater number the ex- travasation originates more deeply and reaches the surface by lacer- ating the easily-torn white tissue. The blood in these cases undergoes coagulation much more rapidly than when it remains in the cerebral substance, unless the base of the brain be the seat, in which case it often remains fluid. The extravasation takes place into the ventricles in about one-half of all the cases. The lateral or fourth ventricle may be the seat, or it may exist in both of the former. The blood extravasated into the ventricles remains liquid a longer time than when effused into any other part. This is probably due to the fact that it is subjected to the action of the ventricular fluid, by which its physical properties are altered. In the majority of cases of haemorrhage into the ventricles, the blood comes originally from the corpus striatum, or optic thalamus, but it may also be derived from the choroid plexus, from the septum lucidum, or from the walls of the ventricles. Sometimes it is im- possible to determine its point of origin. It may enter the ventricle through a small opening, in which case the foyer is distinct, or the wall of the ventricle may be largely lacerated and so broken down that the foyer and the ventricle constitute essentially but one cavity. The septum lucidum is not infrequently torn, and the two lateral ventricles are thus converted into one cavity. As regards what may be called the secondary consequences of an extravasation of blood into the cerebral substances, we find that when it is large the convolutions are flattened against the walls of the cranium, the membranes are usually dry, and a distinct feeling of fluctuation can often be detected. In several cases I have known a large extravasation to cause by its own weight a complete rupture of the lobe in which it existed, through the handling required in removing the brain from the skull. At other times the membranes are evidently congested; the brain- tissue, when incised, exhibits an increased number of red points, and the subarachnoidean or ventricular liquid may be largely augmented over the normal quantity. The state of the arteries is a most important and interesting subject for examination, but, as it has an immediate and direct relation with the pathogeny of cerebral hiemorrhage, it will be more properly consid- ered under the head of pathology. Extravasated blood undergoes certain changes. Instead of di- CEREBRAL HAEMORRHAGE. 105 viding into two parts, the clot and the serum, as does blood when exposed to the atmosphere, it remains for a time homogeneous and gclatiniform. About the fifth or sixth day it separates into two parts ; the one, the serum, is absorbed by the surrounding tissue; the other, consisting mainly of the fibrine and the red corpuscles, contracts and becomes hard. By the fifteenth day it has become fibrinous in texture, and is changed from its former black hue to a yellow color. Micro- scopic examination, made at any period during these changes, reveals the presence of red corpuscles, crystals of hematoidin and sometimes of cholestrin. It never entirely disappears. In the earlier period of the extravasation, the walls of the cavity are rough, and discolored with blood. But, as the changes are going on in the clot, the walls likewise alter in appearance ; the inequalities and irregularities disappear, and a new formation of connective tissue lines the cavity. Blood-vessels appear in it, and aid in the absorption of the fluid portion of the extravasated blood. As the process of separation and absorption goes on, the cavity contracts upon its con- tents, and eventually forms a cicatrix which incloses the remains of the clot. This cicatrix is generally of a yellow color, and firm in texture. Sometimes, however, absorption does not take place. The con- traction of the walls of the cavity does not therefore ensue, and it remains distended with more or less altered blood. This may be the starting-point of secondary lesions, or a new haemorrhage may occur into the same cavity, or an abscess may result. Pathology,—The theory of cerebral haemorrhage brings us to the consideration of several important points. One of the first questions to be solved is, Can the rupture of a vessel of the brain take place— not including traumatic causes—unless the vessel is in a diseased condition ? Both sides of this proposition have their adherents. On the one part, it is urged that cerebral haemorrhage never takes place spontaneously unless the walls of the bleeding vessel have been so injured by disease as to destroy their strength and elasticity ; on the other, that it is perfectly possible for a blood-vessel to give way, owing to the increased tension of the blood or disease of the peri-vascular tissue, without the walls of the vessel itself being in the least diseased. While admitting that, in the majority of cases, the structure of the yielding vessel will be found to be impaired, I am satisfied that either of the other two causes may produce a rupture. The reasons for this opinion will be apparent in the course of the following remarks. One of the most common diseases to which the cerebral arteries are liable is chronic endarteritis, a condition wrhich has been well described by Virchow,1 and which is particularly apt to be met with in those who, 1 “ Ucber die Erweiterung kleinerer Gefasse.” Archiv fur path. Anat. und Physiol B. III., 1848, and “ Cellular-pathologie,” Berlin, 1871, S. 458 et scq. 106 DISEASES OF THE BRAIN. from age or other debilitating influence, have had their nutrition impaired. As the consequence of this state, the vessels lose their elasticity, become brittle, and are therefore often unable to bear the ordinary tension of the blood, much less any severe strain. This disease may terminate in fatty degeneration of the arterial walls, or this last condition may be the primary affection. Fatty degeneration, like chronic endarteritis, is most commonly met with in badly-nourished persons, but who are at the same time cachectic. The inner coat is the point of origin, and hence it sometimes hap- pens that this and the middle coat give wray, leaving the external coat entire, and thus forming an aneurism. But Bouchard,1 who has examined into this matter with great minuteness, denies that such aneurisms are ever found, and asserts that the so-called aneuris- mal sac consists of the lymphatic membrane, lining the cavity in the perivascular tissue, through which the vessel passes; and that the blood, in such cases, has already ruptured the vessel. In reality, how- ever, there is no haemorrhage into the cerebral tissue till this mem- brane gives way. In a subsequent memoir, by MM. Charcot and Bouchard,8 this point is still more thoroughly considered, and the opinion expressed that cere- bral haemorrhage is almost invariably due to what they call miliary aneurisms, which are the result of arteritis, and which are not neces- sarily preceded by atheroma. The existence of these minute aneurisms was first pointed out by Cruveilhier,* and was subsequently recognized by Calmeil.4 Meynert6 appears also to have noticed them, and Heschel6 discovered them in the pons Varolii; but no one previous to Charcot and Bouchard called at- tention to the relation which they bear to cerebral haemorrhage. On March 16, 1866, while examining the foyer of a recent extravasation into the brain, they perceived, on the walls of the cavity in the cerebral tissue, two small globular masses attached to a minute vessel. These were miliary aneurisms. One was ruptured, and its contents were in immediate relation with the mass of extravasated blood constituting the apoplectic clot. Previously to this time these observers had noticed these aneurisms, but not before had they associated them with the pathogeny of cerebral haemorrhage; since then, in numerous commu- 1 “ Etudes sur quclques pointes de la pathogenic dcs hemorrhagies cerebrales.” Paris, 1866. 2 “ Nouvelles recherches sur la pathogenic de Fhemorrhage cerebrate.” Archives de physiologie normale et patliologiquc, 1868, pp. 110-643. 3 “ Anatomie pathologique du corps humain,” liv. xxxiii., PI. 2, Fig. 3. 4 “Traite des maladies inflammatoires du cerveau.” Paris, 1859, tome ii., p. 522. 5 “ Ueber Gefassentartungen in der Yarolsbriieke und den Gehirnschenkelm.” Allgemeine Wiener Wochenschrift, No. 28, 1864. 6 “ Die Capillar-Aneurysmen im Pons Varolii.” Wiener mcdicinischc Wochenschrift, September, 1865. CEREBRAL HAEMORRHAGE. 107 nications, they have called attention to the importance of their dis- covery, and its value is generally acknowledged by neuro-pathologists. Fig. 8. In the accompanying woodcut (Fig. 8), taken from Bouchard’s mem- oir, is represented one of these aneurisms wThich has been ruptured Fig. 9. into a ha3morrhagic clot : a, the aneurism ; b, the clot; c, c, the torn perivascular or lymphatic sheath. Fig. 9 is from the drawing of a vessel which I recently dissect- ed out of the pons Varolii, into the right lobe of which a large ex- 108 DISEASES OF THE BRAIN. travasation had taken place. Both lobes were studded with these aneurisms ; they were also found in the convolutions in the optic thalami and corpora striata, and in the white substance of both hemi- spheres ; a large extravasation had also taken place into the right hemisphere. In sixty-nine cases of cerebral haemorrhage in which po&t-mor- tem examinations were made, atheroma was found but in fifteen, or twenty-two per cent., while these miliary aneurisms were met with in every case. They appear as little globular masses in the small intracranial vessels, and are in size from one-tenth of a milli- metre to one millimetre. If they contain liquid blood, they are red ; but if the blood be coagulated, the color is dark, almost black in some cases. In the order of frequency, they are found in the optic thalami, the corpora striata, the convolutions, the tuber annu- lare, the cerebellum, the centrum ovale, the crura cerebri, and the medulla oblongata. According to Charcot and Bouchard, the arteritis, which re- sults in the formation of these aneurisms, is diffuse in charac- ter. It is found not only in the minute artery, which is the sub- ject of the aneurismal dilatation, but extends to the entire system of minute intracranial vessels. This arteritis is in some respects analogous with what Rokitansky described under the name of chronic peri-arteritis, and is chai’acterized by disease of the membrane, desig- nated by Robin as the perivascular sheath, and by His as the lym- phatic sheath. There are also lesions of the adventitious tunic and of the muscular and internal coats. The diseased action proceeds from without inward, and hence the name of peri-arteritis is a very proper one. Charcot and Bouchard claim that, with the following exceptions, all cases of cerebral haemorrhage are the result of the rupture of miliary aneurisms, viz., fracture with depression ; the haemorrhages which result from thrombosis of the sinuses, and those which occur in the course of certain depraved states of the system. While admit- ting that the majority of cases of cerebral haemorrhage have this origin, I am not prepared to go so far as these observers in ascrib- ing all not embraced in the three categories of exceptions above specified, as being due to this cause. I had recently the opportu- nity of convincing myself that this explanation of the pathogeny of cerebral haemorrhage is too absolute ; for, on examining the brain of a patient who had died from an extravasation of blood into the left corpus striatum, optic thalamus, and left lateral ventricle, not a sin- gle miliary aneurism could be discovered, although they were care- fully sought for in all parts of the brain. The patient, a lady forty- three years of age, had suffered from repeated attacks of acute rheumatism, had frequently been affected with headache and ver- CEREBRAL HEMORRHAGE. 109 tigo, and had been seized with apoplexy while in the water-closet. She had been the subject of heart-disease for over twenty years. I had only the brain submitted to me for examination, but all the arte- ries of this organ were in a state of atheromatous degeneration, and I was able to find what appeared to be the vessel, or one of them, which had given way and produced the extravasation. The accompanying engraving (Fig. 10) represents this artery as. seen with an inch object- ive. It is perceived that several of the aneurismal dilatations have given way; the internal coat of this, as well as of other arteries, was Fig. 10. found, by microscopical examination, to be in a state of fatty degen- eration; the same state existed in the middle coat, and the external coat was thickened and friable. Lancereaux 1 reports a very similar case, of which, as it has an im- portant bearing on the subject, I quote the summary which he gives (page 424): “ Haemorrhage into the left ” [right is evidently meant, and it is so stated on page 252, where the full report of the case is given] “ corpus striatum, producing an irruption into the lateral ventricles, and arteritis, albuminuria, cardiac hypertrophy. “ A woman, aged fifty-eight, died a few days after an attack charac- terized by left hemiplegia, diminution of sensibility, and vomiting. The autopsy revealed the existence of a hasmorrhagic clot at the exterior and posterior part of the corpus striatum, which, after having separated this ganglion from the optic thalamus, had broken into the ventricular cavity. The nervous tissue, besides being torn, was colored yellow, through the infiltration of haematine into its substance. The ventricles contained a small quantity of liquid blood. There existed under the ependyma of the posterior cornu of the right ventricle a haemorrhagic punctation, and a sanguineous suffusion extended over the whole cir- cumference of the cerebellum. The entire encephalic mass was injected. The walls of the cerebral arteries were thick and opaque. On the 1 “ Anatomie pathologique,” texte, pp. 252 and 424; atlas, plates 24 and 43. 110 DISEASES OF THE BRAIN. branches, even those of the smallest size, were perceived moniliferous dilatations, the result of a primitive alteration of the arterial wall, and the probable points of origin of the haemorrhage. The aorta was affected with endarteritis throughout its whole extent, the aortic orifice was slightly insufficient, and the left ventricle was markedly hypertrophied ; the renal arteries were indurated, rigid, and calca- reous. The kidneys, small, atrophied, and granular, were affected with interstitial nephritis. The arterial system was involved through- out almost its entire extent.” It would appear, therefore, that we cannot set aside the results ob- tained by Virchow and others, and that, in the present state of our knowledge, it is safe to adopt the opinion expressed by Durand-Fardel,2 that, although “ the facts observed as described by MM. Charcot and Bouchard have undoubted value, it would, nevertheless, be premature to attribute to miliary aneurisms an exclusive part in the production of cerebral haemorrhage.” The condition of the perivascular tissue, or the brain-substance, has much to do with the occurrence of haemorrhage. One reason why ex- travasation more frequently occurs in the brain than in the liver, for instance, is, that its tissue is softer, and therefore not capable of giving as much support to the blood-vessels as is the latter organ. Now, when the cerebral substance is softened by disease in any part, the natural support of the vessels of that part is still further lessened, and the ten- dency to haemorrhage increased. Again, in the condition sometimes met with in old people, in which the brain becomes atrophied, the ves- sels may undergo dilatation and subsequent rupture. This view is op- posed by Jaccoud,5 but in one case of cerebral haemorrhage, terminating in death, and in which I had the opportunity of making a post-mortem examination, the right hemisphere, the seat of the extravasation, was very considerably atrophied, and weighed three ounces and a quarter less than the left. The possibility of the existence of this cause may, therefore, be admitted, although it cannot be considered as definitely established. The researches of Cotard3 would appear to show that cere- bral haemorrhage is not infrequently a cause of partial atrophy of the brain. In the next place, the state of the blood, as regards quality and tension, must be considered. There can be no doubt that certain dis- eases affecting the general system may so deteriorate the blood as to render it unfit to properly nourish the blood-vessels, and hence their tissue is more readily broken down. Among these conditions are typhus, scurvy, chlorosis, gout, and syphilis. The tension of the blood in the vessels is subject to constant va- 1 Op. cit., p. 262. 2 Op. cit., p. 166. 3 “fitude sur l’atropliie partielle du eerveau,” Paris, 1868. CEREBRAL HAEMORRHAGE. riation from the operation of many physical and mental causes, and may, through their action, be so increased as to overcome the resist- ance afforded by the vascular walls. These influences have been suf- ficiently considered in the section on causes, and need not, therefore, be dwelt upon here at any length. My own opinion of their sufficien- cy, without preexisting disease of the blood-vessels, to produce rupt- ure and extravasation, has been formed after much observation and reflection. Analogous phenomena take place every day, and are not supposed to be due, in any extent, to vascular disease. Thus nasal haemorrhage occurs from strong muscular exertion of such a character as to retard the flow of blood from the brain, from emo- tional or other kind of mental excitement, and from hypertrophy of the left side of the heart, by which the amount of blood in the cerebral vessels is increased. All these causes augment the tension, and it-would be singular if at times a healthy intracranial vessel did not give way through their influence, as well as one outside of the skull. Differential Diagnosis.—A point of very great importance re- mains to be considered as a part of the pathology, and that is whether it is possible or not to determine during life in what part of the brain an extravasation has taken place. While I am afraid we can not be as explicit in this matter as is desirable, I am very sure we can often, from a careful study of the symptoms, arrive at con- clusions more or less accurate, and can sometimes determine the question with absolute certainty. The great difficulty is, that wre are not yet sufficiently acquainted with the physiology of the sev- eral parts of the brain, and hence are not able to ascribe, with as much sureness as is desirable, variations from healthy action, to de- rangement of the proper anatomical part of the cerebral mass. Be- sides, when the extravasation is large, although it may be strictly confined to the anatomical limits of the ganglia or part of the en- cephalic mass in which it originates, it may act by transmitted press- ure upon contiguous ganglia or parts, and hence the symptoms are rendered complex. As we have seen, hsemorrhage is more liable to take place within the ganglia bordering on the motor tract than any other part of the brain. This is mainly due to the fact that this is the most vascular part of the cerebral substance. Generally speaking, when the clot is strictly limited to either of the nuclei of the corpus striatum, the paralysis, however extensive it may have been in the first place, is of a transitory character. More- over, there is no tendency to the production of muscular contractions at a late period of the disease. And there are instances on record in which there has been extravasa- tion into the corpus striatum, and no paralysis of any part of the body. 112 DISEASES OF THE BRAIN. Gintrac,1 of forty cases collected by him, found apparent absence of paralysis in five. But he admits that this number may perhaps be re- duced, for one of the cases was that of an infant one day old, and the other, that of an old man eighty years of age, who had had a cerebral haemorrhage ten years before his death, in both of which an exact di- agnosis of this point could not have been otherwise than difficult. But in one of the others there was no paralysis, and yet after death a clot as large as a pigeon’s egg was discovered in the left corpus striatum. In the second there was no actual paralysis, but a weakness and trem- bling of the right arm. The post-mortem examination revealed the existence of a clot, as large as an almond, in the left corpus striatum. The third wras for a few moments deprived of the power of speech, but he had equal muscular strength on both sides. Then he became wreak and died, without having been actually paralyzed. After death a cav- ity filled with a brown serous fluid was found in the anterior and ex- ternal part of the right corpus striatum, and the whole of the left pos- terior lobe was reduced to a yellowish pulp, and wTas studded with purulent foyers. This was certainly not an uncomplicated case. And thus of the five there was but one in which there was indubitably no paralysis. The optic thalamus is another common seat of extravasation. In such a case the observed symptoms are especially connected with the organs of the special senses. Thus there are double vision, dilatation or convulsive movements of the pupil, blindness, and anaesthesia or hyperaesthesia of the paralyzed parts of the body. As in lesions of the corpus striatum, the paralysis of motion, if present at all, is on the opposite side of the body, and is usually transient in character. The hearing and smell may also be affected. Luys2 has collected a large number of cases in support of the view here enunciated. The researches of Virenque3 also go to show that lesions of the optic thalamus are accompanied with loss of sensibility on the opposite side of the body. His observations, therefore, are entirely confirm- atory of those of Turck,4 who in four very carefully recorded cases found hemi-ansestliesia coexistent with lesion of the optic thalamus and corpus striatum of the opposite side. In those cases of cerebral haemorrhage limited to the optic thala- mus, paralysis of motion when it exists is less intense than when the corpus striatum is also involved, and is often restricted to the inferior limbs. The speech is rarely involved. 1 Op. cit., tome ii., p. 142 et scq. 2 Op. cit., p. 534 et seq. 3 “ De la perte de la sensibility generate et speciale d’un cote du corps (hemianmsthe- site) et de ses relations avec certaines 16sions des centres opto-stries.” Paris, 1874. 4 “ Ueber die Beziehung gewissen Krankheitsherde des grossen zur Anses- thesie.” Sitznngsbcrichte des Kais. Kon. Academie der Wissenschaften, Band xxxvi., 1859. CEREBRAL HAEMORRHAGE. 113 The symptoms just detailed are more the result of lesions affect- ing adjacent regions than of the thalamus itself. The sensory division of the internal capsule and the optic tract are the parts most liable to be injured from haemorrhage in the thalamus. The intelligence is not notably lessened, but there is often a marked proclivity to the supervention of hallucinations of the special senses. Luys1 has very thoroughly worked up this subject,3 and Ritti has recently in a philosophical essay adduced many facts and arguments to show the relations of lesions of the optic thalamus w7ith hallucinations. In thirty-two cases of hallucinations, mainly of the sight and hearing, but some- times of all the senses, post-mortem examinations revealed the existence of some kind of lesion of the optic thalami. It sometimes happens that an ex- travasation, originating in either the corpus striatum or optic thalamus, involves both these ganglia and the intervening part of the internal cap- sule. Hence we have, as the most common symptoms of haemorrhage of this character, loss or impairment of the power of motion, disturbance of sensibility, dilatation or irregular movements of the pupil, aberrations of vision and hearing, etc. As we have seen, a lesion of the posterior half of the internal capsule of one side produces loss of the power of motion and of sensibility in the opposite side of the body. The man- ner in which this is accomplished will be readily understood from an inspec- tion of the accompanying diagram (Fig. 11), in which a indicates the left internal capsule containing both motor and sensory fibres ; b the left half of the pons Yarolii and me- dulla oblongata ; c the left lateral half of the spinal cord ; d a sensory nerve-fibre decussating soon after its entrance into the cord; e a motor nerve-fibre decussating at the lower boundary of the medulla oblongata. A lesion existing at f will therefore cause paralysis of motion and of sensibility at <7, on the right side of the body. Fig. 11. 1 Op. et loc. cit. 2 “ Theorie physiologique de l’hallucination.” Paris, 1874. 9 114 DISEASES OF THE BRAIN. When the extravasation beginning in the left optic thalamus or corpus striatum extends to the fissure of Sylvius so as to involve the posterior part of the third frontal convolution, the island of Reil, or other part supplied by the middle cerebral artery, or when it originates in this region, aberrations of speech occur. These are in- dependent of paralysis of the tongue, and are such as are embraced under the term aphasia. This subject will be hereafter more fully considered. If the lesion be limited to the anterior twro-thirds of the posterior half of the internal capsule, there will be merely paralysis of motion, although there may be, as I have lately had occasion .to know, slight and temporary hemi-amesthesia. If, however, the posterior third of the posterior half of the internal capsule be the seat of the haemor- rhage, there will be wrell-marked hemi-anaesthesia. Of course there are in almost all cases various proportional combinations of loss of the power of motion and of sensibility according to the exact posi- tion of the lesion in the internal capsule. And it invariably happens that with all lesions of the motor tract late contractions of the op- posed muscles supervene. Haemorrhage into the crus cerebri pi*oduces hemiplegia of the opposite side, more or less extensive, according to the size of the clot, with loss of sensibility. The third pair arises in part from the crus, and hence may be paralyzed, producing ptosis and external strabis- mus on the side corresponding to the seat of the lesion, and conse- quently opposite to the hemiplegia. When the pons Varolii is affected, the crossed paralysis is still more marked. The limbs are paralyzed on the opposite side, and the face in whole or in part on the same side as that in which the haemorrhage takes place. If the extravasation is in the mesial line, both sides of the body are paralyzed. According to Trousseau,1 how- ever, crossed paralysis is not always due to a lesion of the pons, as asserted by Gubler,2 and as supported by additional cases collected by Luys.3 Trousseau rests his opinion on one case, in which after death very extensive lesions of the brain were found, but none involv- ing the pons. Nevertheless we find in practice that when an extravasation of blood is confined to one side of the pons, and is not extensive, the face is paralyzed on the corresponding side. The facial nerve makes its exit from the side of the medulla oblongata; some of its roots of origin can be traced as far as the floor of the fourth ventricle, others come from the low'er part of the medulla oblongata, and others 1 “ Lectures on Clinical Medicine,” Bazire’s translation, Part II., p. 833. 2 “ Sur 1’hemiplegie alterne,” Gaz. hebd., October, 1856, and “ Memoire sur les para- lyses alternes,” etc., Gaz. hebd., 1859. 3 Gp. cit., p. 529 et seq. CEREBRAL HAEMORRHAGE. 115 descend from the upper border of the pons, where they probably decus- sate. Now, a lesion existing in a lateral half of the pons will, there- fore, produce a paralysis of the corresponding facial nerve, and of the opposite spinal nerves; whereas, if it occur above the point of decus- sation of the encephalic fibres, the paralysis will be on the opposite side for all parts of the body. These facts are shown in the ac- companying diagram (Fig. 12). It is obvious, from a study of this diagram, that a lesion of one lateral half of the pons (at l) will cause paralysis of motion and of sensibility of the opposite side of the body generally, and of the cor- responding side of the face ; and that a lesion of the hemisphere (at m) will produce paralysis of the opposite side of the face and the body. It is true that it is not definite- ly settled by histological investiga- tion that the decussation of the ascending roots takes place, but pathology is just as capable of determining the question as his- tology. Yulpian1 asserts that the decussation of the roots of the facial occurs in the mesial line of the medulla oblongata at the junc- tion of the two nuclei of origin ; but, if this were the case, a lesion of one side of the pons would neces- sarily be followed by double facial paralysis, a sequence which does not in reality ensue. From the contiguity of the pons to the medulla oblongata, an ex- travasation of blood into it is generally accompanied by the symptoms which result from haemorrhage into this latter organ, though they are not as a rule so strongly marked. The principal phenomena indicating the medulla oblongata as the seat of extravasation are, loss of the power of swallowing, from paraly- sis of the glosso-pharyngeal, difficulty of protruding the tongue, from paralysis of the hypoglossal, and huskiness of the voice, tumultuous Fig. 12. a, the left hemisphere ; b. right half of pons; c. right half of medulla oblongata; d, right half of spinal cord; e., right facial nerve ; /, fibre of origin from nucleus in medulla oblongata; g, descending fibre decussating at upper border of pons; h, ascending fibre; i, sensory root of spinal nerve; k, motor root of sensory nerve ; lesion in pons: m, lesion in left hemisphere; n, paralyzed part supplied by facial; o, para- lyzed part supplied by spinal nerve. 1 “ Essai sur l’origine de plusieurs pairs de nerfs craniens. Th&se de Paris,” 1853, p. 32. 116 DISEASES OF THE BRAIN. action of the heart, dyspnoea and gastric derangements, from paralysis of the pneumogastric nerve. There is in addition paralysis of one or both sides of the body. An extravasation into the cortical substance of the cerebrum is characterized by no very definite aggregation of symptoms. There may be delirium, coma, disorders of speech, convulsions, paralysis, contractions or rigidity of either the paralyzed or sound limbs, vomit- ing, derangement of respiration, and occasionally anaesthesia or hyper- aesthesia. Paralysis when present is upon the opposite side of the body from that of the lesion. When the extravasation is in the white substance of the cere- brum, not included in the direct motor and sensory tracts, there may be no marked symptoms of diagnostic value. I, have known cases in which large foyers have been formed with no other symptoms than intense pain in the head and persistent vomiting. But when blood is extravasated into the white tissue the quantity is ordinarily great, and as a consequence there are often symptoms present which are due to resultant pressure upon other portions of the encephalic mass. Thus there may be coma, paralysis, loss of sensibility, stertorous res- piration, and other phenomena indicating derangement of the motor and sensory ganglia. The passage of the extravasated blood into the ventricles almost invariably causes contractions or convulsions of the muscles of the opposite side of the body. The researches I have made 1 relative to the functions of the cere- bellum would seem to show that its office is not materially different from that of the cerebrum. Still, I think there are some indications which, although not perhaps giving us the right to form a definite conclusion, are yet sufficiently well marked to enable us to arrive at a probable diagnosis between haemorrhagic lesion of the cerebrum and that of the cerebellum. Thus, vertigo is almost an invariable accom- paniment of the cerebellar extravasation ; vomiting is much more gen- erally met with than when the cerebrum is affected ; hemiplegia is not so common ; the sensibility is never disturbed ; and the pain is in the back of the head. Ferrier2 has very clearly shown that irritation of the cerebellum produces nystagmus and defective power of ocular coordination. But I am not aware that these phenomena have been noticed in cases of cerebellar hasmorrhage. Hillairet,3 in his excellent memoir, does not mention them as features of the affection. He distinguishes two 1 “ The Physiology and Pathology of the Cerebellum.” Quarterly Journal of Psycho- logical Medicine, April, 1869. * “ Experimental Researches in Cerebral Physiology and Pathology.” “ West Riding Lunatic Asylum Reports,” vol. iii., 1873, p. 69, et scq. 3 “Hemorrhagie cer6belleuse,” Annuaire de medecine ct cliirurgie pratiques, 1869, p. 39. Also Archives de medecine, 58. CEREBRAL HAEMORRHAGE. 117 forms of this lesion. In the one, the onset is sudden, and death soon follows ; in the other, the coarse of the affection is slow, and life may he prolonged for a considerable period. In this latter, vomiting is a prominent feature. Hemiplegia, according to him, is always crossed. Sensibility remains unaffected till near the close of the disease by death, and there are no convulsions. The speech is not often affected. The special senses he did not find notably deranged, except in the last stage. In this result he differs with several waiters on the subject. Besides a number of cases, some of which are referred to in the memoirs cited, one has occurred in my experience, in which I had the opportunity of making a post-mortem examination.1 A man had suffered from vertigo, occasional convulsions, attacks of nausea, and vomiting, and a constant and violent pain affecting the back of the head. The symptoms had ensued in consequence of a se- vere blow which he had received on the back of the head, by raising himself too soon while the horse he wras riding was passing under a low archway. When this man attempted to walk, he reeled and staggered as if he were drunk. The upper extremities and the organs of speech were not affected ; he had the entire control of his legs when lying down, and there was no diminution of sensibility anywhere. At last, he be- came paraplegic, and shortly afterward died in a convulsion. The post-mortem examination showed the existence of an abscess which had obliterated nearly the wThole of the left lobe of the cerebellum. The other parts of the brain were, so far as could be perceived, per- fectly healthy. Besides the occurrence of local secondary lesions, the immediate re- sults of the presence of a foreign body in the cerebral tissue, there are others, which are due to the interruption of the normal brain-functions, which haemorrhage so generally induces. Thus, atrophy of the cere- bral structure may result, as has been pointed out by Cotard5 and oth- ers, or the degeneration may extend to the spinal cord, as is so well shown by Bouchard.5 In this latter event the process does not begin till about the end of the fourth or fifth month. It is mainly charac- terized by the supervention of permanent contraction of certain of the paralyzed muscles, and by exaggerated reflexes, and will be more appropriately considered under another head. Another point in connection with cerebral haemorrhage requires further elaboration. It is well known that the facial paralysis result- ing from ordinary cerebral haemorrhage is less extensive and less thor- oughly marked than when it is due to disease or injury of the trunk of 1 Op. cit., p. 209. 5 “ fttude sur l’atrophie partielle du cerveau,” Paris, 1868. 3 “ Des degendrations secondaires dc la moelle epiniere,” Archives gen. de medccine, 1866. Also Hun’s translation, American Journal of Insanity, 1869. 118 DISEASES OF THE BRAIN. the seventh pair or to lesion of the pons Yarolii. Thus we have seen that, in the former affection, the orbicularis palpebrarum escapes pa- ralysis,1 and the other muscles supplied by the facial nerve are usually not so profoundly paralyzed as when the pons or the nerve is the seat of the disease. Many explanations have been offered of this remarkable circum- stance, but the one given by Landry8 is more nearly reconcilable with the anatomy and physiology of the parts involved than any other. The nucleus of the facial is entirely comparable to the anterior cornua of the cord. It constitutes a little special motor nerve-centre which possesses a certain amount of autonomy. It is through this centre that the muscles of the face are directly made to contract. The encephalic fibres which connect it with the brain are only at the service of the psychical department, and an impulse sent through them is not of itself capable of exciting contraction in the muscles to which the facial is distributed. But, with the spinal cord, this nucleus pos- sesses reflex excitability, and, as is the case in diseases of the brain in which the anterior columns suppress voluntary movements without destroying the reflex manifestations of which the gray substance of the cord is susceptible, so the cerebral lesion leaves to the nucleus of the facial the power to determine reflex contractions. It therefore con- tinues to be excited by sensitive excitations which reach it from the periphery. Thus, in facial hemiplegia of cerebral origin, we observe, from time to time, certain movements which appear to be voluntary because the provocative sensitive impression, which may only consist of the contact of air, remains unperceived. Accordingly, the orbicularis palpebrarum appears, above all the other muscles, to preserve its mo- bility, for its movements are principally excited by the stimulus of the light, which the lesion of the cerebral lobes does not prevent being reflected to the nucleus of the facial. In extensive diseases of the pons, however, the nucleus of the facial, situated as it is, in immediate proximity to this organ, is almost always compromised with it. In such a case, therefore, both reflex excitability and voluntary power are destroyed, and the paralysis is complete. Treatment.—The means of treatment in cerebral hemorrhage are, first, those which are applicable to the prodromatic stage, with a view 1 Bazire, in his translation of Trousseau’s “ Clinical Lectures,” calls attention to the fact that, in ordinary cases of cerebral haemorrhage, the patient, though able to close the eye of the affected side, cannot do so without, at the same time, closing the other, a fact which shows some loss of power. Since my notice was directed to this circumstance, I have observed that the patient is often sensible of the fact that the eye of the affected side cannot be closed as strongly or as rapidly as the other eye. 5 Quoted by Poincare, “ Lemons sur la physiologic normale et pathologique du systeme nerveux,” tome deuxieme, Paris, 1874, p. 55. CEREBKAL HAEMORRHAGE. 119 of preventing any lesion ; second, those proper during the seizure ; and, third, those which are to be directed against the consequences of an attack. It often happens that an attack may be prevented, even where the threatenings are very decided. The condition of the brain is such that the indications are to lessen the tension of the blood as much as pos- sible. As I have already remarked, under the head of cerebral conges- tion, the bromides of potassium and sodium are peculiarly efficacious in accomplishing this end. Lately, in consequence of the investigations of Dr. S. Weir Mitchell, of Philadelphia, I have made much use of the bromide of lithium in cerebral congestion with or without a tendency to haemorrhage, and have reason to prefer it to either the potassium or sodium salt. One feature of its action, which renders it especially use- ful in such cases as those now under notice, is the short interval which elapses between its administration and the effect. I am very sure I have given it successfully in several cases in which the bromides men- tioned would not have acted so happily. In one of these, a gentleman from the South, who had already had an attack, and who was in con- sequence hemiplegic, was relieved of his vertigo, headache, numbness, and thickness of speech, by one dose of thirty grains, in less than half an hour. The bromide of calcium, a compound to which I have recent- ly called attention,1 is still more eligible. It acts more rapidly than any of the other bromides, and may be given for a longer period with less derangement of the organism. The dose is from fifteen to thirty grains, or even more, if only a single dose is to be administered. The oxide of zinc may also be given with advantage. The bowels, if costive, should be opened by a brisk purgative ; the stomach, if overloaded, should be emptied by an emetic, during the action of which warm water should be freely drunk so as to obviate, as far as possible, all straining ; muscular exertion should be avoided, the head should be kept cool and well elevated, and the mind in a state of the utmost tranquillity. During an attack, and throughout the whole period of reparation of damages, the less that is done in the vast majority of cases the better. The question of the propriety of bloodletting will generally even yet arise, but should in nearly every case be decided in the negative. I say nearly, for I know of but one possible form of attack in which it can by any possibility not only not be useful, but fail to do harm ; and that is in a strong, plethoric person, with a full, bounding pulse, in whom, from the gradual development of the symptoms, we have reason to sus- pect that the haemorrhage is still going on. In such a case, six or eight ounces of blood may be taken from the arm. But, in the case of cere- bral haemorrhage, attended by coma and the ordinary, symptoms of 1 Note relative to Bromide of Calcium. New York Medical Journal, December, 1871, p. 594. 120 DISEASES OF THE BRAIN. the apoplectic condition, there is nothing to be done in the way of medication which can afford the slighest prospect of relief. It is true, a patient thus situated may recover if his attack is not of the severest kind, but it is not through any medicines we give him. Correct views relative to this point are far from being prevalent, and can only be es- tablished by regard being paid to the morbid anatomy and pathology of the subject. A clot in the brain is, to all intents and purposes, a foreign body, and both it and the walls of the cavity must undergo certain fixed and definite changes. In order that these changes may go on with the utmost possible regularity and certainty, all the powers of the system are requisite. The processes are not morbid ; on the contrary, they are in the highest degree conservative. To take blood from a body which is striving by all its agencies to repair an injury, is to deprive it of a portion of its strength without in the slightest degree accelerating the actions at the seat of the lesion. As Trousseau1 remarks, no physician ever thinks of bleeding for an extravasation of blood under the skin, for he knows how perfectly absurd such a practice would be ; and yet, except as regards location, there is no difference between it and the cerebral clot. A prize-fighter, for instance, receives a blow in the face, which ruptures a blood-vessel and gives him a “black eye.” He has an extravasation of blood into the cellular tissue. What would be thought of the physician who would recommend bloodletting from the arm, with a view of causing the absorption of the clot ? The prize-fighter has found out by experience that he can open the skin with a knife, and let the blood out. The practice is excellent, and would be admirable for the brain also, were this organ of no more vital importance than the skin of the face. I have never bled a patient for cerebral haemorrhage since 1849, and I am very sure that I have had no reason to regret the abandonment of the practice. It is a common practice for purgatives to be given, and even so conservative a practitioner as Dr. J. Hughlings Jackson® puts “two drops of croton-oil on the tongue,” why, he does not state, and cer- tainly the practice is in direct antagonism not only with his assertion that “ the chief thing is to keep the patient quiet,” but with the gen- eral tenor of his theory of treatment. I have seen great annoyance and an aggravation of the symptoms from the indiscriminate admin- istration of croton-oil. It is only, in my opinion, admissible when there is obstinate constipation, and when after three or four days the bowels have not been moved. And then as regards iodide of potassium. There seems to be an idea prevalent that this substance exerts a powerful influence in caus- 1 “ Lectures on Clinical Medicine,” Bazire’s translation, Part I., p. 10. 2 Reynolds’s “ System of Medicine,” vol. ii., article “ Apoplexy and Cerebral Haemor- rhage,” p. 541. CEREBRAL HEMORRHAGE. 121 ing the more rapid absorption of the extravasated blood, and hence it is frequently administered in large and frequently-repeated doses. I have often seen patients, at as early a period as possible, while still in a state of profound coma, dosed with the iodide of potassium to the extent of five grains every hour, with the object of causing the imme- diate absorption of the extravasated blood. That such a result is im- possible no one acquainted with the morbid anatomy and the pathology of the subject will deny. In fact, there is nothing to be done beyond keeping the patient per- fectly quiet, with the head well elevated, and in a room, when possible, with a temperature of about 60° and thoroughly ventilated. Indica- tions should be met as they arise. The bowels, if not moved naturally every day, may be emptied by an enema of warm water ; the urine, if not passed by the patient, should be drawn off by the catheter ; the strength, if feeble, as indicated by the pulse, should be kept up by the cautious use of stimulants ; and, if the patient is restless and does not sleep well, some one of the bromides should be administered. Ergot may, on theoretical grounds, be recommended in those cases in which we have reason to believe that the hasmorrhage is still going on ; but I have no personal experience of its power in such instances. If administered, it should be given with no sparing hand. The food should be of the most nutritious character, so as to be small in quantity, and should be taken frequently, day and night. Beef-tea, or the extract of beef, made according to Liebig’s formula, supplies every indication. If symptoms of inflammation make their appearance, cold applica- tions may be made to the scalp, or a blister may be applied to the nape of the neck. Blisters or mustard-plasters to the wrist or ankles are absurd. Nothing should be done for the relief of the paralysis till all signs of irritation of the brain have disappeared, and the patient begins to feel the restraint of confinement, and to make efforts to move his par- alyzed limbs. These evidences of improvement generally begin soon after the eighth day. In about two weeks, therefore, it will be p'foper, in the majority of cases, to take active measures to restore the power of motion, and to prevent those contractions which tend to make a restoration much more difficult. The agents to be employed are pas- sive motion, strychnia, phosphorus, and electricity. The first is accom- plished by flexing and extending the joints of the affected limbs, by friction, and by kneading the muscles with the fingers. These move- ments should be performed every day for five or ten minutes at a time. The patient should likewise be encouraged to move the limbs by his own volition as often as possible short of causing fatigue. Strychnia should be given in doses of the one-twenty-fourth of a grain three times a day, or, preferably, by subcutaneous injection, in somewhat 122 DISEASES OF THE BRAIN. smaller doses once a day. In old cases of hemiplegia, the effects of strychnia thus administered are often well marked, and are exhibited when administration by the stomach has failed to produce a beneficial result. This is seen in the following brief abstract of sixteen cases which will serve as types of numerous others which have occurred in my private practice : Case I.—H. A., aged fifty ; male ; right hemiplegia. Came under treatment January, 1865 ; strychnia ineffectual by the stomach ; thir- teen injections, of from one-thirty-second to one-twenty-fourth grain ; much improved. Case II.—J. S. ; forty-two ; male ; left hemiplegia. February, 1865 ; thirteen injections ; much improved. Case III. —S. T. ; sixty ; female ; right hemiplegia. February, 1865 ; strychnia ineffectual by the stomach ; nine injections ; much improved. Case IV.—I. S. ; sixty ; female ; right hemiplegia. April, 1865 ; five injections ; much improved. Case V.—M. T. ; fifty-two ; male ; right hemiplegia. April, 1865 ; strychnia ineffectual by the stomach ; eleven injections ; cured. Case VI.—O. S. ; sixty-three ; female ; left hemiplegia. April 30, 1865 ; secondary contractions ; twenty-two injections ; no improve- ment. Case VII.—B. R. ; forty-seven ; male ; left hemiplegia. June 11, 1865 ; strychnia ineffectual by the stomach ; seven injections ; much improved. Case VIII.—R. F. ; fifty ; male ; left hemiplegia. June 17,1865 ; strychnia ineffectual by the stomach ; eight injections ; cured. Case IX.—T. W. ; forty-eight; male ; left hemiplegia. Septerm ber 5, 1865 ; eight injections ; much improved. Case X.—T. S. ; forty-nine ; male ; left hemiplegia. Septem- ber 7, 1865 ; secondary contractions ; five injections ; no improve- ment. Case XI.—J. J. ; fifty-seven ; male ; left hemiplegia. September 11, 1865 ; secondary contractions ; no improvement. Case XII.—J. W. ; fifty-two ; male ; right hemiplegia, affecting arm only, at the time treatment was begun. September 27, 1865 ; strychnia ineffectual internally ; six injections ; cured. Case XIII.—W. M. ; forty-five ; male ; left hemiplegia. October 19, 1865 ; strychnia ineffectual internally ; seven injections ; cured. Case XIV.—S. M. ; forty-one ; male ; right hemiplegia. June 17, 1867 ; arm alone affected ; strychnia ineffectual by the stomach ; twenty injections ; cured. Case XV.—M. C. ; forty-four ; male ; right hemiplegia, affecting tongue and face only. July 1, 1867; ten injections ; so much im- proved as to be able to talk with fluency. CEREBRAL HEMORRHAGE. 123 Case XVI.—C. C. ; fifty ; male ; right hemiplegia. May 4,1869 ; strychnia ineffectual by the stomach ; thirty-five injections ; much im- proved. Dr. Charles Hunter1 has called attention to the advantages to be derived from the hypodermic use of strychnia in hemiplegia ; and my former clinical assistant, Dr. R. A. Vance,2 has adduced several cases to the same effect. Instances in support of the views above set forth occur daily in my private practice, and at the New York State Hos- pital for Diseases of the Nervous System. I have every reason, there- fore, to be convinced of the good results to be derived from the practice. Phosphorus administered in the form of phosphide of zinc, sepa- rately or in combination with the extract of nux-vomica, according to the formula given on page 68, is also a useful remedy. But no agent is so valuable in hemiplegia as electricity, and amend- ment almost invariably follows its use, even in old cases, in which there are tonic contractions. If the case is seen soon after the seizure, the induced current will generally be sufficient to produce contractions of the paralyzed muscles. The poles, terminated by wet sponges, should be applied to the skin covering the muscles, or in some cases to the nerves. The current should be strong enough to cause slight pain, or, if sensibility is lessened, to produce contraction. In old cases attended with atrophy of the muscles, and diminished or abolished electro-con- tractility, the primary current may be necessary. It should be applied in such a manner as to be interrupted, for contractions are only caused when the circuit is closed and opened. As the muscles improve in size and irritability, the induced current should be used. Care should be taken not to fatigue the patient, or to cause excessive pain by employ- ing a current of too great a degree of intensity. As regards the restoration of sensibility, it will generally be found to be less difficult than the removal of the motor paralysis. The anaes- thesia very often disappears or becomes much less spontaneously, and it does so from the centre to the periphery ; that is, if there be anaesthesia of the leg, the sensibility returns in the upper part first, and subse- quently in the lower part. The treatment consists mainly in the use of the electric wire-brush, which should be passed gently over the skin previously made dry. The other pole consists of a wet sponge. Either the induced or primary current may be used. If the latter, however, be employed, the wire-brush should constitute the positive pole. The recent advances in brain surgery give us reason to hope for success by operative procedure in those cases in which the clot involves the cortex or in cases of meningeal haemorrhage, the affection next to 1 British and Foreign Medico-Cliirurgical Review, April, 1868. s Journal of Psychological Medicine, April, 1870. The first thirteen cases cited in this work were published in Dr. Vance’s paper. 124 DISEASES OF TIIE BRAIN. be considered. When the symptoms clearly indicate the cortex as the seat of the extravasation it is an easy task to determine its exact location ; and if the situation is such that it can be reached by trephin- ing, the operation is entirely justifiable unless there are strong contra- indications. The question is, however, one which is to be settled for each individual case, and not to be determined abstractly. CHAPTER IV. CEREBRAL MENINGEAL HEMORRHAGE. By the term cerebral meningeal haemorrhage is to he understood— 1. An extravasation of blood between the cranium and the dura mater ; or, 2. An extravasation into the cavity of the arachnoid between the two layers of which this membrane is composed; or, 3. An extravasa- tion into the sub-arachnoideal space between the arachnoid and the pia mater, or into the tissues of this latter membrane, or between it and the brain. There are thus—1. Extra-meningeal haemorrhages ; 2. Intra- arachnoideal haemorrhages ; and, 3. Sub-arachnoideal haemorrhages. The first are almost always the result of traumatic cause, involving injuries of the cranium, by which the vessels of the dura mater are wounded. Extra-meningeal haemorrhage may likewise be produced by the operation of trephining, should any of the vessels of the dura mater be divided. It is, however, beyond doubt that this species may originate independently of wounds and injuries. The distinction between intra- and sub-arachnoideal haemorrhages was first pointed out by Prus,1 to whom we are also indebted for much valuable information on the subject. Of one hundred and seventy- two cases collected by Gintrac,” five were extra-meningeal, one hun- dred and nine intra-arachnoideal, and thirty-four sub-arachnoideal. Symptoms.—The most prominent symptom of meningeal haemor- rhage is coma, which may appear suddenly, or be preceded by premon- itory symptoms, such as headache, vertigo, and general convulsions. The stupor is usually profound, and does not differ from that ob- served in the severe forms of cerebral haemorrhage. The power of motion is generally lost throughout the body, and consequently there is usually no hemiplegia. The reason for this is, that the haemorrhage is so extensive as to press upon both hemispheres. Reflex and auto- matic movements remain, except when the medulla oblongata is in- volved, when some of them are abolished. If the extravasation is in this latter situation, death soon takes place from cessation of respira- 1 “ Memoire sur les deux maladies connues sous le nom d’apoplexie mening6e.” Me- moires de Pacademie de medecine, tome xi., 1845, p. 18. 8 Op. cit., tome i.,p. 732. CEREBRAL MENINGEAL HAEMORRHAGE. 125 tory actions. Anaesthesia is present in the skin of those parts in which the power of motion is lost. In ordinary cases the patient may pass out of the comatose condi- tion from the fact of the brain becoming accustomed to the pressure, and he then may be able to speak, and to move his limbs, but his men- tal and physical faculties are greatly enfeebled, and a renewal of the haemorrhage again plunges him into a state of coma, from which he may again emerge. This sequence may be repeated several times, until death at last takes place. Before this termination there are vomiting, incontinence of urine and faeces, insensibility, and occasionally general convulsions. In a case reported by Dugast,1 a woman entered the Hopital Neckar in a state of marked prostration. Her intelligence was not markedly impaired, but, though she understood almost every thing said to her, she answered only by monosyllables often unintelligible, and pronounced in a low voice. She was affected with paralysis of the left side of the face, and an incomplete paralysis both of motion and sensibility of the right side of the rest of the body. Four days afterward she was in a state of complete prostration, the paralysis was general. Up to this time the intelligence had remained almost intact. She died that day. The post-mortem examination showed the existence of a large sub-arachnoid extravasation at the base of the brain. On the inferior surface of the pons the blood had become consolidated into a clot which pressed upon the left lobe. On the right side of the pons the blood had not coagulated. This case is interesting as bearing upon the subject of cross-paralysis already con- sidered in the previous chapter. It has sometimes happened that meningeal haemorrhage, resulting from an injury of the cranium, has not caused any very prominent symptoms for a considerable period afterward. A teamster was struck on the head by a club in the hands of another man, was stunned for a few minutes, then recovered, and went about his business without complaining of his head. In about twelve hours afterward coma su- pervened, and he died without being aroused. A case is reported by Dr. Gibson,2 in which a still longer period intervened. A man, sixty years of age, was found one morning, about eight o’clock, seated as if asleep at a desk, his arms crossed before him, and his head resting on them. It was discovered that he was profoundly in- sensible. He was sent to the hospital, where he lay comatose, breath- ing stertorously, and paralyzed on the whole of one side. At the end of two days he died. On post-mortem examination there was found fracture of the left side of the cranium, with rupture of the dura 1 “ Quelqucs considerations sur les hemorrhagies meningees cerebrales.” These de Paris, 1869. 2 Edinburgh Medical Journal, September, 18V0, p. 199. 126 DISEASES OF THE BRAIN. mater and middle meningeal artery, from which latter, extensive haemorrhage had taken place. It was ascertained that, five days be- fore, he had fallen down a stone staircase, was stunned for a few minutes, but had soon recovered his senses. Doubtless during the whole of the intervening period the bleeding from the ruptured ves- sel had been going on. Prus, in the memoir cited, attempts to draw a symptomatological distinction between sub-arachnoideal and intra-arachnoideal haemor- rhage. Thus for him headache, dryness of the tongue, fever and de- lirium, are indications of intra-arachnoideal haemorrhage. Somnolence and coma are common to both forms, but, when they are conjoined with the phenomena mentioned, intra-arachnoideal haemorrhage is to be diagnosticated. But most authors doubt if the discrimination can in reality be made during life. Valleix1 declares that the difference is of greater anatomical than symptomatological importance, and Durand-Fardel8 admits that it is difficult to present a characteristic view of the course and phenomena of sub-arachnoideal haemorrhage. I must confess that I see no greater anatomical reason for any differ- ence in the symptoms of the two forms of meningeal haemorrhage than there is for a difference between inflammation of the pia mater and inflammation of the arachnoid. Neither are there any char- acteristic symptoms which would serve to distinguish haemorrhage of the dura mater from either of the other forms. Causes.—Among the predisposing causes of meningeal haemor- rhage age occupies the first place. It is more frequently met with in young infants and in old persons than in those of middle age. Legendre,8 in two hundred and forty-eight cases occurring in infants, and in which post-mortem examinations were made, found no instance of the child being over three years of age. Between one and two years would appear from his researches to be the period in which chil- dren are most liable to the supervention of meningeal haemorrhage. But Gintrac’s4 cases are of different import as regards this point, for of one hundred and sixty-five in which the age was noted, only ten were under ten years of age, while thirty-seven were between the ages of thirty and forty, sixty-seven were between fifty-one and eighty, and two of eighty-seven and eighty-eight years respectively. Meningeal haemorrhage is often produced by injuries of the skull, and results from sudden rupture of a healthy artery or vein. It may follow blows on the head, falls, or injuries with instruments which perforate the cranium, and may or may not be associated with fract- ures of the bones. 1 “Guide de medecine practicien,” tome ii., Paris, 1866, p. 4. 2 Op. cit., p. 173. 3 “ Recherches sur quelques maladies de l’enfance.” Paris, 1846, p. 113 et seq. 4 Op. cit., p. 738. CEREBRAL MENINGEAL HAEMORRHAGE. 127 Extreme heat acting upon the head, venereal excesses, severe mus- cular efforts, excessive mental exertion, amenrrohcea, overfeeding, and constipation of the bowels, have been cited as exciting causes. The larger vessels, or the capillaries, may give way from being diseased, and consequently unable to resist the ordinary tension of the blood. Such a condition may be the result of the long-continued excessive use of alcoholic liquors, or may be due to. hepatic disease. Prognosis.—The ordinary termination of meningeal haemorrhage is death. Of thirty-one cases in old persons, cited by Durand-Fardel, death occurred in twenty-six before the end of the fifth day, in one it took place on the seventh day, in two on the fifteenth, and in two in from twenty to twenty-five days. Legendre, in infants, ascertained the duration to be from eight to twelve days. Prus found death to ensue in cases of sub-arachnoideal haemorrhage before the end of the eighteenth day, but in instances of the intra-arachnoideal form life was sometimes prolonged for over a month. But recovery has occasionally taken place through the formation of false membranes in such a manner as to circumscribe the extravasation, and thus to conduce to the absorption of its fluid portion, and Legendre has described a process occurring in children by which the sanguineous cyst is transformed into one containing serum, thus producing a species of hydrocephalus. Such terminations are, however, so very rare as to mitigate but to a very slight degree the gravity of the prognosis. Diagnosis.—The diagnosis of meningeal haemorrhage is a matter of much difficulty. Still, there are certain characteristics which aid us somewhat in arriving at a correct opinion. Thus, from cerebral haemor- rhage, it may usually be distinguished by the fact that the coma, when it exists, comes on gradually, that the headache is a much more prominent symptom, that there is not often hemiplegia—the paralysis amounting to a general resolution—and above all, by the remissions which so fre- quently mark its course. Durand-Fardel1 declares that when the coma and general abolition of the faculties indicate the existence of strong cerebral pressure not accompanied by paralysis, properly so called, or only by incomplete paralysis, perhaps more strongly marked on one side than on the other, we may suspect the presence of menin- geal haemorrhage ; that a cerebral haemorrhage, or an acute softening sufficiently extensive to produce such pronounced symptoms of com- pression, is always accompanied by complete paralysis involving a lateral half of the body, and that the full development of the phe- nomena is ordinarily preceded by violent headache. From cerebral congestion the diagnosis must be occasionally al- most if not altogether impossible, and the same is true of cerebral softening. The remissions when present in meningeal haemorrhage will afford important assistance in establishing the existence of the 1 Op. cit.} p. 168. 128 DISEASES OF THE BRAIN. disease, but when they are absent the difficulties in the way of an ex- act discrimination may be insurmountable. Morbid Anatomy and Pathology.—An extravasation of blood be- tween the cranium and the dura mater, extra-meningeal haemorrhage, is, as nas already been said, almost invariably the result of traumatic cause. Gintrac,1 however, with his usual industry, has collected five cases in which it appeared to be idiopathic. The first of these he quotes from Dr. J. H. Wythes,3 of Port Carbon, Pennsylvania, but he omits to state that the child had been playing on the door-step, and that a pain in its ankle was supposed by the parents to have been due to a sprain. It is probable, therefore, that the child fell and struck its head. The next morning it was found dead in bed. On post-mortem examination, an extravasation of blood, amounting to about half an ounce, was found between the skull and dura mater, on the upper surface. In the other cases the blood appears to have been effused during extreme congestion of the meningeal vessels, one or more of the latter having given way under the excessive tension to which they were sub- jected. In one" quoted from Abercrombie, there were numerous clots scattered over the interior surface of the dura mater, and which seemed to have come from the Pacchionian bodies. These elevations were very vascular, being gorged with blood. The anatomical characteristics of intra- and sub-arachnoideal haem- orrhages have been very thoroughly given by Prus.3 In the former the blood is extravasated by exhalation, that is, there is no visible rupture of blood-vessels, and, if life be prolonged to the fourth or fifth day, a false membrane is formed by which the clot is retained in appo- sition with either the parietal or visceral layer of the arachnoid. This membrane eventually becomes organized by the formation of vessels in it, and may, therefore, be the source of another haemorrhage; for, as Charcot and Vulpian 4 have shown, these vessels are numerous, large, possessed of very thin walls, and are, therefore, in a favorable condi- tion for giving way under the tension of the blood. Brudet5 previous to Prus had described the false membranes which play so important a part in intra-meningeal haemorrhage, and bad pointed out their resemblance to the arachnoid and their liability to be the source of other haemorrhages, and at about the period of Prus’s publication Mr. Prescott Hewett6 called attention to extrava- sations attached to the free surface of the arachnoid, and kept in 1 Op. cittome i., p. 646. 2 “ Three Cases of Infantile Apoplexy.” North American Medico-Chirurgical Re- vino, January, 1858, p. 70. 3 Op. et loc. cit. 4 Gazette hebdomadaire, 1860, pp. 728, 789, 821. 6 “ Memoire sur l’hemorrhagie des meninges.” Journal des connaissances m'cdico- chirurgicales, 1839. 6 Medico-Chirurgical Transactions, vol. xxviii., 1845. CEREBRAL MENINGEAL HAEMORRHAGE. 129 position by a false membrane not distinguishable by the naked eye from a true serous membrane. The clot may be extensive, covering nearly the whole surface of a hemisphere. The vessels which have given way, and have thus produced an intra-aracjinoideal haemorrhage, are usually found in an atheromatous condition, and the vessels of the neo-membranes are especially liable to be thus diseased. Dr. Sutherland1 in a very interesting memoir gives the details of ten cases of arachnoid cysts occurring in the insane: “ On removing the skull-cap and dura mater, instead of the convolutions of the brain, with its vascular pia mater meeting the eye, there appears a reddish, pulpy, fluctuating swelling on the surface of the brain, having such a uniform appearance that the outline of the convolutions beneath it is invisible. On attempting to strip off the cyst from the surface of the brain it is usually found adhering to the visceral arachnoid along the centre of the longitudinal fissure ; it is easily separated from the convolutions on either side ; but if large enough to embrace the entire hemisphere is found again to be adherent below, but in this situation usually to the parietal layer of the arachnoid membrane.” Of the ten cases reported by Dr. Sutherland, four were in all proba- bility due to injury of the head. In five the mental aberration was organic dementia, in three general paralysis, and in two idiocy and im- becility. In sub-cirachnoideal haemorrhages the blood is, as we have seen, ex- travasated into the space between the arachnoid and the pia mater, and is often entangled in the meshes of this latter membrane. As the blood when extravasated is mingled to a greater or less extent with the cerebro-spinal fluid, it often remains liquid. The quantity thrown out is frequently very large, amounting in some cases to apparently as much as sixteen or even twenty ounces. These figures must, however, be taken with some allowance for the amount of cerebro-spinal fluid with which the blood is combined. The anatomical relations are such as to admit of sub-arachnoideal hemorrhages being very extensively distributed throughout the cranio- vertebral cavity. In one case in which I made a post-mortem exam- ination, it occupied the whole base of the skull, and, in a case cited by Prus, the whole base of the cranium was filled with blood, all the ventricles were in the same condition, and even the sub-arachnoid cavity of the spinal cord was invaded. New membranes are never met with in this form of meningeal hsem- orrhage. Atheroma of the arteries, especially of those at the base of the cranium, is the disease which is ordinarily the immediate cause of the extravasation, and the torn vessel can generally be discovered with- 1 “Arachnoid Cysts.” “West Riding Lunatic Asylum Medical Reports,” vol. i., 1871, p. 218. 130 DISEASES OF THE BRAIN. out difficulty. Aneurisms of the basilar, the internal carotid, or other arteries of the base of the brain, have by their rupture been the cause of sub-arachnoideal haemorrhage. Treatment.—There is nothing to add under this head to the re- marks already made relative to the management of cases of cere- bral haemorrhage, except in those cases where the symptoms show that the clot is confined to a small area. In such instances tre- phining and the subsequent removal of the clot may be successfully accomplished. PACHYMENINGITIS AND HEMATOMA OF THE DURA MATER. A peculiar form of meningeal haemorrhage, called haematoma, is met with under the dura mater. The blood is not diffused, but is collected in sacs which are formed of false membranes, the result of chronic inflammation of the dura mater; or pachymeningitis as it has been designated by Virchow. These capsules are flattened ovals in shape, are three or four inches in diameter, and half an inch thick. They are usually situated at the vertex, and involve both hemispheres. When this is the case, the paralysis which results is bilateral. Symptoms.—The initial symptoms of luematoma of the dura mater are the results of chronic inflammation, and are slow in their progress. In many respects they resemble those indicative of softening, and con- sist of weakness of intellect, vertigo, a dull, circumscribed, persistent pain, and more or less tendency to stupor. The power of motion is generally diminished on both sides of the body, though occasionally there is hemiparesis. Paralysis is scarcely ever complete. Contrac- tions of the limbs and twdtching of the muscles, especially of those of the face, have occasionally been observed. Gradually, through a pe- riod extending over several months, the stupor increases, and finally the patient becomes apoplectic. During the whole course of the dis- ease the pupils are strongly contracted. The patient dies comatose and frequently convulsed. Causes.—Early and old age are both predisposing causes, the dis- ease being met with mainly in children and very old persons. It is frequently seen in the insane, and may probably result from rheu- matism, the excessive use of alcoholic liquors, and fevers. The cause is sometimes to be found in wounds or injuries of the skull. Diagnosis.—It is doubtful if hsematoma of the dura mater can be definitely recognized either in the stage of inflammation or that of hem- orrhage. Legendre1 states that, in children, the most important diag- nostic mark is the permanent contraction of the hands and feet, which is so generally present; but this symptom is certainly met with in other 1 “ Recherches sur quelques maladies de l’enfance,” Paris, 1846. CEREBRAL MENINGEAL HEMORRHAGE. 131 cerebral disorders, and may even result from reflex irritations. The diagnosis is rendered still more diflicult by the fact that tl'e disease under consideration is often associated with other cerebral disorders which mask or modify its symptoms. The absence of fever, the con- traction of the pupils, the slowness and irregularity of the pulse, the facts that there are no vomitings and no general convulsions, that the nerves distributed to the several parts of the face are not paralyzed, that there are constant and very severe headache and a gradually in- creasing tendency to stupor, are, according to Jaccoud,1 sufficient to indicate the presence of haematoma of the dura mater. I am of the opinion that they only enable us to give a guess wrhich has some basis in probability, for I have several times witnessed exactly such a condi- tion as that described, and after death found other morbid conditions than haematoma. Prognosis.—This is unfavorable, death resulting sooner or later, according to the extent of the disease and the natural powers of the patient. Morbid Anatomy and Pathology.—The first stage of hsematoma of the dura mater is characterized by the formation of the false membranes, to which allusion has already been made. These mem- branes are found on the internal surface of the dura mater, and are reticulated, presenting somewhat the appearance of spiders’ webs. They generally have their seat near the sagittal suture, and extend to both hemispheres, being only separated from them by the arach- noid and pia mater. Virchow, who has studied their formation with greater care than any other observer, has found more than twenty layers of them, one on top of the other, and traversed by numerous blood-vessels. Owing to this great vascularity, to the extreme tenuity of the ves- sels, and to the absence of any perivascular support, haemorrhage is liable to occur, and the several lamellae thus constitute a sac into wdiich the blood may be poured. This, pressing upon the cerebrum below, and constantly being enlarged by subsequent haemorrhages, gives rise to the symptoms observed during life. The vessels may be more liable to rupture from the existence of atheromatous degeneration of their coats. Anatomically and pathologically haematoma of the dura mater differs from intra-arachnoideal haemorrhage in the facts that the ex- travasation is between the dura mater and parietal layer of the arach- noid, and that the formation of the membrane precedes the haemorrhage. Those authors who regard the arachnoid as consisting of but a single layer, and who consequently do not admit the existence of intra- arachnoideal haemorrhage, must consequently concede that there are two kinds of extra-arachnoideal haemorrhage, one in which the mem- ' “Traite de pathologie interne,” tome i., Paris, ISTO. 132 DISEASES OF TIIE BRAIN. brane forms subsequently to the appearance of the extravasation, and the other’in which the hemorrhage is the direct consequence of the formation of the membrane. Others again, as, for example, Gintrac and Durand-Fardel, evi- dently regard what they describe as intra-arachnoideal hemorrhage as identical with hematoma of the dura mater ; and it is quite certain that many of the cases adduced by Gintrac as examples of intra- arachnoideal hemorrhage are in reality instances of pachymeningitis with subsequent sanguineous extravasation. The difficulties in the way of a complete understanding of the subject are greatly lessened by remembering the distinction pointed out above, that hoematoma of the dura mater is a secondary affec- tion, the direct result of inflammation and the formation of false membranes ; while in intra-arachnoideal haemorrhage the membrane is derived from the extravasated blood, which is the first step in the morbid process. The size of the cysts is subject to much variation, the quantity of blood ranging from one or two to sixteen or even more ounces. By the pressure which they exert upon the brain, the convolutions are flattened, and even softening of the cerebral tissue may be pro- duced. Treatment.—This requires no amplification at my hands, as I do not believe in the efficacy of any means for curing the affection. All that can be done is to palliate the more violent symptoms, such as the headache and feebleness of mind and body, by anodynes and stimulants, and of these, morphia administered hypodermically, and alcohol in some one or other of its numerous forms, are to be pre- ferred. Bloodletting and blistering are worse than useless. CHAPTER Y. PARTIAL CEREBRAL ANAEMIA FROM OBLITERATION OF CEREBRAL BLOOD- VESSELS (ISCHAEMIA-). Obliteration of cerebral blood-vessels may take place— 1. By thrombosis of the arteries. 2. By embolism of the arteries. 3. By thrombosis of the veins or sinuses. 4. By embolism or thrombosis of the capillaries. I. THROMBOSIS OP CEREBRAL ARTERIES. By cerebral arterial thrombosis is understood a condition in which an artery of the brain undergoes narrowing of its calibre by the depo- PARTIAL CEREBRAL AKLEMIA, ETC. 133 sition of fibrine from the blood on its internal surface. The clot thus formed is called a thrombus. Symptoms.—The phenomena observed in consequence of the forma- tion of a thrombus in a cerebral artery are gradual in their develop- ment, and are often interrupted by stages of apparent improvement. Headache, as in so many other affections of the brain, is a promi- nent symptom and is almost constantly present. It is not usually diffused over the whole head, but occupies a place having a close rela- tion in situation with the seat of the disease. It is rarely of a very aggravated character, and is remarkable rather for its persistency than its severity. In several cases which have come under my notice, the pupil of the eye of the affected side was dilated from the first, and there were ptosis and strabismus, showing that the third nerve was involved. At a very early period in the progress of the disease it is not un- common to meet with marked difficulties in the faculty of speech, and these not only relate to the articulation, but to the memory of words. As regards the first-mentioned form, there may be restraint in the movements of the tongue, the lips, or both, or there may be a loss of coordinating power in the muscles concerned in speech without any actual paralysis. Special inconvenience is, therefore, experienced when attempts are made to pronounce words in which the labial and lingual letters are prominent. The' gutturals in such cases are enunciated without difficulty. In the other form in which the memory of words is impaired, the patient is constantly at a loss for language with which to express his ideas; and, though the proper words may be supplied to him, he almost immediately forgets them again. The full considera- tion of this interesting subject wdll be found under the head of aphasia. Vertigo, though generally present, is not usually severe, at least in the early stages. The incipient symptoms of paralysis soon make their appearance in the majority of cases, and, though there is a gradual advance in the loss of power, there are periods of almost entire remission. Thus the leg, or the arm, or the face, may be the original seat of the paralysis, and eventually the whole of one side be involved. In a case of prob- able thrombosis in a gentleman now under my charge, the paralysis was at first limited to the muscles supplied by the ulnar nerve and those concerned in deglutition. For one period of five days after I first saw him, there w*as an entire remission of his symptoms, and he could move his hand and swallow as well as ever, but gradually the power was again lost, and other muscles became involved. At the present time he is almost entirely hemiplegic. Sensibility is also generally abolished or impaired on the paralyzed side, and thus the various forms of numbness, such as tingling, formi- cation, etc., are present. 134 DISEASES OF THE BRAIN. The mental symptoms are usually apparent from the first, hut may be altogether absent or else so slightly shown as not to attract atten- tion. The memory is impaired, not only as regards words, to which reference has already been made, but also events and circumstances, especially those of recent date. The names of persons and things are likewise readily forgotten. In the case of a gentleman whom I saw in consultation, and in whom I diagnosticated thrombosis, there was left hemiplegia involving both arm and leg, but not the foot, which had begun in the fingers and gradually extended. There was no special difficulty of speech except as regarded the recollection of words, but the memory was wonderfully impaired in every other respect. I en- tered his room upon one occasion just as the servant was carrying out a tray with the remains of his breakfast. Not three minutes had elapsed since he had eaten, and yet he assured me he had tasted noth- ing since the day before. The loss of memory was the first symptom observed in this case. Soon afterward he began to improve, and he is now, after fifteen months, free from paralysis, and with his memory almost as good as ever. The loss of memory in such cases seems to be due in the main to the fact that the power of concentrating the atten- tion upon any subject is very much diminished. There is likewise an indisposition to exert the powers of the mind or body, and thus the patient tends to pass into a condition of apathy. Somnolence is a fre- quent symptom. An interesting case 1 of what was probably cerebral arterial throm- bosis was admitted to the New York State Hospital for Diseases of the Nervous System, August 22, 1870, and came under my observation. The patient, a man forty-one years of age, was temperate, and had never had either syphilis or rheumatism. In March, 1868, he was seized with a dull pain in the right knee, accompanied with numbness. There soon followed formications and pricking sensations, limited to the right foot. These gradually extended upward, and, at the end of two weeks, had reached the shoulder, when he became entirely hemiplegic. Dur- ing this attack his consciousness was not affected, and his organs of special sense, except his touch, were unimpaired. On the 11th of May following, the patient suddenly lost the power of speech, but ex- perienced no disturbance of consciousness. He remained completely aphasic for four months, being only able during this time to utter a few sounds which could not be interpreted into intelligible words. He then began to enunciate a few words, and gradually acquired more facil- ity, though his power of coordination was far from perfect when he came to the hospital. His paralysis remained complete for nearly a year. When admitted there was hemiplegia of the right side of the body 1 See the author’s “ Clinical Lectures on Diseases of the Nervous System,” New York, 1874, p. 1. Case reported by Dr. T. M. B. Cross. PARTIAL CEREBRAL ANAEMIA, ETC. 135 except the face; his eyesight, hearing, and other special senses, were unimpaired, and his intellect was clear. There was no loss of the mem- ory of words, and no impairment of the motor power of the tongue, but simply a defect in the faculty of coordination of the muscles used in articulation. There was more difficulty in pronouncing labials and lin- guals than gutturals. Tactile sensibility, electro-muscular sensibility, and contractility, together with the temperature, were markedly dimin- ished in the right arm, while sensibility to pain and deep pressure was normal. The bladder and rectum were not paralyzed. In talking, he had a peculiar hesitating, stammering manner, highly characteristic of his disease. There were certain words which he was totally unable to pronounce with any degree of accuracy, even after much effort—“Peter Piper”—words which begin with explosive labial letters, and others similarly constructed troubled him greatly. The ophthalmoscope showed the existence of atrophy of both of the disks, and of retinal anaemia. Under the use of strychnine hypodermically administered, phospho- rus, and the primary current to his brain and the faradaic to the para- lyzed parts, very marked improvement in all his symptoms was produced. He regained a considerable amount of power in the arm, became able to walk several miles at a time, and acquired the ability to articulate distinctly any words he wished to say. The sensibility returned, and the nutrition of the affected limbs was manifestly improved. In another case, also the subject of a clinical lecture,1 there was probably thrombosis of the basilar artery. The patient, a woman, aged thirty-five, while at work wringing out clothes and exerting a good deal of force, experienced a sensation of numbness in the right arm and leg, which was attended with slight loss of power, though not enough to cause her to desist from her labor. At the time of the attack there were no head-symptoms of any kind, and she noticed no paralysis of the face. Her speech was not affected. At the time of her admission into the New York State Hospital for Diseases of the Nervous System, there was paralysis of motion and sensibility of the right arm and of motion on the left side of the face. The case was therefore one of cross-paralysis, and it was this fact which mainly induced me to locate the lesion in the pons Varolii. The speech was indistinct, but this was manifestly due to paraly- sis of the tongue and of the other muscles concerned in articulation. In the case in question there had been acute articular rheumatism, but the heart was free from functional or organic disease. The attack was not manifested with the suddenness which characterizes embolism, and there were no loss of the faculty of language, and no mental dis- turbance, which would probably have resulted had the middle cerebral artery been occluded. Besides, the face and the limbs would have 1 Op. tit., p. 130. DISEASES OF THE BRAIN. 136 been paralyzed on the same side, all of which considerations induced me to believe that the case was one of thrombosis of a limited portion of the basilar artery. During the first stage of thrombosis, before the artery is entirely closed, amendment, and even complete recovery, may take place. The remissions in the symptoms already referred to are due to the establish- ment of the collateral circulation, and this may become so complete as to eventuate in cure. It must be confessed, however, that the condi- tion of amemia to which the foregoing symptoms are due, in the great majority of cases ends in softening—a subject which will presently be considered as one of the consequences of thrombosis and other morbid states. Causes.—Thrombosis of an artery may result from atheroma or from endarteritis, by reason of which its elasticity is diminished and the smoothness of its lining membrane destroyed. Both these condi- tions retard the course of the blood, and favor the deposition of fibrine on the internal periphery. The walls of the vessels may be healthy, and a thrombus may then be formed through a weak action of the heart—the result of fatty degeneration or other cause impairing its strength. Certain conditions of the system, such as that which accompanies rheumatism, may induce thrombosis through the excessive amount of fibrine present in the blood and which renders this fluid more readily coagulable. It is probable, also, that other, diseases and particular articles of food—as, for instance, alcohol, fat, and starch—when taken in excess, especially when conjoined with insufficient physical exercise, may so alter the composition of the blood—inducing hyperinosis—as to lead to a like result. Inordinate mental exertion, tending as it does to diminish the tone of the arteries by keeping them in a condition of over- distention, may likewise cause the formation of thrombi. It has apparently resulted from exposure to intense heat, from sup- pression of the menstrual flow, from severe emotional disturbance, and from blows on the head. It is much more common in males than in females, and in persons of advanced years than in the young. Pressure may be exerted upon a cerebral artery by a tumor or other extraneous body, and narrowing of its calibre and a consequent throm- bus be produced. Gintrac1 cites a case of the kind. A young man had suffered for several days with headache and loss of power in the lower extremities. Coma supervened, but he was still able to answer questions. There was then pain in the back of the head, the pupils were dilated, the mouth was drawn to the right, the respiration was laborious but not stertorous, and the left side became completely paralyzed. He died on the fifth day. On post-mortem examination a 1 Op, cit., tome i., p. 444. Quoted from Roupell, Medical Times, 1844, vol. ix., p. 870. PARTIAL CEREBRAL ANJ3MIA, ETC. 137 firm clot was found to occlude the right middle cerebral artery, and it extended to the internal carotid artery, but did not pass into the middle cerebral artery beyond th e point of obstruction. At this place in the fissure of Sylvius a small granulated mass, something like a Pacchi- onian gland, pressed upon the artery and closed it. In such a case the symptoms will of course be developed with much greater rapidity than when the cause of the occlusion resides in the artery itself. Diagnosis.—Arterial thrombosis is distinguished from cerebral con- gestion by the facts that the mental and other symptoms are more pro- found in character, and that the patient has generally passed the prime of life. The existence of paralysis among the early symptoms will likewise tend to the formation of a correct opinion. From cerebral haemorrhage it is diagnosticated by the circumstance of its gradual de- velopment; from encephalitis by the absence of fever and the more chronic nature of the disease; and from embolism by its slow progress and the impossibility of defining the exact period of its beginning. Prognosis.—The prognosis in cerebral arterial thrombosis is unfa- vorable, for the reason that, although the morbid process may advance slowly, and may even be spontaneously arrested in its course before the artery is closed, the tendency to complete obliteration is always great, and the chance of sufficient circulation being carried on by the collateral vessels is very remote. The disposition to softening, there- fore, always exists, and generally cannot be overcome. The inade- quacy of any medical treatment to control the action going on within the artery, or to aid to any great extent in the development of the collateral circulation, is also an element in forming an opinion as to the ultimate result. Morbid Anatomy and Pathology.—Although Virchow1 was the first to write distinctly in regard to the nature of thrombosis, the condition was recognized long before his researches were made, and cases of clots plugging up the vessels are to be found detailed by many of the older medical authors, among whom Abercrombie, Carswell, and Cruveilhier, may be mentioned. Since Virchow began his observations in this direc- tion, many instances have been recorded and a large number of memoirs have been issued upon the subject. An interesting case was related by Dr. Packard,* of Philadelphia, at a meeting of the Pathological Society of that city held in December, 1859. The patient, who had been under the care of Dr. Heller, was a bachelor, fifty-one years of age. At six o’clock in the morning, at the beginning of February, he was seized with paralysis of the left arm and leg. He was a man of very regular habits, and of fanatical love for every thing instructive, and an accomplished scholar in botany, geography, and languages. The paralysis was soon relieved, and he was able, four weeks afterward, to go out again and to 1 Froriep’s Neue Notizen, 1846, Heft xxxvii. 2 North American Medico-Ohirurgical Review, vol. iv., 1860, p. 306. 138 DISEASES OF THE BRAIN. use his arm tolerably well. About the middle of March, in consequence of a fatiguing walk the previous evening, and an attack of diarrhoea during the night, complete paralysis returned. From this he never re- covered, but yet did not die till the December following. Previous to this termination he had confusion of ideas and delirium. Upon post- mortem examination, among other morbid changes, a cavity in the right corpus striatum was found, and this was surrounded by a spot of soft- ening of the cerebral substance as large as an egg. The basilar artery was completely blocked up with clots, as was also the right carotid. These vessels were atheromatous, and the basilar artery was aneuris- mally dilated. The clots had all the appearance of being old. Dr. Dickinson 1 has brought forward five cases of occlusion of arte- ries, several of which I am disposed to think were of embolism, instead of thrombosis, as he considers them to be. Dr. Dickinson nowhere alludes to Virchow’s investigations, but gives the whole credit of the discovery of the relation between emboli and the formation of concre- tions in the heart to Dr. Kirkes. The conclusions which he draws from his cases are by no means original, although he evidently so regards them. The questions to be considered in connection with the morbid anatomy of arterial thrombosis relate to the condition of the artery, the nature of the clot, and the changes which take place in those parts of the brain which are deprived of their due supply of blood. The affections of the artery, being similar to those which render it liable to rupture, need not be dwelt upon at any length here, as they have already been noticed under the head of the morbid anatomy of cerebral haemorrhage. Suffice it, therefore, to say that endarteritis and atheromatous degeneration are the diseased states generally met with. The calibre of the diseased vessel is diminished and the blood is therefore primarily obstructed in its course even before the beginning of the formation of a clot. In addition the internal coat of the artery is roughened, and hence the fibrine of the blood is readily caught and de- posited on the internal periphery. Little by little the layer becomes thicker from fresh accretions, until finally the vessel is entirely occluded. The clot which closes the vessel is, in the beginning, coagulated blood, and hence consists of fibrine and white and red blood-corpuscles. It adheres to the arterial wall and may be of a brown, yellow, gray, or white color. The consistence is greater at the base than at the pe- riphery, and it may contain granules of calcareous matter composed mainly of phosphate of lime.3 The elements, with the exception of the fibrine, are gradually disintegrated and washed away by the current of 1 “ On the Formation of Coagulae in the Cerebral Arteries.” St. George’s Hospital Re- ports, vol. i., 1866, p. 257. 2 Laneereaux, “ De la thrombose et de l’embolie cerebrales. These de Paris,” 1862, p. 86. PARTIAL CEREBRAL ANAEMIA, ETC, 139 blood which continues to flow through the vessel before it is entirely closed, and therefore the layers nearest the arterial wall consist almost entirely of fibrine, and the one nearest the centre of the vessel, which is the latest formed, of fibrine and corpuscles. An examination of such a clot with the microscope shows that the above-mentioned morphological elements are found in its centre, more or less changed, however, accord- ing to the age of the formation. A thrombus may undergo purulent softening and disintegration to such an extent as to result in its break- ing up into fragments, which may lodge in the vessel or its branches farther on, and thus constitute emboli. The region of the brain to which the artery undergoing occlusion is distributed is, of course, deprived to some extent of its blood, and hence presents at first an appearance of anaemia. And this is not prevented by the increase of the collateral circulation, which is never sufficiently vigorous to compensate entirely for the loss by the primary vessel. Microscopic examination shows the capillaries to be smaller and less numerous than in the normal condition, though there is not any palpa- ble softening. But after the artery is entirely closed a change ensues. The anaemic portion of the brain becomes red or pink, and this color is deepest on the borders, owing to the collateral circulation which is now fully es- tablished. This stage has been called red softening, but I am disposed to think the designation erroneous, and that it is liable to convey false ideas of the pathology. For it is perfectly possible at this time for the anaemic portion of the brain to be restored through the activity of the collateral circulation, with the effect of causing a cessation of the symp- toms. If, however, this should be insufficient to provide for the due nutrition of the affected region, softening takes place, and a cure be- comes almost impossible. Obliteration of a cerebral artery by thrombus does not always pro- duce notable symptoms. For these to follow, the morbid process must be set up in a vessel with but few and small collateral branches. Thus, if the internal carotid be obstructed, the circulation is carried on through the circle of Willis by the supply of blood derived from the vertebrals. The basilar artery might also be occluded at any limited region between a pair of transverse arteries, and the circulation still kept up by the carotids on the one side, and the vertebrals on the other. But any closure so as to involve one or more of the transverse arteries must lead to anaemia, and subsequent softening of the pons Yarolii. Thus, in a case reported by Bennett,1 in which there had been vertigo and other head-symptoms for several years, and in which paralysis of the left arm, without loss of consciousness, had suddenly supervened, the basilar artery was found entirely obliterated throughout its entire extent, all 1 “ Clinical Lectures on the Principles and Practice of Medicine,” third edition, Edin- burgh, 1850, p. 370. 140 DISEASES OF THE BRAIN. the transverse arteries were of course closed, and the supply of blood to the pons was cut off on both sides of the mesial line. A somewhat similar case has recently been reported to me by a physician of this city. The patient had suffered with paresis of all the limbs, with pain in the back of the head, occasional vertigo, irregu- larity of the respiration and circulation, and double facial paralysis for several months. He died suddenly while sitting quietly in his chair. On post-mortem examination the basilar artery was found occluded, a, artery of the corpus callosum (anterior cerebral, right); b, middle cerebral artery; c, posterior cerebral artery; a, superior cerebellar artery; e, anterior inferior cerebellar artery; f. posterior inferior cere- .!?£ artery; g, obliteration of artery of corpus callosum (anterior cerebral, right); A, obliteration of middle cerebral artery; i, obliteration of basilar artery; obliteration of vertebral artery (left). and distended by a thrombus which reached from the point of union of tne vertebrals to the posterior cerebral arteries, into the left one of which it extended two or three lines. A very interesting memoir by Hayem1 alleges occlusion of the basilar artery by thrombus to be a cause of sudden death. In all his cases, four in number, the artery was closed throughout a great part of 1 “ Sur la thrombose par arterite du tronc basilaire, comme cause du mort rapide.” Archives de Physiologie Normals et Pathologique, 1868, p. 270. PARTIAL CEREBRAL ANEMIA, ETC. 141 its extent, as the result of extensive arteritis and the formation of dense clots. In the fourth case there was also thrombosis of the left middle cerebral artery, with difficulty of speech. The cerebral vessels most liable to be closed by thrombosis are the internal carotid, the middle cerebral, the basilar and the vertebral; after these come the anterior cerebral, the posterior communicating, and the posterior cerebral. It is by no means rare to find two or more arteries simultaneously affected, and in one case cited by Gintrac1 the whole circle of Willis was obstructed, and, in a remarkably interesting case described by Heubner,3 the right anterior cerebral artery, the left middle cerebral, the basilar, and the left vertebral were obliterated by thrombosis of syphilitic origin (Fig. 13). The arrows in the figure represent the course which the blood took by reason of the several ob- structions to its circulation. The vessels the closure of which produces the greatest disturbance of function are the anterior, middle, and posterior cerebral, which supply the hemispheres, the corpus striatum, optic thalamus, and other impor- tant ganglia. Besides the effect due directly to the anaemia, more or less disturbance results from the congestion posterior to the clot, and the consequent effusion of serum. Treatment.—A knowledge of the morbid anatomy and pathology of cerebral arterial thrombosis must satisfy us of the insufficiency of any medical treatment to cause the absorption of the clot obliterating the channel of the artery. Yet I have several times heard it gravely pro- posed to administer the iodide of potassium, with the view of accom- plishing this object. As regards facilitating the establishment of the collateral circulation, Nature will generally take care of this, and may even so far overdo it as to cause haemorrhage from the rupture of ves- sels not accustomed to the increased tension of the blood. It may therefore be necessary, in this latter condition of excessive action, to give the bromide of potassium in large doses. Should the circulation be feeble, the skin cold, and the patient disposed to somnolence, we have reason to suppose that the collateral circulation is not being formed with sufficient rapidity, and therefore the patient should be kept with the head low, brandy or other spirituous liquors administered, and the body wrapped up in warm blankets. For some time after the successful establishment of the collateral cir- culation there is more or less feebleness of mind and body. For this condition strychnia and phosphorus are especially applicable, and may be administered according to the formulas recommended under the heads of cerebral congestion and cerebral hasmorrhage. Electricity is almost always useful. 1 Op. cit., p. 443. * “Die Luetische Erkrankung der Hirnarterien,” Leipzig, 1874, pp. 87, 194. 142 DISEASES OF THE BKAIN. II. EMBOLISM OF CEREBRAL ARTERIES. Embolism is the term applied by Virchow to the closure of an ar- tery by an embolus, which is a clot formed in some other part of the body and transported by the current of the blood to the vessel which it oc- cludes. It therefore differs from thrombosis in the facts that it is not associated with previous disease of the artery, and that the closure of the vessel is sudden. Symptoms.—In cerebral embolism there are no premonitory symp- toms. As in cerebral haemorrhage, the patient may be sitting per- fectly quiet when he suddenly loses consciousness and falls to the ground, comatose. As the stupor passes off, he finds that he is par- alvzed upon the side of the body opposite to the seat of the lesion. Or there may be no coma, but merely slight confusion of ideas for a moment or two with sudden accession of paralysis on a limited por- tion of one side, involving only the arm or leg. Or, again, the face or the tongue may be the only part paralyzed. Or there may be no paralysis anywhere, and no mental symptoms except as regards the faculty of language, which is entirely or partially lost. Sometimes there are ocular troubles, such as ptosis, strabismus, or blindness. Experience shows that the embolus, for reasons which will be given hereafter, generally lodges in the left middle cerebral artery, and that with the right hemiplegia—if there be paralysis at all—there is often aberration of the faculty of speech. The symptoms of mental derangement, with the exception of the coma of severe attacks, are not ordinarily prominent. I have, however, witnessed several cases in which they formed a very striking feature of the case. In one of these, in which the clinical history of the patient disclosed the pregxistence of several attacks of acute articular rheu- matism, with subsequent endocarditis and mitral and aortic valvular lesions, there were hallucinations and delusions in addition to the complete paralysis of the left side. All these phenomena entirely dis- appeared within thirty-six hours. This case is one of the few in my experience in which the embolus had occluded an artery on the right side of the brain. In another, likewise with valvular disease of the left side of the heart, there was delirium from the first, and this disappeared as the collateral circulation was established. Erlenmeyer has written very excellently of cerebral embolism, but is, I think, incorrect in some points of his symptomatology. He states the ordinary phenomena of an attack to be as follows: There are no prodromata; sudden loss of consciousness, with pa- ralysis of several parts of the body. The facial, the hypoglossal, and the nerves of the extremities, are always more or less affected. Sensi- PARTIAL CEREBRAL ANiEHIA, ETC. 143 bility is abolished in the conjunctiva, but is retained in the cornea. The pupils remain sensitive, and are neither contracted nor dilated, neither are there symptoms of concussion or compression. There are no vomitings and no contractions. The pulse is weak and small, and the temperature rather below the normal standard. Occasionally there are epileptiform convulsions. Psychical troubles do not ordinarily ap- pear till the collateral circulation becomes active, and local hypersemia is thus induced. The principal exception I have to make to the foregoing sequence of symptoms is the too absolute assertion of the paralysis of the facial, hypoglossal, and other nerves. I have seen several cases in which there was no paralysis to be detected in any part of the body by the most careful examination, and several others are on record. In one very interesting instance, occurring in a lady who had had repeated attacks of acute rheumatism, and who had at the time marked aortic insufficiency, headache and vertigo suddenly occurred while she was conversing with a friend, and her speech was cut short with as much suddenness as though she had been shot. There was no paralysis of the tongue, but all idea of language was abolished. In another, that of a gentleman with a similar clinical history, head- ache, vertigo, confusion of ideas, and amnesic aphasia, suddenly super- vened. That both these were cases of embolism can scarcely, I think, be doubted. And then, as regards the state of the pupils, my experience does not coincide with that of Erlenmeyer, for I have frequently found either dilatation or contraction of both pupils, or dilatation of one and con- traction of the other. In examining a case of recent embolism, the ophthalmoscope should always be used to view the fundus of the eye, and even in old cases valuable signs will often be obtained. The middle cerebral artery, the ordinary seat of embolus, arises from the internal carotid, after the an- terior cerebral and ophthalmic have been given off. Occlusion of its channel must, of course, throw an increased amount of blood into these last-named arteries, and, as the arteria centralis retime is derived from the ophthalmic, it and its branches become enlarged. The ophthal- moscope will enable us to discover the congestion thus produced, and will often be the means of helping us to determine, in the absence of pa- ralysis, which side of the brain is the seat of the lesion. In older cases we will frequently find retinal congestion. The following case I quote not only as being the first of which I have any knowledge in which the ophthalmoscope was used in a case of cerebral embolism, but as being interesting from the fact that the embolus was on the right side. It is reported as Cerebral Embolism following Valvular Disease of the Heart.—John Turnbull, aged seventeen, was admitted into the Hull General Infirm- 144 DISEASES OF THE BRAIK ary, on April 25, 1867. He was tall, much wasted, and had a suffering expression, and converging strabismus of the left eye, the mouth being drawn very slightly toward the left side. Pulse 70, very thrilling in character, and a large coarse systolic murmur near the left nipple. He was perfectly sensible, complained of severe frontal headache, with confusion of vision, and stated that he had been in much the same con- dition for seven weeks, his illness beginning spontaneously with head- ache and vomiting, unaccompanied by loss of consciousness or con- vulsions. He had had an attack of acute rheumatism in the previous summer. He was ordered gr. iij of blue-pill and gr. ij of extract of henbane in a pill, and a draught of acetate of ammonia, three times a day, and spirit-lotion to the head. “ No marked alteration in his con- dition, except progressive debility, took place till May 2d, when he complained of increased headache and dimness of vision, and, being un- able to expectorate, from excessive weakness, death from bronchial obstruction threatened. With the aid of some champagne, he rallied in about twenty-four hours, and at the end of a week was much im proved, having a clean tongue and good appetite, but the headache, stra bismus, and deviation of the tongue to the left, remained. On May 16th it was noticed that these symptoms had passed off, with the exception of the last mentioned. He was ordered a mineral-acid mixture. “ A week later, as he still complained of some dimness of sight, he was examined with the ophthalmoscope. The retinal vessels were found much enlarged, and the veins very tortuous; the optic nerve- entrance of an intense red color, not being distinguishable from the surrounding parts except by the entrance of the vessels, the redness being chiefly due to a number of very fine vessels radiating from the centre. There was no morbid effusion in any part. He could spell easily from No. 15 of Jaeger’s test-types (being unable to read and write). He was again examined at the end of another week, when the optic nerve-entrance was observed to be paler in color, so that its cir- cumference could be distinguished, but still much injected, and the vessels nearly as large and tortuous as before; sight was apparently perfect. He was discharged convalescent. “ The peculiar form of paralysis in this case denoted some morbid condition within the cranium, which appeared to have its most easy and natural explanation in cerebral embolism, an opinion further sup- ported by the perfect recovery of the patient. The case received much additional interest from the information afforded by the ophthalmo- scope, for one may fairly believe that the intense congestion of the retinae denoted a similar condition of the brain, perhaps a state of re- action after the circulation had been reestablished through collateral channels.”1 1 British Medical Journal, 1867; also Quarterly Journal of Psychological Medicine, January, 1868, p. 178. PARTIAL CEREBRAL ANAEMIA, ETC. 145 Causes.—The most common first step in the causation of cerebral embolism is acute articular rheumatism, which, by inducing acute en- docarditis, leads to the formation of emboli on the valves of the heart and other parts of the endocardium. Aneurisms of the aorta or other large artery, resulting in the coagulation of the blood in the aneurismal sacs, may likewise induce it, by a portion of the clot being washed off by the current. Esmarch 1 details a case in which, while an examina- tion was being made of an aneurism of the carotid, the patient sud- denly fell back in an apoplectic stupor. The whole right side was at once paralyzed, the facial muscles on the left side were convulsed, and four days afterward death ensued. Post-mortem examination showed that the left internal carotid, the middle cerebral, and the ophthalmic, were completely closed by coagula, which were identical in structure and appearance with the clot in the aneurismal sac. Emboli may also originate in the lungs, and, entering the left auricle through the pulmonary veins, finally lodge in a cerebral artery. Age appears to exercise no influence over the formation of emboli, but men are much more commonly the subjects than women, for the rea- son, undoubtedly, that they are more liable to attacks of rheumatism. Of sixty-two cases under my care, either alone or in consultation, in which I had reason to diagnosticate cerebral embolism, there was organic disease of the heart in all but four. Three of the cases were over sixty years of age; seven between fifty and sixty; eleven between forty and fifty; twenty-nine between thirty and forty; and twelve under thirty. Thirty-nine were males and twenty-three were females. Diagnosis.—From cerebral haemorrhage, embolism may be distin- guished by the following sign's. It occurs without relation to age, while haemorrhage is much more frequent in persons over forty; there are no prodromata; the resultant paralysis is generally on the right side, while in haemorrhage there is no such predisposition; and it is in the great majority of cases associated with organic disease of the left side of the heart. Care, however, must be taken not to over-estimate the value of this diagnostic mark, valuable as it is. In one case under my charge, in which the symptoms pointed strongly to the existence of a cerebral embolus, and in which, after death, the left middle cerebral artery was found occluded, the heart was perfectly healthy; and in one other, in which cerebral embolus was diagnosticated, and in which there was mitral regurgitation, extravasation into the corpus striatum was discovered to be the cause of death. A case has recently been re- ported by Dr. J. Hughlings Jackson,2 in which there was cerebral haem- orrhage with hemiplegia, together with extensive valvular disease of the heart. A patient now in the New York State Hospital for Diseases of the 1 Archiv fur Pathologic, Anatomie und Physiologic, B. xi., Heft 5, 1857. s British Medical Journal, October 29, 1870, p. 459. DISEASES OF THE BRAIN. 146 Nervous System has left hemiplegia, involving face, arm, and leg. It has already lasted seven months, although greatly improved. The hand and arm are much contracted. The attack was apparently in- duced by strong muscular exertion being made while in a stooping and constrained position. Most physicians will be disposed to agree with my diagnosis, that the case is one of cerebral haemorrhage, for the obvious cause of the paroxysm, the lesion being on the right side of the brain, the steady improvement and the muscular contractions, all point to extravasation of blood instead of embolus. Yet he is under twenty years of age, and, before the seizure, had an attack of acute rheumatism, with heart-symptoms. He now has aortic and mitral regurgitation. Such cases as the above are very instructive, and they show us how necessary it is to weigh all the facts, and how great is the possibility of making a mistake after all. For, although I am inclined to the view of haemorrhage, no definite opinion can be given without a post-mor- tem examination. Still in a case of partial or complete hemiplegia, with or without apoplexy, in which the patient was below the age of forty, with the hemiplegia involving the right side, no muscular contractions and or- ganic disease of the left side of the heart, with or without previous attacks of acute articular rheumatism, cerebral embolus may safely be said to be the cause of the symptoms. Moreover, the paralysis from embolism, if it does not disappear within seventy-two hours after the seizure, does not gradually fade away as it so frequently does to a great extent in haemorrhage. It is a somewhat remarkable fact that in cerebral embolism the pa- ralysis may be very extensive and complete without the occurrence of other notable symptoms. Thus in the case of a young lady whom I saw in consultation with Drs. Polk and M. A. Wilson, there had been in childhood a severe attack of inflammatory rheumatism and several minor attacks subsequently. On the last day of September, 1874, she sud- denly became hemiplegic on the left side, but did not lose consciousness. There was no aphasia, pain in the head, convulsive movements, nor mental disturbance. The paralysis, however, involved the left arm and leg, and was exceedingly profound. The face was affected for a short time, but the tongue retained its motor power. Three months after- ward she could stand and walk a little, but was not able to raise the foot from the ground; the arm was absolutely immovablo. Here the clinical history, accompanied as it was with a record of heart-disturb- ance for several years, was such as to leave no doubt as to the lesion being embolism of an artery—probably the middle cerebral—of the right side of the brain. The suddenness with which embolism takes place, to say nothing of the other points in the clinical history, will suffice for the discrimination from thrombosis. PARTIAL CEREBRAL ANJ2MIA, ETC. 147 Prognosis.—The prognosis in cerebral embolism is grave, for the reason that the tendency to softening of the anaemic cerebral tissue always exists. But, if the patient passes over the first four or five days without any aggravation of his symptoms, and especially if they be mitigated in violence, there is considerable hope of a favorable result. Still, a guarded opinion should always be given till all head-symptoms have disappeared. Morbid Anatomy and Pathology.—The first rational explanation of embolism was made by Virchow,1 in 1847, who, in his paper on acute inflammation of the arteries, distinctly explained the manner in which the vessels were occluded by clots transported in the blood from dis- tant parts of the body, and who associated these coagula with valvular disease of the heart. In two of the cases cited by him in which arteries were found closed by such clots, the valves of the heart were discovered to have others still attached to them, and exhibited traces of the sep- aration of those which were found in the vessels. Subsequently (in 1852), Dr. Senhouse Kirkes 4 called special atten- tion to the plugging up of the middle cerebral artery as a cause of soft- ening of the brain. Three cases, in which death followed, are adduced, in each of which the condition of non-inflammatory softening was found to exist in the brain. Dr. Kirkes’s observations appear to have been made without any knowledge of Virchow’s prior researches. He states that the paralysis met with in young persons may be due to the inter- ruption of a due supply of nutriment to the brain by the occlusion of an artery by a plug derived from the left side of the heart. Schiltzenberger,4 among others, has written with great fullness on this subject. Among other conclusions not specially applicable to the particular point now under consideration, he states that fibrinous con- cretions may form in the heart or large vessels, may subsequently be detached and carried by the blood to the cerebral arteries, where they produce symptoms not essentially different from those noticed in cere- bral haemorrhage or acute softening. The only material points of difference under this head between thrombosis and embolism are, the suddenness of the attack, the part of the brain most liable to be affected, the origin of the clot, and the state of the blood-vessel which is obliterated. Relative to the first, the abrupt closure of a vessel as in embolism will, of course, produce more violent symptoms than if the occlusion 1 “ Ueber die akute Entzundung der Arterien.” Archiv fur Pathol. Anatomie, B. i., 1847, p. 272. In a paper on “ Occlusion of the Pulmonary Artery,” published in Froriep’s Neue Notizen in 1846, he enunciated a similar theory. a “ On some of the Principal Effects resulting from the Detachment of Fibrinous Deposits from the Interior of the Heart, and their Mixture with ti e Circulating Fluid.” Medico-Chirurgical Transactions, voL xxxv., 1852. 3 Gazette des Hopitaux, No. 80, 1857. 148 DISEASES OF THE BRAIN. has taken place gradually, and thus time have been afforded for the establishment of the collateral circulation. In the first case, not only is the blood at once shut off from a portion of the brain, but the vessels behind the clot receive a greater quantity than they normally do, and hence the regions they supply are immediately congested. In examina- tion of the brain of a person who has died during the first stage of cerebral embolism, we find those parts of the brain ordinarily supplied by the obliterated vessel paler than natural, with a zone of congested tissue, and perhaps numerous small extravasations of blood on the periphery. The place where emboli are most frequently found is, as has already been stated, the left middle cerebral artery. The left common carotid arises from the arch of the aorta in a line almost exactly coinciding with the course of the blood-current. It therefore happens that an embolus which has formed on the lining membrane of the heart, and which has passed into the aorta after having been detached, enters this vessel instead of the innominata. From the common carotid it passes into the internal carotid and thence with the stronger and more direct current into the middle cerebral artery, which is lodged in the fissure of Sylvius. Of forty-two cases of cerebral embolism collected by Meissner, in thirty-four the left hemisphere was the seat. Of sixty- two cases occurring in my own practice, and to which reference has been made, fifty were accompanied with right hemiplegia, and were consequently on the left side of the brain. Post-mortem examinations were made in eleven of these cases, and in all the embolus occupied the left middle cerebral artery. Of these latter was the case of a prominent elderly gentleman of Providence, Rhode Island, whom I was requested to visit in consul- tation with Drs. Parsons and Collins, of that city. Three days be- fore, while ascending a hill, he had suddenly become semi-unconscious and hemiplegic on the right side. There was also well-marked aphasia. When I saw him he was in a state of partial coma, from which he could be roused so as to be made to comprehend, but was unable to talk, and was entirely paralyzed in the face, arm, and leg, of the right side. The clinical history indicated the existence of disease of the left side of the heart. I diagnosticated an embolus of the left middle cerebral artery, and expressed the opinion that death would ensue within a few hours. In both of these views the other medical gentlemen fully con- curred. The patient died about eight hours afterward. The post- mortem examination was made the following day, and proved the correctness of the opinion that had been expressed, for an embolus completely occluded the left middle cerebral artery, at the point where it divides into the branches which supply the island of Reil and the convolutions of the base of the anterior and middle lobes. The pathology of the genesis of the clot has already been sufficiently PARTIAL CEREBRAL ANAEMIA, ETC. 149 dwelt upon in other connections, and the fact that the artery in which it is found is not diseased has been mentioned. The further consequences of embolism belong to cerebral softening, and will be considered under that head. Treatment.—It is not necessary to make any remarks on this point in addition to those made in regard to the treatment of thrombosis. There is very little to be done besides meeting indications as they arise, and attempting to relieve the paralysis and other symptoms, for which ends my views have been sufficiently expressed in the preceding chapters. III. THROMBOSIS OF CEREBRAL VEINS AND SINUSES. It was, until the researches of Yirchow, generally supposed that the coagulation of the blood in the veins was the immediate result of phlebitis; but through his investigations it is now very well understood that, in the great majority of cases, the inflammation of the veins is a consequence of the formation of a thrombus, and not a cause. For reasons which will be given further on, the sinuses of the dura mater are especially liable to be the seat of autocthonous coagulae. Symptoms.—It is very doubtful if venous cerebral thrombosis pos- sesses such a characteristic symptomatology as to admit of its being identified during the life of the patient. There are headache, convul- sions epileptiform in character, paralysis of different parts of the body, particularly of the ocular muscles, giving rise to squinting and double vision, disturbances of sensibility, and, toward the close of the disease, coma. Occasionally there is apoplexy at an early stage. Certain symptoms have been laid down by authors as indicative of the existence of thrombosis of particular sinuses. Jaccoud,1 however, appears to discredit their importance, and I am disposed to agree with him that, though it may be well to know them, it is safer not to attrib- ute to them an absolute value. Thus, Yon Dusch 2 asserts that epistaxis is symptomatic of obliteration of the superior longitudinal sinus ; Ger- hardt3 finds a difference in the size of the external jugular veins—that of the affected side being more collapsed than the other—indicative of thrombosis of the lateral sinus ; Griesinger4 states that the presence of a painful circumscribed oedema behind the ear is evidence of the existence of thrombosis of the transverse sinus extending into the veins which lead to the sigmoid fossa; and Corazza B thinks obliteration of the superior longitudinal sinus is signified by oedema of the frontal 1 “Trait6 de pathologie interne,” tome premier, Paris, 1870, p. 149. s Henleund Pfeufer’s “Zeitschrift fur ration. Medicin,” B. vii., 1859, p. 161. Also the New Sydenham Translation—“On Thrombosis of the Cerebral Sinuses,” London, 1861. ! Deutsche Klinik, 1857, No. 45. 4 “ Beobachtungen ueber Hirnkrankheiten,” Archiv tier Heilkunde, 1863. 6 “Revista Clinica,” 1866. 150 DISEASES OF THE BRAIN. veins, and exophthalmos. An important point in the symptomatology of thrombosis of the encephalic veins and sinuses is the often simulta- neous presence of suppurative inflammation of the ear. This is ex- plained by the fact that the relations of the mastoid cells and the petrous portion of the temporal bone to the lateral, the cavernous, and the petrosal sinuses, are so intimate that the extension of a morbid process to them, from the parts of the cranium in question, is readily accomplished. Owing to the inflammatory action so frequently set up in the vein or sinus in which a thrombus has been produced, pus enters the gen- eral circulation, and hence abscesses are liable to occur in distant parts of the body. In the very interesting case which forms the basis of Yon Dusch’s important paper, the principal phenomenon observed during the life of the patient—an infant nine months old—was a large abscess occupying the anterior and outer portion of the right thigh, from which half a pint of pus was obtained, by incision, and which continued to discharge for several days. Death occurred in a few days without being preceded by convulsions, coma, or other head-symptoms. On examination after death, the anterior part of the superior longitudinal sinus was found to be completely closed by a firm, pale, triangular clot of blood, adherent to the walls. Posteriorly the clot did not entirely fill the calibre of the sinus, and was softer. Similar clots were also found in the left lateral sinus, and in the veins terminating in the superior longitudinal sinus. In a case reported by Abercrombie1 as “ Suppuration within the Left Lateral Sinus,” the affection undoubtedly resulted from an exten- sion of inflammation from the cranium to the veins. The patient, a young lady aged sixteen, complained of severe headache, which ex- tended over the whole head. She had an oppressed look, and great heaviness of the eyes; pulse 120; tongue clear and moist; face rather pale. She had been liable to suppuration of the ears, and the left ear had been discharging pus for three weeks; had complained of head- ache for a fortnight. A few days afterward, her strength began to fail, there was a tendency to stupor, and slight delirium was present. There was constant complaint of pain in the head. Finally, she became more comatose, but was sensible when roused, and knew those about her a few minutes before her death. On post-mortem examination the membranes of the brain were found congested, but the brain-substance was not diseased. The left lateral sinus was inflamed throughout its whole extent. “ Its inner coat was dark-colored, irregular, and fungous. At one place the cavity was nearly obliterated. The disease extended into the torcular Herophili, 1 “ Observations on Chronic Inflammation of the Brain and its Membranes.” Edin- burgh Medical and Surgical Journal, vol. xiv., 1818, p. 288. PARTIAL CEREBRAL ANAEMIA, ETC. 151 o.nd affected a little the termination of the longitudinal sinus. Behind the auditory portion of the temporal bone, near the foramen lacerum, and in the course of the left lateral sinus, a portion of the bone nearly the size of a shilling was dark-colored and carious on the inner table. It was at this place that the sinus appeared to be most diseased.” It is stated that the walls of the sinus were so thickened as to pre- vent the passage of the blood, and that evidently no blood had trav- ersed it for some time. Although Abercrombie failed to recognize the real nature of the morbid process, there can be no doubt that the sinus was closed by an old coagulum, which had been adherent to the walls, Prichard1 reports the case of a girl sixteen years of age, in whom epileptic convulsions had existed for two years, and recurred very fre- quently, sometimes several times a day. There appeared to have been no other symptoms indicating cerebral disturbance except that it is mentioned that at one time she was slightly delirious, and then was free from fits. She was treated actively for nine months, and then died in a convulsion, of the usual character. Examination after death showed that “the left lateral sinus, through its whole extent, was filled up by a substance very different in its nature from a recent coagulum, and apparently consisting of a deposi- tion of lymph, which had become organized. It appeared so com- pletely to occupy the calibre of the sinus as to have entirely impeded the passage of the blood through it.” Another case, reported by the same author,2 is that of a girl twenty - two years of age, whose mother had been insane, and whose complaint “began by a feverish disorder, under which she labored about nine weeks. It was followed by a melancholy and pensive habit. She was observed to spend most of her time in reading religious books, and attended a meeting of Calvinistic dissenters.” When she first came under treatment, her appearance was very wild; she was mischievous, and fond of destroying her clothes. In about three months and a half she was discharged cured, but was readmitted a month afterward, and remained in the hospital till her death, which took place about three years subsequently. During this period her constitutional tendency to scrofula showed itself in a decided manner. The glands of the neck were frequently swollen and inflamed, and she was repeatedly attacked by pneumonic symptoms. When these disorders became a little relieved, her mental alienation was aggravated. She generally sat with her hands folded, and her eyes fixed downward. She died from general debility and exhaustion, but without additional head-symptoms. Post-mortem examination revealed the existence of thickening of the dura mater, serous effusion between this membrane and the pia mater, fluid within the pia mater, and thickening of this membrane. 1 “ A Treatise on Diseases of the Nervous System.” London, 1822, p. 1'76. 8 Op. citp. 357. 152 DISEASES OF THE BRAIN. The substance of the brain was very firm, the pineal gland was large. “ The longitudinal sinus contained a firm coagulum, resembling a poly- pus, which extended into the lateral sinus.” In only one instance have I had the opportunity of making a post- mortem examination in a case of thrombosis of a cerebral sinus. The patient, a man forty years of age, had been upon a drunken debauch for several days, when he gradually passed into a condition of stupor, which was at first mistaken for the continued effect of alcoholic intoxi- cation. As it continued for two days after all stimulants had been withheld, this idea was abandoned, and the diagnosis of cerebral hmmorrhage was made. I saw him at this time, and was disposed to agree with this opinion. There were profound stupor, stertorous breathing, and complete resolution of all the limbs. Much to my surprise, however, the state of coma gradually passed off, and as sensi- bility returned the patient complained of intense pain in the forehead and vertex, which was accompanied by twitchings of the muscles of both sides of the face, and of both upper extremities. On the tenth day right hemiplegia suddenly ensued, unattended with loss of con- sciousness, though there was a slight disposition to stupor manifested as soon as the attention failed to be engaged. The pupil of the left eye was dilated. On the twelfth day a severe epileptiform convulsion ensued, which was succeeded by another on the same day, during which the tongue was very severely bitten. Control of the bladder and rectum was now lost, and on the fourteenth day the convulsive state became permanently established, and the patient died that night without regaining consciousness though the convulsions became somewhat less violent. The post-mortem examination was made the following morning. The pia mater and arachnoid were somewhat congested, though the subarachnoideal fluid was not notably increased in quantity. The sub- stance of the brain was healthy, and there was no extravasation of blood anywhere to be found. But, on laying open the longitudinal sinus, a firm coagulum was found completely occluding it, from its beginning anteriorly, to its termination in the torcular Herophili, partly filling this cavity, being attached to its anterior wall, and extending for the distance of an inch and a quarter into the left lateral sinus. The thrombus was much more dense and compact in its anterior than in its posterior part, and that portion which occupied the lateral sinus was evidently of more recent formation than the rest. A consideration of the symptoms exhibited by these cases will serve to show the truth of the assertion made in the beginning of my remarks on the subject, that there are no such characteristic symptoms of thrombosis of the cerebral sinuses as will suffice for the identification of the disease. The most that can be premised is a not very decided probability. PARTIAL CEREBRAL ANJiMlA, ETC. 153 Causes.—Among the causes of thrombosis of the cerebral veins and sinuses, those affections of the heart in which the force of its systole is lessened, and those in which there is an obstacle to the return of the venous blood, occupy a prominent place. Through the action of either of these categories of diseases the circulation within the cranium is retarded, the blood tends to accumulate in the large veins and sinuses, and, its course being abnormally slow, coagulation is liable to ensue. Tumors in the neck, by compressing the internal jugular veins, also tend to the same result by backing up the blood in the lateral sinus. An intra-cranial tumor may exercise a like effect by direct pressure upon a sinus. Thrombosis may result from the extension of inflammation from the cranium or the cerebral tissue to the sinuses. Such is the case when the suppuration of the ear terminates by the formation of a thrombus in the lateral, cavernous, or petrosal sinus, or when abscess of the brain or an extravasation of blood produces a like effect. The condition in question may also be caused by injuries of the skull; it has been known to follow the operation of trephining and other surgical procedures on the cranium, and may also result from carbuncles, of or near the head, and from erysipelas occurring in like situations. Age appears to be of some influence as a predisposing cause of venous cerebral thrombosis. Thus, of thirty-seven cases cited by Gin- trac,1 fourteen were between the ages of three weeks and ten years, eleven between eleven and twenty years, six between twenty-one and thirty years, four were forty-five, fifty-five, sixty-five, and sixty-eight years old respectively, and two were of advanced age, not exactly known. As Gintrac remarks, the first period of life is that which is most favorable to the occurrence of venous cerebral thrombosis, adoles- cence and adult age are a little less favorable, and old age is the least so of all. Sex seems to be of no predisposing power: of thirty-one cases in which the sex was stated, fifteen were males and sixteen females. Prognosis.—The elements for forming a prognosis being of a very indeterminate character, it is difficult to form an opinion relative to the probable result in the case of a person presenting the symptoms which have been mentioned. It is perhaps, however, warrantable to say that thrombosis of the cerebral veins or sinuses must from the very nature of the lesion be a most grave disorder, if not one necessarily fatal, sooner or later. If the vein or sinus in which the clot exists be small, and if the causes be of such a character as to admit of removal, and thus the extension of the coagulation be preventable, the prognosis would of course be more favorable than if an opposite state of affairs exists. After all, the only data from which a judgment can be formed are the severity of the symptoms and the course and duration of the 1 Op. et loc. cit., p. 528. 154 DISEASES OF THE BRAIN. disease. The symptoms themselves can be of little service in this respect, for, as we have seen, they have no such pathognomonic value as to indicate to us the pathological condition with which we have to deal. Diagnosis.—After the remarks already made incidentally with ref- erence to this point, there is nothing to say which can elucidate the subj ect. Morbid Anatomy and Pathology.—The ordinary seat of the affection under consideration, when not the result of some other contiguous lesion, is the superior longitudinal sinus ; when due to suppuration of the ear, the clot is usually first found in the lateral sinus ; when resulting from injury, it has a near topographical relation to the seat. Through the occlusion of the sinus it becomes distended on the distal side of the clot, and the blood is thus thrown back upon the capillaries and eventu- ally upon the arteries. A state of cerebral ischaemia is therefore in- duced, to which the symptoms of the first stage of the disease are, in the main, to be ascribed. This ischaemia may lead to extravasation of blood, to inflammation, or to softening. An increased effusion of serum into the sub-arachnoid space and into the ventricles is an almost neces- sary consequence. The clot differs in character according to its age. When recent, it is soft in consistence and almost black in color, and is not adherent to the walls of the sinus in which it is situated. When old, it is grayish, dense, and unresisting, and attached to the wall of the vessel. If it be divided, a soft, broken-down mass is often found occupying the centre. This consists of fat and other elements of the regressive metamorphosis which the substance of the thrombus has undergone. It was undoubtedly this matter which Abercrombie and other writers mistook for pus. Other points in the morbid anatomy and pathology of venous cere- bral thrombosis have been sufficiently considered in the remarks which have already been made. Treatment.—There are no means at present known to science by which the affection can be cured, or its consequences prevented. All that can be done is to treat the symptoms as they arise, to search for their cause, and to remove the latter if removal be possible. Life may, in some cases, be prolonged by the judicious use of quinine and stimu- lants. Convulsions may be lessened in force and frequency by the em- ployment of the bromides, and pain assuaged by hypodermic injections of morphia, by a pill containing half a grain of codeia, given at bed- time, and repeated if necessary, or by directly taking off a part of the intra-cranial vascular tension by leeches to the inside of the nostrils, or cups to the nape of the neck. The capillaries of the brain may be occluded either by embolism or thrombosis, as are the larger vessels. But the phenomena of these IV.—EMBOLISM AND THROMBOSIS OF THE CEREBRAL CAPILLARIES. PARTIAL CEREBRAL ANAEMIA, ETC. 155 lesions are so in definite and obscure that it is impossible, in the present state of our knowledge, to identify them during the lifetime of the sub- ject. There is, therefore, little to be said relative to partial cerebral anaemia resulting from obstruction of the blood in the capillaries, other than to call attention to the genesis, the morbid anatomy, and the pathology of tl e processes in question. It will, accordingly, be more convenient to consider the subject without subdivision into symptoms, causes, etc. Embolism of he cerebral capillaries may be the result of deposit of pigment, oifat of pus, or of the debris of various tissues, normal or abnormal, which have undergone decomposition. Pigment may be deposited in the capillaries whenever the blood— as it does in certain diseases—contains an abnormal amount of pig- mentary corpuscles. Meckel1 appears to have been the first to call attention to the condition in question. In the case of a lunatic, he dis- covered the spleen to be enlarged, and to be covered with dark pig- ment. Virchow2 soon afterward, in the case of a patient who had been subject to ague, found the spleen enlarged, black, from excess of pig- ment, and the blood in the heart to contain cells with pigment. Meckel attributed a great degree of importance to the occurrence of melanac- mia—as the blood-disease is called—for the reason that he considered the pigmentary obstruction of the capillaries a condition liable to result therefrom, and, as a consequence, when those of the brain are thus af- fected, the supervention of head-symptoms. Virchow, however, while admitting the possibility of such a sequence of phenomena, is not able to add any facts tending to elucidate the subject. Frerichs 3 has called attention to the pigment liver as associated with pigmentary emboli in the capillaries of the brain. Thus he says: “The next organ in point of frequency to the liver, which undergoes important organic and functional derangements, is the brain. Numer- ous particles of pigment, which have passed unarrested through the vessels of the liver and the lungs, accumulate in the narrow capillaries of this organ, and particularly in those of the cortical substance. Even by simple inspection of the shade of color, we can form an approximate notion of the quantity of coloring-matter which has been deposited, and of the extent of the vascular obstruction. We must not, however, rely entirely upon inspection, for slight accumulations of pigment in the capillaries easily escape notice, particularly when viewed with an un- practised eye, and can only be distinguished with the assistance of the microscope. In addition to the above, it is not at all uncommon for the vessels to become obstructed by a colorless fibrinous-like coagulum which of course does not affect the shade of color. The mechanical 1 Ally. Zeitschrift fur Psychiatric, 184'7, cited by Virchow. “ Die Cellular-Pathologic,” Berlin, 1871, p. 263, and Jaccoud, op. cit., p. 144. 2 Op. cit. 8 “Klmik der Leberkrankheiten,” Sydenham Society Translation, vol. i., p. 314. DISEASES OF THE BRAIN. interruption to the circulation which is produced in this way, not unfrequently gives rise to rupture of the small vessels, and the forma- tion of numerous capillary apoplexies. Meckel long ago made observa- tions of this nature. Planer described eight cases in which small ex • travasations were scattered through the gray and white substance of the brain. These numerous haemorrhages have not com e under my own observation ; but in two cases I have observed extravasation into the meninges.” Frerichs states that he has seen three cases in which there were functional derangements indicative of material changes in the cortical substance of the brain. One of them was that of a lady in her fortieth year, who, after an attack of quotidian fever, accompanied by somno- lence, suffered from protracted loss of memory. The functions of vege- tative life resumed their normal condition, and there were no derange- ments of motion or sensation present. The headache and giddiness gradually diminished after the removal of the intermittent fever, by means of quinine ; but the weakness of memory, ind the inability to .find suitable words for objects and ideas, were still on the increase two months after the cessation of the ague. Another case was that of a girl, aged nine years, living in the same district, where, according to the evidence of two medical men, intermit- tent fever, terminating fatally, was at the time very prevalent. This girl, whose mental powers had previously been normal, had undergone several attacks of tertian fever. After a protracted use of preparations of bark, she recovered in her bodily symptoms ; but her mental facul- ties gave way, and a state of complete idiocy, accompanied by a raven- ous appetite, supervened. In regard to these cases, Frerichs further remarks that it is un- certain whether atrophy of the brain had resulted from occlusion of the capillaries, or whether it had been induced by the extensive capillary apoplexies 'consequent upon this occlusion, or whether the intermittent fever was complicated with other accidental changes in the brain. He gives the details of several other cases of intermittent fever, accompa- nied by head-symptoms, and in which, after death, the cerebral capilla- ries—principally those of the cortical substance—were occluded by de- posits of pigment, originating in the liver and spleen, and transported to the brain by the current of the circulation. A case is reported by Bright,1 of a man, who died of paralysis fol- lowing fever, in whom the cortical substance of the brain was the color of black-lead. Sydenham had not failed to notice the fact that mental derange- ment sometimes remains after intermittent fever, which, if treated by depletion, passed into imbecility. Cases of like character have frequently come under my notice. In 1 “ Reports of Medical Cases,” London, 1801, chapter ci., plates xvii. and xix. PARTIAL CEREBRAL ANAEMIA, ETC. 157 one of these there had been repeated attacks of intermittent fever, and the spleen was greatly enlarged. The patient, a young man twenty- two years of age, had suffered from epilepsy for several months, the first paroxysm ensuing shortly after a severe seizure of fever, and being preceded by headache, vertigo, confusion of ideas, and twitching of the muscles of the face. When I first saw him his mind was considerably impaired, and he was having three and sometimes four or five epileptic fits every week. All his mental symptoms were improved by the use of arsenic; his fits ceased, and his spleen became much reduced in size. Those physicians who have practised in malarious regions can scarcely have failed to notice the fact that the enlarged livers and spleens, which are so frequently produced by repeated febrile attacks, are often coexistent with cerebral symptoms, such as have been de- scribed.1 The vessels of the cortical substance appear to be more liable to oc- clusion from pigmentary emboli than any other part of the brain. Some recent researches of my own would seem to show that the vessels of the retina are also apt to be so obstructed, and that some cases of pigmen- tary deposit in the eye are in reality instances of pigmentary embolism of the intra-ocular vessels. Although the symptoms of the affection in question have nothing characteristic about them, yet its existence may be suspected with some show of probability, when pain in the head, delirium, convulsions, ver- tigo, paralysis, and other disturbances of sensibility and motility, coexist with enlarged spleen or liver, and when there is the previous history of malarial fever. Embolism of the cerebral capillaries from migration of fat is a con- dition which certainly occurs, but which has not as yet been very thoroughly studied. Todd,2 in a woman who died comatose and hemi- plegic, found after death an extravasation of blood into the right corpus striatum, and that “ the vessels of the softened portion of the corpus striatum, immediately surrounding the clot, were thickly studded with oil-globules, which in some situations were aggregated into dark masses so large as here and there almost to fill up the vessels. The minutest capillaries, as well as the larger arteries, exhibited these deposits, and few could be discovered without them. Bergmann,3 who has devoted much attention to the subject of fat embolism, has recently 4 reported a case in which a man, who died in consequence of injuries received from a fall, was found to have many 1 A further consideration will be given to this very interesting subject in the forthcom ing memoir of the author, on “ Pigmentary Cerebral Embolism, and other Affections of the Nervous System the Results of Malarial Poisoning.” 3 “ Clinical Lectures,” London, 1861, p. 733. 3 “Zur Lehre von der Fettembolie.” Dorpat, 1863. 4 “Ein Fall tbdlicher Fettembolie.” Berliner klinische Wochenschrifl, No. 83, 1873, 158 DISEASES OF THE BRAIN. haemorrhagic extravasations into the lungs, and numerous oil-globules in the pulmonary capillaries. The brain does not appear to have been examined, but probably the cerebral capillaries would have been found in a like condition. In order to throw additional light on this subject, I have performed a number of experiments upon animals, of which the description of one will be sufficient, as the results were analogous in all essential respects. Into the left ventricle of the heart of a medium-sized dog sixty min- ims of olive oil were ipjected.1 The animal was killed six hours after- ward by section of the medulla oblongata. The brain was removed from the skull and carefully examined. The membranes were decidedly congested. The arteries of the base of the brain contained numerous oil- globules, and this was especially the case with both the middle cerebral Fig. 15. Fig. 14. arteries. The minute terminal branches ot these vessels were filled with fat, and several of them were entirely occluded. The microscope showed the capillaries throughout the brain, both of the cortical and medullary substance, to be gorged with fat-globules, aggregated in masses, so as to prevent, in many instances, the passage of the blood. In other experiments I allowed a longer time to elapse before kill- ing the animals, and in one death took place spontaneously during a state of profound coma. The post-mortem appearances were more strongly marked, and in the latter several centres of incipient softening had been set up. 1 The heart was penetrated through the thoracic wall by the needle of an hypodermic syringe, and the injection made very slowly. The left ventricle was chosen in order to avoid, as far as possible, the stoppage of the oil in the lungs. PARTIAL CEREBRAL ANEMIA, ETC. 159 Nothing is known relative to the symptomatology or pathology of fat-embolism of the cerebral capillaries, or of the elements of a correct diagnosis or prognosis of the affection. The cerebral capillaries may be obliterated, as Virchow1 has shown, by deposits of pus or of the debris of organic structures undergoing disintegration. Thus a thrombus undergoes such a transformation that a puriform mass originates in its centre through changes taking place in the central layers of the clot, and the whole eventually beeomes con- verted into a finely-granular substance which is capable of being trans- ported to distant parts of the body and occluding the smaller vessels and the capillaries; or, for instance, ulceration following endocarditis takes place in one of the cardiac valves, as a consequence of acute or chronic softening. The minute fragments of the valve are carried away by the current of the blood, and are deposited in the vessels of remote parts, such as the eyes, the brain, the kidney, and spleen. The accom- panying cuts (Figs. 14 and 15) represent these capillary emboli in the penicillii of the splenic artery, following endocarditis. In Fig. 14 the vessels are magnified ten diameters ; in Fig. 15 three hundred. Whether such emboli are capable or not of transferring specific dis- ease to other parts where they are deposited, or whether, as some authors, differing from Virchow, assert, they merely act in a mechanical manner, is as yet undetermined. The weight of evidence appears to favor the view of Virchow, that they act not only by occluding the capillaries, but also by their inherent specificity originating new centres of local disease. Theombosis.—Thrombosis of the cerebral capillaries may, like the same condition of the larger vessels, result from any cause capable of inducing a stoppage or retardation in them of the circulation of the blood. One of the most common of these factors is calcareous deposit, a state which is only to be detected after death, and which, like many other analogous morbid processes, was first clearly pointed out by Vir- chow.8 According to him it depends upon the failure of the kidneys to excrete the mineral matter which is taken up by the blood from the bones, and which in consequence is deposited in other organs. Some authors regard calcareous deposit as being a process more anal- ogous to embolism than to thrombosis, but it must be recollected that the mineral substance is not in a morphological state in the blood, but is held in solution up to the time of its separation at the places where it is found. It would, in my opinion, be equally logical to regard the deposition of fibrine upon the internal coat of a vessel as embolism, for it is held in solution till it becomes attached to the wall, and in this respect does not differ from the condition of the calcareous matter. 1 “Die Cellular-Pathologie,” Berlin, 1871, p. 237, et seq. * Op. cit., p. 252. DISEASES OF THE BRAIN. In the first place, the serum of the blood holding' the mineral sub- stance in solution is probably infiltrated through the vascular walls in- to the peri-vascular tissue and the deposition effected there. Eventual- ly, as the change in the surrounding substance tends to prevent further transudation, and as the vessels degenerate from their normal struct- ure, the metastatic deposit is made around their internal circumference and the channel is finally occluded. At the same time the capillaries lose their elasticity and become hard and brittle. The brain in the vicinity of these centres of morbid action may be so saturated with the calcareous matter as to give a distinct grating sound when cut, and the molecules of phosphate or carbonate of lime may even be seen with the naked eye and distinctly felt when a portion of the brain is rubbed be- tween the fingers. Marc6 1 reports the case of a man, fifty-five years of age, who died in a state of complete dementia. On post-mortem examination the mem- branes were found adherent to the brain; in the centrum ovale of both sides there existed large lacunae of a yellow color and with the appear- ance of elder-pith. In addition, there were numerous calcareous incrus- tations forming sharp protuberances and giving a sensation to the finger like that experienced when the tongue of a cat is gently rubbed. . The capillaries were likewise incrusted. The cerebral substance contained several old haemorrhagic foyers. The calcareous concretions were found to consist of crystallized carbonate of lime and of the same substance in globular masses. Subjected to the action of dilute hydrochloric acid, they were dissolved with the evolution of carbonic-acid gas; an organic substance analogous in its characteristics to the corpora amylacea re- mained; it was not, however, colored blue by iodine. The capillaries surrounding these masses had undergone various de- grees of calcareous incrustation. On some, the crystals were scattered here and there on the walls ; on others they formed groups or plaques, more or less enveloping the circumference of the vessel. There were some in which the channel was entirely obstructed by the colorless crys- tals, without any other foreign matter, fatty, granular, or pigmentary, being present. Thrombosis of the cerebral capillaries may also be the consequence of atheromatous degeneration and of moniliform dilatation. The white substance of the cerebrum, the cortical layer, and the cor- pora striata are more liable to be the seats of this process than the other parts of the encephalic mass. 1 “Bulletin de la socidte anatomique,” 1863, p. 468, cited by Gintrae, op. tit., p. 473. CEREBRAL SOFTENING. 161 CHAPTER VI. CEREBRAL SOFTENING As a consequence of several of the conditions described in the fore- going pages, and especially as resulting from thrombosis and embolism in their various forms, cerebral softening naturally comes next in order for consideration. Most authors treat of it in direct connection with obliteration of the cerebral arteries; but, although frequently due to this cause, it may be produced by others, and occlusion is not always followed by softening. For these reasons I have preferred to consider it as it really is, a distinct pathological condition—as much so as sclero- sis or any other morbid anatomical state. Symptoms.—When softening is the result of haemorrhage, of arterial embolism, or of arterial or venous thrombosis or embolism, the symp- toms peculiar to those affections are first met with. Thus there are troubles of the intelligence, the sensibility, and the power of motion, suclnas have already been described under the heads mentioned, and, if the morbid process goes on within the cranium to its full development, there are peculiar aggravations and the evolution of new symptoms. If coma has existed from the beginning, it may continue with little or no remission, and the patient may die without regaining consciousness, or may become only partially sensible. The condition of softening is not usually set up after either haemorrhage, thrombosis, or embolism, till about the tenth day, though some cases are more rapid in their progress, and the symptoms now to be mentioned are those which are coincident with what some pathologists have designated the “second stage;” the “yellow softening” of others. The “first stage,” or “red softening ” of these writers, is, in my opinion, not in reality softening, but rather the congestion due to overaction in the collateral circulation. In addition to the continued paralysis of motion and the loss of sensibility which exist on one side of the body, the mental symptoms become more strongly marked. There may be delirium with the occur- rence of hallucinations and delusions, though these are generally eva- nescent. Occasionally a fixed idea obtains possession of the patient’s mind, and for a while influences him in his conduct, but his mental tenacity is not strong enough to enable him to retain it for any length of time, so it soon yields to another. The intelligence is notably diminished, so that the patient is unable to conceive an exact idea of his situation, or to obtain a moderately complete notion of quite simple matters which may be submitted for his mental action. Thus he refuses to credit the assertion that he is ill, declares that his health, both in mind and body, is excellent, and that 162 DISEASES OF THE BRAIN-. he is fully capable of transacting his business or of performing any intellectual operation. The memory is invariably impaired, and things of the greatest familiarity are forgotten. Thus a patient laboring under cerebral softening, the result of embolism, could not tell his wife’s name, nor by what means he came to my office. Another, sent to me by Dr. Michel, of St. Louis, in whom thrombosis was the probable cause, could not tell me where he came from, nor the names of his children. He insisted with great vehemence that he was perfectly able to at- tend to his ordinary business, and yet was unable to add three numer- als together. In another case, likewise having the clinical history of thrombo- sis, which I saw in consultation with my friend Dr. J. W. Ranney, of this city, the patient, a gentleman about sixty years old, could not tell his age ; declared that Dr. Ranney, whom he bad known for many years, was a grocer, “who lived around the corner”; and held to the delusion that his sons had made several forcible attempts to rob him. The power of giving the attention to subjects is very greatly less- ened. The patient may seem to be listening to what is said, or observ- ing what is passing about him, but, if he be questioned he at once shows that he really has not been heeding ; even when things are for- cibly brought to his mind, and he is told to mark them, he is incapable of doing so to any considerable extent. The speech is almost invariably affected either in the form consti- tuting aphasia, or from paralysis of the tongue and other muscles con- cerned in articulation. There is a disposition to misplace words, or to clip them by cutting off the last syllable. Thus a patient reading the title of a book in my library called it the “ Unit. Stat. Dispenst.” for United States Dispensatory; another was the “Philosoph. as Absol. Scien.” for Philosophy as Absolute Science; and he told me he was “a lawy. by professi.,” when he meant to say he was a lawyer by profes- sion. The same fault is shown in reading from a printed page, and in writing. Only a few days ago I received a letter from a gentleman, in which the final letter of nearly every word was omitted. The emotions, especially those of a sorrowful character, are very easily excited, and therefore the least untoward event causes the exhibition of feeling. Sometimes the patient sheds tears without being able to assign any cause, or may get into uncontrollable fits of weeping; occasionally of laughing. All these symptoms indicate failure of the mental power, but it is, nevertheless, true that softening of the cerebral tissue may exist with- out the manifestation of the least degree of imbecility. It not unfre- quently happens that, while there is a general loss of intelligence, some one or two faculties of the mind are notably increased in vigor. CEREBRAL SOFTENING. 163 I have a patient now under my charge whose intellectual force is greatly reduced, who cannot pronounce the simplest sentence correctly, who is paralyzed throughout the whole of one side, and who has so lost the sense of propriety that if he feels the desire to urinate he yields to it at once, no matter where he may be or who are present, but whose volitional power is even greater than before the accession of his disease. Thus he will read volume after volume, turning over the pages regu- larly, and scarcely, except by oversight, skipping a word, although it is very certain he does not comprehend a tenth part of what he reads, and that what he does for a moment understand is immediately for- gotten. The strength of his will is also shown in the impossibility of inducing him to do any thing which either caprice or habit prompts him not to do. His appreciation of harmony has become so sensitive that a discord of sounds made on the piano causes him real mental suffering, whereas when he was in health his musical taste and discrimination of the pitch and quality of sounds were below mediocrity. Drowsiness is very generally present; at first, perhaps, to a slight extent, but sooner or later as a prominent feature. Headache is very common, and is usually dull and circumscribed. The forehead is its most common seat. Other sensations in the head, such as vertigo, full- ness, weight, and constriction, are scarcely ever absent. Gradually, the condition of the patient, mentally and physically, becomes weaker and weaker, and death ensues, immediately preceded by coma, convulsions, delirium, or a combination of these phenomena. Not unfrequently, softening of the brain is not preceded by haem- orrhage, thrombosis, embolism, or other evident affection, but begins obscurely, and advances very gradually. Such cases are often directly due to disease and obliteration of the cerebral capillaries, as described in the immediately preceding chapter, or they may be the result of a slow inflammatory process. In this form the symptoms make their ap- pearance in succession; but the paralysis, instead of being present from the inception, comes on very slowly, commencing as a slight weakness, conjoined with numbness, in one or more of the extremities, or in the face. Ordinarily, the first evidence of paresis is discovered in the leg, which is not lifted clear of the ground. The toe consequently strikes against the inequalities of the pavement, and the patient is apt to fall. Sometimes the weakness is shown by the leg suddenly giving way at the knee. I have had several patients with cerebral softening, in whom this accident was of common occurrence, and who had thereby received severe injuries. Or, when the arm is the paretic member, the grasp, as shown by the dynamometer, is materially lessened in strength, and things held in the hand are dropped. I have now a patient in charge in whom the affection is in its very earliest stages, and of which the only manifestations are, clipping of the words in speech and paresis of one arm. 164 DISEASES OF TIIE BRAIN. This inability of the muscles to maintain a continuous contraction for a short time, though met with in several other affections, is to some extent characteristic of cerebral softening, and, in conjunction with the other phenomena, is a valuable indication. Even before it has become so far developed as to attract the attention of the patient or those about him, its existence may be ascertained by means of the dynamometer described in the preliminary chapter of this treatise. The paralysis usually goes on to complete loss of power, though its progress is often very slow, and is marked occasionally by periods of decided improvement. At these times the patient’s friends imagine that he is about to recover, and if, as is sometimes the case, the mental symptoms are likewise mitigated, their hopes are still further exalted. It is necessary that the physician should not be deceived. In a case which I saw in consultation with Dr. Chamberlain, of this city, I diag* nosticated chronic softening. At the time, there were feebleness of memory, paresis of one side of the body, and difficulties of speech. I gave an unfavorable prognosis, but soon afterward amendment began, and the patient, who was an insurance agent or appraiser, resumed his business to some extent. I nevertheless adhered to my opinion, for I had seen too many cases of similar character to be deceived in so clear a one as this. I never saw the patient again, and am therefore unac- quainted with the subsequent phenomena, except that about a year afterward I was invited by Dr. Chamberlain to be present at the post- mortem examination. His brain contained a foyer of softened tissue as large as a walnut, apparently the result of obliteration of the posterior branch of the left middle cerebral artery, and involving a portion of the middle lobe of the left hemisphere. In another case, which I had very thorough opportunity for study- ing, the patient, a gentleman thirty-five years of age, was the subject of chronic softening, without any history of previous lesions. The dis- ease had come on very insidiously, first showing itself by a slight im- pediment of speech and impairment of memory. Gradually he lost power in both arms and both legs, though the right side was more affected than the left. His gait became titubating, and although he never lost the ability to walk, yet he did so with great and increasing difficulty. But his stages of apparent improvement were at first nu- merous and well marked. His memory at such times was stronger, his countenance brighter, his articulation distinct, his emotions more under command, his power of attention increased, his intelligence equal to all ordinary occasions, and his walk free from any sign of debility. Then all these steps would be suddenly lost, and he would again become imbecile and weak. Finally, a severe convulsion, more evident on the right side than the left, supervened one evening after dinner, as he was quietly smoking a cigar. Between seven and twelve o’clock that night he had over a hundred fits. He died at the latter hour. The post- CEREBRAL SOFTENING. 165 mortem examination revealed the existence of a large centre of soft- ening, involving the middle lobe of the left hemisphere. Sometimes the course of the disease is still more irregular. No evidence of cerebral disorder is perceived beyond aphasia, and the patient remains in the full possession of his intellect, and without pa- ralysis, up to a short time before death. Durand-Fardel1 cites the case of a man, thirty years of age, who entered the Hotel Dieu, presenting all the signs of pulmonary phthisis. In a few days afterward he expe- rienced difficulty of articulation, in thirty hours he became comatose, and, in twenty more, died. The post-mortem examination revealed the existence of softening of the inferior surface of the left middle lobe of the cerebrum. Although it is not so stated—Durand-Fardel hav- ing written previous to Virchow’s observations—there is little doubt that the cause of the softening was an old embolus in the left middle cerebral artery. Lallemand,1 in his first letter, cites several cases in which the dis- ease was marked by singular symptoms, such as convulsions, contrac- tions, and delirium. In a case which I saw in consultation with Prof. C. A. Budd and Dr. J. T. Taylor, occurring in a gentleman about thirty-five years of age, there were coma and violent hemi-convulsions, evidently due to softening from embolism, of which there had been two attacks, the last several weeks previously. Death ensued, but no post-mortem ex- amination was, I believe, obtained. A gentleman is now under my charge who has valvular disease on the left side of the heart, the consequence of rheumatic endocarditis, and who, six months since, had an apoplectic attack conjoined with aphasia and right hemiplegia. He soon became able to speak pretty well, and regained power and sensibility to a great extent in the para- lyzed limbs. During the past two weeks, however, he has exhibited symptoms of mental derangement, as shown by the existence of hal- lucinations and delusions, and is gradually losing the power of motion and of sensation on the right side. His speech is as perfect as it ever was, and there is yet no sign of dementia. It has happened that individuals have died who, on post-mortem examination, were found to have softening of the brain, but who, during life, had exhibited no symptoms of this or any other cerebral disorder. Rostan, who was the first to write systematically on the disease, refers to such cases, and Durand-Fardel is still more explicit. The latter says : “We meet with softening of the brain in persons who, up to the time of death, had presented no appreciable derangement of the cere- 1 “ Traite du ramollissement cerebrale,” Paris, 1843. 2 “ Recherches anatomico-pathologiques sur l’encdphale et ses dependanees,” Paris, 1824. DISEASES OF THE BRAIN. bral functions, and in whom softening has been developed without having given any evidence whatever of its existence.” In such in- stances the white matter of the hemisphere can alone be involved. One such case verified by post-morten examination has occurred within my own experience. The patient, a soldier of the Second United States Infantry, died at Fort Riley, in Kansas, of which post I was medical officer, of chronic dysentery, the result of exposure. There were no mental symptoms, no difficulty of speech, no paralysis; nothing, in fact, indicating the existence of brain-disease. He died in full pos- session of his intellectual faculties. The post-mortem examination re- vealed the existence of ulceration of the small intestines, and, as the cause of death was very evident, the brain was not examined. I re- served it, however, for purposes of study, and, on making a section of the right hemisphere an hour afterward, discovered an encysted centre of softening, including more than two-thirds of the posterior lobe. The right posterior cerebral artery was entirely obliterated by thrombosis. The man had been at the fort several months, and had never made complaint of any illness till he was attacked with dysentery six weeks before. The duration of cerebral softening is very variable. Rostan found it to range from a few days to several years. Andral, from an analysis of one hundred and five cases, found that the period was from twelve days to three years. The most rapid case occurring in my experience terminated in death at the end of eighty hours. Some confusion on this point has arisen from the fact that some authors regard embolism and thrombosis as essentially identical with softening, a doctrine which is clearly erroneous, as, in many cases of these affections, recovery or death may take place without the stage of softening being reached. In the case above referred to, post-mortem examination showed that the condition known as yellow softening was just making its appear- ance. As I have already stated, I cannot regard the alteration called by some pathologists red softening any thing more than the congestion due to the active collateral circulation. The case of longest duration, of which I have any personal knowl- edge, was that of an eminent scientific gentleman, who had suffered from the symptoms of softening of the brain for nearly four years, when he died. There was no post-mortem examination, but the history of the case was that of thrombosis of the left middle cerebral artery, and the course of the disease left no room for doubt as to its nature. The symptoms of cerebral softening which I have specified are those which are in general the result of the morbid processes existing in the cortical substance of the hemispheres, or in the optic thalami, or corpora striata. Generally, as Laborde 1 has shown, whenever the cortr 1 “ Le ramollissement et la congestion du cerveau principalement consid6res chez le rieillard,” Paris, 1866, p. 1, et &eq. CEREBRAL SOFTENING. 167 cal substance is the seat of softening1 there is at least one other centre occupying the central part of the brain, or especially the corpus stria- tum or optic thalamus. But the other portions of the encephalic mass are liable to be similarly affected, and then the phenomena are of a dif- ferent character. Thus the pons Varolii may undergo softening from occlusion of the basilar artery, or of one or more of its transverse branches, or from disease of its capillaries, or from chronic inflammation of its substance, and if the disease be limited to this ganglion there is no marked mental deteriora- tion or other evidence of intellectual derangement. The symptoms are in the main connected with sensibility, and the power of motion with ar- ticulation, and with the respiratory, circulatory, and stomachal functions, as evidenced by dyspnoea, irregular action of the heart, and nausea and vomiting. In the case of an elderly gentleman whom I saw in the early part of 1874, and who had been affected for about a year, there was almost complete paralysis of the lower part of the face on both sides, there was great difficulty of swallowing, the tongue could not be pro- truded, speech was very indistinct, the respiration and action of the heart were irregular, and the limbs were partially paralyzed. There was a general loss of sensibility throughout the whole body, and attacks of vertigo and epileptiform convulsions had been frequent. At the same time the intellect was as clear and exact in its operations as it ever had been. I diagnosticated glosso-labio-laryngeal paralysis, and expressed the opinion that the patient would not live over a month. He died in two weeks. The post-mortem examination showed the hemispheres and cerebellum and the membranes to be healthy. The basilar artery was entirely closed by a thrombus. The pons Yarolii was as soft as cream, and the membranes peeled off as easily as if they had never been at- tached to it. Examined microscopically after due preparation, the cap- illaries were found to be in a state of atheromatous degeneration. The medulla oblongata was not softened, but extreme atrophy of nerve-cells had taken place in the nuclei of the facial nerve of both sides. This point will be further considered under the head of atrophy of nerve-cells. Softening of the cerebellum can scarcely, in the present state of our knowledge, be diagnosticated from any other affection of that organ. The rapid form, such as results from embolism of the larger vessels, pre- sents so many analogies with haemorrhage that there are no sure signs by which a discrimination can be made; and the slow form due to disease of the capillaries or to chronic inflammation is not distinguished from abscess or tumor. But it may be inferred that the cerebellum is the seat of structural change when the category of symptoms cited under the head of cerebral hiemorrhage is preseat, and the history of the case will often aid us in forming an opinion of its nature not very wide of the mark. When death results from cerebral softening, it may be directly due 168 DISEASES OF THE BRAIN. either to the disease itself, or to some intercurrent affection. Thus the patient may die from pure exhaustion or from slow asphyxia caused by the imperfect action of the respiratory function, or he may choke to death either by being unable to swallow food which he has taken into his mouth, or by the regurgitation of the contents of the stomach during a convulsion, or a severe convulsive seizure may cause immediate as phyxia, or a series of convulsions may produce a more gradual asphyxia, or he may die in a state of profound coma. The intercurrent affections may be either meningitis or hypostatic congestion of the lungs from long confinement to the recumbent pos- ture, or diarrhoea, or a fresh attack of thrombosis or embolism. Causes.—The etiology of cerebral softening has already been con- sidered to some extent under the heads of cerebral haemorrhage, and obliteration of cerebral arteries and veins and of the capillaries, from embolism and thrombosis, of which conditions it is so often a sequence; but, as it may occur without having been preceded by either of these or other noticeable affections, a few additional observations are necessary. Age is certainly a strong predisposing, if not an actual exciting cause, although the disease is observed at all periods of life. Rostan, whose cases were collected at the Salpetriere, a hospital containing only old women, found that there were ten cases in persons between the ages of sixty and sixty-nine, twenty between seventy and seventy-nine, and ten between eighty and eighty-seven. Andral, excluding cases occur- ring in infants, found that, of one hundred and fifty-three cases, there were between the ages of 15 and 20 10 20 “ 30 18 30 “ 40 11 40 “ 50 19 50 “ 60 27 60 “ 70 34 70 “ 80 30 80 “ 89 4 Durand-Fardel, from an analysis of fifty-five cases, found between the ages of 30 and 40 3 40 “ 50 8 50 “ 65 2 60 “ 70 14 70 “ 80 23 80 “ 87 5 The period of life, therefore, at which softening is most apt to occur, is from the age of fifty to eighty. During the past ten years, forty-five cases of cerebral softening, not CEREBRAL SOFTENING. 169 the result either of haemorrhage, arterial embolism, or of arterial or ve- nous thrombosis, have been under my care or been seen by me in consulta- tion. Of these, one was under twenty years of age; four were between twenty and thirty years; nine between thirty and forty; twelve between forty and fifty; eight between fifty and sixty; eight between sixty and seventy; and three between seventy and eighty. The general results, therefore, go to show the greater proclivity which advanced age gives to the occurrence of the disease. In one of those between seventy and eighty, the mind was scarcely impaired till about two months before death, though there had been paresis, headache, and aphasia, for two years. No definite statistics have been collected relative to the influence of sex, although the opinion appears to prevail that the affection is more liable to occur in females than in males. Of the forty-five cases just cited, twenty-nine were males and sixteen females. The season of the year does not appear to exercise much influence. Durand-Fardel, from sixty-three cases, found that seventeen occurred in winter, thirteen in spring, twenty in summer, and thirteen in autumn. I have found it difficult in many cases, from the insidious or latent charac- ter of the early symptoms, to fix the period of beginning with accuracy. Intense and long-continued intellectual exertion is one of the most common causes of cerebral softening. Eleven of the cases occurring in my experience were clearly the result of this cause. Severe and pro- tracted emotional disturbance was apparently the cause in four cases. Eostan, among the causes, cites insolation, the action of intense cold, blows upon the head, and excessive use of alcoholic liquors. The influence of obliteration of the cerebral arteries, sinuses, veins, and capillaries, in producing partial cerebral anaemia, and hence as lead- ing to the supervention of softening, has already been dwelt upon at suf- ficient length. Diagnosis.—The history of haemorrhage, thrombosis, or embolism, when these conditions have either of them given rise to softening, will aid in the diagnosis. The signs which serve to distinguish these affec- tions from others have already been amply considered. When there is no such previous clinical history, softening of the brain may be confounded with chronic meningitis, meningeal haemor- rhage, or tumors. From chronic meningitis it is to be distinguished in many cases by the facts that in the former the headache is generally diffused, while in softening it is fixed, that the paralysis is more limited, that there are frequent spasms of the limbs, that there are well-marked febrile exacerbations, and that there is not the progressive enfeeble- ment of the intellect so characteristic of the vast majority of cases of cerebral softening. At the same time it must be admitted that the diag- nosis sometimes cannot be clearly made out. In meningeal haemorrhage coma occurs as an early symptom, gradu- 170 DISEASES OE THE BRAIN. ally increasing1 in intensity, whereas in softening it comes on at a late period. Hmmatoma of the dura mater, however, may readily be con- founded with softening. The history of the case will aid in the forma- tion of a correct diagnosis. In tumors the most prominent symptoms are pain and convulsions, while the intellect usually remains unaffected. The pain is exceedingly intense, while in softening it is dull. The speech in tumors is generally unaffected. Prognosis.—Cerebral softening in general ends in death. Neverthe- less, it is not altogether hopeless. If the patient be young, of good constitution, and of temperate habits ; if the centre of softening be small, and not involving the more important parts of the brain, there is some encouragement to expect a favorable termination. Some of the cases cited in this chapter go to show that recovery is possible, and I have certainly seen others with the ordinary initial symptoms of cere- bral softening recover with appropriate medication. Such patients, however, were all under the age of forty, and were of good constitution and habits. In softening due to embolism, and occurring after rheuma- tism and endocarditis, the liability to future attacks must not be over- looked. I have seen as many as six attacks of embolism occurring in the same patient, and yet no morbid condition beyond that of anaemia set up, and again cases in which a single embolus has caused softening and death. Morbid Anatomy.—In the softening of the brain which results from the obliteration of arteries or veins by embolism or thrombosis, the first stage after that of congestion from the excessive action of the collateral circulation is what is called yellow softening. This is not, as some authors have supposed, produced by the infiltration of pus into the cerebral substance, but is caused by regressive metamorphosis of the brain-cells into fat, the granules of which are mixed with the coloring matter of the blood which gives rise to the peculiar yellow color. The white corpuscles of the blood also undergo degeneration into fat. These altered white corpuscles were described by Gluge 1 as inflam- mation corpuscles, under the idea that softening was always the result of inflammation. Laborde,2 who has studied this subject with great success, shows, however, very conclusively that the transformation is a true degeneration, a part of the fat-corpuscles being derived, as stated above, from the nervous fibres, the cylinders of which disappear, the contents being extravasated, and with the myeline being converted into fat; and another part consisting of altered white blood-corpuscles. At this time the cerebral tissue is pulpy, constituting a centre of softening or a foyer, the consistence of which is greater at the circumference than at the centre. Tiie blood-vessels passing through the disorganized por- 1 “ Atlas of Pathological Histology.” Translated by Leidy. Philadelphia, 1853. 1 Op. cit. CEREBRAL SOFTENING. 171 tion are easily separated from the perivascular tissue and are covered with oil-globules. The second stage is designated white softening, and in it the brain- substance loses altogether its morphological characteristics, and appears as a white, cream-like matter so soft that a weak stream of water, al- lowed to impinge upon it, washes it away. In this semi-liquid matter, whitish flakes of denser tissue are suspended. Microscopical examina- tion shows that all traces of nervous structure have disappeared, and that no anatomical elements remain except oil-globules and organic cor- puscles somewhat resembling leucocytes. When the morbid process involves the cortical substance of the cerebrum, the convolutions undergo a peculiar kind of transformation first pointed out by Cruveilhier, and then by Durand-Fardel1 as occur- ring in the senile form of softening. This is characterized by the formation of yellow plates, irregular in form, soft to the touch, but yet sufficiently dense to resist the action of a thin stream of water. Microscopically they are seen to consist of nucleated fibres, fat-corpuscles, fat-globules, and degenerated capillaries, with blood-crystals and granular matter. Essentially, therefore, they are formed of connective tissue. The degenerated nerve-tissues, constituting a focus of softening, may undergo absorption. In such a case, a cicatrix, similar in general characteristics to that resulting from the curative process of haemorrhage, remains. In the softening resulting from inflammation, a somewhat different set of morbid appearances exists. Thrombosis and embolism produce a true death of the parts previously supplied by the occluded vessels, a ne- crobiosis, as it has been called by Virchow. The process is accompanied, as we have seen, by degeneration of the nervous tissue, but in the soft- ening due to inflammation new formations result. Sometimes the two coexist, but the latter is occasionally an entirely independent action. When such is the case, connective tissue is generated, and the ner- vous substance is rapidly broken down. An exudation of an albumi- nous fluid containing fine granules, the disintegrating nervous substance and numerous flakes of coagulated fibrine, takes place, and with blood- corpuscles causes the centre of softening to present the appearance of a reddish pultaceous mass, easily washed away by the action of a weak stream of water. With age the color of this softened tissue becomes brown or yellow. Sometimes, when the inflammation has extended to the deeper parts of the cerebrum, the contents of the cyst are pene- trated by the new connective tissue. The pulpy mass undergoes partial absorption, and is replaced by a white turbid liquid, called by Cruveil- hier and Dechambre “ milk of lime” (lait de chaux). Durand-Fardel designates this form of softening “ cellular infiltration.” 1 “ Maladies des vieillards,” Paris, 1854, p. 72. 172 DISEASES OF THE BRAIN. The softening resulting from occlusion of the capillaries, a condition not recognizable during life, does not differ essentially, except in its situation, from that which follows embolism or thrombosis of the larger vessels. The centres of the process are, however, smaller, are generally numerous, and usually met with either in the cortical or white sub- stance, or in the corpora striata. The morbid anatomy of the affected vessels has been sufficiently considered in the previous chapter. When disease of the capillaries has been the cause of the softening, these may be ruptured, and we meet with minute extravasations of blood in the disintegrated perivascular tissue, constituting the “ capillary haemorrhage ” of Cruveilhier. Pathology.—The first definite accounts of cerebral softening were given by Lallemand 1 and Rostan,3 both of whom published their works in the same year, 1820. In the very beginning of his first letter, Lallemand awards to MM. Recamier, Bayle, and Cayot, the credit of describing the condition under consideration, and of giving it the designation by which it is so general- ly known, even out of France, of ramollissement. Lallemand then pro- ceeds to define the term by saying that, by ramollissement of the brain, he understands a kind of liquefaction of a part of its substance, the re- mainder preserving its ordinary consistence. He then quotes cases from Morgagni and Abercrombie, and cites others from his own experi- ence; and then concludes by declaring that he does not hesitate to range cerebral softening among the inflammations, in which opinion he is supported by Abercrombie.3 Rostan 4 regarded the disease as some- times being due to inflammation, and sometimes to degeneration of the blood-vessels. Bouillaud 6 viewed it as an anatomical feature of inflam- mation. Cruveilhier6 considered what he called red softening as result- ing from the capillary haemorrhage previously mentioned, and that other forms were certainly due to inflammation. Andral7 recognized the fact that softening might result from inflam- mation or capillary haemorrhage, but he also insisted that it might be due to special alterations of nutrition, caused by different morbid influ- ences, such as obliteration of the arteries supplying the brain, or im- poverishment of the blood. MM. de la Berge and Monneret8 adopted in part the views of Ros- tan relative to degeneration of the cerebral vessels as a cause of soften- 1 “ Recherches anatomico-pathologiques sur l’enccphale,” Paris, 1820. 2 “Recherches sur le ramollissement du cerveau,” Paris, 1820. My references to Rostan’s work are to the second edition, of 1823. 3 Op. cit., p. 205. 4 Op. cit., chapter vii. 6 “ Traite de l’encephalite,” Paris, 1825. 6 Art. “ Apoplexie,” in “ Dictionnaire de medecine et de chirurgie pratiques.” T “ Clinique medicale.” s “Compendium de medecine pratique.” CEREBRAL SOFTENING. 173 mg. Carswell1 regarded softening occurring during life as being af- fected by these circumstances—inflammation, obliteration of arteries, and modification of nutrition. Fuchs2 appears to think that inflammation is not a necessary ante- cedent, but that congestion is. He also admits obstruction of the arteries at the base of the brain to be a cause. The studies of Durand-Fardel3 have been very thorough, and have contributed greatly to our knowledge of cerebral softening. According to him, the affection is an inflammation which does not differ essentially from other inflammations occurring in the young or old. White soften- ing he regards as the chronic form of the disease. Other pathologists published the results of their observations and generally to the same effect as those which have been quoted, viz., that cerebral softening was an inflammatory process, and sometimes one re- sulting from obliteration or disease of the arteries. A few, however, held to the view of Lallemand and Durand-Fardel, that inflammation was always the starting-point. In 1847 Virchow published his observations relative to embolism, and the partial cerebral anaemia produced by occlusion of an artery thus be- came a recognized fact. In reality, it came to be regarded as the only cause capable of giving rise to softening, and many pathologists of the present day entertain such an opinion. But I think this is carrying the theory further than facts will warrant. I cannot altogether disregard the researches of Durand-Fardel,4 Calmeil,6 Rokitansky,6 Wedl,T and others, and although I cannot agree that all cerebral softening is a con- sequence of inflammation, I am very sure it has this and other causes besides thrombosis and embolism. Calmeil’s work is a monument of careful observations and scientific deductions, and his fifth chapter (tome ii.), entitled “ Du ramollissement ckr'cbrdl local aigu, ou de Venctpha- lite locale aigue sans caillots sanguins si'egeant sous la forme dhm foyer ou des plusieurs foyers circonserifs, soil a la surface, soit dans la pro- fondeur de la masse enckphaliquef contains cases which are amply sufficient to establish the point for which he contends. He shows, too, in other chapters of his treatise, that softening results about the periph- ery of clots due to cerebral haemorrhage. The weak feature of Calmeil’s otherwise very complete work is, that he altogether ignores Virchow, and those after him, who have confirmed his facts and theories. 1 Art. “ Softening of Organs,” in “ Cyclopaedia of Practical Medicine,” vol. iv., p. 176, American edition. 2 “ Beobachtungen und Bemerkungen iiber Gehirnerweicliung,” Leipzig, 1838. 3 “ Traits du ramollissement du cerveau,” Paris, 1843. 4 “Maladies des vieillards,” Paris, 1854. 6 “ Traite des maladies inflammatoires du cerveau,” Paris, 1859. 6 “ Pathological Anatomy,” Sydenham Society translation, 1850. ’ “Rudiments of Pathological Histology,” Sydenham Society translation, 1855. 174 DISEASES OF THE BKAIN. Soulier,1 on the other hand, can see in softening nothing of the nature of inflammation. For him it is always a necrobiosis, produced by the cessation of the physiological action of the blood, obliteration by embolus or thrombus, by diminution of the calibre of the vessels, or oc- clusion resulting from atheroma or obstruction of a vein or sinus. He admits that the obliteration of an artery may cause congestion behind the point of obstruction, by which the coagulation and capillary hemor- rhage of acute softening—the capillary apoplexy of Cruveilhier—are to be explained. This red ramollissement has, however, nothing of the nature of inflammation about it. The only points in which I differ with Soulier are, that I cannot regard softening as being solely due to occlusion of blood-vessels, and that I am very sure the congestion which follows thrombosis or embo- lism is not necessarily the first stage of softening. There is no more reason why partial cerebral anaemia should always result in softening, than that ligation of the femoral artery should always lead to gangrene of the parts below. Obstruction of veins and sinuses in the brain may be followed by softening. The clot is usually the result of injuries or disease of the cranial bones or cerebral membranes, especially the dura mater. It may also be caused by certain cachectic conditions in which the blood is deteriorated in quality, such as typhus and typhoid fevers and cholera. Four cases, in which this latter affection was followed by thrombo- sis of the superior longitudinal sinuses, with consecutive softening, have come under my observation. In two of them there were also thrombi in both femoral veins. The upper surfaces of both hemispheres were the seats of the softening, which involved the gray matter only. Thrombosis of the veins or sinuses may also in general terms be produced by whatever cause is capable of retarding the current of blood. Mr. Toynbee,2 in his chapter on diseases of the mastoid cells, has brought forward several cases in which the lateral sinus was occluded by coagula, and in which there was cerebral softening. Cerebral softening may also result from the formation of adven- titious growths, or from the presence of foreign bodies in the brain. In such cases the process begins with inflammation, and is similar to the action which sometimes goes on around an extravasation of blood. Acute cerebritis or meningitis may likewise result in softening. This fact is admitted by Drs. Russell Reynolds and Bastian, in their admirable essays on cerebritis and softening of the brain, though with evident reluctance. We see, therefore, that cerebral softening may be caused either by annemia or inflammation, and that it is of two kinds, inflammatory and 1 Journal de medecine de Lyon, Fevricr, 1867. * “Tue Diseases of the Ear, their Nature, Diagnosis, and Treatment,” London, 1860. CEREBRAL SOFTENING. 175 non-inflammatory. The seat of the softening may be in any part of the brain, although some regions are more liable than others. When due to thrombosis, there appears to be no predilection for any particular location, but, as embolism is generally found on the left side in the middle cerebral artery, the parts of the brain supplied by this vessel are more liable than the corresponding parts of the right side. Durand-Fardel, however, did not arrive at this conclusion. Of one hundred and sixty-nine cases of softening, he found the left hemisphere the seat in sixty-nine, the right in seventy-one, both in twenty-six, and the middle line in three. The gray matter is generally supposed to be more frequently the seat of softening than the white. It is true that, of thirty-three cases of acute softening observed by Durand-Fardel,1 the convolutions were involved in thirty-one, but in nine only were they the sole part af- fected. In fifty-three cases which the same author collected from the writ- ings of Rostan, Lallemand, and others, the centres of softening were found to be as stated in the following table. Occasionally more than me region was involved. Convolutions and white substance 22 Convolutions alone 6 White substance alone 5 Corpus striatum and optic thalamus 6 Corpus striatum alone 11 Optic thalamus alone 4 Pons Varolii 3 Crux cerebri 1 Corpus callosum 1 Walls of the ventricles (septum) 1 Fornix 1 Cerebellum 1 Rostan, on the other hand, found the corpora striata and the optic tnalami to be the parts most frequently affected, and after these the central part of the hemispheres. He met with but few cases involving the median line. As regards the frequency with which the convolutions with the white substance were involved, as compared with the motor tract, he found that, of one hundred and seventy-seven cases of acute and chronic softening, the convolutions and white substance were affected in one hundred and nineteen, and the corpora striata and optic thalami in fifty eight. The middle lobe is more liable than any other, as is seen in the fol- lowing statement of Durand-Fardel, based upon an analysis of ninety- five cas^s: 1 “Trait6 du ramollissement du cerveau,” Paris, 1843. 176 DISEASES OF THE BKAIK Posterior lobe 18 Middle 61 Anterior 13 Posterior and middle 7 Posterior and anterior 2 Middle and anterior 2 Whole convexity of hemisphere 1 Middle line 1 Tn more than one-half of the cases, therefore, the middle lobe was the seat of the disease. A question connected with the pathology of cerebral softening, as with haemorrhage, is, “ Can we determine, from a consideration of the symptoms, what part of the brain is the seat of the lesion ? ” The answer must be the same. We can do so with some approach to ac- curacy, but, till we are better acquainted with the physiology of the different ganglia composing the brain, we cannot expect to do so with absolute certainty. Indeed, owing to the greater extent of tissue in- volved, compared to that affected in haemorrhage, we have a more com- plicated .set of phenomena to deal with. I have nothing further to add to the remarks made on a similar point, under the head of cerebral haemorrhage. Treatment.—The treatment proper for cerebral softening should de- pend very much upon the cause from which it has arisen, and must more or less be directed against the symptoms which are manifested. Thus, if there is reason to suspect the existence of thrombosis or embo- lism, and a consequent anaemic condition of a portion of the brain, the judicious use of stimulants and tonics is advisable, wrhile the body should be kept warm by additional clothing, or the application of artificial heat—at the same time the recumbent posture should be assumed, and the head supported on a low pillow. Mental exertion should, of course, be absolutely interdicted. If there be much headache, it is probably due to too great an activity of the collateral circulation, and in such a case some one of the bromides may be given in large doses, repeated as often as may be necessary. I have frequently seen great relief follow their administration. Delirium is often due to a like cause and may be similarly treated. Dr. Reynolds 1 speaks highly of the Indian hemp in doses of a quarter to half a grain of the extract; but I have found the bromide of potas- sium, in doses of thirty grains every three or four hours, more effica- cious. It is also the most beneficial remedy in the convulsions which frequently precede a fatal termination. In that form of softening which is obscure in its origin and gradual in its progress, there is a little more hope of a favorable result, though even here it must be confessed that treatment is not often effectual. 1 Article, “ Softening of the Brain,” in “ System of Medicine,” vol. ii. CEREBRAL SOFTENING. 177 Still, as I have said, when speaking of the prognosis, there are un- doubtedly cases in which recovery has taken place, and I am very sure that I have several times succeeded in curing individuals who, so far as I have been able to judge, were affected with cerebral softening. As these cases are interesting in themselves, and as the histories will show the means of treatment employed, I do not hesitate to transcribe the fol- lowing typical ones from my case-book: I.—Mr. R., a gentleman, twenty-four years of age, awoke one morn ing about the middle of March, 1870, with a sensation of numbness ex tending through the whole of the left arm and leg, and with a feeling of vertigo which was insupportable when he arose from the bed. He sat down in a chair, and while in this position was conscious of a buzz- ing sound in the right ear. In the course of half an hour the vertigo passed off, but the numbness and sound in the ear remained, and he oc- casionally saw double. In a few days afterward he noticed a slight difficulty of articulation, owing to apparent thickness of the tongue, and about the same time observed that in the morning the pillow was wet with the saliva which had run from his mouth during sleep. His uncle, a wealthy gentleman of this city, sent him off traveling, but he Teturned in a few weeks with loss of power in the left arm and leg, which had be- gun to be manifested to a slight extent before his departure. He came under my charge May 15, 1870. At this time the paralysis, of both motion and sensation, was well marked on the left side, as shown by the assthesiometer and dynamom- eter. The line made by the dynamograph with the right hand was perfectly straight, while that made by the left was at an angle of forty- five degrees with the other. In his conversation he clipped his words, and sometimes left out the smaller ones. His memory he stated was materially impaired. There was almost constant headache over the whole frontal region, and attacks of vertigo were frequent. There was no marked paralysis of the face, though the muscles of both sides were paretic, and he often had double vision. The right pupil was largely dilated and was insensible to light. Ophthalmoscopic examination showed the left eye to be perfectly normal, but the retinal vessels of the right were smaller and straight, and the choroid was paler than natural. Upon inquiry I ascertained that he had given extraordinary atten- tion to his business for a period of several months before the attack of numbness, frequently being up making calculations till three o’clock in the morning, and thus depriving himself of the necessary amount of sleep. My opinion was, that he was suffering from incipient softening of the brain due to disease of the capillaries, which, in its turn, resulted from cerebral congestion and exhaustion. I was further of the opinion that the lesion involved the right hemisphere and motor tract. 178 DISEASES OF THE BRAIN. I prescribed the phosphide of zinc in the dose of the tenth of a grain, with half a grain of extract of nux-vomica in pill three times a day, with the constant galvanic current three times a week, the latter to be derived from fifteen of Smee’s cells, and to be passed from fore- head to occiput for three or four minutes at a time. At the end of ten days he had lost his diplopia, the pupil of the right eye had regained its natural diameter and irritability, and the vertigo and headache had notably diminished. The treatment was continued, and at the end of a month he had recovered the sensibility and power on the paralyzed side to such an extent, and had improved so much in other respects, that I advised him to take a short journey. He was absent two weeks, during which period he continued to take the pills as before, and on Ills return was, to all appearance, well. He has since remained in ex- cellent health. II.—Mr. R. W., a merchant of this city, consulted me in April, 1868, under the following circumstances: After a long period of great domestic anxiety, during which he had been engaged in some heavy commercial transactions, and had suffered from wakefulness, he experienced one afternoon, while riding in the park in his carriage, a slight quivering motion at the apex of the tongue. It continued until he reached home; and then, upon looking in a mir- ror, he could see the fibrillary movement very distinctly. He was not alarmed, and went to bed at his usual hour. In the morning he noticed a little thickness of speech, but the movement had ceased. That after- noon he had a violent headache, attended with vertigo and nausea. Be- coming alarmed, he sent for his family physician, who ascribed the symptoms to indigestion, and administered a mild cathartic. The fol- lowing day, on attempting to rise from the bed to go to the water- closet, he was attacked with such a severe vertigo that he was obliged to lie down again; and, though he did not for a moment lose conscious- ness, his fasces escaped from him involuntarily. From this time he gradually lost strength in both arms and legs, and his speech became very defective. His memory suffered to such an extent that he forgot the names of his children. There was very little headache, the vertigo had ceased, there was no disturbance of vision, and no loss of power over the sphincters. About six weeks after the occurrence of the first symptom noticed, he came under my care. At this time there was anaesthesia of both sides of the body, both legs and both arms had lost power; he clipped his words, and frequently substituted others of similar sound or meaning for those he ought to have used. His memory was much weakened, and there was a strong tendency to stupor. There were no troubles of the special senses— ophthalmoscopic examination revealed nothing abnormal—there was no facial paralysis. I diagnosticated softening of the brain from general cerebral amemia consequent upon congestion and cerebral exhaustion, CEREBRAL SOFTENING. 179 and I prescribed a liberal allowance of wine, a full and nutritious diet, carriage exercise, and amusements of various kinds. This was the very reverse of the treatment to which he had been subjected. In addition, I recommended the constant galvanic current, to be applied as in the previous case, and gave the following prescription: . Olei phosphorat. § ss; mucil. acaciae, §j; ol. bergamii, gtt. xv. M. ft. emulsio. Dose, gtt. xv. ter die. The treatment was carried out with the result of obtaining a gradual and permanent improvement, so that at the end of about six months the patient was well. He then went to Europe, where he now is, with as good health as he has ever enjoyed. Other cases, similar in their general features, have been under my care with a like result in each, and several others have been very decid- edly improved and relieved of the more prominent symptoms of the disease, without, however, regaining full health. The means of treat- ment thus far consist in the use of tonics, stimulants, and especially phosphorus and strychnine, the avoidance of all severe mental exertion, and all excessive emotion, open-air exercise, and the use of the constant galvanic current. The beneficial effects of maintaining the physical strength were several years since pointed out by Mr. F. Skey1 in a clinical lect- ure delivered at St. Bartholomew’s Hospital, but it must be con- fessed that the opposite plan of treatment has been very generally followed. Softening from the effects of thrombosis or embolism is, as I have said, not much under the control of the physician. Patients recover from it, however, when they are of good constitution, and when the focus of softening has not been extensive. The mind and body may, and in such cases generally do, remain feeble, and we are therefore consulted for the relief of the condition. In such cases tonics, and among them phosphorus, strychnine, and wine, occupy a prominent place; the constant galvanic current to the head, and the induced to the paralyzed muscles, will rarely fail to be of service. III.—Thus a gentleman, who had been a distinguished officer of the army, suffered from loss of memory, defective articulation, ptosis, double vision, and right hemiplegia, probably the result of embolism. Several years before he came under my charge, he had been treated by Dr. J. T. Metcalfe, for heart-disease, the result of acute rheumatism. I gave the phosphide of zinc and extract of nux-vomica according to the for- mula previously mentioned, advised a liberal use of wine and beef- steaks, applied the primary current to the brain, and the induced cur- rent to his paralyzed arm and leg, and in a few weeks had the satisfac- tion of seeing such a degree of improvement as almost to constitute a 1 “ On the Yalue of Tonic Treatment in some Diseases of the Brain, more especially Cases of Ramollissement,” Dublin Hospital Gazette, November, 1858. 180 DISEASES OF THE BRAIN. cure. The ocular troubles had disappeared, his memory had improved, he talked as well as ever, and the numbness and loss of strength were no longer remarked unless he over-exerted himself, which, owing to his general feeling of bien aise, he was very apt to do. He remained in this condition for over a year, when he had several other attacks of embolism, each of which left him more weak, mentally and physically, than before, and of which he eventually died. There were some interesting features connected with this case, which will be referred to at greater length under the head of aphasia. IV.—In another case, in which there was reason to think a foyer of softening had been absorbed, a marked relief from the sequelae was obtained. The patient, a literary gentleman of distinction, had, several years previously to my seeing him, suffered from an attack of acute rheumatism with endocarditis. About a month after his recovery, as he was sitting in his library before the fire, he felt a sensation as if one side of his face had suddenly become much heavier than the other. Al- most immediately afterward he lost consciousness, and fell to the floor. He could not have been in this condition longer than five minutes when he came to himself, to find that he was paralyzed in the right arm and leg. Attempting to call for assistance, he found he could not articulate. His wife soon afterward entered the room, and medical aid was obtained. He was bled to the extent of sixteen ounces, and purged with croton-oil. The following day he was much better; could move his arm and leg, and articulate with some degree of distinctness, but toward even- ing headache ensued, he became delirious, and the paralysis increased. Of the condition immediately following, he could give no very clear account. He only knew that he was confined to his bed for several weeks, was delirious part of the time, and that, after the acute attack passed off, he was left with an enfeebled mind, imperfect articulation, and paralysis of the arm and leg on the right side. He went to Europe, traveled extensively, and returned at the end of a year very much improved,, but still with some degree of mental weakness, defective speech, and paralysis, remaining. When he came under my observation, the following were the prin- cipal symptoms observed: The strength of the right arm, as measured with the dynamometer, was not one-third that of the left; the exten- sors of the leg and foot were almost entirely paralyzed, so that in walking he abducted the leg so as to cause the foot to clear the ground ; electro-muscular contractility was much weakened, though the induced current caused feeble contractions. His speech was af- fected mainly as regarded the memory of words. He spoke with a good deal of volubility, but constantly used the wrong expressions. Thus, when he wished to tell me that he had visited Europe for the CEREBRAL SOFTENING. 181 benefit of his health, he said : “ I went to Elope for the bequest of my hedge,” and then went on—continually making other mistakes—to tell me a long story which I could scarcely understand. His emotions were easily disturbed: he cried because he had to wait a few minutes in my reception-room before seeing me. Ophthalmoscopic examination showed pale choroids and straight and attenuated retinal vessels. Auscultation revealed the existence of both mitral and aortic regurgitation. Taking into consideration the history of the case and the present condition of the patient, I diagnosticated embolism of the left middle cerebral artery, subsequent softening and eventual absorption of the diseased part of the brain. My idea was that the brain, as a whole, was anaemic, and that, with improved nutrition of it and the paralyzed limbs, amelioration of the symptoms was possible. I therefore prescribed the phosphide of zinc and nux-vomica pills as before mentioned, directed the use of wine to the extent of half a bottle of champagne daily, and advised that animal food should form the principal portion of each meal. Since his illness he had, by direc- tion of his physician, left off the use of coffee. I directed it to be resumed, and to be taken strong. The primary galvanic current was passed through the head in the manner previously indicated in this chapter, and the induced current was applied for half an hour three times a week to the arm and leg, each paralyzed muscle receiving a full share of attention. It was not long before signs of amendment were noticed. His strength became greater in the arm, and he was able to extend the leg and to raise the foot after half a dozen electrical applications. His speech next gave evidence of improvement, and his mind became stronger. The treatment was continued for about four months, with only an intermission of a week. At the end of that time his gait was almost natural, though he still swung the foot a very little, his arm was nearly as strong as the other, his mind was not perceptibly weaker than that of other persons of his age (fifty-five), and his speech was excellent except when he was excited and very anxious to express himself correctly and fluently. There is one point in regard to which a few words are perhaps necessary, and that is to enter a protest against the use of counter- irritation of any kind, and to discountenance, as far as I can, the em- ployment of the actual cautery. I have never seen the least advantage follow the application of croton-oil to the shaven scalp, nor can I con- ceive how such a measure can be recommended on rational grounds. I have several times witnessed its action, and have invariably seen it aggravate the symptoms. In the case of a gentleman from St. Louis, affected with cerebral softening, the effect was to make his speech still more imperfect and his mind weaker. A lady, who was affected 182 DISEASES OF THE BRAIN. with all the more prominent symptoms of softening of the brain, had all the phenomena increased in violence after the application of the actual cautery to the nape of the neck. I could easily adduce otncr examples to the same effect, were it necessary. CHAPTER VII. APHASIA. The subject of aphasia is of such interest, and so much attention has recently been given to it by physiologists and pathologists, that, although it is only a symptom common to several morbid conditions, a treatise on diseases of the nervous system would scarcely be re- garded as complete without its being fully considered. By aphasia is understood a condition produced by an affection of the brain by which the idea of language, or of its expression, is im- paired. The word is derived from the Greek—a, privative, and (paaig, speech—and, as stated by Trousseau, was proposed by M. Chrysaphis, a distinguished Greek scholar, as a substitute for alalia, used by Lor- dat, and aphemia, employed by Broca, to designate the same condition. In the definition which I have given of aphasia, the term is limited to impairment of the idea of language or of its expression. It does not, therefore, include those cases in which the individuals are able to speak, but will not; such as are met with among the insane. The idea of language is as perfect as ever, and is doubtless entertained, but the person does not speak because he does not will to do so, and this fail- ure may arise either from a lack of the necessary power, or from a stubborn determination not to speak. A lady was a short time since under my charge who had been treated by a homoeopathic physician as a case of aphasia. A very slight examination was sufficient to con- vince me that the case was one of hysteria. She had not spoken for several months, but upon one occasion she came to my office with her maid, whom she required to repeat the alphabet, and when the right letter was reached she signified the fact by raising her hand. She thus spelled out the words she wished to use. Subsequently she procured a card with all the letters on it, such as are used for children learning their alphabet, and she composed her words from this. Of course all these facts showed that her idea of language was intact, but she still might have lost the power of coordinating the muscles concerned in articulation so as to express herself in spoken words. Although I was sure this was not the case, I failed to make her speak, until one morn- ing she became very much interested in something I was saying, and, finding her alphabet too slow a means of expression, dropped it and APHASIA. 183 began to speak with great fluency. After talking with energy for a quarter of an hour, she suddenly recollected herself and took up her card of letters again, but the charm was broken, and by degrees she resumed her speech. At one time this lady was under the care of my friend Prof. Flint, for some chest or throat difficulty, and on one occa- sion spoke very well. Neither does aphasia embrace cases of inability to speak from paral- ysis of the tongue or other muscles of articulation. Defective speech from this cause is frequently met with in hemiplegia, in glosso-labio- laryngeal paralysis, and some other affections. In such instances the idea of language remains, but the patient does not speak because he is unable to put the organs of articulation in motion. A few days ago a gentleman, a prominent merchant of the city, was sent to me as a case of aphasia. As he entered my consulting-room, I saw that he was hemiplegic on the left side, and, on telling him to put out his tongue, found that he could not get it beyond the teeth, or touch the roof of his mouth with it. The history of the case was that of ordinary cere- bral haemorrhage, and he regained the power of speaking after several applications of the primary and induced galvanic currents had been made to the tongue and muscles of the face. The distinction between aphonia and aphasia must also be made. In the one the idea of speech is undisturbed, and articulation is not inter- fered with except as regards phonation. Aphonic patients can whisper, but are unable to speak in full voice, owing to some laryngeal affection impairing the tone of the vocal chords. The fact that the faculty of speech may be deranged independently either of the will, paralysis, or loss of voice, appears to have been noticed at a very early period in the progress of science. Thus Isaiah 1 says, “ For with stammering lips and another tongue will he speak to this people;” and again,8 “Thou shalt not see a fierce people, a people of a deeper speech than thou canst perceive; of a stammering tongue that thou canst not understand.” Thucydides mentions that many, who suffered from the plague which raged at Athens, found on recovering that they had not only forgotten the names of their friends and relations, but also their own names. Pliny,3 in the chapter entitled Memories, Exemplci, says, in speak- ing of this faculty: “For nothing is so weak in man; disease, falls, injuries, even sL fright, may impair it partially, or destroy it altogether. A blow from a stone has abolished the memory of the alphabet. A fall from a high roof has caused a man to cease to recognize his mother and neighbors, another even forgot his slaves, and Messala Corvinus, the orator, could not recall his own name.” 4 1 Chapter xxviii., 11. * Chapter xxxiii., 19. 3 Lib. vii., cap. xxiv. 4 Trousseau has translated this passage somewhat differently. I quote from an illu- minated copy printed at Tarvisium (Treviso), in October, 1479. 184 DISEASES OF THE BRAIN. Suetonius 1 relates that Claudius so far lost his memory that he for- got the names of persons to whom he desired to speak, and could not even recollect the words he wished to use. Passing over several authors of later times who have recognized the existence of the difficulty in question, we come to Crichton,3 who re- marks as follows: “ There is a very singular defect in memory, of which I have myself seen two remarkable instances. It ought rather to be considered as a defect of that principle by which ideas and their proper expressions are associated, than of memory, for it consists in this, that the person, although he has a distinct notion of what he means to say, cannot produce the words which ought to characterize his thoughts. The first case of this kind which occurred to me in practice was that of an attorney much respected for his integrity and talents, but who had many sad failings to which our physical nature too often subjects us. Although nearly in his seventieth year, and married to an amiable lady much younger than himself, he kept a mistress, whom he was in the habit of visiting every evening. The arms of Venus are not wielded with impunity at the age of seventy. He was suddenly seized with great prostration of strength, giddiness, forgetfulness, insensibility to all concerns of life, and every symptom of approaching fatuity. His for- getfulness was of the kind alluded to. When he wished to ask for any thing, he constantly made use of some inappropriate term. Instead of asking for a piece of bread, he would probably ask for his boots ; but, if these were brought, he knew they did not correspond with the idea he had of the thing he wished to have, and was therefore angry. Yet he would still demand some of his boots and shoes, meaning bread. If he wanted a tumbler to drink out of, it was a thousand to one he did not call for a certain chamber-utensil, and, if it was the said utensil he wanted, he would call it a tumbler or a dish. He evidently was con- scious that he pronounced wrong words, for, when the proper expres- sions were spoken by another person, and he was asked if it were not such a thing he wanted, he always seemed aware of his mistake, and cor- rected himself by adopting the appropriate expression. This gentleman was cured of the complaint by large doses of valerian and other proper medicines.” Dr. Crichton subsequently met with another case similar to the fore- going, and he quotes the following from Prof. Gruner, of Jena, in vol. vii. of the Psychological Magazine. The patient, a learned gentleman, after his recovery from an acute fever, suffered a loss of memory for words. Among the first things he desired to have was coffee (Icoffee), but, instead of pronouncing the letter he substituted in its place a z, 1 “ C. Suetonii Tranquilli,” xii. Caesarea. 8 “An Inquiry into theNatare and Origin of Mental Derangement, comprehending a Concise System of the Physiology and Pathology of the Human Mind, and a History of the Passions and their Effects,” London, 1798, vol. i., p. 371. APHASIA. 185 and therefore asked for a cat (katze). In every word which had any he committed a similar mistake, substituting a z for it. He also cites, from Van Goens, the case of Madame Hennert, wife of the professor of mathematics at Utrecht, who suffered a similar de- fect of memory. When she wished to ask for a chair she asked for a table, and when she wanted a book she demanded a glass. But, what was singular in her case was, that when the proper expression of her thought was mentioned to her, she could not pronounce it. She was angry if people brought her the thing she had named in- stead of the thing she desired. Sometimes she herself discovered that she had given a wrong name to her thoughts. This complaint continued several months, after which she gradually recovered the right use of her recollection. It was only in this particular point that her memory seemed to be defective, for M. Van Goens assures us that she con- ducted her household affairs with as much regularity as she ever had done, and that she used to show her husband the situation of the heavens on a map with as much accuracy as when she was in perfect health. The following case, in Gesner’s Entdeckungen der Neuesten Zeit in der Arzneigelehrheit, is likewise quoted by Crichton: “ A man, aged seventy, was seized, about the beginning of January, with a kind of cramp in the muscles of the mouth, accompanied with a sense of tickling all over the surface of the body, as if ants were creep- ing over it. On the 20th of the same month, after having experienced an attack of giddiness and confusion of ideas, a remarkable alteration of his speech was observed to have taken place. He articulated easily and fluently, but made use of strange words, which nobody understood. The number of these does not at present seem to be great, but they are frequently repeated. Some of them he seems to forget entirely, and then new ones are formed. When he speaks quick he sometimes pro- nounces numbers, and now and then he employs common words in their proper sense. He is conscious that he speaks nonsense. What he writes is equally faulty with what he speaks. He cannot write his name. The words he writes are those he speaks, and they are always written conformably to his manner of pronouncing them. He cannot read, and yet many external objects seem to awaken in him the idea of their presence.” Dr. Rush,1 in the work the title of which is cited below, in chapter xii., which treats of Derangement in the Memory, refers so specifically to affections of the speech that I quote his language with some degree of fullness, and I do so with the less hesitation as his observations appear to have escaped notice, both in this country and in Europe. He says: “ 1. There is an oblivion of names and vocables of all kinds. “ 2. There is an oblivion of names and vocables, and a substitution 1 “ Medical Inquiries and Observations upon Diseases of the Mind.” Fourth edition. Philadelphia, 1830, p. 2*74. The first edition was published in 1812. 186 DISEASES OF THE BRAIN. of a word no ways related to them. Thus, I knew a gentleman afflicted with this disease, who, in calling for a knife, asked for a bushel of wheat. “ 3. There is an oblivion of the names of substances in a vernaculai language, and a facility of calling them by their proper names in a dead or foreign language. Of this, Wepfer relates three instances. They were all Germans, and yet they called the objects around them only by Latin names. Dr. Johnson, when dying, forgot the words of the Lord’s prayer in English, but attempted to repeat them in Latin. Delirious persons, from this disease of the memory, often address their physicians in Latin or in a foreign tongue. “ 4. There is an oblivion of all foreign and acquired languages, and a recollection only of vernacular language. Dr. Scandella, an ingenious Italian, who visited this country a few years ago, was master of the Italian, French, and English languages. In the beginningof the yellow fever which terminated his life in the city of New York in the autumn of 1798, he spoke English only ; in the middle of his disease he spoke French only; but on the day of his death he spcke only in the language of his native country. “ 5. There is an oblivion of the sound of words, but not of the let- ters which compose them. I have heard of a clergyman in Newburyport, who, in conversing with his neighbors, made it a practice to spell every word that he employed to convey his ideas to them. “ 6. There is an oblivion of the mode of spelling the most familiar words. I once met with it as a premonitory symptom of palsy. It oc- curs in old people, and extends to an inability, in some instances, to remember any more of their names than their initial letters. I once saw a will subscribed in this way by a man in the eightieth year of his age, who during his life always wrote a neat and legible hand. “ 9. There is an oblivion of names and ideas, but not of numbers. We had a citizen of Philadelphia many years ago, who, in consequence of a slight paralytic disease, forgot the names of all his friends, but could designate them correctly by mentioning their ages, with which he had previously made himself acquainted.” Dr. Rush remarks of these cases, that “ there appears to be some- thing like a palsy of the mind, quoad these specific objects.” Thus far there had been no attempt to define with precision the seat of the faculty of language, or even to establish its existence; but, in the early part of the nineteenth century, Dr. Gall, a German physician, an- nounced that such a faculty did exist, and that it was seated in those convolutions of the brain which rest upon the posterior part of the supra-orbital plate, and that a large development of the organ was indi- cated by prominence and depression of the eyes. He was first led to believe in the existence of such an organ by observing that some of the scholars with whom, as a young man, he had to compete, excelled him APHASIA. 187 in the ability to learn by heart, and he noticed that those thus endowed with great memory for words possessed prominent eyes. From these circumstances, he was gradually carried on to the foundation of his phrenological system. In reality, however, Gall considered that there were two organs of language in each hemisphere—the one originating the idea of words, the other the talent for philology, and for acquiring the spirit of lan- guages. The former organ he describes as lying on the posterior half of the supra-orbital plate, as before mentioned. It gives a talent for learning and recollecting words, and persons possessing it large, recite long passages by heart after reading them once or twice. The other is placed on the middle of the supra-orbital plate, and when it is large the eyeball is not only rendered prominent but is depressed, causing the lower eyelid to assume the appearance of a bag or fold. Persons having this organ large have not only an excellent memory for words, but a particular talent for the study of languages, for criticism, and in gen- eral terms for all that has reference to literature. Dr. Spurzheim, however, admits but one organ, lying transversely on the posterior portion of the supra-orbital plate, and this view is ac- cepted by Combe and other distinguished phrenological authorities.1 In support of his theory that there is such an organ, Gall cites the case of a notary reported by Pinel.2 The latter, in speaking of apo- plexy, says this affection may be limited in its action to the words which are used to express ideas. In the case mentioned, the patient forgot, after an attack of apoplexy, his own name, that of his wife, those of his children and friends, although there was not the least paralysis of his tongue. He no longer knew how to read or write, and yet his memory as regarded other things was unimpaired. Dr. Gall3 refers also to the case of a soldier, sent to him by Baron Larrey, who was affected in a manner similar to that of the notary. It was not his tongue which was involved, for he was able to move it about in all directions, and to pronounce words, but he had lost the memory for words, although he recollected other things as well as ever. I shall presently have occasion to refer to a still more interesting case, reported by Larrey, and one which appears to have escaped the notice of all writers on the subject of aphasia. Spurzheim mentions the case of one Lereard, of Marseilles, who, caving received a blow from a foil on the eyebrow (which one is not stated), lost the memory of proper names entirely. He sometimes even forgot the names of his intimate friends, and even of his father. 1 For a full account of the subject, the reader is referred to a “ System of Phrenol- ogy,” by George Combe, Boston, 1834, or to “Phrenology,” etc., by J. S. Spurzheim, Boston, 1833. 2 “ Traite medico-philosophique, sur l’alienation mentale.” Second edition. Paris, 1809, p. 90. 3 “Physiologie du oerveau,” vol. iv., p. 84. 188 DISEASES OF THE BRAIN. Gall, therefore, located the organ of language in a limited part of the anterior lobe of each hemisphere; but he adduced very little evi- dence to support his opinion, and hence his views did not meet with any thing like general acceptance. A number of cases, however, re- ported by Lallemand, Rostan, and others, support it, while several ad- duced by the same authors are opposed to it. In 1825 Bouillaud,1 who had collected a great number of cases of affections of the brain, was surprised to find how frequently the loss of speech coexisted with disease or injury of the anterior lobes. He also confirmed, what others before him had noticed, that the loss of the power of expressing ideas in articulate language was often the only evi- dence of a brain-affection. He made one very important step in advance, and his views on this particular point are adopted—and often without credit—by the majority of the present writers on aphasia; he divided the faculty of speech into two distinct categories of phenomena: 1. The faculty of creating words as representatives of our ideas, and of recollecting them—internal speech. 2. The power of coordinating the movements necessary for the ar ticulation of these words—external speech. This classification forms the basis of the division of aphasia into the two varieties, the amnesic and the ataxic. The cases which Bouillaud adduced in support of his theory were many of them in patients who exhibited no other symptoms than the loss of the power of articulate language. They preserved their intelli- gence, comprehended perfectly questions put to them, and knew the value of words; but, although there was no paralysis of either the tongue or the lips, they were unable to utter a word. At the post- mortem examination, the lesion was always found in the anterior lobes. Sixty-four cases formed the basis of his conclusions. A part was direct, and went to show that lesion of the anterior lobes was accompanied by derangement in the faculty of speech; the other part was indirect, and established the fact that, when the anterior lobes were not affected, the lesion being in some other region of the brain, the faculty of speech remained intact. Cruveilhier opposed Bouillaud’s views, and, in a paper read at the Athenee de Medecine in the same year, brought forward seven cases of persons, some of whom had lost the faculty of speech, but who, on post- mortem examination, were found to have no disease of the anterior lobes; and others who had spoken, but in whom there were more or less profound changes in these parts. Subsequently Andral2 reported the results of the analysis of thirty- 1 “ Traite de l’encophalite,” Paris, 1825 ; and also, “ Recherches cliniques, propres a d6montrer que la perte de la parole correspond k la lesion des lobules anterieurs du cer- yeau,” Archives de med., 1825. 2 “ Clinique medicale,” tome ii., p. 185. APHASIA. 189 seven cases of lesion of one or both anterior lobes. Of these, speech was abolished twenty-one times, and preserved sixteen times. Lalle- mand1 also opposed Bouillaud with several cases; but the latter rejoined3 with a fresh array of thirteen cases in support of his doctrine, and with many arguments against the validity of those brought against him. Longet3 declares that Bouillaud appears to have refuted many of the objections of his adversaries, and to have demonstrated that some of their cases were badly interpreted. At the same time, while admitting that it is possible that different parts of the brain preside over different voluntary movements, he affirms that there is nothing positively estab- lished as regards the localization of the active principles of these move- ments. Subsequently, in other memoirs, Bouillaud brought forward addi- tional cases in support of his theory, making a total of one hundred and three, and offered a prize of five hundred francs to any one who would adduce an instance of profound lesion of the anterior lobes without troubles of speech. Many years subsequently Velpeau announced that he should claim this prize, for that, in March, 1843, he had related the case, and presented the brain, of a wig-maker who had come under his care for prostatic disease. This man was in full possession of his reasoning faculties, and, moreover, was noted for his unconquerable loquacity. Pie died a few days subsequently, and on post-mortem ex- amination a scirrhous tumor was found to have entirely taken the place of the two anterior lobes of the brain. Very little faith seems to have been put by physiologists or pathologists in the history of this case. If it proves any thing, it is that the anterior lobes are useless appendages to the rest of the cerebral system. But Bouillaud was not content with the deductions to be drawn from pathology. In a series of experiments, he endeavored to establish the truth of his idea, and thus bring the science of physiology to his support. These experiments were detailed in a paper4 read before the Academy of Sciences, in September, 1827, which was subsequently (1830) published in the tenth volume of Magendie’s Journal de Physi- ologie, from which I quote. The experiments relative to the anterior lobes were made on dogs. Only one was entirely successful—the animals in the others dying too soon after to admit of satisfactory deductions being made. But the twentieth experiment was more satisfactory. On the 28th of June, 1826, he passed a gimlet through the anterior 1 Op. cit., lettres 6, Y, 8. a “ Exposition de nouveaux faits k 1’appui de 1’opinion qui localise dans les lobes an- t6rieurs du cerveau le principe legislateur de la parole.” “ Bulletin de l’Academie de Medecine,” 1839, tome iv., p. 282. 3 “ Traite de la physiologie,” tome ii., p. 438. • “ Recherches experimentales sur les fonetions du cerveau (lobes cerebraux) en gene- ral et sur celles de sa portion ant6rieure en particular.” 190 DISEASES OF THE BRAIN. part of the brain of an active, docile, and intelligent dog. Immediately afterward the animal was convulsed, and could not rise from the ground. Sight and hearing remained. Symptoms of compression soon came on; the result, probably, of the haemorrhage. Eventually, the animal re- covered, but it was found to have lost much of its intelligence and agility. The faculty of memory seemed to have been entirely abolished; and there was a decided expression of imbecility in its countenance. It could no longer ascend or descend a staircase; the fore-legs were lifted very high in walking, and its movements were all badly coordinated. 'Vhcn struck or made to walk, it uttered sharp cries, but it had lost entirely the ability to bark. As Bouillaud remarks, “it no longer barked, either to show its affection, or to drive away strangers who came to the house.” Once only, on the 18th of July, it tried to bark at a passer-by, but failed in the attempt. This is the only experiment I have been able to find which has any bearing upon the question of the localization of the faculty of language. And I do not quote it as proving much on the subject. The difficulties in the way of experimentation are almost insuperable, to say nothing of the fact that it is doubtful if any of the sounds made by animals can be compared with human speech. But unintentional experiments have been performed upon the human subject, which tend to show that, though the faculty of lan- guage may be located in one or both anterior lobes, either may be seriously injured without the faculty of language suffering to any ap- preciable extent. Two of them have happened in this country, and, although referred to in connection with aphasia by Seguin and Harris, I take satisfaction in bringing them forward on account of their great importance to the question under consideration. The first is related by Dr. Harlow,1 of Vermont: The subject was a strong, healthy man, twenty-five years of age, and was engaged in ramming down a charge of powder in a rock to be blasted, when an explosion took place, and the tamping-iron was driven clear through his head. In a few minutes he recovered his consciousness, was put into a cart and carried three-quarters of a mile to his residence, where he got out and walked into the house. Two hours afterward he was seen by Dr. Harlow. He was then quite conscious and collected in his mind, but exhausted by extensive hasmorrhage from the hole in the top of his head. Blood, pus, and particles of brain, continued to be discharged for several days, but by January 1, 1849, the wound was quite closed and his recovery complete. There was no pain in the head, but a queer feeling, which he could not describe. As regarded his mind, he was fitful and vacillating, though obstinate, as he had always been. He 1 Boston Medical and Surgical Journal, December, 1849, vol. xxxix., p. 389. Also, “Descriptive Catalogue of the Warren Anatomical Museum,” Boston, 1870, p. 145. APHASIA. 191 oecame very profane, never having been so before the accident. He lived till May 21, 1861, twelve and a half years subsequent to the acci- dent, when he died, after having had several convulsions. His cranium was obtained, and, with the bar, is now preserved in the Warren Ana- tomical Museum at Boston. Dr. J. B. S. Jackson1 thus describes the skull: “ The whole of the small wing of the sphenoid bone upon the left side is gone, with a large portion of the large wing, and a large por- tion of the orbital process of the frontal bone, leaving an opening in the base of the skull two inches in length, one inch in width poste- riorly, and tapering gradually and irregularly to a point anteriorly. This opening extends from the sphenoidal fissure to the situation of the frontal sinus, and its centre is an inch from the median line. The optic foramen and the foramen rotundum are intact. Below the base of the skuil the whole posterior portion of the upper maxillary bone is gone. The malar bone is uninjured; but it has been very perceptibly forced outward, and the external surface inclines somewhat outward from above downward. The lower jaw is also uninjured. The opening in the base, above described, is continuous with a line of old and united fracture that extends through the supra-orbitary ridge in the situation of the foramen, inclines toward and then from the median line, and terminates in an extensive fracture that was caused by the bar as it came out through the top of the head. This fracture is situated in the left half of the frontal bone, but inferiorly it extends somewhat over the median line. In form it is about quadrilateral; but it measures two and a half by one and three-quarter inches. Two large pieces of bone are seen to have been detached and upraised, the upper one having been separated at the coronal suture from the parietal bone, and being so closely united that the fracture does not show upon the outer surface. The lower piece shows the line of fracture all around. Owing to the loss of bone, two openings are left in the skull; one that separates the two fragments has nearly a triangular form, extends rather across the median line, and is four inches in circumference ; the other, situated between the lower fragment and the left half of the frontal bone, is long and irregularly narrow, and is two and five-eighths inches in circum- ference. The edges of the fractured bones are smooth, and there is nowhere any new deposit.” From this account it will be seen that the left anterior lobe of the brain suffered severely by this terrible injury, and yet it is not stated that the subject had ever shown any difficulties of speech. If the faculty of language resides in the whole of the lobe, such an immunity could scarcely have existed. It must be noted, however, and the photo- graph of the cranium establishes the fact, that the third frontal convo- lution and the island of Reil escaped all injury. Another interesting 1 “Descriptive Catalogue of Warren Anatomical Museum,” loc. cit. 192 DISEASES OF THE BRAIN. circumstance is the addiction to profanity after the accident. A like phenomenon has been noticed in cases of aphasia. The second instance is almost as extraordinary. I quote the history of the case, 952, from Dr. Jackson:1 “ Cast of the head of a man who was transfixed through the head by an iron gas-pipe, and who, to a very considerable extent, recovered from the accident. “The patient, a healthy and intelligent man, about twenty-seven years of age, was blasting coal when the charge exploded unexpectedly, and the pipe was driven through his head, entering at the junction of the middle and outer thirds of the right supra-orbitary ridge, and emerg- ing near the junction of the left parietal, occipital, and temporal bones. One of his fellow-miners saw him upon his hands and knees, and strug- gling as if to rise ; and, going to his assistance, he placed his knee up- on his chest, supported his head with one hand and with the other with- drew the pipe. This last projected about equally from the front and back of the head, and much force was required for its withdrawal.” Brain escaped from the anterior opening, and coma and collapse supervened. “ In seven weeks he sat up, and in one more walked about. The right hand he used somewhat, but less well than the left. For about ten months after the accident his memory for some things was nearly lost, but during the next two months there was a considerable improvement.” The accident happened on May 14, 1867, and in June, 1868, the patient, with the gas-pipe, was exhibited to the Massachusetts Medical Society. “The man appeared to be in a good state of general health; and, though his mental powers were considerably impaired, there was nothing unusual in his expression, nor would there be noticed, in a few minutes’ conversation with him, any marked deficiency of intellect.” It is very evident that in this case the right anterior lobe was seriously injured—the left escaping—and yet there does not appear to have been any aberration of speech. It is to be regretted, however, that the history is not more specific as to the things in regard to which the memory was deficient. There are other cases which militate against Bouillaud’s doctrine. Thus, M. Peter2 states that a drunken cavalry-soldier fell from his horse on the back of his head, and fractured his skull. Stupor set in at once, followed by the most violent delirium. The man kept constantly shout- ing the worst possible oaths, and held connected conversation with im- aginary persons. He died at the end of thirty-six hours, without hav- ing recovered his reason. On dissection, a fracture of the roof and base of the skull was discovered in all its length. The posterior lobes of the 1 Op. cit., p, 149. * Quoted by Trousseau, “ Lectures on Clinical Medicine.” Translated by Bazire, vol, L, p. 256. APHASIA. 193 brain were found, on post-mortem examination, to have sustained no injury, but both anterior lobes were in a pulpy condition, through a most violent contusion, caused by their being knocked against the an- terior wall of the cranium. The whole thickness of the lobes was dis- organized. As Trousseau remarks, this case shows that the two frontal lobes may be destroyed in their anterior portion without causing a loss of the faculty of speech. Trousseau also cites the case of two officers, who, after a quarrel, fought a duel. One of them fired first, and the ball entered his adversary’s head at one temple, passed through the brain, and then raised the temporal bone on the opposite side. The ball was extracted, and the patient immediately made a sign with his hands, and expressed his thanks in a very low voice. He recovered, for the time being, and, during five months thereafter, could speak perfect- ly well, and was remarkable for the wTit and fluency of his conversation and writing. He subsequently died of softening; and it was found, on post-mortem examination, that the ball had passed through the two frontal lobes in their middle portion. A still more striking case is re- ferred to by Dr. Bazire, in a note to Trousseau’s lecture on aphasia, in the work cited. It was reported in 1843 by M. Aug. B6rard, to the Anatomical Society of Paris. The patient, a miner, was knocked down and severely injured by an explosion in a mine. He did not lose con- sciousness, but managed to creep out of his hole and to call to his help some men who were working a short distance off. He begged them to fetch a cart and to take him to M. Berard’s house. He was there ex- amined. The whole frontal region was laid open, the integuments hung in shreds, the bones were splintered and in detached fragments, and the brain was exposed. Both anterior cerebral lobes were completely de- stroyed, and in their stead was a mixture of blood, of bony splinters, and brain-substance. In spite of this frightful injury, the man could relate in all its details how the accident had occurred. He died the next day. Whether or not we accept this case in all the import claimed for it, there can be no doubt that Bouillaud is wrong in claiming that injury of the anterior lobes is necessarily followed by some derangement in the faculty of speech. It is only fair, however, to state that latterly he has admitted that the organ of language may occupy the posterior part of either lobe. Dr. M. Dax, in 1836, read a paper before the medical congress which met that year at Montpellier, in which he came to the conclusion that the faculty of language “ was seated, not as Gall and Bouillaud had contended, in both anterior lobes of the brain, but that it occupied only the left anterior lobe.” He based this opinion on one hundred and forty cases of aphasia attended with paralysis, and in which the loss of power was on the right side; showing, therefore, that the lesion which produced the aberration of speech also caused the hemiplegia, and that 194 DISEASES OF THE BEAIN. this lesion must have been on the left side. This paper at the time at- tracted very little attention, and was forgotten till the year 1861 wit- nessed the reopening of the discussion.1 It would be very easy to quote a large number of cases confirmatory of Dr. Dax’s doctrine, but a few will suffice to show the general bearing of a great many others: The following case seems to have escaped notice. It is not the one referred to by Gall as being sent to him b} Larrey. In that case the left anterior lobe was injured and there was aphasia, but the lesion was caused by a sword. Baron Larrey 2 presented to the Academy the cranium of a subject with the following history: Toward the end of the year 1815 an officer of dragoons came to the hospital with a wound from a ball which he had received at Waterloo. The missile had entered the left side of the cranium at a point about six or eight millimetres from the eyebrow and near the temporal ridge. At first he had suffered loss of consciousness and profuse haemorrhage, but had recovered, with but slight loss of motor power. So far as his mind was concerned, there was no derangement except as regarded the faculty of speech; he had lost the memory of substantives. For this reason he was unable to drill his company, and, though able to distin- guish his men by their size, their form, their complexion, or their voice, he could not call them by name. He refused to allow the operation of trephining to be performed, and in 1827 died of phthisis. A post-mortem examination was made. The ball was found em- bedded in the thickness of the bone, having elevated and fractured the internal table. The dura mater was strongly adherent to the whole of the left anterior cranial fossa; it was also thicker and denser than in the natural state. A spheroidal excavation, five centimetres in its horizontal and seven or eight in its vertical diameter, was discovered at the summit and on the temporal side of the left anterior lobe of the brain. Mr. Thomas Hood 3 reported the history of a patient, a sober, intel- ligent man, sixty years of age, who, on the evening of September 2, 1822, suddenly began to speak incoherently, and became quite unintelli- gible to those around him. It was discovered that he had forgotten the name of every object in Nature. His recollection of things seemed to be unimpaired, but the names by which men and things were known were entirely obliterated from his mind, or rather he had lost the faculty by which they were called up at the control of the will. He was by no means inattentive, however, to what was going on, and he recognized 1 Dr. Marc Dax’s memoir was republished in the Gazette hebdomadaire, No. IV, April, 1865. 2 “ Blessure du cerveau avec perte de memoire des noms substantives,” Journal dc physiologic de Magendie, tome viii., 1828, p. 1. 8 “ Phrenological Transactions.” Quoted by George Combe in his “ System of Phre- nology,” Boston, 1834, p. 429. APHASIA. 195 friends and acquaintances perhaps as quickly as on any former occasion; but their names, or even his own or his wife’s name, or the names of any of his domestics, appeared to have no place in his recollection. “ On the morning of the 4th of September,” says Mr. Hood, “ much against the wishes of his family, he put on his clothes and went out to the workshop, and when I made my visit he gave me to understand, by a variety of signs, that he was perfectly well in every respect, with the exception of some slight sensations referable to the eyes and eyebrows. I prevailed on him with some difficulty to submit to the reapplication of leeches, and to allow a blister to be placed over the left temple. He was now so well in bodily health that he would not be confined to the house, and his judgment, in so far as I could form an estimate of it, was unimpaired, but his memory of words was so much a blank, that the monosyllables of affirmation and negation seemed to be the only two words in the language the use and significance of which he never en- tirely forgot. He comprehended distinctly every word which was spoken or addressed to him; and, though he had ideas adequate to form a full reply, the words by which these ideas are expressed seemed to have been entirely obliterated from his mind. By way of experiment I would sometimes mention to him the name of a person or thing, his own name for example, or the name of some one of his domestics, when he would repeat it after me distinctly once or twice; but generally before he could do so a third time the word was gone from him as completely as if he had never heard it pronounced. When any person read to him from a book, he had no difficulty in perceiving the meaning of the passage, but he could not himself then read, and the reason seemed to be that he had forgotten the elements of written language, viz., the names of the let- ters of the alphabet. In the course of a short time he became very ex- pert in the use of signs, and his convalescence was marked by his im- perceptibly acquiring some general terms which were with him, at first, of very extensive and varied application. In the progress of his recov- ery, time and space came both under the general application of time. All future events and objects before him were, as he expressed it, ‘ next time ; ’ but past events and objects behind him were designated £ last time' One day, being asked his age, he made me to understand that he could not tell; but, pointing to his wife, uttered the words, ‘ many times ’ repeatedly, as much as to say that he had often told her his age. When she answered sixty, he answered in the affirmative.” On the 10th of January he suddenly became paralytic on the left side [this is evidently a typographical error for right side]. On the 17th of August he had an attack of apoplexy, and on the 21st he expired. In the Phrenological Journal, vol. iii., p. 28, Mr. Hood has reported the dissection of his brain: “ In the left hemisphere, lesion of the parts was found, which terminated at half an inch from the surface of the brain, where it rests on the middle of the supra-orbital plate.” Two 196 DISEASES OF THE BRAIN. small depressions or cysts were found in the substance of the brain, “ and the cavity considered as a whole expanded from the anterior part of the brain till it opened into the ventricle in the form of a trumpet. The right hemisphere did not present any remarkable appearance.” Dr. Thomas Hun,1 of Albany, in detailing a case of amnesia in which there were no symptoms of paralysis, and in which there was no post-mortem examination, cites the case of a lady who died of cancer of the brain, occupying, at the time of her death, the greater portion of the left anterior lobe. In the early stages of her disease she was often unable to call the most familiar objects by name, and had to ex- press herself by signs or by pointing at the object. When the word she wanted was pronounced before her, she recognized it, and was able to repeat it. Other cases, and especially several which have occurred in my own experience, are reserved for future consideration. Up to this period we have the organ of articulate language limited to the left anterior lobe of the brain, but in 1861 its location was still further restricted. In that year M. Gratiolet, in discussing before the Anthropological Society of Paris a question relative to the comparative development of the brain and mind among different races, brought up the subject of cerebral localization, to which he announced himself as being strongly opposed. M. Auburtin, on the contrary, contended that the localization of the faculty of speech at least was definitely estab- lished, through the researches of Bouillaud, in the anterior lobes. In support of this view, he adduced cases which had already been brough forward, and cited others in addition, which went to show that loss of speech was the consequence of traumatic lesion of these parts of the brain. His adversaries cited other cases in which persons had preserved the faculty of language notwithstanding extensive lesions of the an- terior lobes. M. Auburtin responded that, if such profound and exten- sive injuries had not interfered with speech, it was because that part of the lobes in which the organ is situated was not involved. And he then cited the case of a patient in the Hospital for Incurables, who for many years had been deprived of the power of speech, and he declared that he would renounce the doctrine of Bouillaud if the autopsy of this patient did not reveal disease of the anterior lobes. The patient in question was under the charge of M. Broca, and the latter, a decided opponent, accepted the challenge of M. Auburtin, and declared that, when the man died, the examination should be made. Some time afterward the patient died, the post-mortem examination was made, and the lesion was found to occupy the left anterior lobe.* From this time forward, M. Broca, who had been a most determined 1 American Journal of Insanity, vol. vii., 1850-51, p. 859. 2 See “ Etude sur la localisation de la faculty du langage articule.” Th&se de Paris de M Carrier, 1867. APHASIA. 197 opponent of Bouillaud’s views of localization, became converted, and carried them to a still more extreme point than even M. Marc Dax had done. Taking, as his principal case, the one to which M. Auburtin had pinned his faith, he read, in 1861, before the Anatomical Society of Paris, a memoir,1 in which he discusses the question of the location of the faculty in question with all his perspicuity and directness. As the two cases cited by him are of historical interest, I give the chief details of them: A man named Le Borgne, who had been an inmate of another de- partment of Bicetre for over twenty years, was transferred to one of the wards under M. Broca’s care, to be treated for a severe attack of phlegmonous erysipelas. The man was a confirmed epileptic, and had not spoken, since his entrance into the hospital, more than a few words, which he employed for the expression of all his ideas. It is stated that in other respects his intelligence was good. Le Borgne was known in the hospital by the name of “ Tan,” a word which he habitually used, and which, with the oath, “ Sacrb noin de Dieu,” constituted his entire vocabulary. “ Tan,” owing to the constancy with which he used it, was the name by which he was known in the hospital; and, when he could not make himself understood by his signs, he employed the oath, and gave other manifestations of anger. For several years he had remained in the hospital with no other lesion than that of speech, with an occasional epileptic paroxysm; but, after a few years, his right arm became paralyzed, and four years sub- sequently the leg of the same side was involved; his sight was likewise enfeebled, and for the past seven years he had been entirely confined to his bed. Notwithstanding the fact that he was almost in a dying condition when M. Broca first saw him, some important points in his cerebral difficulty were noted. To any question put to him, he replied, as usual, “ Tan” but at the same time endeavored to make himself understood by signs. Thus he raised six fingers to indicate that six days had elapsed since the inception of his erysipelas, and by opening and shut- ting his hand four times and then raising one finger signified that he had been twenty-one years in Bicetre. Sensibility was lessened on the affected side; there was no deviation of the tongue, which could be moved freely in all directions, and no paralysis of the face beyond a slight weakness shown by the swelling of the left side when he breathed; there was a little difficulty of swallow- ing, from the fact that the muscles of the pharynx were gradually be- coming implicated. After a few days the man died. As I have said, the autopsy showed that the lesion was situated in the left anterior lobe. More exactly, however, it should now be stated 1 “ Sur le siege de la faculty de langage articule avec deux observations d’aphemie.” Bulletin de la society anatomique, tome iv., 1861. DISEASES OF THE BRAIN. that it involved the inferior marginal convolution of the temporo- sphenoidal lobe, the convolutions of the island of Reil, and in the fron- tal lobe, the frontal transverse convolution, and the posterior half of the second and third frontal convolutions. The left corpus striatum was also affected. According to Broca, the disease had in all probabil- ity begun in the third frontal convolution, and had gradually extended T to the other parts; the paralysis marking the implication of the island of Reil and the corpus striatum. The other case was that of a man named Le Long, aged eighty-four years, who had entered the hospital for a fracture of the neck of the femur. Eighteen months before, he had been treated in the medical service for a temporary apoplexy, which had deprived him of the faculty of speech, but had caused no paralysis. Le Long, whose intelligence, facial expression, and ability to gesticulate, were very striking, made himself perfectly well understood, although able to pronounce indistinct- ly a very few words, but which were nevertheless properly applied. These words were “ oui” “ non, toujovrs, tois ” for trois, and Lelo for Le Long. Thus when asked, “ Can you write ? ” he answered, “ Oui.” “ Have you any children ? ” “ Oui.” “ How many ? ” “ Tois,” but at the same time, as if aware that he was not answering correctly, he raised four fingers. “ How many boys ? ” “ Tois,” raising two fingers. “ How many girls ? ” “ Tois,” holding up two fingers. “ What time is it by this watch ? ” “ Tois,” at the same time raising ten fingers to signify that it was ten o’clock. “ How old are you ? ” To this question he replied by two gestures ; the one consisting of raising eight fingers, the other of four fingers, by which he meant that he was eighty-four years old. Aside from this application of the word tois to all numbers, his answers were perfectly correct. The tongue was neither paralyzed nor thickened; on one side the larynx was mobile, and his limbs possessed their normal power for his age. It was therefore a case of pure aphasia, or, as Broca then designated the affection, aphemia. Twelve days after the accident, the patient died. The post-mortem examination revealed the existence of lesions, almost identical in situa- tion with those of the former case. The posterior part of the third left frontal convolution, and the contiguous part of the second, had been absorbed and replaced by a serous fluid. Two cases can scarcely decide any point in pathology; but, without venturing to assert positively that the organ of language resides exclusively in the posterior part of the third frontal convolution, M. Broca expressed the opinion that the in- tegrity of this convolution, and perhaps of the second, is indispensable to the normal operation of the function of speech. Many cases were adduced by Charcot,1 by Falret,2 by Perroud of 1 Gazette hebdomadaire, 1863, pp. 473, 625. 2 Archives de medecine, tome iv., Mars et Mai, 1864. 8 Journal de medecine de Lyon, Janvier et Fevrier, 1864. APHASIA. 199 Lyons, by Trousseau,1 and others, in support of the localization of the faculty of articulate language in the left side of the brain. Most of these cases were accompanied by right hemiplegia, and, in several, post- mortem examinations showed the lesion to exist in the parts designated by Broca. In the early part of 1833, M. G. Dax, son of the M. Dax who had placed the organ of language in the left hemisphere, presented, through M. Lelut, a memoir to the Academy, in which he claimed with his father that aphasia was always the result of lesion of the left hemisphere, but he assigned a still more restricted position, by limiting it to the anterior and exterior part of the middle lobe. He cited forty cases of loss of the power of speech, coincident with lesion of the left hemisphere. Now, besides these direct cases, there are others which bear with almost as much effect on the affirmative of the doctrine in question, Thus M. Fernet, in 1863, presented a case to the Soci6t§ de Biologie, in which there was left hemiplegia, but no aphasia. After death, soften- ing of the right hemisphere, from thrombosis of the right middle cere- bral artery, was found to exist. M. Parrot * adduced another case in which there was complete atrophy of the island of Reil, and of the third convolution of the right side, but in which there was no trouble of speech. These cases go to show that the organ of articulate language is not situated in the right hemisphere. M. Lesur3 has reported a case which is of very great interest. A child was kicked on the head by a horse, and a fracture of the frontal bone was thus produced. The operation of trephining was performed at a point about an inch and a quarter above the left eye. After the operation and during the progress of the case, it was observed that, whenever pressure was made upon the brain through the hole in the cranium, the child lost the power of speech, and that when this pressure was removed she regained it. A similar case occurred several years ago in my own practice. Among British writers, Dr. Hughlings Jackson nas given the histo- ries of thirty-four cases of loss of speech coinciding with right hemiple- gia. He is entitled to the credit of making a beautiful application of anatomy and physiology to the pathology of the subject under considera- tion. The part of the brain designated by Broca as the seat of the organ of articulate language is nourished by the left middle cerebral artery. An obstruction of this artery would of course interfere with the perfect action of that region, and thus aberrations of speech would be produced. But the same artery also supplies blood to the corpus striatum of the same side. Hence the frequency with which aphasia is associated with right hemiplegia. The cause of the obstruction is gener- ally, according to Dr. Jackson, embolism, for in twenty of his cases the 1 Clinique m’edicale. 2 Gazette hebdomadaire, 1863, p. 606. 3 Gazette des hopitaux. 4 “ London Hospital Reports,” vol. L DISEASES OF THE BRAIN. heart was more or less affected, and in thirteen of them there was valvu lar disease. Among other British writers, some of whom will be more fully re- ferred to hereafter, must be mentioned, Dr. Sanders,1 Dr. Moxon,2 Dr. Ogle,3 Dr. Bateman,4 and Dr. Bastian.5 The matter does not appear to have attracted much attention from German physiologists and pathologists, since the discussion in the French Academy in 1861. Previous to that period several excellent memoirs upon the physiology of speech were published by Germans, among which that of Dr. Bergman8 is preeminent. A memoir by Nasse7 is also interesting. In 1865 Yon Benedict and Braunwart8 published a very thorough paper on the subject, and other observers have reported cases. In this country there have been several very excellent memoirs upon aphasia, and, as we have already seen, the subject early attracted atten- tion, and the fact that such a condition could exist without other mani- fest symptoms was fully recognized. Thus Prof. A. Flint9 detailed the histories of six cases, in one of which post-mortem examination showed extensive disease of the left anterior lobe, and in four, in which the situation of the hemiplegia was noted, the right was the affected side. Dr. H. B. Wilbur,10 in a memoir on aphasia, treats of the aberrations of the faculty of language as they existed in certain idiots under his observation. His cases, though interesting, are scarcely in point, as the difficulties of speech were clearly the result of mental deficiencies. A very important memoir is that of Dr. E. C. Seguin,11 in which a very excellent history of the subject is given, with the citation of forty- eight cases from the records of the New York Hospital, in which there were difficulties of speech coexisting with hemiplegia, and two in which there was no hemiplegia. In several of these cases, however, as Dr. Seguin states, the loss of the faculty of speech was due to paralysis of the tongue and other muscles concerned in articulation. Another excellent paper is by Dr. T. W. Fisher,12 of Boston. Dr. Fisher has studied the subject very philosophically, and records thirty- 1 Edinburgh Medical Journal, August, 1866. 2 British and Foreign Medico-Chirurgical Review, April, 1866. 3 “St. George’s Hospital Reports,” vol. ii., 1867. * Journal of Mental Science, January, 1868, and subsequent numbers. 5 British and Foreign Medico-Chirurgical Review, January and April, 1869. 6“Einige Bemerkungen iiber Storungen des Gedachtniss und der Sprache. Ally* .mine Zeitschrift fur Psychiatric, 1849, s. 657. I Allgemeine Zeitschrift u. s. w., 1853, s. 523. 8 Canstatt’s “ Jahresbericht,” 1865, s. 31. 9 Medical Record (New York), March 1, 1866. 10 American Journal of Insanity, July, 1867. II Quarterly Journal of Psychological Medicine, etc., January, 1868. ,2 Boston Medical and Surgical Journal, September 1, 1870, and subsequent numbers. APHASIA. 201 eight cases in which post-mortem examinations were made with defi- nite results. Cases have also been published by Bartholow1 and others. With this outline statement of the history of the subject of aphasia, we are in a position to inquire more fully into the evi- dence which locates the organ of language in a particular region of the brain. Aphasia, as it is now understood, comprises several distinct vari- eties. At the time Wernicke’s2 scientific work appeared, aphasia was classified as either ataxic or as amnesic. But Wernicke’s care- ful study of the subject led him to discard these terms and to sub- stitute in their place the terms motor aphasia and sensory aphasia. Kiissmaul3 shortly afterward made a further advance by separat- ing sensory aphasia into its two component parts, word-deafness and word-blindness. In addition to motor aphasia, wTord-deafness, and word-blindness, we also recognize agraphia, paraphasia, amnesia, and apraxia. Each one of these forms will now be considered in detail. Motor aphasia consists of the loss of the memory of how to make the muscular movements of the lips and tongue necessary for the articulation of words. When this form of aphasia exists alone, the power of voluntary speech is abolished, and also the power of repeating words that are heard. There is no difficulty in comprehending written or printed letters or words, or of understanding words that are heard. The individual has simply forgotten how to place his tongue and lips in the proper positions for producing articulate speech, but can readily express his ideas by signs, by selecting the proper letters from an alphabet to spell out w’ords, and also by writing, if the lesion is not cortical, and if the muscles of the arm are not too paretic. Word-deafness consists of the loss of the memory of the sound of words. To a person affected with word-deafness his own lan- guage sounds to him like a tongue with which he is totally un- familiar. He hears, but does not comprehend the meaning of the sounds. Word-deafness must not be confounded with word-amnesia. In the latter case the word is forgotten, but is immediately recognized as soon as it is heard, wThile in word-deafness it is not understood at all. Word-deafness and auditory amnesia usually accompany each other. Word-blindness is the loss of the memory of the appearance of words. As the form of the letters and of the words arouses no rec- 1 Medical Repertory, Cincinnati, January, 1869. 2 Wernicke, “ Die apatische Symptomen Complex,” 1874. 3 Kiissmaul, “ Disturbances of Speech,” Ziemssen’s “ Cyclo.,” vol. xiv. 202 DISEASES OF THE BRAIN. ollection in the mind of an individual suffering from word-blindness, he is, of course, totally unable to read. For the same reason also writing becomes an impossibility. It sometimes happens that though the memory of the appearance of printed or written words is lost, the memory of the form of the various letters may remain. In this case the patient can read aloud and can copy, but, of course, does not un- derstand what he has read or written. It is similar to a person who, without understanding Latin, can read aloud Latin words and per- haps pronounce them faultlessly, and yet not comprehend the meaning of a single word he has read. Agraphia is the loss of the faculty of writing, and may be either sensory or motor. Sensory agraphia accompanies word-blindness, for it is manifestly impossible to write a word if the memory of the shape of the letters is lost. Motor agraphia is the loss of the memory of how to make the muscular movements necessary in guiding the pen or pencil in the formation of letters. Motor agraphia usually occurs simultaneously with motor aphasia. Paraphasia is the loss of the power of speaking coherently. There is little or no difficulty in pronouncing words, but the words uttered fail to express their author’s meaning, and usually have no sig- nificance at all. Thus one patient referred to his boots as his “ top- sails,” while another, in trying to tell the time, called half-past twelve “ half-past candle-stick.” Amnesia is the inability to voluntarily recall memory-pictures and may involve any of the special senses. A person affected with this form of aphasia finds it impossible to recollect the names of people, or of objects which should be familiar to him. The memory-picture is not destroyed, as it is in word-deafness or in word-blindness, for the forgotten word is immediately recognized as soon as it is heard or seen, but in most instances it is immediately forgotten again and can not be recalled by any voluntary effort of the will. Thus a person affected with amnesic aphasia is shown a knife and the question is put to him “ What is it ? ” Immediately he shows by intelligent signs that he knows what the object is used for. He will go through the motions of opening and shutting the knife, or as if he was cutting a piece of stick, and you can frequently see from the expression of the countenance that he is making every effort to think of the proper name. You ask him: “Is it a watch?” “No.” “Is it a hat?” “No.” “Is it a knife?” “Yes, yes, a knife, a knife—that is it.” In a moment you hold up the knife again and ask him to name it, only to find that he has again forgotten it. Apraxia, though not a form of aphasia, frequently occurs with it ; particularly with word-blindness and word-deafness. Apraxia is the term used to designate the inability of an individual to comprehend APHASIA. 203 the uses or imports of objects. This condition was first described by Kiissmaul1 and more recently by Starr,2 who reports nine cases of apraxia occurring with word-blindness, in all of which autopsies were obtained. To detect apraxia it is simply necessary to show to the person to be tested several objects with which all people are more or less familiar, and see if he recognizes them and uses them for the pur- poses for which they were intended. If he fails to do this, then apraxia is present. Apraxia is not necessarily confined to psychical blindness. There may be apraxia of hearing, of smell, of taste, and of the tactile sense. Pathology.—The lesions producing the different forms of apha- sia are invariably situated in the left hemisphere of the brain in right-handed persons, and in the opposite hemisphere in left-handed persons. The lesion resulting in motor aphasia is situated in the posterior part of the inferior frontal convolution, or Broca’s convolution as it is sometimes called, and perhaps in the contiguous region of the an- terior central convolution wdiere the centres for the lips and tongue have been located. Lesions in the motor conducting paths below this region of the cortex also produce motor aphasia, and, as Gow- ers3 points out, if the lesion is immediately below the cortex, the aphasia becomes permanent, since a lesion in this position would involve the commissural fibres, as well as the fibres of the direct speech tract, and thus there would be no pathway for the outward transmission of motor speech impulses. But if the lesion affects the speech tract lower down, as, for instance, in the internal capsule, then the aphasia will be transient, because the motor impulses can pass from the centre on the left side to the corresponding centre in the right hemisphere, thence through the right internal capsule to the lips and tongue. Word-decifness is due, as was first pointed out by Wernicke, to a lesion involving the posterior two-thirds of the first temporal convolu- tion. It is probable that a lesion of the posterior part of the second temporal convolution will also result in word-deafness. Word blindness is produced by a lesion involving the angular gyrus and the supra-marginal convolution. The situation of the lesion resulting in motor agraphia has not been definitely determined, but recent investigations lead to the belief that it is to be found in the motor centres for the fingers in the posterior central convolution. The accompanying diagram (Fig. 16), modified from Naunyn, illustrates the position of the lesions in the forms of aphasia just de- scribed. T Kiissmaul, op. tit. 2 Starr, Med. Rec., October 27, 1888. 3 Gowers, “ Diseases of the Nervous System,” 1888, 204 DISEASES OF THE BRAIN. In paraphasia we are again indebted to the careful researches of Wernicke for the first absolute knowledge of the situation of the lesion resulting in this form of aphasia. Wernicke’s cases led him to believe that paraphasia was due to a lesion of the association tracts between the word-speaking centre in the posterior part of the inferior frontal convolution and the word-hearing centre in the temporal con- volutions. Recent post-mortem investigations confirm this view. Fig. 16. The lesion is usually found to involve the island of Reil and the parts directly under it. The island of Reil lies directly over the association tract passing between the word-speaking and the word-hearing centres. Although the lesion is usually situated in the position just mentioned, a lesion which involved this association tract in any part of its course would be attended by the same result. In simple amnesia the situation of the lesion is not definitely known. Starr 1 advances the theory that “ auditory amnesia is caused by a lesion in the association tracts leading to the temporal convolu- tions, in distinction fi’om word-deafness due to a lesion in those convo- lutions.” This theory is plausible, but is unsubstantiated, as its author admits, by post mortem evidence. It would certainly seem probable, when the appearance of an object fails to arouse the recol- lection of its name, and that feeling it, tasting it, or smelling it, if these are possible, enables the individual to recall the name desired, that the lesion must be in the association tracts and not in the cortical centre. But when it becomes impossible for an individual to spon- taneously think of a word, of the name of an object, or of the name of 1 Starr, op. cit. APHASIA. 205 a person, in which case neither the special senses nor the association tracts are necessarily used at all, then Starr’s theory becomes unten- able. The lesion in such a case probably lies in the same situation as the lesion for word-deafness—that is, in the posterior part of the first and second temporal convolutions, but, unlike the lesion producing word-deafness, it does not destroy the memory-picture, but simply inhibits its regeneration. The lesion producing apraxia with word- blindness is situated in the tempoi-o-occipital region. Apraxia is not confined to psychical blindness. There may be apraxia of any of the senses, but as yet there is no post-mortem evidence to prove the location of any of these forms of apraxia except apraxia with word- blindness. The following cases illustrate the different forms of aphasia. Case I. Motor Aphasia.—W. W., aged forty-one, entered the New York State Hospital for Diseases of the Nervous System, August 22, 1870, hemiplegic on the right side, and affected with ataxic aphasia. In the month of March, 1868, as ascertained by Dr. Cross, the resi- dent physician of the hospital, he was seized with a dull pain in the right knee, accompanied with numbness, formication, and pricking sensations, limited to the right foot, while general numbness of the whole side soon supervened. These, with loss of power, gradually extended and increased till at the end of two weeks the patient was entirely hemiplegic. There was at no time any loss of consciousness nor any mental aberration. On the 11th of May following, the patient suddenly lost the power of speech, but his mind remained per- fectly clear, and, though he could not utter a word, he understood well everything that was said to him. He remained nearly com- pletely aphasic for four months, being only able during that time to utter a few sounds, which could not be interpreted into intelligible words. About September, 1868, he began to enunciate a few words, at first very slowly and indistinctly, and gradually acquired more facility. When I presented him before the class at the Bellevue Hospital Medical College, in November, 1870, although he could talk, his power of co-ordination was very imperfect, and many words were articulated with great difficulty. This trouble was chiefly manifest- ed in regard to labials and linguals, such wrords as “ truly rural,” “ Peter Piper,” “ baker,” and others of the kind, causing him to make repeated efforts before he could even imperfectly pronounce them. There was no paralysis of the tongue, no deviation when it was pro- truded, and but very slight if any paresis of the orbicularis oris or other facial muscles. The arm and leg on the right side were pro- foundly paralyzed. In this case there was no loss of the memory for words, and no difficulty in writing. It was, so far as the aphasia was con- 206 DISEASES OF THE BRAIN. cerned, entirely motor in character, and accompanied by right hemi- plegia. My opinion is that there had been a lesion involving the motor division of the internal capsule and that the recovery from the aphasia was due to the fact that the lesion was too low down to affect the commissural fibres passing through the corpus callosum, and that the speech impulses were eventually transmitted through this channel in the manner previously mentioned. Case II. Amnesia and Partial Motor Aphasia.—A. E., formerly a bookseller, consulted me in the autumn of 1869 for what was con- sidered by his friends to be, and what probably was, softening of the brain. Before any symptom of disease appeared he had been noted for his remarkable memory, but was now exceedingly forgetful, especially as regarded words. Thus he had forgotten his first name, and could not tell me the names of his children. His conversation was marked with great hesitancy, from his not remembering the words he wushed to use, and there was, besides, marked difficulty of articulation, and some words he could not pronounce at all. There was right hemiplegia, wThich had gradually been getting worse, and which, when I saw him, was extensive enough to interfere materially with the movements of his arm and leg. The left side was not affected, and the tongue and face were apparently not paralyzed. He was sub- sequently lost at sea in the City of Boston. This case, therefore, exhibited both the amnesic and motor forms of aphasia, and was accompanied by right hemiplegia. I regard the condition as being due to thrombosis, probably of the left middle cere- bral artery. Case III. Word-deafness with Auditory Amnesia, Word-blind- ness, and Apraxia.—C. D., aged forty-six, consulted me in October, 1886, for epilepsy. He was a Frenchman, but had been in America many years and spoke English fluently. He had had epileptic attacks for two years, at first infrequently, but lately as often as five or six times a day. Under treatment the attacks diminished to about one a month. On Christmas Day, 1888, he had a sudden attack of hemipa- resis on the right side of the body, which was, however, unattended by loss of consciousness. Examination showed that he was word-deaf, but only for English words. Any remark addressed to him in French was readily comprehended and replied to in French, but he was totally unable to understand anything said to him in English. There was also amnesia for English words. When asked in French to tell the English names of different objects which were shown to him, he could not do so, although he promptly named them in French. He was also word-blind, but only for English icords. French books he could read and discuss intelligently, but English books he could not read at all. There was no apraxia present at this time. APHASIA. 207 I saw him again on May 5, 1889. The right arm -was completely paralyzed, the right leg partially so. Word-deafness was complete for both English and French words. He could talk fairly well in the French language, but was totally unable to understand a single word that was said to him. Word-blindness was now present for both Eng- lish and French words. He was therefore iinable to read in either language. Apraxia was also observed. He did not know what a match was used for. At his meals it was noticed that he did not know what his fork was for, although he could have used it perfectly well, as his left arm was not paralyzed in the slightest degree. Many other objects, the uses of which he had formerly understood, were now shown to be utterly unknown to him. I saw him for the last time on July 3d. There was no change in his condition except that the right leg had become completely para- lyzed. He died the following month, but no post-mortem examination could be obtained. Case IV. Motor Aphasia, Paraphasia, and Word-blindness.— H. I., a merchant, consulted me in August, 1869, for hemiplegia, with inability to speak. While sitting at his desk, six weeks previously, he suddenly became vertiginous, and lost consciousness for a few moments. On recovering his senses, he discovered that he was paralyzed on the right side, and that he could not speak a word. He was exceedingly anxious to make known some wish, and one of his clerks brought him paper and a pencil, but he could not write a letter. An alphabet was then written, but he was unable to select the letters to form the words he wanted to use. A physician was sent for, and Mr. I. wras bled to the extent of six- teen ounces, without any favorable result. He remained hemiplegic and completely aphasic for about two weeks. He then began to walk, and acquired the ability to say “wThat,” “ certainly,” and “ saw my leg off,” which he contracted into “ sawmelegoff,” accentuating strongly the ultimate syllable. These words he used without apparent intelli- gence, though he clearly understood all that was said to him, and laughed at any joke as heartily as ever. His condition was about the same when I saw him. He could protrude his tongue and move it actively in all directions, but could not articulate any words but those mentioned. Thus, when I asked him to say “ table,” he said “ Certainly ” ; and when I said “Well, say it, then,” he exclaimed, “Sawmelegoff!” At the same time, to show that he understood what I said, he went across the room and put his hand on a table, uttering, at the same time, his full stock of words, “ what,” “ certainly,” “ sawmelegoff.” I then asked him if he could write ; he replied, “ Certainly.” I placed paper before him, and gave him a pen with ink, but he was unable to write his name as I requested, although he could use his 208 DISEASES OF THE BRAIN. fingers for other things tolerably well. I asked him to draw a series of parallel lines, and he did so without difficulty. On my insisting that he should now make an effort to write his name, he made the attempt with the result shown in the accompanying woodcut (Fig. 17). I told him that was not his name, at which he gesticulated Fig. 17. violently, exclaimed “ Sawmelegoff ! ” and gave me one of his vis- iting-cards. This gentleman continued under my care for some time, but with no perceptible change, lie had had two attacks of acute articular rheumatism, and had, when I saw him, both aortic and mitral insufficiency. My diagnosis was embolism of the left middle cerebral artery. Case V. Paraphasia.—Captain C., an officer of the mercantile marine, was attacked in September, 1874, with sudden loss of the power of speech, attended with confusion of ideas, and vertigo. He soon recovered, but had several subsequent seizures, characterized by vertigo, impairment of language, and slight delirium. I first saw him on the 31st of October, and on the 28th of November he went with me to the University of New York, where he was one of the subjects of my clinical lecture on aphasia, delivered to the medical class. At this time, and for several wTeeks previously, he had constantly used words which were without relation to the things he washed to name. Thus, if he wanted his boots, he would ask for his top-sails, or wTould be apt to employ some other word designating part of a ship. In bis con- versations with me he continually exhibited this peculiarity. There was no want of memory for any other parts of speech than substan- tives. For instance, I held up a penknife before him ; he at once said it was to cut with, but when I pressed him to name it, he called it a “ boat.” A thermometer was an “ anchor,” and a watch was a “capstan.” When I asked him to say “National Intelligencer,” he said “National intelligence-office,” and, no matter how often I repeated the words, he always said “National intelligence-office.” The reason for this v’as very obvious : he had frequently had occasion to say “intelligence-office,” but had probably never before in his life been asked to say “National Intelligencer.” After a time he succeeded in acquiring the powrer to utter the final “ e r,” but then he placed it in the wTrong position, and said “ National intelligence-officer.” Syllable by syllable, he could speak these wrords correctly, but they were at once forgotten. Case VI. Paraphasia, and Agraphia.—Mrs. L., forty-three years APHASIA. 209 of age, consulted me in December, 1888. About a month previous to my seeing her she had awakened at her usual time in the morn- ing and found that her right arm and leg were very much weak- ened. At that time the peculiarity of her speech was observed and had continued ever since. She was able to pronounce many words perfectly, while other words were frequently mispronounced. Thus, “ pouring ” was “ pawling,” a “ battery ” was a “ battlewag,” and “ vaseline ” was “ very green.” There was also a tendency to sub- stitute a word or words in a sentence in place of the proper words, so as to make the sentence incoherent. Thus she said that “ she had just been to peppermint,” meaning, however, that she had just been to church. “ Half-past twelve ” she called “ half-past candle- stick.” She was also unable to write a single word. With a pen or a pencil she could draw fairly well, and could copy letters with con- siderable accuracy. Case VII. Motor Aphasia and Word-blindness.—G. E., a noted physician of this city, was suddenly stricken with apoplexy. On re- gaining his consciousness it was observed that, although he compre- hended everything that was said to him, he could not speak a single word spontaneously, neither could he repeat words when asked to do so. Thinking that he might be able to express his thoughts by means of letters formed into words, an alphabet was brought to him, but he could not arrange the. letters so as to form words. He had lost the visual memory of the letters. When words were formed from the letters and shown to him, he failed to comprehend them. He had therefore lost the visual memory for words also. This con- stitutes a perfect example of word-blindness accompanied by motor aphasia. Case VIII. Amnesia and Agraphia.—During the winter of 1868-’69 a man came to my clinic, at the Bellevue Hospital Medical College, who was aphasic, and from whose friends, his own gest- ures, and the few words he could speak, I obtained the following history: Some months previously he had been working in a stone- quarry, and was struck by some piece of machinery on the left side of the head, at about the junction of the frontal with the temporal bone. For a short time he was unconscious, recovering, however, without paralysis, but with loss of the memory of words. When he came under my observation he was very intelligent, comprehended every word said to him, and made repeated and persistent efforts to talk, but he could not utter a word spontaneously beyond “ yes ” and “ no,” which he always used correctly. Thus, when I asked him where he was born, he became much excited, gesticulated violently, and appar- ently made every effort to tell me. The perspiration stood out in large drops on his forehead, but no sound came from his lips. Then the following conversation took place: “Were you born in Prus- 210 DISEASES OF THE BRAIN. sia?” “No.” “In Bavaria?” “No.” “In Austria?” “No.” “In Switzerland?” “Yes, yes, yes—Switzerland, Switzerland,” at the same time laughing, and moving his hands actively in all direc- tions. He could pronounce words wrell, but could not write. I took occasion to speak at length on the subject of aphasia, and gave it as my opinion that there had been a fracture of the internal table of the skull, and that a fragment of bone was pressing on the posterior and lateral part of the anterior lobe. Prof. Sayre was pres- ent, and I advised him to trephine the patient, with the view of elevat- ing any depressed piece of bone, and restoring the normal function of that part of the brain. The operation was performed a few days afterward, the patient being placed under the influence of ether. The internal table was found to be fractured, and a splinter wras pressing on the anterior central convolution. It was removed, and, as soon as the patient emerged from the anaesthetic condition, he spoke perfectly well. Case IX. Motor Aphasia and Agraphia, folloioed by Parapha- sia.—J. II., a captain of a coasting-vessel, consulted me in November, 1804, for difficulty of speech with which he had been affected for sev- eral months. Upon inquiry, I ascertained that one morning early he had been called from his bed upon some duty connected with his ves- sel ; that he had risen rather hastily and gone on deck ; that while giving an order he suddenly became very dizzy, and fell, unconscious. He soon regained his senses, but found that he was paralyzed on the right side, and had lost the ability to speak. It was subsequently ascertained that he had also lost the ability to write. He could under- stand all that was said to him and could read. His agraphia and aphasia were therefore both motor. He soon afterward reached port, and remained at home for three months, during wdiich period the paralysis disappeared almost entirely, and he reacquired the ability to speak and to write. He then went to sea again as a passenger to Cuba, and while in Havana had another attack similar to the first, but without paralysis of motion, though there was loss of sensibility on the right side. The memory for words was entirely destroyed, though he could pronounce distinctly any Avord he Avas told to say, if he did not allow too long a period to elapse between the direction and the response. About four months after his last seizure he consulted me. At this time he could say a few words, and he employed them to express all his ideas, assisting himself with very energetic gestures, Avhich, however, were rarely expressive of his thoughts. The words he thus constantly used were “ sifi,” which signified both “ yes ” and “no,” and “time of day,” which he employed when he had any other answer than a simple affirmative or negative to give. Besides these expressions, he had an oath, “ Hell to pay ! ” which he ejaculated APHASIA. 211 whenever he did not succeed in making himself understood, and some- times without any such exciting cause. These were the only expres- sions he could originate, but he could pronounce distinctly any word he was told to say, and even as many as three short successive words. When told to write, he took the pen, and, on my telling him to give me his name and address, wrote “ Time of day,” and then, seeing that that was not the correct answer, immediately followed it with “ Hell to pay ! ” On my remarking to him that he had given me wrong information, he immediately wrote “ sifi.” Any word, however, which I told him to write, he did without any difficulty, and thus I obtained several long sentences from him. From his brother, who came with him, I obtained the facts in his history I have mentioned. Examining his heart, I found that he had a strong systolic murmur, and was told by his brother that he had had, fifteen years ago, a first attack of acute articular rheumatism, which had been followed by several other attacks. Many other cases of aphasia have come under my observation, but it is scarcely necessary to mention them in detail, as they present no features differing in any material point from those cited. It will be observed, however, that simple uncomplicated cases of any one form of aphasia are uncommon. Motor aphasia occurs more frequently than any other form, and is more liable to occur independ- ently of any other variety of aphasia. The reason for this is obvious. Motor aphasia frequently accompanies ordinary hemiplegic attacks resulting from a cerebral hemorrhage, involving the anterior two- thirds of the internal capsule. In such a case only the motor tract is injured, and, of course, only motor aphasia is produced. This aphasia is usually transient, which is in direct contrast to motor aphasia of cortical or immediately subcortical origin. On the other hand, word- deafness, word-blindness, and amnesia are more frequently caused by embolism or thrombosis of an artery which results in the softening of quite an extensive area of the cortex. It is for this reason that word- blindness and word-deafness are so frequently associated. As to the causes, the prognosis, diagnosis, morbid anatomy, and pathology, they have been sufficiently considered in the remarks made, and the treatment is of course that of the pathological condition to which it is due, whether this be cerebral haemorrhage, embolism, throm- bosis, softening, hysteria, wounds, the bites of poisonous serpents, syph- ilis, or other cause. One point, however, should be mentioned in this connection, and that is that constant efforts should be made to develop the uninjured speech-centre, and to exercise the vocal organs by con- stant attempts to speak. The application of the galvanic or faradaic currents to the tongue and other muscles concerned in articulation is a measure of usefulness. 212 DISEASES OF THE BRAIN. CHAPTER VIII. ACUTE CEREBRAL MENINGITIS. By acute cerebral meningitis is understood inflammation of two membranes of the brain—the pia mater and arachnoid. Some writers have made the attempt to discriminate between inflammation of the arachnoid and inflammation of the pia mater, but there are no diagnostic marks by which such a distinction can be made, and we find from post- mortem examination that neither membrane can be inflamed without the other participating in the morbid process. Inflammation of the dura mater is never included under the term meningitis. The ancients made no distinction between the several inflammatory affections of the intra-cranial organs, but comprehended them all in one disease, which they called frenzy— << Progressive Facial Hemi-atrophy,” Journal of Nervous and Mental Diseases, Octo ber, 1876. 532 DISEASES OF THE SPINAL CORD. ministered strychnia and other tonics without benefit. This treat- ment, however, seems to be indicated, and is in general urged by those who have written on the subject. No cure has yet been re- ported. It must be borne in mind that diseases which arc slow to advance are also slow to recede. III. INFLAMMATION LIMITED TO THE POSTEEIOB TEACT OF GEAY MATTEL OF THE SPINAL COED. The posterior tract of gray matter, the columns of Burdach, or the postero-external columns, and the columns of Goll, or postero-median columns, are probably the only channels by which sensations reach the brain from the parts below. Recently Gowers1 has described a tract on the periphery of the cord, situated externally to the crossed pyramidal tract in lower levels of the cord, and anteriorly to it in higher levels, which degenerates upward. This distinguished investi- Fig. 64. A. C., anterior commissure. P. C., posterior commissure. I. g. s., intermediate gray sub- stance. P. Cor., posterior cornu. C. C.P., caput cornu posterioris. L. L. L., Lateral limiting layer. A.-L. A. T., antero-lateral ascending tract, which extends along the periphery of the cord. Diagram ot a section of the spinal cord in the cervical region. (Gowers.) gator considers that the sensations of pain and temperature are trans- mitted to the brain through this tract, but as yet this view has not been confirmed by sufficient evidence to make it conclusive. The fibres which constitute the posterior nerve-roots do not, on their en- 1 “ Diagnosis of Diseases of the Spinal Cord,” INFLAMMATION OF THE POSTERIOR TRACT OF GRAY MATTER. 533 trance into the cord, follow any uniform course. Some of them pass directly over to the motor cells in the anterior horn of the same side ; others terminate in the cells of the posterior horn either at the level at which they enter the cord, or else after passing upward or down- ward for a short distance ; some seem to approach and probably end in the group of cells situated near the junction of the posterior horn, and the posterior commissure known as the vesicular column of Clarke ; others pass by way of the posterior commissure to the column of Bur- dach on the opposite side ; and others again enter the columns of Coll and Burdach on the same side. The column of Goll, and possibly part of the column of Burdach, are made up of long fibres which pass up the entire length of the cord and decussate in the pons. This tract unquestionably is the conduct- ing path for the muscular sense. The tracts through which sensations of pain, touch, and temper- ature are transmitted to the brain are not definitely determined. To Brown-Sequard we are indebted for a knowledge of the fact that the sensory tract, with the exception of the muscular sense, decussates almost immediately after entering the cord. If, therefore, a lateral half of the spinal cord be divided so as to include the whole of the gray matter, the animal upon which the experiment is perfoi’med loses sensibility in the parts below, on the opposite side of the body, and—which is not, however, a matter of present inquiry—motion on the same side. Brown-Sequard’s investigations led him to believe that sensory im- pressions were conducted to the brain through the posterior horns of gray matter ; but the probability is, though the question is not yet definitely settled, that sensations of pain and temperature reach the brain through Burdach’s column, passing up on the side opposite to that on which the nerve-roots enter the cord. The sensation of touch may be transmitted through the same channel, but there is some evidence which points to the partial confirmation of Brown- Sequard’s theory, and perhaps it may yet be shown that the sense of touch may reach the brain through the posterior columns of gray matter. Cases in which phenomena of loss of motion on one side and of sensibility on the other are coexistent from spinal disease are by no means very infrequent. Several such have been under my care in hos- pital and private practice, and I have always attributed them to a lesion of one lateral half of the cord disturbing the power of motion on the same side and of sensation on the other. But experiment shows that, w*hile one part of the posterior nerve- roots passes over to the opposite side immediately on its entrance into the cord, another part passes upward and another downward. The effect, therefore, of a limited lesion involving one lateral half of the 534 DISEASES OF TIIE SPINAL COED. cord would be profound aneosthesia of the opposite side of the body and a slight degree on the same side. Accordingly, in such cases as those I have referred to, there is always a trace of numbness on the side the motion of which is paralyzed. The action of a lesion of one lateral half of the cord in only slightly diminishing sensibility on the side of the alteration while greatly lessening it on the opposite side will be readily understood from an examination of Fig. G5 : a, the left half of the spinal cord, b the right half ; c, a right posterior root, with its ascending fibres d, its descend- ing e, and its decussating fibres f; g, decussating fibres from the op- posite side. A lesion of the right side of tbe cord at h will produce great loss of sensibility on the op- posite side, and slight loss on the same side. With this brief statement of the physiology and pathology of the subject, I leave the further consideration of the diseases of the poste- rior tract of gray matter till science has given us more definite in- formation than we now possess relative to its functions and de- rangements. Fig. 65. IV. INFLAMMATION OF THE ANTERIOR AND POSTERIOR TRACTS OF GRAY MATTER OF THE SPINAL CORD. The gray matter of the spinal cord as a whole, is subject to at least one disease—tetanus—which, according to recent investigations, is in reality a central myelitis. Since Lockhart Clarke in 1864 gave the re- sults of his examinations on this subject, other data to a like effect have been published, and, though differences in the lesions have been observed these are of secondary importance to the main fact that in tetanus the central gray matter is the chief seat of the alterations. The circum- stance that the white matter has also been found diseased no more in- validates the correctness of the statement than the fact that a patient dying with the symptoms of pneumonia, still has that disease, even though there be a patch or two of inflamed pleura as a secondary lesion. Two varieties of tetanus are generally described by systematic writers—the idiopathic and the traumatic; but, as they are character- a. Tetanus. TETANUS. 535 ized by similar phenomena, differing mainly as to their modes of origination and severity of their symptoms, there would be no advan- tage in considering them separately. Symptoms.—The first symptom to make its appearance in cases of tetanus is a feeling of pain or oppression in the epigastric region. In the beginning it does not attract much attention, but, as the disease advances, it becomes exceedingly severe, and adds greatly to the dis- comfort of the patient. Soon after the occurrence of this pain uneasiness is generally ob- served about the throat. This is, perhaps, no more than a sense of stiffness of the muscles concerned in deglutition, but it is not long before swallowing is impeded to a considerable extent. With these symptoms there are ordinarily mental and physical depression, sensa- tions of chilliness, and a general feeling of malaise. The foregoing constitute a prodi’omatic or formative stage, which may last a few hours or several days, and which is occasionally over- looked when the disease is intense and rapid in character. In the next stage the epigastric pain is still a prominent symptom. It is seated just below the sternum, and generally extends backward to the spinal column. It appears to be due to spasm of the diaphragm, so that this muscle is among the first, if not the very first, to be affected in the vast majority of cases. The difficulty of swallowing increases, and then the muscles of the jaws become contracted, constituting the condition known as trismus or lockjaw. At first there is only stiffness of these muscles with those of the neck, but gradually they become rigid, and the patient experiences difficulty, if not impossibility, in opening the mouth. The facial muscles do not escape, and an expres- sion like the risus sardonicus is produced from the retraction of the angles of the mouth, the elevation of the alee nasi, and the expansion of the nostrils. At the same time the eyes are staring, the brows cor- rugated, and the countenance anxious or wearied in appearance. Sometimes gradually, at others suddenly, the morbid action extends to other muscles. Generally it passes to those of the neck, the back, and the loins, causing violent contraction, and bending the body back- ward. This state is called opisthotonos. The contraction of the power- ful muscles referred to is so great as to cause the body to assume the form of an arch, the head being thrown far back, the abdomen pro- truded, and thus, if the patient were placed on his back, only the occiput and heels would touch the bed. Opisthotonos is the usual va- riety of spasm. Two other formg are occasionally met with. In one of these—em- prosthotonos—the body is bent forward from the contraction of the thoracic, abdominal, and pelvic muscles. In the other—pleurosthotonos— it is bent laterally. This latter may be met with in opisthotonos, owing to the muscles on one side being more strongly affected than on the 536 DISEASES OF THE SPINAL CORD. other. Both emprosthotonos and pleurosthotonos are rare. Of very- many cases of tetanus that have been under my observation, I have only seen the former four and the latter three times. The spasms characteristic of the disease are tonic; hut, though they do not entirely relax, they are marked by more or less exacerbation, accord- ing to the severity of the attack and the care taken of the patient. Any cause calculated to excite reflex action will induce an acces- sion. Thus the contact of the bedclothes with the body—the legs especially—the touch of the hand, the forcible shutting of a door, the rumbling of carriages in the street, even the blowing of a breath of air on the skin, may produce an aggravation of the spasm. Even without any apparent excitation these fits occur. They are marked by great pain, and may be so violent as to break the teeth, and the bones of the legs, and tear the large muscles of the thigh. During their continuance, and often when they are not present, the pain at the pit of the stomach becomes unendurable, and the patient may lose consciousness through its intensity. I have several times seen this event occur. The tonic rigidity of the muscles of respiration induces diffi- culty of breathing, and the same result may ensue from spasmodic closure of the glottis. Death has frequently taken place suddenly from one or other of these causes. With all this muscular excite- ment and mental disturbance there is in the early stages rarely any fever. Toward the close, however, the skin is hot,, and the ther- mometer often ranges from 105° to 110° Fahr., or even higher, but the pulse remains small and weak. Owing to the difficulty of swallowing, the patient suffers from hun- ger and thirst, and thus the powers of the system are still further re- duced. The bowels are always obstinately constipated. Wakefulness is generally present from the first. When the patient does sleep, it usually happens that the muscles are relaxed, to be again suddenly affected with spasm as soon as he awakes. The mind is clear throughout, even in the most severe cases. When loss of consciousness occurs from extreme pain, it is from syncope, and not from any implication of the brain in the essential nature of the disease. Death usually takes place by apncea. It may, however, re- sult from exhaustion, and, according to some authorities, from the spasmodic action attacking the heart. The duration of the disease is very variable. The shortest case on record is one observed by Prof. Robinson, of Edinburgh. The patient, a negro wTaiter, cut his finger with a piece of broken china. He was immediately seized with tetanus, and died within fifteen minutes. Mr. Poland quotes a case in which death took place in five hours ; in a case cited by Lepelletier in a few hours ; in one by Dr. Jackson in twelve ; in one by Dr. Leith in eighteen; and in one observed by Mr. Curling TETANUS. 537 in nineteen.1 The shortest duration in any case I have witnessed was twenty-six hours, though I believe there were several much shorter, which occurred during the recent war in this country. The average period of duration in fatal cases is from the third to the fifth day. Instances in which it has been prolonged far beyond this limit are not uncommon. Hennen2 reports a case in which it lasted six weeks, and then the patient died of another disease. He reports another case in which it lasted seven weeks, and ended in recovery. I have seen three cases in which it extended to the fifth week. The period which elapses between the reception of the cause and the beginning of the symptoms is also subject to a great variation. In a case already cited it was only fifteen minutes ; in another, quoted from Dr. Randolph by Reeves,3 the spasms ensued immediately after the patient was stung by a bee ; and in another, which occurred in his own experience, they came on in a sensitive female immediately after running a needle into her finger. There is doubt, however, as to such cases really being tetanus. In the last one cited it is stated that “the body and extremities 'were rigid, mouth closed, and the jaws fixed, the eyes the same. At short intervals the whole body was affected with convulsive shocks; the administration of a dose of chloroform removed them, but the back and neck remained rigid for three days.” This attack was probably a manifestation of hysteria. In eighty-one cases collected by Mr. Curling, the disease began between the fourth and fourteenth days, both inclusive, and in nine- teen on the tenth day. The following table from Reeves shows the period of the occur- rence of the disease in three hundred and forty-three cases : Within 6, 12, 18, or 24 hours 12 From 1 to 2 days 12 “ 3 “ 5 “ 37 “ G “ 8 “ 94 (( g « jo « “ 12 “ 14 “ 52 From 15 to 1*7 days 25 “ 18 “ 20 “ 9 “ 21 “ 23 “ 9 “ 24 “ 2G “ 6 “ 27 “ 29 “ 9 “ 30 “ 32 “ 1 Causes.—The inicrobic origin of many cases of tetanus seems to be beyond dispute. It is claimed by many, and perhaps with a great deal of reason, that all cases of tetanus, whether traumatic or idio- pathic, are due to the presence in the system of the tetanus bacilli. The power of this microbe to induce tetanus was first successfully 1 All the above instances are quoted from Reeves’s “ Diseases of the Spinal Cord and its Membranes,” London, 1858, p. 387 ct scq. 2 “ Observations on some Important Points in the Practice of Military Surgery,” etc., Edinburgh, 1818, p. 263. 3 Op. til., p. 377. 538 DISEASES OF THE SPINAL CORD. demonstrated by Rosenbaoh1 in 1886, and confirmed later by Iloch- singer,2 Yanni and Garri,3 Bonome,4 and others. Bonome describes the bacillus as “ slender and bristle-like, with a small colorless swell- ing at each end like the head of a pin.” This bacillus had previously been described by Nicola'ler6 in connection with cases of tetanus. Pus containing these bacilli, when injected into the muscles or be- neath the skin of an animal, invariably induced tetanus, but when injected into the blood failed to do so. Hochsinger,6 however, in a later article on this subject, claims to have discovered that although the tetanus bacilli is not found in the human blood in subjects suffer- ing from tetanus, yet the blood possesses poisonous qualities, and, when injected into animals, invariably induced tetanus. The tetanus microbe is found in the earth, and, according to Bonome, in the dust and mortar of old buildings. It is only necessary for the microbe to be deposited in some open wound, or to be introduced into the sys- tem in some other manner, in order that tetanus should be developed. According to this theory, tetanus cannot be considered as traumatis- mal in the proper sense of the word, the wound simply being the means of the introduction of the tetanus microbe into the system. The most common cause of tetanic infection is bodily injury of any kind, from the' slightest to the most severe, and of any part of the body; although wounds of some parts, as of the thumb and great-toe, are more apt to be followed by the disease than those of other regions. Jt has been known to result from the bite of a tame sparrow, from the sticking of a small fish-bone in the pharynx, from a seton in the thorax, from the stroke of a cane across the back of the neck, from the blow of a whip-lash, from fractured bones, and from every other imaginable wTound or injury. In a case under my charge in this city, it was caused by a splinter of wrood slightly scratching the palm of the hand; in another, a slight punctured wound of the foot produced it. Next in frequency to wmunds, tetanus is induced by exposure to cold and damp. This is the exciting cause in the majority of cases of idiopathic tetanus, and it increases liability in those w7ho have suffered from wTounds. It was not uncommon, during the recent war, for the number of cases of tetanus to be much increased immediately after a sudden change of the weather from dry and mild to wet and cold. It has also apparently been caused by wrorms, by abortion and labor, and by diseases of the womb. Terror has the reputation of having in- 1 Archiv fur klin. Cliir., Berlin, 1SS6—’87, xxxiv., p. 306. 2 Centralblatt fur Bacteriol. und Parasitenk., Jena, 1887, x., p. 1068. 3 Spcrimentalc, Firenze, 1887, lix., p. 617. 4 Gior di Ii. Acad, di Med. di Torino, 1886, 3d S., xxxiv., p. 759. 5 “ Beitrage zur Aetiologie des Wundstarrkrampfe,” Gottingen, 1885. 6 Fortschritt der Med., February 5, 1888. TETANUS. 539 duced tetanus in one case reported by Dr. Willan, and in others ob- served by Hennen. In the form occurring in very young children, and known as tris- mus nascentium, it appears to be induced by inattention to the cut um- bilical cord. The tendency to tetanus, especially among soldiers and others who have been wounded, is increased by poor diet, confinement in ill-venti- lated hospitals, inattention to cleanliness, and neglect to give proper care to the wounds they may have received. Diagnosis.—The only affections with which tetanus is liable to be confounded, by any but the most ignorant, are the hysterical simulated affection, and the condition induced by poisoning with strychnia and other substances of its class. That hysteria can simulate tetanus, as well as almost all other dis- eases, we have abundant evidence. A case has already been referred to in this chapter which was evidently hysterical, and several others have come under my observation. A lady now under my charge has repeated attacks of hysterical spasms, during which her jaws are tight- ly closed, she is unable to swallow, and her body is bent backward so as to assume the position of opisthotonos. Such seizures are readily distinguished from tetanus by the facts that they are unaccompanied by pain or real distress, are of very tran- sient duration, and are accompanied by other manifestations of hys- teria. From the artificial tetanus caused by strychnia, the diagnosis is more difficult; for, so far as the more obvious symptoms go, there is such a great similarity that even the most skillful diagnosticians might be, for a time, undecided. It is well known that strychnia is not unfre- quently used for the purpose of committing murder or suicide, and it is possible so to employ it for either of these purposes as to cause its effects to extend over a long period of time, and thus to add to the difficulties attending the discrimination. Even in such a case, however, the diagnosis can be made if due care and a thorough inquiry into the history of the case be made. In the first place, the tetanus of strychnia always shows itself in the lower extremities before trismus ensues. The legs are stretched widely apart, and the hands are generally involved. In natural tetanus, trismus precedes spasm in the extremities; indeed, the lower extremi- ties are rarely affected to any great extent. The arms generally escape altogether. The epigastric pain, which constitutes so prominent a feature of true tetanus, is not present in the toxic variety. I have witnessed three cases of poisoning by strychnia, and this pain was not complained of in either of them. In the tetanus of strychnia, the symptoms are developed with great 540 DISEASES OF THE SPINAL CORD. rapidity, and death takes place generally within a half an hour, al- though life may be prolonged, in exceptional cases, somewhat beyond this period. In true tetanus it is very rarely the case that death takes place within twelve hours, and ordinarily not till several days have elapsed. In those cases of poisoning by strychnia in which the doses have been small, and administered at comparatively long intervals, the symp- toms are mitigated in violence, and consequently one of the distinguish- ing features of the two affections is lost. Still, the general character and sequence of the phenomenon are the same, and it is not improbable that careful observation and inquiry will fail to elicit the true nature of the case. Prognosis.—The longer the time that has elapsed between the recep- tion of the injury or subjection to other cause, the greater is the prob- ability of a favorable termination. When the paroxysms are slight, and the intervals between them long, the prognosis is also more favorable. A low bodily temperature is a favorable indication. On the contrary, an elevated temperature is of fatal augury. The duration of the dis- ease is likewise an important element in the prognosis; and, when it has lasted over a week, death does not often take place. Cases are, however, on record in which a fatal result has supervened after the affection has existed for several weeks. Tetanus is, nevertheless, one of the most fatal of maladies. Dr. O’Beirne1 witnessed two hundred cases without a single recovery. Ilennen2 never saw a case of acute symptomatic tetanus recover. McLeod 3 has collected and analyzed twenty-three cases which occurred in the British army in the Crimea, of which but two recovered. Demme4 refers to eighty-six cases in the hospitals in Italy during the campaign of 1859, of which six were cured ; and Hamilton 6 has observed eight cases, of which three recovered. Nine cases have been under my immediate care, of which there were three recoveries. Of the many cases which I observed in the course of my inspections of camps and hospitals in the army during the recent war, I do not know how many terminated favorably. I am disposed, however, to believe that the number was not great. Hamilton states that his information leads him to think that, of one hundred and fifty cases which occurred during the war, the recoveries were few. Morbid Anatomy and Pathology.—As regards the cord, the results of post-mortem examination of patients who have died of tetanus have 1 “ Dublin Hospital Reports,” vol. iii., pp. 343, 378. 2 Op. cit., p. 262. 8 “Notes on the Surgery of the War in the Crimea,” London, 1858, p. 153, et scq. Also table, p. 439. 4 “ Militar-chirurgische Studien,” Wurzburg, 1861. 8 “A Treatise on Military Surgery and Hygiene,” New York, 1866, p. 595. TETANUS. 541 tip to a comparatively late period been very unsatisfactory. Roki- tansky,1 in chronic cases, found a proliferation of connective tissue. Wedl,4 in one case, discovered increased redness of a portion of the spinal cord. Curling3 declared that serous effusion with increased vas- cularity was generally observed in the membranes investing the medulla spinalis, and also a turgid state of the blood-vessels above the origin of the nerves ; and Wunderlich4 regarded the lesions as consisting in a proliferation of the connective tissue of the cord, the medulla oblongata, and the cornua cerebri and cerebelli. But, in 1864, Dr. Lockhart Clarke,5 after a careful examination of the spinal cords of six persons who had died of tetanus, found as the uniform results an abnormally enlarged condition of the blood-vessels throughout the gray matter, especially in the posterior horns, and granular disintegration of the nerve tissue. He expresses the opinion that tetanus depends (first) upon an excessively excitable state of the gray nerve tissue of the cord induced by the hyperasmia, and morbid condition of the blood-vessels, and the exudation and disintegration resulting therefrom, and (second) that the spasms are the result of the persistent irritation of the peripheral nerves by which the exalted excitability of the cord is aroused, and thus the cause which at first induced in the cord its morbid susceptibility to reflex action is subse- quently the source of that irritation by which the reflex action is excited. Subsequently, Dickinson * found enlargement of the blood-vessels throughout the gray substance of the cord, with perivascular exuda- tion, rupture of the blood-vessels in many places, and granular disin- tegration. Dr. Clifford AllbuttT has reported the results of his examination of the spinal cords in four cases of tetanus. He found diminution of the consistence of the cord of various degrees and situation ; haemorrhage in two cases visible to the naked eye ; enlargement of the blood-vessels; exudation of a granular plasma surrounding the vessels ; enlargement of the cells of the gray matter, and the granular degeneration of Clarke. Outside of this cord he found the nerve thickened and con- 1 “ Beitrage zur Pathologie des Tetanus,” Virchow's Archiv, tome xxvi., 1862. ! “ Rudiments of Pathological Histology,” “ Sydenham Society Translation,” London, 1855, p. 276. * “A Treatise on Tetanus,” etc., London, 1836. 4 Archiv der Heilkunde, 1862. 6 Lancet, 1864; Medical Times and Gazette, 1865; also, more fully, “On the Pathology of Tetanus,” Medico-Chirurgical Transactions, vol. xlviii., 1865, p. 255. 6 “Description of the Spinal Cord in a Case of Tetanus,” Medico-Chirurgical Trans- actionsi, vol. li., 1868, p. 267. 7 “ On the Changes of the Spinal Cord in Tetanus,” “ Transactions of the Patho- logical Society of London,” vol. xxii., 1871, p. 27. 542 DISEASES OF THE SPINAL CORD. gested, and bathed in inflammatory products. These results were con- firmed by the subsequent examination of Drs. Clark and Dickinson. Dr. Fox 1 made post-mortem examinations of four cases. In one the only abnormality remarked was dilatation and distention of the vessels of the spinal pia mater. In the others there were softening, hmmorrhage, amyloid bodies, in the gray substance, and thickening of the vessels. Michaud2 examined the cord in four cases. He found that the gray matter presented a general red appearance. The vessels were enor- mously enlarged. There were numerous free nuclei and foci of perivas- cular exudation. The gray substance, and especially the posterior commissure, was the seat of these alterations which, according to him, consist essentially in a proliferation of the nuclear elements of the con- nective tissue. The appearance which Lockhart Clarke considers to be a granular degeneration, Michaud regards as being due to these nuclei existing in the exudation around the blood-vessels. He considers teta- nus to be an acute inflammation of the gray tissue of the cord. When either of the upper extremities is the seat of the wound, which is the primary cause of the disease, the lesions of the cord are found in the cervical enlargement, and, when either of the lower limbs is injured so as to induce the affection in question, the spinal lesions are found in the lumbar enlargement. The nerves coming from the wounded part have been found the seat of inflammation by Airlong and Tripier,8 and by Michaud. In other cases they have not exhibited any change. The muscles of the body suffer secondarily. The violent spasmodic contractions to which they are subjected often produce ruptures of their tissue and extravasations of blood. On the other hand, it has often happened, especially in very rapid cases, that nothing has been found which could fairly be regarded as constituting the essential feature of the disease. Billroth 6 affirms that his examinations of the spine and nerves, in cases of tetanus, have thus far given only negative results, and this is in accordance with the ob- servations of the great majority of pathologists. But these discrepan- cies are, I think, to be ascribed to defective methods of examination, and in no event can they disprove the positive data obtained by others. It is contended by some authors that tetanus, like hydrophobia, is due to blood-poisoning. The fact, that a condition, so nearly resem- bling it as to be with difficulty diagnosticated from it, may be caused 1 “ Recherches anatomo-pathologiques sur l'etat des systemes nerveux central et peri* pherique dans le tetanus traumatique,” Archives de Physiologie, 1871, p. 59. 2 “ The Pathological Anatomy of the Nervous Centres,” London, 1874, p. 355. 3 Archives de Physiologie, 187°, p. 244. 4 Op. cit. 5 “General Surgical Pathology and Therapeutics, in Fifty Lectures,” Hackley’s translation, New York, D. Appleton & Co., 1871, p. 353. TETANUS. 543 by the injection of strychnia into the blood, appears to favor this view. However this may be, the character of the symptoms, as well as the anatomical lesions, indicates the spinal cord to be the seat of the disease. The first symptoms of tetanus—spasm of the diaphragm and tris- mus—indicate that the initial disturbance in the spinal cord is to be found at as high a level in the cerebro-spinal system as the nucleus of the fifth nerve. The increase in temperature may be accounted for by the implication of the heat-producing centre which Ott1 has shown exists in the pons. The spinal cord is both an organ for the generation of nerve-force, and for conducting impressions to and from the brain. In tetanus it is this first-named function which is deranged, and this is shown by the great exaltation of reflex excitability which exists. Evei'ything capable of 'causing a reflex movement of the slightest kind, and even excitations which in health would be altogether unperceived by the cord, augments its intrinsic action to a great extent where tetanus exists. Now, we are able to produce a similar increase of reflex action by strychnia ; and, in those cases of disease in which the amount of blood in the cord is increased, very small quantities of strychnia produce the characteristic phenomena of stiffness in certain muscles, and of aug- mented reflex excitability. The condition is aggravated by the medi- cine ; and, if we had no other facts to support the theory, we should be warranted in concluding that, in cases of strychnia-poisoning, the amount of blood in the cord and the excitability of the organ are both increased. From a consideration of all the points bearing on the sub- ject, we are warranted in concluding that tetanus essentially consists in a morbid exaltation of the functions of the spinal cord as a nerve- centre. Bernard2 has investigated this matter with his usual exactness. He says : “ Strychnia produces convulsions by exaggerating the sensibility of certain parts ; it also causes reflex movements. We have seen that the point of departure is in the sensitive system ; for, where the pos- terior roots of the nerves are cut, the animal dies without convulsions.” An experiment performed by myself and my friend and collabora- tor, Dr. S. Weir Mitchell,3 shows that the action of strychnia is to destroy the nervous excitability from the centre to the periphery. Its influence, therefore, must first be exerted on the spinal cord. '“The Heat-Centres of the Cortex Cerebri and Pons Yarolii,” Journ. Nerv. and Ment. Bis., February, 188S. 2 “Lc9ons sur les effets des substances toxiques et m6dicamenteuses,” Faris, 1857, p. 386. 3 “ Experimental Researches relative to Corroval and Yao; Two New Yarieties of Woorara, the South American Arrow-Poison,” American Journal of the. Medical Sciences, July, 1859 ; also “ Physiological Memoirs,” Philadelphia, 1863, p. 181, ct seq. 544 DISEASES OF THE SPINAL COP.D. “ Under the skin of a large frog, whose left sciatic nerve was pre- viously divided, a few drops of a strong solution of strychnia were in- troduced. Tetanic spasms ensued in two minutes. After forty-five minutes the nerves were irritated by galvanism. That of the left side, which had been cut, responded energetically, while no motions could be produced through the uncut nerve. The former remained excitable for two hours later.” Bernard1 asserts that the action of strychnia extends no farthei than the spinal cord ; and any one who has seen a frog under the influ- ence of this substance cannot have failed to notice that all the symp- toms indicate exalted spinal action. We are therefore led by observation and experiment to the conclu- sion that the lesion of tetanus is seated in the gray matter of the spinal cord, and that, although we cannot at present affirm an absolute identity of the lesions, in each case we have enough data to enable us to say in general terms that tetanus is essentially an inflammatory affection of the gray matter of the spinal cord. Vulpian3 has shown that strychnia does not produce organic lesions of the cord. He kept a frog for a month under its influence, and on kill- ing the animal found the cord in all its parts in a perfect state of integ- rity. But on this point there is a difference of opinion, Jacubowitsch and Roudanowsky asserting that the processes of the nerve-cells are torn, and that the cells themselves are often ruptured. It is not, how- ever, probable that the condition of the cord, in poisoning by strychnia, ever goes beyond the point of hypermmia, which, being of recent oc- currence, would disappear on death supervening. It is also extremely probable that, in the cases of tetanus in which recovery takes place, the organic derangements discovered by Lockhart Clarke do not occur. This is his opinion : Hyperemia is the first stage of all inflammations, and it is of course entirely possible that the morbid process should be aborted at this stage. Indeed, it is a matter almost of certainty that in some fatal cases of tetanus the pathological action has not gone beyond the hyperasmic stage, and hence the absence of lesions in the cases ex- amined by Billroth and others. But a hypera3mia of this kind is of course as much of the nature of inflammation as though the process had reached its full development. How does a wound of the extremity or trunk of a nerve cause tet- anus ? It has been supposed by some authors that there was a neuri- tis in each case which advanced centripetally till it reached the spinal cord. In regard to this point, Mitchell3 says : “ There is a prevalent belief that tetanus is more apt to arise when 1 Op. cit., p. 359. 2 “ Convulsions pendant un mois chez unc grenouille empoisonee par la strychnia; in- tegrity complete de la moelle epiniere,” Archives de Physiologic, 1868, p. 306. 3 “ Injuries of Nerves and their Consequences,” Philadelphia, 1872, p. 147. TETANUS. 545 large nerves are slightly hurt than on other occasions ; hut, although there are on record many cases where this terrible malady has followed the inclusion of nerves in ligatures, in the mass of tetanic histories the causal irritation has arisen in the extreme distribution of nerves, and where there has been no proof of precedent injury to large trunks. "Were it otherwise, I must more often have seen tetanus, whereas, in two hundred recorded instances of wounds of great nerves which passed under my eye during the war, not a single case of lock-jaw, was seen, although in perhaps one-half, the injuries were recent, and we actually witnessed a part of the process of healing. In fact, the tendency tow- ard irritation resulting in spasm seems to increase as the nerves divide and approach the skin. Brown-S6quard succeeded once in causing te- tanus by leaving a rusty tack in the foot of an animal. I have never been able to get this result by any method, nor, in some seventy sec- tions or wounds of nerves in animals, have I ever encountered it.” The experience of Dr. Mitchell on this point is sufficient to deter- mine it against the existence of a neuritis extending to the cord. Were there any such cause it would undoubtedly be more apt to arise from a wound of the trunk of a nerve and to extend to the cord, than from an injury of the terminal extremities. Moreover, the facts that tetanus has been known to follow in a few minutes after the reception of a wound, and that there is no pain along the course of the nerve, are directly at variance with the idea of a peripheral and ascending neuritis as the cause of the spinal lesions. Treatment.—There is scarcely a sedative or stimulant remedy in the pharmacopoeia which has not been employed and recommended in teta- nus. Aconite, ether, belladonna, chloroform, cannabis Indica, conium, opium, tobacco, Calabar bean, ice, counter-irritants, alcohol, and many other substances, have been used, and cases reported which have appar- ently recovered under their administration. Then, of surgical means, excision of the injured nerve and amputation of the wounded member have also been recommended, but are not, I believe, practised now. Latterly the bromide of potassium and hydrate of chloral have been employed with favorable results. A case in which the latter agent was successfully used in tetanus is reported by Dr. Wirth,1 of Columbus, Ohio. In about a month the pa- tient took nine ounces and two drachms, in doses of from thirty to forty grains, at times as often as every one and a half hour. In this case opium in large doses had been administered without effect. A number of other cases, in which chloral was administered, are cited in the same number of the JVew York Medical Journal in which Dr. Wirtli’s case appears, in several of which it was successful. A very thorough analysis by my friend Dr. D. W. Yandell,2 of Louis- 1 New York Medical Journal, November, 1870, p. 419. 3 American Practitioner, September, 1870, p. 152. 36 546 DISEASES OF THE SPINAL CORD. ville, of an unpublished report on tetanus, by Dr. R. O. Cowling, em- braces so much valuable information on the subject that I quote the summary entire. The term acute is applied to tetanus occurring within nine days of the injury, and chronic to cases ensuing after nine days : “ Calabar bean was given in thirty-nine cases, with thirty-nine per cent, of recoveries. Of these reported cures, but one was of acute teta- nus ; five others were in cases which recovered before the expiration of fourteen days. Per contra, there were ten deaths from chronic tetanus. “ Indian hemp used in twenty-five cases, with sixty-four per cent, of recoveries, of which three cases were acute, and six recovered before the symptoms lasted fourteen days. “ Chloroform relieved seventy per cent, of thirty-five cases, nine of which were acute, and eight recovered before fourteen days. Three chronic cases died, and two after symptoms lasted fourteen days. “ Ether.—Sixty per cent, of fifteen cases recovered ; five acute ; seven inside of fourteen days. One chronic case died. “ Opium.—Fifty-seven per cent, of one hundred and sixty-five cases recovered ; twenty-two acute ; twenty-nine before the fourteenth day. Twenty-six chronic cases were lost, and four after the disease had con- tinued fourteen days. “ Tobacco relieved fifty per cent, of forty-one cases ; six acute ; six before fourteen days of the disease. Four chronic cases died, and one after fourteen days. “ Quinine.—Seventy-three per cent, of fifteen cases recovered ; one acute ; three before fourteen days. Three chronic cases ended fatally, and one after fourteen days’ duration. “ Aconite.—Eight per cent, of fourteen cases recovered; none acute; none recovered before fourteen days. Death in one chronic case. “ Stimulants.—Eighty per cent, of thirty-three cases recovered ; four acute ; six within fourteen days. Six chronic cases died, and three after fourteen days. “ Mercury.—Fifty-seven per cent, of seventy-five cases got well ; twelve before fourteen days. Seventeen chronic cases were lost, and two after fourteen days. “ Bleeding.—Fifty-five per cent, of fifty-eight cases recovered ; nine acute ; ten before the fourteenth day. Seven chronic cases were lost, and two after fourteen days. “ Cold Affusion.—Seventy-three per cent, of eleven cases recov- ered ; three acute ; three before fourteen days. Two chronic cases died. “ Ice-bags.—Seventy-seven per cent, of nine cases recovered ; one acute ; two in less than fourteen days. “ Amputation.—Sixty per cent, of seventeen cases recovered ; four acute ; four in less than fourteen days. Three chronic cases died, and one after fourteen days. TETANUS. 547 “Division of nerve relieved seventy-five per cent, of three cases; one acute ; one before the fourteenth day. One chronic case died. “Purgatives.—Sixty-six per cent, of seventy-four cases recovered ; thirteen acute ; twelve before fourteen days. Ten chronic cases died, and three after fourteen days. “ Turpentine relieved seventy per cent, of sixteen cases ; six acute; four before fourteen days. Five chronic cases died, and two after fourteen days.” Among the conclusions arrived at by Dr. Yandell from these data are, that “ recoveries from traumatic tetanus have been usually in cases in which the disease occurs subsequent to nine days after the injury ; that when the symptoms last fourteen days recovery is the rule, and death the exception, apparently independent of the treatment; that chloroform, up to this time, has yielded the largest percentage of cures in acute tetanus ; that the true test of a remedy for tetanus is its influ- ence on the history of the disease : does it cure cases in which the dis- ease has set in previous to the ninth day ? does it fail in cases whose duration exceeds fourteen days ? and that no agent, tried by these tests, has yet established its claims as a true remedy for tetanus.” It is, perhaps, scarcely necessary to say that I fully accord with these opinions. Judging from its effects upon the spinal cord, it was supposed by Mr. Morgan that woorara injected into the blood might prove efficacious in tetanus. Experience, however, has not confirmed this view ; and the researches of Dr. Cowling show that it is one of the most inefficient of remedies. In a case which was under my charge fifteen years ago, when I was one of the surgeons of the Baltimore Infirmary, I injected corroval—a remedy which the investigations of Dr. Mitchell and myself had proved to be antagonistic to strychnia—into the blood. The patient, a colored boy, became affected with tetanus two days after his arm had been am- putated by my friend and colleague Prof. Nathan R. Smith. Cannabis Indica, morphia, and chloroform, had been used without effect, when at my request Prof. Smith turned the case over to me, in order that cor- roval might be administered. Two drops of a strong solution of the substance in water were injected into the cellular tissue of the forearm. At the time the pulse was 160, and the respirations about 75. There was very decided opisthotonos. In three minutes the pulse had fallen to 152. Two more drops were then injected, and the pulse fell to 144. As it soon rose again, two more drops were injected, when it fell to 132, and the respirations to 64. The spasms still continuing, two more drops were injected. In five minutes the pulse began to decline rap- idly, and in ten minutes had fallen to 90. At this time the patient had a violent tetanic spasm, and during its continuance the pulse became intermittent. It then rapidly went down to 40, then to 30, and during 548 DISEASES OF TEE SPINAL CORD. a violent spasm the patient died. From this record it will be seen that at no time did the corrovnl exercise the least effect over the disease.1 As I have stated, three successful cases have occurred in my prac- tice. One of these I saw in consultation with Dr. J. Lewis Smith, of this city. It was traumatic, and had ensued two weeks after a wound of the foot by a nail. The patient was treated by cannabis Indica, and the persistent application of ice to the spine. The spasms were greatly lessened in force and frequency, and recovery took place within two weeks. Another, which was also traumatic and acute—that is, making its appearance within nine days after the injury—was treated accord- ing to the same plan, and recovered in sixteen days, though the jaws remained stiff for several weeks afterward. The wound was caused by an ice-pick being accidentally thrust through the hand. The third case was that of an eminent musician of this city, who, while drilling with the regiment to which he belonged, injured his thumb with a splinter from the stock of his rifle. The first evidence of tetanus appeared on the twelfth day. The attack was not very severe. I administered the extract of cannabis Indica (Squires’s) in doses of half a grain every two hours, and kept up the application of ice to the spine continuously for six days. There were several violent spasms during this period, and the opisthotonos was well marked. At the end of a week the cannabis Indica was omitted for a day, but, the spasms becoming more frequent and severe, it was resumed as before, and continued with tolerable regu- larity for ten days longer. During this period there were but two spasms, and the opisthotonos became less. It was then gradually di- minished, and on the twenty-fifth day was left off altogether, the patient being convalescent. I am disposed to think that, whatever internal medication be adopt- ed, the application of ice to the spine is a measure which should always form a feature of the treatment. IV. INFLAMMATION OF THE ANTERIOR COLUMNS OF THE SPINAL CORD (SCLEROSIS OF THE COLUMNS OF turck). Tiirck2 has shown that the anterior columns of the spinal cord are subject to a chronic inflammation such as is now known under the name of sclerosis. In the cases which he described the morbid process in- 1 “ Traumatic Tetanus; Inoculation with Corroval; Death,” by Edward Milholland, M. D., Resident Physician at the Baltimore Infirmary. In Maryland and Virginia Medi- cal Journal, January, 1861, p. 13. 2 “ Ueber Degeneration einzelner Riickenmarksstrange, welche sich ohne primiire Krankheit des Gehirnes oder Riickenmarks entwickelt,” Sitzungsberichte der kaiserlichen Academie der Wissenschaftcn, Mat. nat. Cl., 1856, p. 112. INFLAMMATION OF THE LATERAL COLUMNS. 549 volved symmetrically a small region on each side of the anterior me- dian fissure—that part which is designated the column of Tiirck. Microscopical examination showed proliferation of the neuroglia, with degeneration of the true nerve-elements. The course of the disease, the symptoms, causes, etc., together with the morbid anatomy and pathology, do not differ essentially from the corresponding affection of the lateral or crossed pyramidal tract which is more frequent and is more thoroughly understood. Our present knowledge leads us to the inference that the columns of Tiirck are in function similar to the lateral columns. The number of cases in which they have been found altered is as yet small, and they have not been very thoroughly worked up. In some cases they have been sclerosed in conjunction with a like condition of the lateral columns. I shall, therefore, pass at once to the consideration of the next division of the subject. Y. INFLAMMATION OF TIIF LATERAL PYRAMIDAL TRACT OF THE SPINAL CORD ; SPASTIC SPINAL PARALYSIS (PRIMARY SYMMETRICAL LAT- ERAL sclerosis). Tiirck,1 who, as we have seen, demonstrated the fact that the ante- rior columns of the cord could be the primary seat of sclerosis without any other region participating in the lesion, also showed that the lateral columns could be similarly affected. Turck’s investigations were al- lowed to remain scarcely noticed for ten years, when Charcot2 made like observations and since then has aided in establishing it as a dis- tinct pathological condition. Symptoms.—The chief phenomena of the disease under considera- tion are paralysis and contraction of the affected limbs. The lower ex- tremities are, more than the upper, liable to be the seat of these symp- toms. The loss of power is very gradual, and there is no atrophy be- yond the general emaciation consequent upon diminished use of the muscles. Sensibility is not in general affected, but in some cases there is more or less pain in the paretic limbs and in the back near the seat of the disease. The paralysis is rarely complete. At first the patient merely tires more readily, slight exertion fatigues him, and this is especially noticed in the muscles which flex the leg upon the thighs, and the consequent sensation of weariness is experienced in the popliteal space. Some- times it is shown in the sudden relaxation of the extensor muscles of the leg and the fall of the patient thereby ; at others, in the fact that the extensors of the foot become weak, allowing the toes to drop, and hence causing stumbling. The gait then becomes characteristic. 1 Op. tit., p. 112. 2 L'Union Medicate, 1855. DISEASES OF THE SPINAL CORD. Owing to tlie fact that the patient’s extensor muscles are weak, he is unable to lift the feet high enough to clear the ground, and hence he throws them out by means of the abductor muscles of the thigh, and thus causes them to describe an arc of a circle. Then in putting them down the heel strikes the ground a longer time before the sole than it does in the natural gait, and hence the foot comes down with a jerking motion. This is the ordinary manner of walking practised by a person affected with the disease under notice. In another form of locomotion, the body is moved laterally on the thighs, first to one side and then to the other, in such a way as to cause the feet to be raised high enough without the complete action of the extensor muscles. The gait is there- fore similar to that of a duck, or of a woman with a very wide pelvis. The motion of the body is almost serpentine., and the feet glide over the ground barely lifted high enough to avoid contact. In both the methods of walking the patient requires support. At first a cane answers, then he comes to crutches, and eventually the as- sistance of an attendant becomes necessary. As a consequence of the paralysis, and the contractions which event- ually ensue, the movements are often complicated and sometimes ren- dered impossible by the legs becoming interlocked at every attempt to walk. In a patient from Connecticut under my care, not long since, this difficulty was a very prominent feature, and though the muscles of flexion and extension were sufficiently strong to allow of his walking, those which abduct the thighs were so materially paralyzed, and the adductors were so greatly contracted, as to produce the condition mentioned. Reflex movements, so far from being lessened, are generally exalted ; and this is especially true of the “ tendon reflex,” as exhibited when one leg is crossed over the other and a smart blow given with the edge of the hand over the tendon of the quadriceps extensor, just below the patella. The leg is suddenly extended, and bounds much higher than it normally does under like excitation. An exaggerated “ knee-jerk,” however, unaccompanied by other symptoms of disease of the lateral pyramidal tract, is of no importance whatever. The electrical con- tractility of the muscles remains unimpaired. The “ ankle clonus,” which consists of an alternating spasm and relaxation of the gastroc- nemius, can always be obtained, except in some well-advanced cases, by supporting the weight of the patient’s leg and then, grasping the foot firmly, suddenly extending it, when, if the conditions are favor- able, the foot will be thrown into rapid vibrations of flexion and ex- tension. In some patients who have been afflicted with the disease under consideration for a long time the muscles of the leg become so stiff and rigid that the ankle clonus cannot be obtained, and even the exaggeration of the knee-jerk cannot be demonstrated. Sometimes the contractions, which are so prominent a feature, re- INFLAMMATION OF THE LATERAL COLUMNS. 551 lax, but they again supervene, and generally persist with more or less intensity till the closing stages of the disease, when the power of the cord becoming exhausted entirely, and all the muscles being paralyzed, the spasmodic action ceases. A very remarkable case is one reported by Charcot,1 of a woman who, after several hysterical attacks, was seized, after having been greatly frightened, with a violent paroxysm of hysteria, which was soon followed by a general trembling, accompanied by a weakness of the limbs. At the end of a month the feebleness was such that she could not leave her bed. About the same time the trembling ceased, but was succeeded by a contraction which affected at first the extremi- ties of the left side, but in the course of three weeks involved those of the right side also. The neck also became rigid. All these phenomena persisted, they even increased so that in the early part of 1850 she was admitted into the Charite. At that time she was confined to her bed in the dorsal decubitus, not being able to move her limbs. Her general health was good, and her cerebral functions were normal. The muscles of the neck were painful and stiff. The skin on the left anterior part of the thorax was hyperaesthetic, the condition being exactly bounded by the median line. The tactile sensibility was a little obtuse in the left superior extremity, but the sensibility to pain was exaggerated. The muscular sensibility was also more marked than in the normal state. The superior extremities were strongly contracted; the forearm was flexed on the arm, and the fingers were also strongly flexed. Attempts made to extend the limbs were only partially successful and caused pain. The contracted muscles were the seat of continuous spontaneous pains, and from time to time sudden movements took place in these members, either spontaneously or as a consequence of reflex action. Neither of these limbs could be moved by voluntary power. The trunk was rigid and its muscles were painful to pressure. Pressure on the cervical region of the skin also caused pain. Both inferior extremities were also strongly flexed. Pressure on the muscles caused pain, and there wrere also darting pains through these limbs. The case was regarded as one of hysteria. The patient remained in the hospital two years, and left in about the same state as when she entered. Subsequently the symptoms almost entirely disappeared, nothing remaining but a weakness of the lower extremities and a slight degree of contraction of the upper. But in 1855 she had another hys- terica] attack, and this was followed by a return of the former con- dition. In 1856 she entered the Salpetribre, and in 1862 her case was studied by M. Charcot. The symptoms w7ere similar to those wThich _ 1 Cited by Bourneville, l' De la contraction hysterique permanente,” Paris, 1872, p. 77, 552 DISEASES OF THE SPINAL CORD. have been described, though even more pronounced. In 1864 she died during an attack of erysipelas. The post-mortem examination showed the essential lesion to consist of sclerosis of the lateral column from the medulla oblongata to the lower boundary of the lumbar enlargement. The gray matter was healthy throughout. A study of this case shows that the principal symptoms of primary symmetrical lateral sclerosis are as Tiirck described them in his mem- oir—paralysis, contractions, and pain in the back and limbs. To these must also be added the exaggerated knee-jerk and the ankle clonus. Causes.—The causes of the disease are probably similar to those producing so many other spinal affections—cold, dampness, over-exer- tion, syphilis. Nothing very definite is known on the subject. Diagnosis.—The elements of the diagnosis of primary symmetrical lateral sclerosis of the spinal cord are the presence of contractions with paralysis but without atrophy, and the absence of any organic disease of the brain or superior part of the cord (bulb) which could give rise to the condition as a secondary disorder. It must, however, be borne in mind that contractions are the expression of degeneration of the lateral pyramidal tract. It is only by attention to the clinical history of the case that we can ascertain whether the lesion is primary or secondary. But it must be remembered that it is a matter of the most rare occur- rence for the motor tracts of both hemispheres to undergo degenera- tion simultaneously, while in the spinal cord it is equally rare to find the disease limited to one lateral pyramidal tract only. The distinction between the disease in question and progressive muscular atrophy is so clear as scarcely to require comment, and from amyotrophic lateral spinal sclerosis, the absence of atrophy and its ac- companiments, and of a tendency to attack the nuclei of the bulbar nerves, will serve to make the discrimination. It has more affinities, so far as its symptoms are concerned, with chronic spinal meningitis, multiple spinal sclerosis, and with tumors which, by their pressure on the cord, may give rise to very similar phenomena to those exhibited in lateral sclerosis. I am afraid the difficulties of making a diagnosis between it and these affections are, in the present state of our knowledge, almost insurmountable. I know of no sure signs by which the discrimination can be made. Prognosis.—Although remissions may take place, the prospect of an entire cure is not very great. The progress of the disease is, how- ever, slow in the majority of cases, and its course may, I am satisfied, be materially retarded if not altogether arrested in some cases. Morbid Anatomy and Pathology.—Tiirck was the first to associate sclerosis of the lateral columns with a definite set of symptoms. In three of the cases of the twelve on which his memoir is based he found these regions of the cord the seat of symmetrical sclerosis. It has been INFLAMMATION OF THE LATERAL COLUMNS. 553 very definitely settled that the lateral columns are, in embryonic life, anatomically distinct from the rest of the cord ; and, though in the process of development this anatomical separation is apparently lost, pathology shows us that it in reality exists. Charcot,1 in considering this subject, calls attention to the fact that transverse sections of the cord in cases of primary symmetrical Fig. 66. Fig. 67. Fig. 68. lateral sclerosis made through the cervical enlargement show that the alteration embraces a greater extent of the cord than when any other pai't is affected. Thus, when the region in question is the seat of the lesion, the sclerosis extends anteriorly as far as, and even beyond, the external angle of the anterior horn, w'hile posteriorly it almost en- croaches on the posterior tract of gray matter. On the outside it is always separated from the cortical layer by a tract of white tissue which remains intact. In Fig. 66 is represented a transverse section of the cord made through the cervical enlargement, a denotes the sclerosed portion ex- tending beyond the external angle of the anterior tract of gray matter reaching to the posterior tract behind, and separated from the cortex hy a layer of unaltered white substance. In the dorsal region the lesion is more circumscribed, as is seen from an examina- tion of Fig. 67, which represents a section of the cord through the middle of that part. In front it scarcely reaches the posterior boundary of the anterior tract of gray matter. As in the section just described, the sclerosed portion does not extend to the cortical layer of the cord. In the lumbar region the lesion is still less extensive, occupying only about a quarter of the area of the lat- eral columns. Unlike the lesion in the cervical and dorsal regions, it touches the cortical layer of the cord (Fig. 68). The undegenerated white matter situated on the periphery of the lateral pyramidal tracts from the lower dorsal region upward is the direct cerebellar tract. This tract is not found in the lumbar region. Finally, in those cases in which the morbid process extends to the medulla oblongata, we find it seated in the anterior pyramids, Fig. 69. 1 Op. cit., p. 220. 554 DISEASES OF THE SPINAL CORD. not in the nuclei of the bulbar nerves, as in cases of amyotrophic lat- eral spinal sclerosis to be presently considered. Fig. 09 represents a transverse section of the medulla oblongata through the middle part of the olivary bodies ; A A, the anterior pyramids in a state of sclerosis. In primary symmetrical lateral sclerosis the initial stage, as in other inflammatory affections of the spinal cord, whether acute or chronic, is probably congestion. This congestion begins in the axis cylinders of the nerve tubes and eventually becomes a chronic inflam- mation. From the axis cylinder the inflammation extends to the nerve and sheath and eventually to the connective tissue, which undergoes proliferation and, by its increase in volume, presses upon and gradually destroys the nerve tubes. This evidently accounts for the paresis which is the initial symptom of the disease. As the nerve fibres descend they are continually branching off to connect with the motor cells in the anterior horn of gray matter. This accounts for the gradual diminution in the area of the lateral pyramidal tracts as Fig. 70. Diagrammatic representation of the connection between the lateral pyramidal tract and the motor cells in the anterior horn; also the reflex fibres. (Modified from Bramwell.) pmc, Posterior median column, or column of Goll. pec, Posterior external column, or column of Burdach, through which a deep reflex fibre (R) passes to join the motor cell at 3. S, A superficial reflex fibre passing through the posterior horn of gray- matter to join the motor cell at 2. Ip t, Lateral pyramidal tract, from which a motor nerve-fibre (1) passes to the motor cell. 4, Motor fibre to a muscle. 5, Fibre to neighboring cells. 6, Fibre to motor cells in opposite horn. they descend. The inflammatory process is transmitted by these fibres to the motor cells in the anterior horn which are thereby kept in a state of continual irritation. INFLAMMATION OF THE LATERAL COLUMNS. 555 All motor cells by constant vibration keep the muscles which they supply moderately contracted, or, as it is commonly termed, “ in tone.” This is beautifully demonstrated in Bell’s facial paralysis, where one side of the face is paralyzed. The normal “ tone ” of the paralyzed side having been abolished, the face is drawn toward the sound side. When the motor cells are in a constant state of irritation, the nor- mal “ tone ” of the muscles which they supply is enormously increased. Hence the stiffness and rigidity of the limbs. The exaggerated knee- jerk and the ankle clonus are, in my opinion, both due to the irritable condition of the motor nerve-cells. It is claimed by most authors that these two symptoms are caused by the abolition of the power of transmitting inhibitory impulses through the lateral pyramidal tracts owing to their diseased condition. It is claimed that when a healthy individual is struck on the patellar tendon that he can restrain the knee-jerk if he desires to, and that, in any case, there is a certain amount of involuntary restraint ; and that in disease of the lateral pyramidal tract this power of inhibition is lost. This theory is not, to my mind, supported by evidence. A healthy individual controls the manifestation of the tendon reflex by contracting the flexors of the leg, but not by any mental influence directed against the knee- jerk impulse. As for involuntary inhibition, if there is such a thing, its loss should be manifested immediately after a cerebral haemorrhage, which, as Althaus1 points out, is not the case. The exaggerated knee- jerk and the ankle clonus do not appear until the descending degener- ation has reached the lateral pyramidal tract. On the other hand, it is not difficult to believe that irritable nerve- cells will send out irritable impulses under stimulation. Hence, if a blow is struck on the patellar tendon of an individual suffering from sclerosis of the lateral columns of the cord, and in whom the motor cells in the anterior horn must necessarily be in a constant state of irritation, and the sensory impulse from the blow reaches these cells, an irritable motor impulse will result and an exaggerated knee- jerk will necessarily follow. (See Fig. 70.) The ankle clonus is the exaggerated reflex of the gastrocnemius. Treatment.—In the early period of the disease large doses of ergot will rarely fail to be of service. I have several times succeeded in relieving the paralysis and arresting the spasms of the limbs in cases presenting all the initial phenomena of lateral sclerosis by the persistent and free use of this remedy. But to be efficacious it must be given in the very first stage, before the paralysis becomes extreme, or perma- nent contractions are present. A drachm of the fluid extract three times a day is the smallest dose likely to prove efficacious. If there is reason to suspect the influence of syphilis in producing the disease, the iodide of potassium in large and gradually-increasing 1 “ Sclerosis of the Spinal Cord.” DISEASES OF THE SPINAL CORD. 556 doses should be administered. Charcot and Gombault1 have proved the existence of disseminated sclerosis of the cord in a woman affected with syphilis, and there is of course reason to believe that the diffused form such as that now under consideration may have a like origin. In such cases mercury may also be given, preferably in the form of the bichloride, with the iodide of potassium. Later, no treatment is, so far as we know, calculated to materially arrest the progress of the disease. Nitrate of silver and cod-liver oil have also occasionally improved the strength of the patient and less- ened the rigidity of the contractions, but only for a short time ; and the primary uninterrupted galvanic current to the spinal column and the contracted muscles has also proved serviceable in the same way and to a like extent. Up to quite a recent period I had never derived any benefit in cases of lateral sclerosis from counter-irritation, but I am disposed to think from some late experience that the actual cautery, applied on each side of the spinous processes throughout the entire length of the vertebral column and frequently repeated, is useful. For the relief of pain, morphia may be administered, or what is, I think, preferable, as it does not appear to be an excitant of the cord, codeine. Half a grain or more may be given as required. Hypodermic injections of atropia, beginning with the one hundred and twentieth of a grain and increasing gradually, are beneficial in mitigating the spasms of the muscles. VI. INFLAMMATION OF THE LATERAL COLUMNS OF THE SPINAL CORD AND OF THE ANTERIOR TRACT OF GRAY MATTER (AMYOTROPHIC LAT- ERAL SPINAL SCLEROSIS. For the recognition of this affection and the patho-anatomical data relative to its identity, we are indebted to Charcot, who, with his cus- tomary ability, has presented a mass of facts abundantly sustaining his views in regard to its autonomy. Cases exhibiting the phenomena of amyotrophic lateral spinal sclerosis were noticed, and their details published before he enunciated his doctrines on the subject; but the relations of the lesions to the symptoms were not known previous to his observations. Symptoms.—The first symptom to make its appearance in the affection under notice is paralysis, which occurs ordinarily gradually, advances steadily, and may involve at the same time one or more of the limbs. Generally atrophy ensues soon after the appearance of the 1 “ Note sur une cas des lesions disseminees des centres nerveux observees chez une femme syphilitique,” Archives de physiologic, 1873, p. 143. AMYOTROPHIC LATERAL SPINAL SCLEROSIS. 557 paralysis, and, as in infantile spinal paralysis, and the spinal paralysis of adults, involves whole groups of muscles at once—not the individ- ual muscles in succession, as in progressive muscular atrophy. After a time the morbid process in its ascending course reaches the medulla oblongata, and, thus implicating the nuclei of the facial, spinal accessory, hypoglossal, and pneumogastric nerves, especially the two latter, causes atrophy of the tongue, and many of the other symptoms met with in progressive muscular atrophy affecting these centres. Finally, death takes place from interruption to the processes of respiration and circulation. The muscles which are the seat of atrophy are subject, as in pro- gressive muscular atrophy, to fibrillary contractions, which, however, as in the last-named affection, precede the atrophy, and advance and attain their greatest development pari passu writh the wasting. The electrical reactions of the affected muscles show both qualita- tive and quantitative degenerations. As the atrophy progresses the muscles respond less and less to the faradaic current, and finally cease to respond to it at all. At first there is a gradual decline of the gal- vanic contraction, but at the expiration of a few weeks’ time it will be observed that moderately strong currents produce good contrac- tions ; but it will also be noticed that the anodal closure contraction equals or excels the cathodal closure contraction. In other words, the polar reactions of degeneration (see page 28) are present. But the feature which is most characteristic of amyotrophic lateral spinal sclerosis is the permanent contractions of which the affected limbs are the seat. These, though in part due, as Charcot1 says, to the paralysis of certain antagonistic muscles, are mainly caused by spas- modic contractions of the non-paralyzed or partially paralyzed muscles, so that the joints are rigidly flexed. The position assumed when the forearm and hand are the seat of this deformation, is shown in Fig. 71. The fingers are flexed upon the palm, the thumb adducted, and the hand strongly bent upon the arm. In the case of a gentleman who came under my observation in Sep- tember, 1874, the position of the left hand was very similar to that shown in the figure. The arm was semiflexed, and the whole member held firmly against the walls of the chest, by the action of the pectoral and latissimus dorsi muscles. Any attempt to overcome the contrac- tions was strongly resisted by the muscles, and caused very consider- able pain. The atrophy of the paralyzed muscles was well marked, and fibrillary contractions were easily excited, even if not present when the inspection was made. In this case the disease had appeared suddenly six months previous- ly, after exposure subsequent to a debauch. The upper extremities 1 “ Lecjons sur les maladies du systfeme nerveux,” 3me fascicule, Paris, 1874, p. 234. 558 DISEASES OF THE SPINAL CORD. only were affected, but there was, even when I saw the patient, a little restraint in the movements of the tongue. I did not see him again, but I heard that death had ensued from dysentery three months after Fig. 71. his visit to me. I also learned that his tongue had become atrophied, and that there was difficulty of swallowing. In another case the contracted muscles were the pectorals, and the left arm was, in consequence, drawn strongly across the front of the chest. This patient, a man forty years of age, was paralyzed in both upper extremities, but the contraction, when I first saw him, was limited, as stated, to the pectoral muscles. He visited me again about six months afterward, and then the right upper extremity was also contracted throughout its extent. The fingers were bent on the palm to such a degree that they could not be opened by any force which it was safe to apply, and pressed so strongly on the palm as to cause pain. If the nails were allowed to project beyond the ends of the fingers—and it was very difficult to keep them short—they entered into the skin and caused painful sores. The hand was flexed on the wrist, the elbow half bent, and the arm was held firmly against the side of the chest. At the time of the first visit of this patient there was no evidence of any alteration of the medulla oblongata, but at the second visit there were several indications of incipient bulbar paralysis. Deglutition was effect- ed with difficulty, the tongue could not be carried to the roof of the mouth, was protruded only slightly upon great effort being made, and was the seat of constant fibrillary contractions. The atrophy of the paralyzed muscles was well marked, and fibril- lations were so strong as to be a source of great discomfort. The lower extremities were not then involved, and the bladder and sphinc- ters were intact. I have not seen the patient since—now about seven months—and am ignorant of the subsequent course of the disease. AMYOTROPHIC LATERAL SPINAL SCLEROSIS. 559 The contractions are not always similar, either in extent or strength, in the corresponding limbs, and they may for a time, especially in the early stages of the disease, disappear. But they reappear later, and tend to become more and more rigid as the affection advances ; still, in the most extreme period of the malady, as the atrophy becomes pro- nounced, they disappear wholly or in part, there being little if any muscle left to maintain the contraction. Another feature is a spasmodic extension of the paralyzed limbs, especially the lower, which is most strongly marked as the patient lies in bed ; or the members may be involuntarily flexed and remain in that condition for several minutes or longer. These movements are not ordi- narily accompanied with pain, as are those of spinal meningitis, which in many respects they resemble. The patient very generally experiences severe pains in the affected limbs, which are aggravated or excited by pressure or traction in the muscles. Numbness is also usually present to a greater or less degree, but there is never complete anassthesia. A peculiar kind of tremor is sometimes seen in the limbs, the mus- cles of which are partially paralyzed and atrophied. This is in reality not so much a tremor as it is a more extensive movement, resembling that which is present in some old cases of hemiplegia from cerebral haemorrhage. It is only, like that, manifested when voluntary move- ments are attempted. As previously stated, the disease, unless death ensues from some in- tercurrent affection, eventually extends to the medulla oblongata. In none of my cases has this circumstance been present to any marked degree while the patients were under my observation ; but in two, as we have seen, there were indications of such extension when they passed from under my notice. Charcot states it to be an invariable se- quence, so far as his observations extend, and he sums up the subject as follows : The paralysis of the tongue, inducing a difficulty of swal- lowing and of articulation, may cause a complete loss of the power of speech. The paralyzed tongue presents very soon, in general, a cer- tain degree of atrophy ; it is shrunken, wrinkled, and agitated with vermicular movements. The paralysis of the veil of the palate makes the voice nasal, and, with the laryngeal paralysis, renders the act of deglutition difficult, The orbicularis oris being paralyzed, an alteration in the form of the countenance takes place. The mouth is considerably enlarged transversely, through the predominance of the action of the muscles which are not involved. The naso-labial furrows are depressed. The symptoms give to the physiognomy a sad expression. The mouth, es- pecially after laughing or wgeping, remains for a long time half open, and allows the viscid saliva to flow continually. Finally, by reason of the implication of the pneumogastries, grave DISEASES OF THE SPINAL CORD. troubles of the respiration and circulation supervene, and cause the death of the patient, already weakened by insufficient nourishment. In some cases there are variations from the ordinary course of the disease. It has begun in the lower extremities instead of the upper, and again has been restricted in its domain for a long time to a single limb or to one side of the body. In two cases, according to Charcot, it has begun with the bulbar symptoms, which in general appear only at the end. In regard to such instances as these last, there is doubt of their being examples of amyotrophic lateral sclerosis. Causes.—Exposure to cold and dampness appears to be the most efficient exciting cause of the disease. In one of Charcot’s 1 cases, the patient, an itinerant showman, was exposed during a journey to cold and rain. The following morning he was taken with a chill, which was repeated thirty-six hours afterward, and then he was seized with pains along the course of the nerves, and in the joints mainly of the upper extremities. Fibrillations accompanied them, and paralysis and atrophy soon followed. In the case occurring in my own experience, the patient became intoxicated, and wandering into the Central Park, lay all night on wet grass, exposed to a cold, drizzling rain. In the morning he was arrested and taken to the police court, and sent to Blackwell’s Island for ten days. On his way up, he was subjected to the influence of a cold wind, which, blowing on his wet clothes, chilled him more and more. The following morning he was discharged, his friends having ascertained his situation and paid his fine. But he already felt a degree of weak- ness in his arms, and in the course of a week they were to a great extent deprived of motor power. Fibrillary contractions were present from the first, but there was no pain anywhere. In the majority of cases no cause can reasonably be assigned. There appears to be no hereditary influence to the disease. Diagnosis.—The diagnosis of amyotrophic lateral spinal sclerosis presents many features of interest. A consideration of the essential phenomena shows that they are as follows : 1. Paralysis occurring in symmetrical parts of the body, unaccom- panied by anaesthesia. 2. Atrophy following the paralysis, and attacking masses of mus- cles. 3. Spasmodic rigidity, eventually leading to permanent contrac- tions, lasting up to the last stage of the disease. 4. Extension of the affection to the lower extremities, and the su- pervention of intermittent and tonic contractions or rigidity. 5. The implication of the medulla oblongata, and death in the course of two or three years. Thus, we see that the affinities of amyotrophic lateral spinal sclero- sis are with spinal paralysis of adults and progressive musoular atrophy, 1 “ Deux cas d’atrophie musculaire progressive,” Archives dephysiologic, 1869, p. GST. AMYOTROPHIC LATERAL SPINAL SCLEROSIS. 561 with which latter, disease it was confounded by Dumesnil,1 Charcot,2 and others, up to quite a late period. But the differences between it and both these diseases are suffi- ciently striking to prevent much danger of confounding them. Thus from spinal paralysis of adults it is discriminated by the facts that reflex excitability is not impaired, nor the electric excitability of the muscle diminished, as in the former affection ; that the atrophy is more profound and constant; that fibrillations are present, and especially by the existence of t.he spasmodic contractions of the limbs which form so prominent a feature of amyotrophic lateral spinal sclerosis. From progressive muscular atrophy the distinction can be readily made out. In the facts that paralysis precedes the atrophy, that the wasting takes place in groups of muscles, and that spasmodic contrac- tions occur in amyotrophic lateral spinal sclerosis ; while in progres- sive muscular atrophy the paralysis is consequent on the wasting, the muscles shrink singly and irregularly, fibre by fibre, and spasmodic con- tractions do not occur, we have sufficiently precise diagnostic marks of differences between the two affections. Prognosis.—There is no case of cure on record. The course of the disease is progressively onward. In the majority of cases the fatal ter- mination occurs within two years; occasionally, it is deferred for a few months longer. Morbid Anatomy and Pathology.—As I have said, amyotrophic lateral spinal sclerosis has, until quite lately, been regarded as, at most, an eccentric form of progressive muscular atrophy. It is among the reports of cases of this affection, therefore, that we must search for early data relative to the morbid anatomy of the disease under consid- eration. Dumesnil,* in 1867, reported the details of five cases of spinal disease under the name of progressive muscular atrophy, two of which were, undoubtedly, instances of amyotrophic lateral spinal sclerosis. In both of these, symptoms such as have been described were present, and, on post-mortem examination, lesions of the lateral columns and anterior horns of gray matter were found to exist. Charcot and Joffroy 4 have given with fullness of detail the particu- lars of two cases of amyotrophic lateral spinal paralysis, in which the post-mortem examination was very thorough. 1 “ Nouveaux faits relatifs h la pathogenie de l’atropbie musculaire progressive,’’ Gazette hebdomadaire, Nos. 27, 29, 30, 1867. 2 “ Deux cas d’atrophie musculaire progressive avec lesions de la substance grise et des faiseaux antero-lateraux de la moelle epiniere,” Archives de physiologie, No. 4, 1869. 3 “Nouveaux faits relatifs h la pathogenie de l’atrophie musculaire progressive,* Gazette hebdomadaire, Nos. 27, 29, 30, 1867. 4 “ Deux cas d’atrophie musculaire progressive avec lesions de la substance gri3e et des faiseaux antero-lateraux de la moelle epiniere,” Archives de physiologic, 1867. 562 DISEASES OF THE SPINAL CORD. The first of these is reported as a case of progressive muscular atrophy, especially marked in the upper extremities, with atrophy ol the muscles of the tongue and of the orbicularis oris and paralysis with rigidity of the inferior limbs. On post-mortem examination the nerve- cells of the anterior horns in the cervical and dorsal regions were found atrophied, while many had disappeared. In the bulb there were atrophy and disappearance of the nerve-cells, constituting the nucleus of the hypoglossal. The anterior roots of the spinal nerves and the roots of the hypoglossal and the facial were also atrophied. In addition, there was symmetrical diffused sclerosis of the lateral columns. In this case the bulb was affected after the lower parts of the cord, and the lesion of the nuclei of the hypoglossal and facial was of such a nature as to cause atrophy of the tongue and orbicularis-oris muscle. The instance was, therefore, of a typical character. The second case has already been cited under another head of this chapter. It is entitled—Progressive muscular atrophy especially mani- fested in the upper extremities; acute pains in the limbs coming on in paroxysms ; anaesthesia in certain parts of the body ; paralysis with rigidity of the inferior extremities; lesions of the nerve-cells of the anterior horns of gray matter; centres of gray degeneration in the posterior horns; symmetrical diffused sclerosis of the lateral columns ; considerable thickening of the spinal dura mater and pia mater of the cervical enlargement. This case was not an uncomplicated one, but still the essential lesions of the anterior horns of gray matter and of the lateral columns are perceived to have been present. Gombault1 reports the case of a woman in whom the symptoms were not developed with any suddenness, but in whom there gradually supervened loss of power with atrophy and contractions in the upper extremities, then paralysis with atrophy in the lower limbs, and finally atrophy of the muscles of the tongue and lips, with difficulty of swal- lowing, and the other symptoms of glosso-labio-laryngeal paralysis. Post-mortem examination showed the lateral columns to be symmetri cally sclerosed, and in the anterior horns of gray matter symmetrical lesions, exactly limited to this region, and consisting of atrophy, pig- mentary degeneration, and disappearance of the nerve-cells. In the bulb, the nuclei of origin of the bulbar nerves were similarly altered. It is perceived, therefore, that in amyotrophic lateral spinal sclero- sis the essential lesions are seated symmetrically in the lateral columns and in the anterior horns of gray matter, and that when the morbid process extends—as it always does, if the patient does not die in the mean time of some intercurrent affection—to the medulla oblongata, it 1 “ Sclerose symetrique des cordons lateraux de la moelle et des pyramides anterieurs dans la bulbe; atrophie des cellules des cornes anterieures de la moelle ; atrophie mus» culaire progressive; paralysie glosso-laryngee,” Archives de physiologic, 1872, p. 589. AMYOTROPHIC LATERAL SPINAL SCLEROSIS. 563 invades the nuclei of origin of the nerves which are affected in glosso- labio-laryngeal paralysis. The accompanying woodcut from Charcot Fig. 72. represents a section of the bulb made at the level of the middle part of the nucleus of the hypoglossal ; a b to the right of the imaginary line R R’ represents the normal condition ; a, the nucleus of the hypo- glossal composed of about thirty multipolar ganglion-cells; e, a vessel circumscribing the nucleus; c, the floor of the fourth ventricle; cl, the fasciculus teres ; b, nucleus of the pneumogastric. On the left the letters a' b', etc., represent the corresponding parts in a case of amyo- trophic lateral spinal sclerosis. It is perceived that only five or six cells exist in the nucleus of the hypoglossal. The nucleus of the pneu- mogastric is, on the contrary, normal. Now, it appears to me that M. Charcot is wrong in considering, as he apparently does, every case of glosso-labio-laryngeal paralysis ac- companied by progressive muscular atrophy of the muscles lower down, as one of primary amyotrophic lateral spinal sclerosis. Those cases of glosso-labio-laryngeal paralysis which, at a later period, exhibit the phenomena of progressive muscular atrophy in the muscles of the upper extremities and of other parts of the body are, in my opinion, not cases in which there is primitive lesion of the lateral columns, but examples of secondary degeneration of the cord, being produced as a consequence of the superior lesion. The case reported by Dr. Hun,1 of Albany, is quoted by Charcota as an instance of amyotrophic lateral spinal sclerosis, but, according to the 1 “ Labio-Glosso-Laryngeal Paralysis,” American Journal of Insanity, 1871, p. 194. s “Lecjons sur les maladies du systeme nerveux,” Paris, 1874, p. 229 DISEASES OF THE SPINAL CORD. 564 view above expressed, it was in reality a case of glosso-labio-laryngeal paralysis with secondary degeneration of the spinal cord. The patient, a man aged fifty-eignt, first noticed that the saliva dribbled from his mouth when speaking or writing. Shortly afterward he was conscious of a difficulty in the pronunciation of words, and then there were evi- dent hesitation and defect in the articulation of certain words, and his voice became nasal. * A year afterward there were complete loss of speech, difficulty of deglutition—any effort at swallowing being attended with paroxysms of coughing and suffocation—and paralysis of the tongue, which could only be protruded a quarter of an inch beyond the edge of the teeth. There was partial loss of motion in both arms, but no atrophy. A month subsequently it was noticed that he dragged his feet a little, but he could still walk alone for a considerable distance. The pa- ralysis advanced until he was unable to walk, and the difficulty of deglu- tition increased. When seen by Dr. Hun, January 4, 1871, “ he was sitting in a chair propped up by pillows, being unable to lie down on account of dyspnoea; complete loss of motion except a little nodding of the head and a little movement of the right hand; sight and hearing unimpaired; speech entirely lost; mouth partly open; and lips immovable, except a slight twitching of the left angle of the mouth; cheeks flaccid; tongue completely paralyzed and lying on the floor of the mouth; respiration feeble, and occasional coughing ; pulse 90 per minute and regular ; both arms paralyzed and slightly flexed, and attempts to straighten the fingers caused pain; lower extremities completely paralyzed, and feet and ankles cedematous ; defecation natural; micturition slow and fre- quent; attempts to swallow occasioned distressing cough and suffoca- tion, and the aliments were often rejected through the nose. “ He remained in this condition until the afternoon of the same day, when an attempt to swallow some porridge brought on severe coughing and strangling. At seven o’clock that evening he died without a strug- gle. “ Autopsy twenty hours after death. “ External Appearances.—Rigor mortis well marked. Body spare but not emaciated, no very evident signs of muscular atrophy. “ Head.—Scalp very dry. Skull-cap removed with great difficulty, owing to adhesions of the dura mater, which was torn in trying to sepa- rate it from the bone. Dura mater very much thickened. Arachnoid normal with considerable serous infiltration of the sub-arachnoidean connective tissue. Pia mater much injected. The cerebral substance, both cortical and medullary, appeared to be of normal color and consist- ency but exceedingly hyperEemic. The following conditions of the cranial nerves were found : 1. Olfactory normal; 2. Optic normal; 3. Motor oculi normal; 4. Patheticus small; 5. Trigeminus, on the left AMYOTROPHIC LATERAL SPINAL SCLEROSIS. 565 side flattened, gray, and softened; on the right side larger and very hy- peraemic; 6. Abducens atrophied especially on the left side; 7. Facial atrophied and gray on both sides ; 8. Auditory normal ; 9. Glosso-pha* ryngeal normal; 10. Pneumogastric atrophied on both sides; 11. Spinal accessory much atrophied; 12. Hypoglossal so much atrophied on both sides as to resemble mere threads or filaments of connective tissue. The corpora striata and optic thalami were normal. The cerebellum was very hyperaemic, but otherwise presented nothing unusual. The pons Yarolii and medulla oblongata appeared to be of firmer consistency than usual. “ Spinal Cord.—Spinal meninges much injected. The anterior spinal roots were atrophied, especially on the left side. Transverse sec- tions of the cord showed the anterior cornua of gray matter, as well as the left anterior and right lateral column, to be of a dark rose-color, as if very hyperaemic. “ Portions of the brain, cerebellum, and spinal cord were immersed in absolute alcohol, preparatory to making sections for microscopic exami- nation. When sufficiently hardened, thin sections were made, stained with Carmine, rendered transparent with benzole, and mounted in bal- sam. “The sections of the brain revealed nothing abnormal. The sec- tions of the cerebellum showed a very hyperaemic condition of the part, and a granular degeneration of the large ganglionic cells forming the middle layer of the cortical portion. “ Thirty sections were made at various levels of the medulla oblon- gata, involving the roots and nuclei of implantation of the cranial nerves, especially those of the facial and hypoglossal. Careful micro- scopic examination of these specimens, with objectives varying from fifteen to nine hundred diameters, demonstrated that the portion of medulla forming the floor of the fourth ventricle was the seat of several pathological lesions. “ There was a decided hypertrophy or overgrowth of the connective tissue, which appeared to have encroached upon and to some extent replaced the several groups of ganglionic cells which form the nuclei of implantation for the facial and hypoglossal nerves. The individual cells comprising these groups were separated from one another, and in many instances had lost their stellate appearance ; their radiating pro- cesses having been destroyed, so that each cell remained isolated and disconnected from its neighbors. These cells had also undergone a de- generative process, which in many cases rendered them simply a collec- tion of fine granules, and a deposit of brownish-yellow pigment had taken place to such an extent as to give the cells an appearance almost precisely similar to those which are normally found in the locus niger of Soemmering ; they were fewer in number than usual and diminutive in size. 566 DISEASES OF THE SPINAL CORD. “ Sections of the cord made in the cervical, dorsal, and lumbar re- gions, showed a sclerosis with increase of the connective tissue in the anterior and lateral columns, which was most marked in the left ante- rior and lateral columns. The multipolar ganglion cells, situated in the anterior cornua of gray matter, were fewer in number than usual, and many of them appeared granular and very much pigmented.” As Dr. Hun subsequently remarks, there was here “ a descending degeneration of the motor tracts of the cord consecutive to a primary lesion situated in the medulla. This is fully in accordance with the views presented by Bouchard in his work on secondary degenerations of the spinal cord, and accounts for the progressive paralysis of the trunk and extremities which follows the original loss of motion in the lips, tongue, and palate.” The cases cited by M. Charcot from Leyden1 are similar in general characteristics. To repeat, glosso-labio-laryngeal paralysis is a paralysis without atrophy. Paralysis and atrophy consequent to it of other parts lower down, are due to secondary degenerations of the cord. Amyotrophic lateral spinal sclerosis is a paralysis with atrophy. It has a tendency to ascend and to involve the nuclei of the bulbar nerves, causing the atrophy of the muscles of the lips, tongue, and palate, and accompanied with fibrillary contractions, which latter are not phenomena of glosso- labio-laryngeal paralysis. Such cases as those of Hun, Leyden, and others, as well as several which have come under my own experience, are, so far as their lower spinal phenomena are concerned, to be classed not with the protopathic, but the deuteropathic spinal amyotrophies of Charcot, the secondary spinal degenerations of Bouchard, to which attention will be given hereafter. Even if we adopt M. Charcot’s view that in such cases there is a real atrophy of the tongue, which is concealed by the hyperplasia of the perimysium, and the deposit of fat between the muscular fibres, we could not avoid perceiving the difference between such instances and those of true progressive muscular atrophy attacking the tongue, and in which there are fibrillations, and no interstitial fat to mask the ver- itable condition. The lesions of the muscles in amyotrophic lateral spinal sclerosis are similar to those met with in progressive muscular atrophy. The peri- mysium is increased in quantity and the muscular fibrillre undergo fatty degeneration and atrophy. In considering the relation of the phenomena to the lesion, the ques- tions to engage attention are mainly those which have already been suffi- ciently dwelt upon, when the other affections characterized by paralysis and atrophy were under notice. One symptom, spasmodic contraction, 1 “Ueber progress?ve bulbare Paralysie,” Archiv fur Psychiatrie, Band ii., S. iiL PROGRESSIVE LOCOMOTOR ATAXIA. 567 a concomitant of primary symmetrical spinal sclerosis, is, as has been pointed out when that disease was under consideration, the direct con- sequence of the lesion of the lateral columns. Treatment.—In regard to a malady of so hopeless a character as amyotrophic lateral spinal sclerosis, there is little or nothing to say under this head. We have no means at our command capable of arresting the onward tendency of the disease. VII. INFLAMMATION (SCLEROSIS) OF THE POSTERIOR ROOT-ZONES OF THE SPINAL CORD (PROGRESSIVE LOCOMOTOR ATAXIA), (TABES DORSALIS). In the former editions of this work I described locomotor ataxia tinder the designation—based upon its patho-anatomy as then under- stood—of posterior spinal sclerosis. The recent investigations of Charcot and his pupils have, however, shown that the morbid process which gives rise to the remarkable group of symptoms known as loco- motor ataxia is in reality situated in the subdivisions of the posterior columns, lying between the columns of Goll and the posterior horns of gray matter, and called the posterior root-zones. In accordance, therefore, with its exact morbid anatomy, tabes dorsalis should be designated by the term placed at the head of this section. But, for convenience, I shall generally use the name locomotor ataxia, and no confusion can arise from this course, so long as we bear in mind the relation which it bears to the more exact pathological designation. Although other writers, and especially Romberg,1 had described a disease answering to that now generally known as locomotor ataxia, we are mainly indebted to Duchenne 2 for giving a full and distinct ac- count of an affection which, before his studies, had scarcely attracted attention. Since then, the morbid anatomy, the pathology, and the symptomatology, have been so thoroughly studied by Charcot, Pierret, Westphal, and others, whose labors will be presently more specifically referred to, that the disease in question may be said, with truth, to be one of the most thoroughly understood in the whole range of medical science. Symptoms.—Locomotor ataxia has no uniform set of initial symp- toms. Sometimes it begins with dull, heavy p&ins in the small of the back or other part of the spinal column, which are very soon followed by sharp, electric-like pains, which shoot down the limbs along the course of the nerves, and which are very generally taken by the patient for twinges of neuralgia or rheumatism ; or it may be first manifested 1 “Lehrbuch der Nervenkrankheiten,” Berlin, 1840; also, “Sydenham Society’s Translation,” London, 1853. 2“Del’ataxie locomotrice progressive,” Archives Generates de Medecine, 1858; also, ■* De l’electrisation localisee,” Paris. 1861. 568 DISEASES OF THE SPINAL CORD. by a feeling of constriction around the body like that which is so com- mon in acute myelitis. Again, the first symptoms are cerebral, and may consist of attacks of vertigo, pains either in the front or back of the head, epileptic fits, disturbances of vision, such as diplopia, ptosis, and defective accom- modation, In this form the pupils are contracted often to mere points, or occasionally they will be found to be, one contracted, and the other dilated. At other times the stomach and bowels are disordered ; vomiting is frequent, and there may be diarrhoea or obstinate constipation. Or, finally, the initial phenomena may be connected with the sensibility, giving rise to angesthesia, and the various abnormal sensations con- nected therewith. In whatever way it may begin, locomotor ataxia is soon chiefly manifested by disorders of motility, but inquiry reveals the fact that these are in reality secondary, being dependent upon the diminished sensibility which always exists. As this is the essential feature of the disease, I propose to inquire into its characteristics at some length. If the lesion, as it usually does, exists in the dorso-lumbar region of the cord, the first evidences of anaesthesia or of perverted sensibility are noticed in the feet. A common feeling is as if the toes are too large for the shoe, or as if pieces of some plastic material are between them. Sometimes there are burning pains in the soles of the feet, and very generally “ pins and needles ” and other forms of numbness. A curious symptom is that, not only is the sensibility lessened, but the transmission of sensitive impressions to the brain does not take place with the normal degree of activity. I have noticed this phenomenon in rather more than half the cases that have come under my observation. In a lady, now a patient, a pin stuck into the calf of the leg is not felt for fourteen seconds on the right side and sixteen on the left. In a patient with posterior spinal sclerosis, under treatment in the New York State Hospital for Diseases of the Nervous System, if the feet were put into hot water the sensation was not felt for almost three minutes. As he said, “ My feet might be scalded till the flesh dropped off and I would not know it till the mischief was done. Then I should feel it sharply.” The explanation of this symptom is to be found in the fact that the conducting power of the posterior columns is lessened by the lesion, and hence the brain does not receive in the usual time the im- pressions made upon the nerves. The ability to feel pain is therefore diminished, but there is, besides, a marked abatement of the tactile sensibility. The extent of this can only be accurately measured by the gesthesiometer. When this instru- ment is used, we find that the two points can be widely separated and a single impression only be felt on parts of the body which in the nor- mal condition would give the sensation of two points at a much less PROGRESSIVE LOCOMOTOR ATAXIA. 569 distance apart. A gentleman from Virginia consulted me recently, in whom I diagnosticated locomotor ataxia, and who, instead of being able to perceive the two points with the end of the index-finger, when the twelfth of an inch apart, could feel but one point, though the two were separated to the extent of an inch and a half. Sometimes, even in the early stages of the disease, the loss of sensibility is so great that the patient hardly feels the points at all. This loss of sensibility gives rise to some curious sensations, espe- cially in the soles of the feet. These are usually such as might be pro- duced by the interposition of some substance between the foot and the shoe, or between the shoe and the ground. One patient feels as if he has cushions on the soles of his feet, another as if bladders of air are, interposed, another as if he is constantly treading on sticks, or, if riding in an omnibus, as if the hem of a lady’s dress had got under his feet, and one a short time since described the sensation to me as being like that which he thought he would feel if his feet had been dipped into tar, and then into sand. In some-cases the ability to distinguish differences of temperature, or to appreciate the sensations produced by the application of hot or cold bodies to the skin of the affected parts, remains, but this is not, as some authors assert, a constant phenomenon, for in the majority of cases the sensations produced by heat or cold are just as unappreci- able as those caused by any means capable of giving rise to sensitive impressions. But the symptoms by which locomotor ataxia is recognized most readily are those which relate to motility, and the phenomena often make their appearance at a very early stage of the affection. At that time there is no loss of motor power, but there is an inability to coordinate the muscles—to bring them to harmonious action, and thus to execute with precision the various voluntary movements. Thus, in the act of standing, a great many muscles are simultaneously made to contract, and each one to just that necessary degree which is essential to maintain the body in the erect posture. Very often the first evidence of any motor trouble is experienced in regard to this faculty of standing. This impediment is, however, not one of paralysis, for, if the patient looks at his feet, he has no more trouble in standing alone than a perfectly sound man. A gentleman connected with the city government of Brooklyn con- sulted me a short time since for an affection which was very evidently locomotor ataxia. The first indication of disease, as he informed me, was that it had been his habit, while at his morning ablutions, to shut his eyes, and he had noticed, about two months previously, that when he did so he could not maintain his equilibrium. When he visited me he was unable to stand with his eyes shut, and his gait was perfectly characteristic of locomotor ataxia. 570 DISEASES OF THE SPINAL CORD. Before the locomotion of the patient becomes obviously affected, he experiences inconvenience in placing his feet upon small surfaces. Thus, when he attempts to enter a carriage, he finds it difficult to guide his foot to the step, and in mounting a horse he cannot readily hit the stirrup. A gentleman from Maryland, who is now a patient of mine, and who is affected with the disease in question, tells me that among the first symptoms which he noticed was the difficulty he experienced in putting his foot into the stirrup. He was obliged to use his hand as a guide. A like trouble is frequently experienced in ascending a stair- case. The gait of a person suffering from locomotor ataxia is very much changed from that which is natural. Instead of the foot being placed upon the ground with an easy motion, the heel a little in advance of the sole, and the latter gliding down gently, the leg is, as it were, jerked forward, the heel comes down suddenly, and the sole follows, at a con- siderable interval, with an abrupt flapping motion. In ordinary walking the placing of the foot on the ground consists of one movement—there being no stoppage between the touching of the ground by the heel and the planting of the sole of the foot; but, in the gait of a person affected with posterior spinal sclerosis, the foot is placed on the ground by two distinct movements, one for the heel and another for the sole of the foot. But, besides these irregularities of the progressive movements, there are others which are likewise notable. The leg is not carried directly forward, but is thrown out a little from the median line, and this gives the patient a motion like that of one walking on a tight-rope, and bal- ancing himself with a pole. The object of this movement is doubtless to widen the base, and thus to enable the patient to preserve more readily his centre of gravity within it. In standing, he, for the same reason, always separates the feet to a greater than normal distance. In walking or standing, it will be observed that the patient affected with sclerosis of the posterior root-zones of the spinal cord keeps his eyes fixed on his feet, or on the ground a little distance in advance. He is obliged to do this for the reasons—which with others will be more fully considered under the head of pathology—that the sensibility of the soles of the feet being diminished, and the muscular sensibility being also lessened, he is deprived, to a great extent, of the chief means by which he was formerly enabled to recognize the position of his feet, and of the dynamic condition of his muscles. He hence is obliged to make use of another sense—his vision—in order to obtain the necessary information. Therefore, when he shuts his eyes, or is obliged to walk in the dark, he is deprived of the assistance of his eyesight, and, having only his diminished tactile and muscular sensibility to guide him, moves in an exceedingly timid and disorderly manner, or else is unable to walk at all. PROGRESSIVE LOCOMOTOR ATAXIA. 571 Under some circumstances he is unable to go forward, even with the assistance of his eyesight. Experience has taught him that he can- not rely on very important senses, which formerly he implicitly trusted. He loses confidence in them, and is not reassured, even with vision to assist him. He therefore uses extraordinary caution in walking over a tiled floor, on the ice or snow, in descending a staircase, or in crossing a street crowded with vehicles. In a recent clinical lecture,1 delivered to the class of the Bellevue Hospital Medical College, I called special attention to this phenomenon of loss of confidence, and adduced severa. cases in illustration of this point. That there is little paralysis of motion to account for these abnor- malities, can be readily shown by a few inquiries and experiments. Thus it will ordinarily be found that the patient who is unable to stand with his eyes shut, or take a step in the dark, can push strongly with his legs, or walk a short distance with a good deal of vigor. He is still good for a “ spurt,” but long-continued muscular effort fatigues him. When the lesion is above the origin of the nerves which go to form the brachial plexus, the upper extremities are the seat of symptoms which are similar to those described as manifesting themselves in the legs. There are numbness and other indications of anaesthesia, together with more or less difficulty in coordinating the muscles into harmonious action. The patient finds that the ends of his fingers have lost, to some extent, their acute tactile sensibility, and that there is restraint in the management of the fingers. He experiences these difficulties in button- ing his clothes, in picking up a pin, in writing, and in other actions requiring nice manipulation. If he attempts, for instance, to carry a glass of wine to his lips, he spills a portion of the contents ; and, if told to place his finger on any particular part of his face, the movement is accomplished with a wabbling motion, and the finger is darted suddenly to the part as it approaches it. All persons possess a knowledge of where the different parts of their bodies are situated, which does not depend upon the sense of sight, although probably acquired by that sense and experience. There is such an intimate and exact relation be- tween the ends of the fingers and the cutaneous surface of the body that, if a spot no bigger than the head of a pin be made with a pencil on the forehead, a person can close his eyes and touch it with the end of his finger without difficulty every time he makes the attempt. He can also, with the eyes shut, carry the end of his fingers straight to the tip of his ear, the middle of his eyebrow, or any other part of his body within reach. A person, however, laboring under sclerosis of the pos- terior root-zones of the spinal cord, cannot do any of these things. He loses, at a very early period of the disease, that intimate topographical relation which exists between the ends of the fingers and the rest of the 1 “ Clinical Lectures on Diseases of the Nervous System,” Journal of Psychological Medicine, January, 1871. 572 DISEASES Ofr THE SPINAL CORD. body ; and hence, when he closes his eyes, and attempts to put the tip of his index-finger on the end of his nose, he misses his aim, sometimes by as much as two or more inches. M. Onimus 1 has called attention to the fact that important indica- tions are afforded by an examination of the handwriting of ataxies, the defective power of coordination being well shown even when the eyes are open, but being still more strongly manifested when they are shut. The difficulty which they experience is in making the round letters, such as «, c, and o. Besides the incoordination there is a jerking movement of the pen, and a kind of impidse to continue writing after the word is finished. Finally, when the ataxia of the arm is at its height, there is an impossibility of writing a single word, and we obtain only a set of traces confused and without order. I am able, after many ex- periments, to confirm the foregoing obser- vations. In Fig. 73, «, is seen the attempt of a patient with his eyes open, and look- ing at his pen, to write the word “ Civiliza- tion.” At b is a like attempt made when the eyes were shut. As in the legs, when the lesion is so low down in the cord as only to affect them, there is no well-marked paralysis. The grip of the pa- tient is strong, and the dynamometer shows the existence of consider- able strength. He is, however, not capable of continued muscular effort; and, though he may be able to lift several hundred pounds, or to carry another person around the room, his muscles are exhausted with the gradual and regular expenditui'e of a much less amount of force. A phenomenon is often noticed as regards the upper extremities, which also exists with the lower, but which cannot be so readily mani- fested—and that is, that the patient loses the ability to distinguish even considerable differences between weights. In the normal condi- tion, if two weights, differing in the ratio of thirty-nine to forty, are put one in one hand and one in the other, the difference is perceived without difficulty. The lower extremities, according to Jaccoud, are not so sensitive, and cannot distinguish a less difference than from about fifty to seventy grammes. A person affected with lo'comotor ataxia, due to sclerosis of the posterior root-zones above the origins of the nerves which form the brachial plexus, may have an ounce-weight put into his hand, and Fig. 73. 1 Gazette medicate, February 21, 1874; also, Chicago Journal of Nervous and Mental Diseases, April, 1874, p. 254.. PROGRESSIVE LOCOMOTOR ATAXIA. if in a few seconds it be removed, and one of half an ounce be substi- tuted, he will not be able to tell correctly which is the heavier. Or both hands may be extended, and the two weights placed simul- taneously in them. The eyes should, of course, be closed. Some- times less differences can be perceived, but ordinarily greater ones are not distinguished. In the case of a gentleman now under my charge, there is an impossibility of telling which of two pieces of lead, the one weighing one ounce and the other a pound, is the heavier. Spiith 1 states that, in a case under his charge, the patient could not distinguish between two weights, wThich differed as one to one hundred. No means for measuring the extent to which the patient is able to determine the state of muscular contraction is at all comparable to the dynamograph. The range of its usefulness is, however, limited—owing to the fact that posterior spinal sclerosis is not very frequently seated high enough in the cord to affect the muscles of the upper extremities. When the lesion is not above the origin of the nerves which go to form the brachial plexus, the line is straight, as in the accompanying figure, Fig. 74. which represents the tracing made by a patient suffering from sclerosis of the posterior root-zones in the lower dorsal region of the cord. But, when the seat of the disease in the cord is anywhere between the fifth cervical and first dorsal vertebrae, the ability to maintain a uniform degree of pressure is impaired, and lines resembling the following are produced : Fig. 75. Both the above were made by the .same patient, the upper with the right and the lower with the left hand. He was perfectly confi- dent, till I showed him the tracings, that he had exerted a uniform pressure while the paper was traversing the pencil. 1 “ Beitrage zur Lehre von der Tabes dorsalis,” Tubingen, 1864. DISEASES OF THE SPIXAL CORD. Under the name of barmsthesiometer, Eulenberg1 has described an instrument for estimating the sense of pressure, by means of which very accurate determinations can be made for different parts of the body. He succeeded in demonstrating a considerable impairment of the sense of weight in the great majority of cases of locomotor ataxia exam- ined, even Avhen sensibility to pain, tickling, or electric irritation, was but slightly affected, and the sense of temperature was normal. The reflex excitability of the skin is generally notably increased. The touch of the bedclothes, or even the rubbing of one leg against the other, is sufficient to cause strong contractions. Involuntary movements of the limbs, independent of those due to reflex excita- tions, are rarely met with. A symptom first pointed out by Westphal2 is the absence or nota- ble diminution of the reflex excitability of the tendons. It is generally best exhibited by causing the patient to cross one leg over the other and then to strike with the side of the hand the tendon of the quadri- ceps extensor just below or just above the patella. It will be found that there is very slight and often no movement whatever of the leg. In the healthy subject, involuntary extension of the leg at once takes place. This symptom, though occasionally absent, as I have found, is yet so generally present, even in the early stage of locomotor ataxia, as to make it a sign of considerable diagnostic importance. The electro-muscular contractility is generally increased. In some few instances I have found it normal, and in still fewer diminished. There are no polar degenerative reactions. It has already been mentioned that there are frequently ocular troubles. These generally occur among the early symptoms, and relate either to vision, to the movements of the eyeball, or to both. Indeed, the very first symptoms may be connected with the eye or the nerves supplying its muscles. Thus there may be amaurosis due to gray atrophy of the optic nerve, or of the disk, a condition readily detected by the ophthalmoscope ; or the third pair of nerves may be involved, causing ptosis, divergent strabismus, and dilatation of the pupil; or the sixth pair of nerves alone may be affected, causing convergent strabismus ; or there may be only contraction of the pupil and promi- nence of the eyeball from the irritation propagated from the cilio- spinal centre through the sympathetic nerves. In the majority of cases the iris loses its reflex action to light, but, as Argyll-Robertson first pointed out, still retains the power of contraction and dilatation for accommodation. These ocular troubles never take place in sclero- sis of the posterior root-zones'existing below the cilio-spinal centre— the upper dorsal region of the cord. 1 Allg. Med. Cent.-Zeitung, No. 93, 1869; also, Journal of Psychological Medicine, October, 18Y0, p. 622. 2 “Archiv fur Psychiatrie und Nervenkrankheiten,” B. v., s. 819. PROGRESSIVE LOCOMOTOR ATAXIA. 575 Galezowski1 has called attention to a very important fact in con- nection with the ocular disturbances of ataxies, and that is, the loss of the ability to distinguish certain tints and colors. Thus patients affect- ed with locomotor ataxia, and who are at the same time amaurotic from gray atrophy of the optic nerves, are unable to distinguish the secondary tints of the scale (1 to 5, Plate F), and lose the perception of red and of green. The perception of yellow and blue is not lessened ; on the contrary, it appears in some cases to be rendered abnormally delicate. I have frequently verified the extreme value of these tests, and have often observed the phenomena referred to when there was no other disturbance of normal vision, so far as all type-tests were concerned. Another organ liable to functional derangement and even organic disease as effects of locomotor ataxia is the heart. Attention was first directed to this point by Berger and Rosenbach,8 who, in a monograph based on seven cases, arrived at the conclusion that aortic insufficiency was the condition induced. But in a recent paper on the subject of the relation between locomotor ataxia and cardiac lesions, M. Gras- set 3 shows, from two cases occurring in his own experience, and the citation of fifteen others from different writers, that the influence is not such a restricted one as supposed by Berger and Rosenbach, and that the influence is such as would be produced by acute suffering of any kind. He shows very conclusively that there is no direct relation between the spinal affection and the heart, but that the agonizing pains which the patient affected with locomotor ataxia usually suffers, are the cause of the heart-troubles. To use his own language : “ Ex- periments prove the undoubted influence of peripheral excitations and painful sensations on the heart. They show that it is possible that, with man, pains, if long continued, affect the heart in an abnormal way and induce disease of the organ. Physiology simply indicates the possi- bility ; clinical experience establishes the reality.” The disturbances in the healthy action of the stomach and intes- tines, which have already been alluded to as common initial symptoms, are sometimes very distressing. As the pains in the limbs are often taken for evidences of neuralgia or rheumatism, so these gastric and intestinal troubles are frequently regarded as indicating the existence of dyspepsia. I have had a number of patients under my charge who, with double vision, ptosis, contracted or unequal pupils, incoordination, and the other symptoms of locomotor ataxia, had been told that “ it was all dyspepsia,” because vomiting and gastric pain were prominent 1 “ Dii diagnostic des maladies des yeux par la ehromatoscopie retinienne,” etc., Paris, 1868; also, “Echelles typographiques et chromatiques pour l’examen de l’acuite visuelle,’’ Paris, 1874. 2 “ Ueber die Coincidenz von Tabes Dorsalis und Insufficienz der Aorten-Klappen,” Ber- liner Min. Wochenschrift, No. 27, 1879, p. 402. s “ Ataxie locomotrice ct les lesions eardiaques,” Montpellier Medical, Juin, 1880. 576 DISEASES OF THE SriNAL CORD. features of the disease. These symptoms are also due to the relations of the sympathetic nerves with the spinal cord, and are not present in cases where the lesion is low down in the lumbar region. When, however, this part of the cord is involved, there are very remarkable disorders of the genital system. These consist of frequent nocturnal emissions with or without erections, or of an inordinate desire for sexual intercourse. A gentleman who consulted me a few weeks ago, and who was affected with the disease in question, informed me that he had several times had as many as eight seminal emissions in one night, and that his sexual desire was almost inextinguishable. Paralysis of the bladder is a common circumstance, and the sphinc- ter is not infrequently likewise affected. The bowels are usually obsti- nately constipated. The feeling of constriction around the body, which is so common a symptom in acute myelitis, and wrhich is met with in other organic affections of the cord, is rarely absent in cases of sclerosis of the pos- terior columns. Although the course of the disease in the great majority of cases is onward to a fatal termination, there are often periods of remission, as in other spinal affections, and it rarely happens that the duration is not several years. A gentleman from Westchester County, in this State, has been affected for over twenty years, and still walks tolerably well. Another from Boston had been subject to the disease for over twelve years. When I first saw him he could not stand with his eyes shut, had the characteristic ataxic gait, was subject to genital and urinary troubles, but yet was no worse than he had been six years previously. He visited me again in October, 1875, walking as well as when I saw him originally, but still subject to the electric-like pains in as great degree as ever. Another, from Pittsburg, has been in a stationary condition for several years ; and another, from Binghamton, in this State, remains about as he was three years ago. I could easily cite twenty others whom I occasionally see professionally, who hold their own, and who have been affected for from five to ten years. Romberg gives the average duration at from ten to fifteen, Jaccoud at from six to eight, and all authors agree that the course is slow. Of the many patients affected with sclerosis of the posterior columns of the spinal cord who have been under my charge during the last ten years, five only have as yet died, so far as I am aware. Of these, one had been affected seven years, one eight years, two about ten years, and one eight and a half years. There are several cases now under my charge in which the affection has existed longer than either of these terms. The advance of the disease in the cord causes an aggravation of all the symptoms, and the appearance of others not previously noticed. The loss of motor power is now a prominent feature, the muscles be- come atrophied, bed-sores make their appearance, there is anasarca, and PROGRESSIVE LOCOMOTOR ATAXIA. 577 the patient, if not carried off by some intercurrent affection, dies of tbe extreme exhaustion induced by his disease. Among the anomalies of sclerosis of the posterior root-zones of tbe spinal cord, the joint affections are especially worthy of attention. Their connection with posterior spinal sclerosis was first indicated by Charcot.1 Previous to his observations, they had been noticed, but they were ascribed to an intercurrent rheumatism, and, many years before locomotor ataxia was recognized as an independent disease, the asso- ciation of spinal disease with inflammation of the joints was pointed out by Prof. J. K. Mitchell,2 of Philadelphia ; and his son, Dr. S. Weir Mitchell, with Drs. Morehouse and Keen,3 had also related cases in which wounds of the spine had been followed by arthritis. Since Charcot’s paper was published, Dr. Benjamin Ball4 has cited cases of like affections coexisting with locomotor ataxia. In the cases in ques- tion there is no fever, redness, or pain. Generally these accidents dis- appear without leaving permanent organic changes behind them, but in some cases the head of the bone may be absorbed, and spontaneous dislocation be the result. Of the cases of locomotor ataxia which have come under my obser- vation, in nine only were there any troubles of the joints. Death may take place either as the direct consequence of the lesion of the spine, or as the result of some intercurrent affection, such as pneumonia, dysentery, phthisis, or cystitis, or by disturbances of respi- ration and circulation, or paralysis of the muscles of deglutition by the extension of the disease upward, so as to reach the phrenic nerves, or medulla oblongata. A psychical form of locomotor ataxia mentioned by some authors can scarcely be said to exist. It is true that some patients are pecul- iarly subject to mental depression, and to attacks of temporary excite- ment, with wakefulness ; but the rule, according to my experience, is that by far the greater number preserve a very calm and equable frame of mind, and such is the conclusion of Steinhal6 and Erb.8 But mental disorder of a very decided character is occasionally, though rarely, developed toward the latter stages of locomotor ataxia. I have not, however, been able to ascertain that this is particularly liable to assume any special form. It may be intense melancholia, or 1 “Sur quelques arthropathies qui paraissent dependre d’une lesion du cervcau ou de la moelle 6piniere,” Archives dc physioloc/ie, No. 1, January, 1868, p. 161. s American Journal of the Medical Sciences, vol. viii., 1831, p. 65. 3 “ Gunshot-Wounds and other Injuries of Nerves,” Philadelphia, 1864. 4 “ On Diseases of the Joints connected with Locomotor Ataxy,” Medical Times and Gazette, October 31, 1868. 5 “ Beitrage zur Geschichte und Pathologie der Tabes Dorsalis,” Hufeland's Journal, Hand 98, 1844. 8 “ Graue Degeneration der Hinterstrange,” Ziemssen's Handbucli, elfter Band, zweite Hiilfte, p. 184. 578 DISEASES OF THE SPINAL CORD. general mania, or general paralysis of the insane. It is necessary to bear in mind, especially as regards the last-named complication, that it is altogether different from a brain-disease with ataxic phenomena. There is a form of general paralysis of the insane in which there are difficulties of coordination and other tabetic symptoms, but here the cerebral manifestations are first in order ; whereas, in locomotor ataxia, the spinal disorder is the primary trouble, and the cerebral altogether secondary. Westphal1 was the first to direct attention to the ataxic- form of general paralysis of the insane, and to show that the disorders of movement which are exhibited are due to degeneration of the pos- terior columns of the spinal cord. Several instances of mental disorder supervening toward the ter- mination of locomotor ataxia have come under my observation, and in one of them the development was so rapid as to preclude the idea that it was due to any extension of the disease directly to the brain. The form of mental derangement in this case was acute mania, and the patient died, after a paroxysm of intense excitement, in a condition of profound coma. In another case there were repeated epileptiform convulsions, with stupor during the intervals, and in which latter condition death ensued. Friedreich2 has called attention to an affection of the spinal cord occurring very rarely in children, which he regards as a hereditary or family form of locomotor ataxia, but which, from an experience of four cases, and detailed descriptions of six others occurring in the practices of Drs. W. C. Warren, of Holly Springs, Mississippi, and E. S. Coleman, of Hollywood, Arkansas, I am disposed to think is not locomotor ataxia, but a hitherto unrecognized spinal disease. It begins in early life, and is, at least in the early stages, not so much characterized by incoordination as by muscular weakness. In the cases I have witnessed, the children, brothers in two instances, presented the appearance of old men, but were able to walk as well with the eyes shut as with them open, and to stand with closed eyes without any unusual swaying of the body. In none of the cases was there any hereditary tendency, but, as I have said, my cases are two pairs of brothers. Dr. Warren’s cases, three in number, were children of the same parents ; as were also Dr. Coleman’s three cases. All my cases are males ; of Dr. Warren’s cases two were boys and one a girl ; of Dr. Coleman’s cases all were boys. Friedreich is of the opinion that this form is more common in girls than in boys. I think it somewhat doubtful whether the cases he cites are of the same character as those which have come to my knowledge, and I re- frain from any further discussion of the subject till I have more thor- 1 “ Tabes Dorsualis und Paralysie universal progressive,” Zeitschrift fur Psychiatric, Band xx., 1863; und xxi., 1864. 2 “ TJeber ataxia mit besonderer Beriicksichtigung der hereditaren Formen,” Virchow's Arcliiv, Band 68, 1876 ; Band 70, 1877. PROGRESSIVE LOCOMOTOR ATAXIA. 579 oughly studied the symptoms and pathogeny, through the instances within the range of my own observation. Causes.—I have been very unsuccessful in my efforts to ascertain the cause in the greater number of persons affected with progressive locomotor ataxia who have been under my observation. The opinion is very prevalent that it is generally the result of excessive venereal in- dulgence ; and, although this is undoubtedly sometimes a cause, it cer- tainly is not so common a one as is generally supposed. I have care- fully inquired into the etiology of all the cases I have seen, and have only been able to assign inordinate sexual indulgence as the cause in a very small proportion. The impression has probably arisen from the fact that there are frequently aberrations of the sexual function as phe- nomena of the disease. Injuries and exposure to cold and dampness were apparently the causes in some cases, standing in a constrained po- sition—three cases in railway conductors—in others, the excessive use of alcoholic liquors in a larger proportion, and syphilis in probably one- twentieth of the cases. In the majority, however, no cause can reason- ably be assigned. As regards the predisposing causes, it is certainly more common in men than in women—four cases only in my experience pertaining to the female sex. The age from twenty-five to forty is that in which it most frequently appears. There seems to be no direct hereditary influence to the disease. Diagnosis.—A consideration of the symptoms detailed in the fore- going pages will prevent posterior spinal sclerosis from being confound- ed with any other affection of the spinal cord. It may, however, be difficult at times to discriminate between it and the lesions of the cere- bellum, and the distinction has frequently not been made by very skill- ful diagnosticians. At one time Duchenne held the view that locomo- tor ataxia was really the result of a lesion of the cerebellum, but he subsequently 1 retracted this opinion, and accepted the doctrine that the spinal cord is the seat of the disorder. In a recent memoir2 I have endeavored to point out the differences between cerebellar disease and the affection now called posterior spinal sclerosis. In that essay I have said : “ Derangement of locomotion certainly does result from injury or disease of the cerebellum. Experi- mental physiology, as well as pathology, proves this. Beyond a doubt the disorder is, however, clearly due to vertigo. There are, moreover, headache, vomiting, and eventually in some cases hemiplegia, generally of the opposite side to that of the cerebellar lesion, a fact at variance with Larrey’s assertion. The gait of a person thus affected is exactly 1 “ Diagnostic differential des affections cerebelleuses et de 1’ataxie locomotrice pro- gressive,” Gazette hebdomadaire, 1866. * “ The Physiology and Pathology of the Cerebellum,” Journal of Psychological Medi cine, April, 1869. 580 DISEASES OF THE SPINAL CORD. similar to that of a drunken man. As Carre says, the movements are not abrupt, jerking, and exaggerated, as they are in locomotor ataxia. They are more uncertain, and do not depend upon any defect of co- ordination, but upon weakness of the voluntary power. “When either of the peduncles of the cerebellum is affected there is an irresistible impulse to go sideways, and sometimes gyratory move- ments are produced.” The characteristic symptom of cerebellar lesion is vertigo; and, although this is sometimes met with in sclerosis of the posterior root- zones, it is not a prominent feature, and is rarely present at all except in the very earliest stage. In the cerebellar lesions the cutaneous sensibility is unimpaired, whereas in posterior spinal sclerosis it is always diminished. A patient with disease of the cerebellum can stand and walk better with his eyes shut than with them open, for the vertigo is not in the former condition felt to the same extent. The reverse is true of loco- motor ataxia. The history of the case will also serve as a good guide to the diagnosis. In the latter or even in the developed stage of loco- motor ataxia it would be difficult to mistake it for any other affec- tion. Prognosis.—The prognosis is no more favorable than that of ante- rior or lateral spinal sclerosis. A few cases are cured, more are relieved, but the great majority go on unchecked. Of the cases which have come under my observation, seven were cured, and they were subjected to treatment from a very early stage. Of these, four were probably of syphilitic origin, but in the other three no such cause was at all probable. One of them was a woman. The cases in which amelioration has been produced are more numer- ous. In fact, it is not at all uncommon to succeed in retarding the on- ward progress of the disease, and of thus prolonging the life of the patient. Morbid Anatomy.—Within the last few years many very important contributions have been made to the morbid anatomy of locomotor ataxia mainly by the pathologists of that great French school of the Salpetriere with Charcot at its head. For the complete understanding of these a few words relative to the normal anatomy of the parts con- cerned are necessary. In embryonic and early infantile life the posterior columns are di- vided into two unequal parts by a fissure extending from the angle formed by the posterior median fissure and the posterior commissure of gray matter. The internal or median part is wedge-shaped, is of greater extent in the cervical region than in the dorsal, and greater in this than in the lumbar. It is called the posterior median column, or the column of Goll. The external part of the posterior column is all that region PROGRESSIVE LOCOMOTOR ATAXIA. 581 bounded externally by the posterior horn of gray substance and in- teriorly by the posterior median columns. It is called the poste- rior external column, or the posterior root-zone, or the column of Burdach. In adult life the fissure separating these two regions no longer ex- ists, but its situation is generally marked by a furrow on the periphery of the cord, and a histological ditference exists between them, in that the posterior median columns contain a greater amount of connective tissue than do the posterior external columns, and the nerve-fibres in them are long and continuous, while those in the latter contain many short fibres, which, after passing upward or downward for a short dis- tance, leave it; the majority of them entering the posterior horn of gray substance, the minority terminating in the posterior median column. Now, although it often happens that both these subdivisions of the posterior columns are the seat of the alteration giving rise to loco- motor ataxia, it has been very positively shown that the essential lesion is that of the posterior external column, and that it is to the disease of these regions that the majority of the peculiar symptoms of locomotor ataxia are due. The posterior internal columns transmit the muscular sense for the lower limbs and trunk only. The muscular sense tract for the upper extremities probably lies in the median portion of the posterior exter- nal columns. It is therefore possible, if the ataxia is limited to the upper extremities, to find the lesion confined to the posterior external columns. This point has been determined by a case very thoroughly investi- gated by Pierret,1 in which a woman named Moli suffered from the electric-like pains, and incoordination of locomotor ataxia, which were mainly experienced in the upper extremities. On post-mortem exam- ination that part of the cord—the cervico-dorsal—in relation with the upper extremities was found to be sclerosed in a thin lamina existing only in the posterior external columns. The posterior median columns were perfectly healthy. In another case the same observer had the opportunity of confirm- ing the view that the posterior median columns do not transmit sen- sory impressions from the upper extremities. A woman (Cutta) had suffered for many years with electric-like pains in the lower extremi- ties, plantar anaesthesia, and incoordination. Standing and walking were impossible. In late years she had experienced constricting pains around the body. The superior extremities were not in the least in- volved. On post-mortem examination the posterior columns in the lumbar region were sclerosed throughout their whole extent, except 1 “ Sur les alterations do la substance grise do la moelle epiniere dans l’ataxie loco- motricc,” etc., Archives de physiologie, 1870, p. 597. 582 DISEASES OF THE SPINAL COED. that on each side a little islet of healthy tissue remained. At the sixth dorsal vertebra the sclerosed tissue was less extensive and almost entirely confined to the posterior median columns, the posterior ex- ternal columns only exhibiting on each side a little islet of sclerosed tissue. A little higher these islets disappeared, and the lesion was entirely limited to the posterior median columns.1 Now, if the posterior median column is not exclusively occupied by fibres transmitting sensory impressions from a lower level, we should not be able to account for the entire exemption of the superior extremities from all ataxic phenomena, for the posterior median col- umns in that part of the cord in relation with them were the seat of marked lesion. When the posterior median columns are the seat of marked dis- ease, it is more than probable that the lesion originates in the poste- rior external columns, and therefore affects the former secondarily. Pierret expresses the opinion, in which Charcot concurs, that the im- plication of the posterior median columns is a phenomenon analogous to that which produces an ascending median sclerosis as a result of partial myelitis, and that the lesion is only produced in those cases in which the morbid process is very strongly pronounced in the lumbo- dorsal region of the cord. As has been shown, the initial lesion of tabes begins in the poste- rior external columns. Now, it is through these columns that a large proportion of the sensory fibres pass immediately after their entrance into the spinal cord, and it is the slow inflammation and destruction of these fibres that give rise to the group of symptoms previously described. Sensory tracts in the cord degenerate upward, and usually degenerate slowly; hence, as the disease generally begins in the lower segments of the coi’d, a considerable interval of time elapses before symptoms of the disease appear in the arms, and a still longer time before cerebral symptoms are observed. It is not always the case that the morbid process stops with the posterior columns ; the posterior horns of gray matter, the lateral columns, and even the anterior horns, may be reached. As to the spinal nerves, it will almost invariably be found that the posterior roots are atrophied and the sensory ganglia diseased. The intra-cranial lesions are important. Indeed, there is reason to think that they are often the starting-point of the disease. They have been very carefully studied by many observers, and the fact that one of the most striking of them—that of the optic nerve—can be observed with the ophthalmoscope, gives additional interest to the subject. The alteration which the optic nerves undergo is a slow progressive 1 “ Note sur la sclerose des cordons posterieurs dans l’ataxie locomotrice progres- sive,” Archives de physiologic, tome iv., 1871—’72, p. 364. PROGRESSIVE LOCOMOTOR ATAXIA. 583 sclerosis, causing atrophy of the disks and of the nerves themselves. From the color which the nerves assume, the condition is known by ophthalmologists as gray degeneration. According to Leber, and Weck- er and Jaeger, the essential changes met with in gray degeneration of the optic nerve are a marked increase in the quantity of connective tissue, especially of the* cell-elements, and the appearance of numerous grumous cells. The lesion is therefore of the same character as sclero- sis affecting the other parts of the nervous system. The ophthalmoscopic appearances have been so clearly stated by Wecker and Jaeger,1 that 1 quote from them the following details : “ The clinical characters are especially revealed by the particular appearance of the papilla and by the narrowing of the visual field. “ An essential sign which we have claimed for the ophthalmoscopic image of gray degeneration, is the more or less complete absence of an atrophic excavation. It is of course easy to understand that such ex- cavation is much less apt to be formed when there is a substitution of cellular tissue than when, as in simple atrophy, the entire nervous struct- ure disappears. “ In gray degeneration of the nerve the initial signs of the disease consist in a simple change in the color of the papilla without any exca- vation. It becomes pale, as is perceived by the examination of the erect image with Helmholtz’s plates, and it assumes a more or less pro- nounced bluish tint. “With this change of color there is a coincident change in the transparency of the tissue of the disk. It becomes impossible to fol- low the central vessels in their ramifications ; they seem to be applied to the bluish-white tissue of the papilla, and the whitish sclerotic ring offers a marked contrast to the opaque tissue of the nerve.” According to these authors, the ophthalmoscopic appearances in cases of gray degeneration are sufficiently characteristic to enable the diagnosis of locomotor ataxia to be made with certainty from them alone. This is, however, I am inclined to think, too positive a state- ment. We may, however, safely conclude that when they are coexist- ent with the disturbance of chromatic perception previously referred to ; when the pupils are contracted—they are dilated in ordinary optic neuritis and atrophy of the optic nerve—and especially when electric- like pains are present, we have as positive indications of the existence of locomotor ataxia as are desirable. Besides this atrophy of the optic nerve, there is another condition to which it is subject, as a consequence of a preexisting sclerosis of the posterior root-zones, and that is a chronic neuritis. This state is in- duced when the spinal lesion is seated in that part of the cord known as the cilio-spinal centre. The ophthalmoscope in these cases reveals 1 “ Traite des maladies du fond de l’ceil,” Paris, 1870, p. 73. 584 DISEASES OF THE SPINAL CORD. in the early stages the existence of choked disk, and subsequently sim- ple atrophic changes. This condition is not peculiar to locomotor ataxia, but may be caused by other chronic affections of the spinal cord. It is referred to by Dr. Clifford Allbutt1 in his excellent mono- graph as “ simple or primary atrophy of the optic nerve, sometimes ac- companied at first by that slight hypersemia and inactive proliferation which make up the state I have called chronic neuritis. This sort of change I have never found as a result of spinal injuries, but I have often met with it in chronic degeneration of the cord, and in locomotor ataxy.” Besides the optic, others of the cerebral nerves may be affected. Those most commonly involved are the third, the sixth, and the audi- tory; the lesion of this latter causing deafness and other disturbances of hearing. The lesions found in the brain never affect primarily the hemi- spheres. To be sure, it is sometimes the case that there are mental troubles, but they come on toward the close, and are probably the result of defective nutrition and sympathetic action. The other cerebral lesions, like that of the optic nerve, are in very intimate anatomical relation with the posterior columns of the cord. They are, therefore, met with in the lower cerebellar peduncles, in the restiform bodies, and in the optic thalami, and consist of degeneration and atrophy. The situations of the spinal lesions and their general character were well known to Romberg 2 before the researches of Duchenne, Charcot, and others. Thus, he states that he was present at the post-mortem examination of the cord of a former patient. The organ was reduced one-third in diameter, and the atrophy was confined to the lower part of the posterior columns. The posterior nerve-roots were also atro- phied, but the anterior columns were healthy. He was also acquainted with the fact that the cerebral nerves were similarly affected. Although it is probable that the sympathetic is atrophied in some part of its extent, in many cases of locomotor ataxia, the fact has not been demonstrated, except as regards one instance reported by Donnezan, in which a filament from the superior cervical ganglion was found atrophied. The ganglion itself was healthy. In the later stages of the affection the muscles may exhibit a con- dition of atrophy. In such cases their tissue will be found on micro- scopical examination to have undergone fatty degeneration and substi- tution to a greater or less extent. 1 “ On the Use of the Ophthalmoscope in Diseases of the Nervous System,” etc., Lon- don and New York, 1871, p. 198. 3 “ Lehrbuch der Nervenkrankheiten des Menschen,” “ Sydenham Society TraDsla tion,” London, 1853, vol. ii., p. 399. PROGRESSIVE LOCOMOTOR ATAXIA. 585 The morbid anatomy of the joint-affections which sometimes result from the spinal lesion consists in an accumulation of water in the synovial cavity, and a general oedema of the soft parts. The most common seat of this alteration is the knee, and next after that the shoulder. The hip, the el- bow, the wrist, and the smaller joints, may also be involved. Occasionally the trouble does not stop here, but the articulat- ing surfaces may become rough from atrophy of the proper bone-tissue, and eventually a considerable part of the osse- ous substance disappears, giv- ing rise to spontaneous laxation. The accompanying figures, from Charcot, illustrate the nature of the change. In Fig. 76 is represented the superior extremity of the healthy humerus, and in Fig. 77 the corresponding part of a humerus exhibiting the lesions produced by locomotor ataxia. Pathology.—The theory of posterior spinal sclerosis which is gen- erally held is, that the lesion impairs a faculty by which the muscles are brought into harmonious action—a faculty of coordination. According to this view, the first thing to be done was to locate this faculty in an organ, and Puchenne, with whom it originated, adopting the ideas of Flourens and others, placed it in the cerebellum, and therefore regard- ed what he designated progressive locomotor ataxia as a disease of the cerebellum.1 Thus he said : “ In conclusion, regarding the order of appearance, and the habitual progress of the symptoms which mark the three periods of progressive locomotor ataxia, we find that the central morbid action which produces the phenomena symptomatic of this disease begins in general in the motor nerves of the eye, and in the tubercular quadrigemina, extending thence to the superior and inferior cerebellar peduncles and finally to the cerebellum.” As already stated, Ducbenne has abandoned this view of the loca- tion. But, although it has been established by numerous post-mortem examinations that the cerebellum is not the seat of lesion in cases of locomotor ataxia, and although the differential diagnosis between dis- eases of the cerebellum and posterior spinal sclerosis has been very clearly made out, there are some who still hold the view that, although the cerebellum shows no traces of disease, and that, although the poste- rior columns of the spinal cord may be in a state of sclerosis, the symp- toms are the result of an interruption to the passage, from the cere- Fig. 76. Fig. 77. 1 “ De Electrisation localisde,” deuxi&me edition, Paris, 1861, p. 611. 586 DISEASES OF THE SPINAL CORD. bellum through the posterior columns to the spinal nerves, of that force which coordinates the muscles into harmonious action. In the memoir to which reference has already been made, I have entered at length into the consideration of the question of the location of a coordinating faculty in the cerebellum, and have, I think, adduced sufficient facts and arguments to show that coordination is not one of its functions. Without going into a full account of the subject, a synopsis of the con- clusions arrived at will probably not be deemed out of place : 1. The consequences of removal of the cerebellum, if the animal survi ves the immediate effects of the injury, are not enduring. This conclusion is supported by experiments by Flourens,1 Harting,3 Wag- ner,3 Dalton,4 myself,6 and others. The physiological inference, of course, is, that, if the faculty of coordination resided in the cerebellum, it ought to be permanently removed with the ablation of the organ. 2. The entire removal of the cerebellum from some animals does not apparently interfere in the slightest degree even for a moment with the regularity and order of their movements. I have performed a num- ber of experiments with reference to this point, on different classes of animals. They prove very clearly that the cerebellum is not the gen- erator of coordinating power in all animals that have it: a fact in com- parative physiology which is fatal to the hypothesis that this is its function in man. 3. The disorder of movements which results in birds and mammals immediately after injury of the cerebellum is not due to any loss of coordinating power, but is the result of vertigo. If the cerebellum be removed from a pigeon it exhibits disorder in its movements, but a careful examination of the phenomena exhibited, shows that it is suffering from a vertiginous sensation. Even when placed upon its breast and allowed to remain at rest, there is a trem- bling and swaying of the body, such as is produced by alcoholic in- toxication. Exactly such symptoms can be caused by giving pigeons bread soaked in alcohol. 4. The phenomena of cerebellar disease or injury, as exhibited in man, are not such as show any derangement of the coordinating power. Many cases are on record which support this proposition. Andral6 states that, of ninety-three cases of cerebellar disease which he has studied, only one appeared to support the theory which locates the co- ordinating power in the cerebellum. 1 “ Recherches experimentales sur les proprietes et les fonctions du systome ner- veux,” Paris, 1842. 2 “Experimenta quaedam de affectibus laesionum in partibus encephalc,” 1826. 8 “ Nachrichten von der Universitat und der Konigl. Gesellschaft der Wissenschaften zu Gottingen”; also, Journal de la physiologic de Vhomme et des animaux, Avril, 1861. 4 American Journal of the Medical Sciences, January, 1861, p. 83 ; also, “Treatise on Human Physiology,” fourth edition, 1867, p. 416. 6 Op. cit., p. 24. 6 “ Clinique m6dicalc,” seconde edition, tome v., p. 735. PROGRESSIVE LOCOMOTOR ATAXIA. 587 Many special instances might he brought forward, and several have occurred in my own practice. The case of Alexandrine Labrosse, reported by Combette,1 is, however, worth referring to more specific- ally. His paper is entitled, “ Case of a young girl who died in her eleventh year, in whom there was complete absence of the cerebellum, of the posterior peduncles, and of the annular protuberance.” Magen- die examined the brain after her death, and satisfied himself that the defect was congenital. As M. Combette remarks in regard to this case, Alexandrine Labrosse had been able to walk for several years, but always in an uncertain manner. Gradually her legs lost their strength, and she became paraplegic. She preserved the use of her upper extremities to the last. It is very evident, therefore, that the weakness of her legs was due to paralysis ; for, had it been the result of incoordination, the arms must necessarily have participated. For these reasons, I think, it cannot be considered, with any degree of probability, that the cerebellum has anything whatever to do with the symptoms manifested in sclerosis of the posterior root-zones of the cord. Neither is it, in my opinion, necessary to assume the existence of an organ whose office it is to exercise a coordinating power. The incoordination which is so prominent a phenomenon of scle- rosis of the posterior columns is unquestionably due to the loss of what is called the muscular sense. Sir Charles Bell2 has argued strongly in support of the existence of such a sense. He enunciates his theory in the following sentence : “ Between the brain and the muscles there is a circle of nerves; one nerve conveys the influence from the brain to the muscle, another gives the sense of the condition of the muscle to the brain.” It is by this connection that we are enabled, according to Sir Charles Bell and other physiologists, to form an idea of the state of contraction of a muscle, and to lessen or increase the contraction as may be necessary. In locomotor ataxia the patient loses this muscu- lar sense, or is unable to exert it, for the reason that the posterior median columns in lower levels of the cord, and the median portion of the posterior external columns at a higher level, through which the muscular sense-perception reaches the brain, are by disease rendered incapable of transmitting it. Before proceeding to the further discussion of this subject, clear ideas should be entertained relative to the anatomy and physiology of the spinal cord. In Fig. 78, which represents a transverse section through the spi- 1 Journal de physiologie experimentale et pcithologique, par F. Magendie, tome xi., Paris, 1831, p. 27. a “ On the Nervous Circle which connects the Voluntary Muscles with the Brain,” Philosophical Transactions. Also, “ The Nervous System of the Human Body,” London, 1830, p. 225. 588 DISEASES OF THE SPINAL CORD. nal cord, the posterior nerve-fibres are seen to enter the posterior horn of gray matter and the posterior external column. Some of these fibres (1 and 2) connect directly with the sensory cells in the posterior horn. These fibres probably conduct sensory impressions of pain, temperature, and touch. Others (4) terminate in Clark's columns, whence the fibres spring which form the direct cer- ebellar tract. Others, again (3), which en- ter the poste- rior external column, aft- er ascending or descending for a short distance, en- ter the pos- terior medi- an column and ascend to the medulla. It is through this tract that muscular sense is conducted. Some (5), which enter the posterior external column, pass directly over to the motor cells on the same side. These fibres undoubtedly transmit the deep reflexes. The superficial reflexes reach the cells in the anterior horn through the posterior horn (7). In Fig. 79, which represents a longitudinal section of the cord, the course of the nerve-fibres within the cord is clearly demonstrated. Such being the connection of the posterior nerve-roots with the posterior division of the cord, it is evident that no part of the length of these columns can be damaged, either by injury or disease, without involving destruction of a corresponding number of nerve-roots, and, as these fibres transmit all sensory impressions, their functions must necessarily be interfered with ; hence the sharp shooting pains from irritation of the sensory roots ; the anaesthesia from destruction of the nerve-fibres ; the inability to stand with the eyes closed, on account of the anaesthesia of the plantar surface of the feet and from the loss of the muscular sense ; and the ataxic gait, which is likewise due to the impairment of the muscular sense ; and, since reflex action depends upon the preservation of the continuity of the reflex arc, the loss of the knee-jerk and of other deep reflexes is readily explained. Pig. 78. Diagrammatic representation of the nerve-fibres entering the cord. (Modified from Edinger.) PROGRESSIVE LOCOMOTOR ATAXIA. 589 In sclerosis of the posterior root-zones of the spinal cord the lesion generally involves the posterior nerve-roots, the posterior white sub- stance, and the posterior cornua of gray substance. Hence the cord loses the ability to transmit nervous force. Those unconscious acts Fig. 79. Diagrammatic representation of the course of the nerve-fibres in the spinal cord. (Edinger.) of muscular coordination which are regulated by the gray substance of the spinal cord can no longer be perfectly accomplished, and the brain is brought to assist in the determination through the sense of sight. The patient cannot stand well with his eyes shut, or walk in the dark, or determine differences of weight, because he is relying altogether on the perceptive faculty of the brain, and this organ is not in a condition to perform its work with precision, because sensory 590 DISEASES OF THE SPINAL CORD. impressions do not reach it on account of the destruction of the sen- sory pathway in the spinal cord. An interesting point connected with the pathology of locomotor ataxia is the fact that the spinal lesions sometimes exist in conjunc- tion with the cerebral lesions which are the anatomical basis of general paralysis of the insane. This subject was alluded to when the last- named disease was under consideration. Westphal,1 who was the first to give special attention to this matter, does not believe that there is any direct relation between the morbid process in the cord and that in the brain. Neither of them is, in his opinion, secondary to the other. They simply coexist as the expression of an excessive proclivity to dis- ease of the nervous system, just as any other two diseases may be pres- ent, one in the brain and the other in the cord, without there being any direct interdependence between them. This is undoubtedly correct. Locomotor ataxia is by no means uncommon in patients affected with the other forms of insanity. Several such cases have come under my own observation, and Dr. Patrick Nicol,2 in an excellent memoir, has adduced several instances which have occurred in his experience. As we have seen, the lesions in sclerosis of the posterior root-zones are not always confined to the original seat. Among other parts of the cord liable to be involved is the anterior tract of gray matter. Hence we have the more complete development of paralysis and the superven- tion of atrophy in the affected muscles. A remarkable instance of loco- motor ataxia combined with muscular atrophy formed the subject of a clinical lecture,3 which I delivered at the Bellevue Hospital Medical College, in the winter of 1871—’72. In this case there were electric-like pains, incoordination, ocular troubles, ptosis, double vision, plantar an- aesthesia, etc. After about two years muscular atrophy set in, begin- ning in the left leg, then involving the right corresponding member, then the left arm, and finally the right upper extremity. In this case the lesion of the posterior root-zones was the primary lesion, the anterior tract of gray matter subsequently becoming sym- metrically implicated. There were no contractions like those present when the lateral columns of the cord are the seat of disease. In the case of the woman Moli, reported by Pierret,4 to which refer- 1 “ Ueber den gegenwartigen Standpunktder Kentnisse von der allgemeinen progressive!] Paralyse der Irren,” Griesinger’s Archiv fur Psychiatrie und Nervenkrankheiten, Heft i., Band i., 1867. 2 “ On Progressive Locomotor Ataxy and some other Forms of Locomotor Deficiency, as found in the Insane,” “West Riding Lunatic Asylum Medical Reports,” vol. i., 1871, p. 178. 3 “ Clinical Lectures on Diseases of the Nervous System,” New York, 1874, p. 166. 4 “ Sur les alterations de la substance grise de la moelle epiniere dans l’ataxie locomo- trice considerees dans leurs rapports avec l’atrophie musculaire,” Archives de physiologic. 1870, p. 690. PROGRESSIVE LOCOMOTOR ATAXIA. 591 ence has already been made, there were also the combination of the symptoms due to the lesion of the posterior root-zones, and those re- sulting from the extension of the morbid process to the anterior horns of gray matter—the right side being the seat of profound muscular atrophy. On post-mortem examination it was found that the right an- terior horn of gray matter in the dorsal and cervical regions was the seat of degenerative changes in the nerve-cells, many of which had dis- appeared. The horn was markedly diminished in size. These changes are shown in the accompanying figure (Fig. 80) from Pierret—a, the posterior roots ; b, the internal radicles, the sclerosis being limited to their area ; c, the right anterior horn of gray matter atrophied. This association of muscular atrophy with sclerosis of the posterior root- zones is to be explained by the fact, first pointed out by Kolliker,1 that some of the internal fibres of the posterior roots pass toward the ante- rior horns of gray matter, and can be traced as far as the large cells forming the external group. The connection of the fibres of the pos- terior roots with the anterior horns of gray matter is also referred to by Lockhart Clarke2 and Gerlach.3 Fig. 80. Treatment.—It must be remembered that locomotor ataxia often spontaneously remits in the violence of its symptoms. Indeed, the re- mission may at times amount to almost a complete intermission. But taking1 this fact into full consideration, I am quite sure that the disease is not m every case uninfluenced by medical treatment. A great many medicines have been recommended, and numbers of cures have been re- ported. Careful inquiry, however, suffices to show either that the al- 1 “A Manual of Human Histology,” “Sydenham Society Translations,” vol. i., 1853, p. 415. 8 “ Philosophical Transactions,” 1853. 3 Strieker’s “Manual of Histology,” American edition, New York, 1872, p. 645. 592 DISEASES OF THE SPINAL CORD. leged cures were merely instances of more or less complete remission, or that the cases were really not examples of the disease in question. To even mention the assumed remedies would be profitless labor. In the very earliest period of the disease ergot is calculated in some cases to be of decided benefit. It should be administered in doses of at least a drachm three or four times a day, and continued for several months. The bromide of potassium, sodium, or calcium, is an effica- cious adjuvant. Under the combined use of these remedies I have repeatedly seen the electric-like pains diminish in violence or even altogether disappear. The gastric disturbances may often be allevi- ated by bismuth, or, what is usually still more efficacious, by Fair- child’s pepsin in doses of three or four grains with each meal. With these measures the primary galvanic current applied to the spine, on each side of the spinous processes, is an agent which ought to be used. Cases have been reported by Meyer, Benedict, and others, in which it alone has apparently effected cures—or arrest of the mor- bid process—and Rosenthal1 speaks highly of its beneficial influence. I have used it with success in several cases in conjunction with the means previously mentioned. Ordinarily, it has not appeared to me to be of any material service. The pains in the back and the sharp shooting pains in the legs or arms and around the abdominal and thoracic regions may be com- bated with phenacetine in ten- or twelve-grain doses, or antifebrine in five-grain doses, either of which can be repeated in an hour if neces- sary, or by codeine in doses of from half a grain to one or even two grains, or with hypodermic injections of morphia. If the case comes under observation when the motorial troubles are well marked, or if, after having used it for a month, no decidedly beneficial effect follows the treatment just specified, I omit the ergot, and frequently use instead, the nitrate of silver in doses of the quarter of a grain three times a day. According to Rosenthal,5 Wunderlich, Charcot and Vulpian, Herschell, Klinger, Duguet and Vidal, have ex- tolled its merits. This remedy has in my hands apparently proved ser- viceable in several cases which were well advanced, but I am not able to speak definitely on the subject, for the reason that with it bromide of potassium, and especially galvanism, were used. Two cases were cured by the combined remedies—one of them was that of a distin- guished journalist, who, in the first place, was treated with ergot, and subsequently, when this medicine appeared to be of no furthe'r effect, with the nitrate of silver. At the present time, seven years having elapsed, this gentleman is well, free from pains, able to coordinate, and with no symptom of the affection remaining. The disease was first manifested by an epileptic paroxysm, and soon afterward ocular trou- bles made their appearance. The electric-like pains, abdominal con- 1 “ Klinik dcr Nervenkrankheiten,” Stuttgart, 1875, p. 394. 2 Op. vit., p. 390. PROGRESSIVE LOCOMOTOR ATAXIA. 593 striction, and incoordination in the upper and lower extremities, were well marked. He was under treatment for about four months. The other case was that of a lady of this city. The disease in her began with pain in the back, and electric pains in the lower extremities Ptosis, dilatation of the right pupil, and diplopia followed, and then gradual loss of sensibility in the soles of the feet, and difficulty in coor- dinating the muscles of the legs. The disease had lasted two years and a half when the patient came under my charge. She was treated with the nitrate of silver and the other remedies mentioned, for nearly a year, and throughout the whole period gradually improved till her recovery was complete. The nitrate of silver was suspended for a week after each month of its administration. In a third case ergot and nitrate of silver were given together with- out the bromide of potassium. This case was that of a gentleman, a merchant of this city, residing in Bridgeport, Connecticut. He had had ocular troubles, and was suffering from pains, incoordination, plantar anaesthesia, paralysis of the bladder, and swelling of the right knee, when he came under my charge, being sent to me by my friend Dr. Hubbard, of Bridgeport. The disease had then lasted only a few months. With the medicines, the constant galvanic current to the spine and spinal nerves was employed. He was entirely cured in less than three months. In all cases inquiry should be made with reference to the existence of a syphilitic taint. If affirmative results follow the investigation, the iodide of potassium should be administered in gradually-increasing doses as recommended for acute spinal meningitis, or in combination with corrosive sublimate, according to the formula given on page 308, recol- lecting that galvanism is likewise to be used, and such other treatment as the special symptoms may seem to require. Two cases were cured by this treatment; one of them was that of a gentleman from the West —a fully-developed case—who had been treated by my friend Dr. Bumstead, for other syphilitic troubles, and who sent him to me for his spinal disease. The incoordination, plantar anaesthesia, pain in the lumbar region, and the electric pains, were all present, together with slight diplopia. He was under treatment for about ten months. I met him a few weeks since in a railway-car, the picture of health, and, as he told me, perfectly well. The other case occurred in the person of a gentleman of this city, and was similar in general features to the preceding. A cure was ob- tained, after like medication, in six months. In the majority of cases, whether there is a syphilitic taint or not, I administer the iodide of potassium. Beginning with moderate doses, it should be gradually increased up to the point of toleration, which differs vastly in different individuals. The iodide of potassium is very efficacious in preventing the formation of new connective tis- 594 DISEASES OF THE SPINAL CORD. sue. In this manner, I am convinced, the progress of the disease is often arrested, and in the early stage, which is probably one of simple congestion only, destruction of the nerve-fibres may be avoided. In another case, after ergot had been used for several months with- out apparent benefit, the nitrate of silver was administered with the effect, to all appearance, of checking the further progress of the disease, and producing decided amelioration of the existing symptoms. The patient, a distinguished member of the dramatic profession, by my ad- vice withdrew from the stage, and, being in Philadelphia, he consulted at my suggestion Dr. Weir Mitchell, who unhesitatingly confirmed my diagnosis. He took the nitrate persistently for about six months, and was so greatly improved that I gave my consent to his resuming his profession. There are now no pains; his coordination is good, and his general health leaves nothing to be desired. In several cases I have obtained ameliorations by the use of phos- phoric acid, phosphorus, and chloride of barium, but after extensive experience with these agents, I am unable to report any permanently good results. If the vesical sphincter be paralyzed, belladonna may be used with advantage, preferably in the form of hypodermic injections of atropia gradually increased daily, from the one hundred and twentieth of a grain to the thirtieth. Hydro-therapeutics in all forms, and faradization, have never, ac- cording to my experience, been of the slightest benefit, except as re- gards the use of the latter to the affected muscles. The ether-spray recommended by Jaccoud has been entirely inefficacious in my hands, and the same may be said of all plasters and embrocations. One auxiliary means of treatment I have lately employed with ad- vantage, and that is, keeping the patient as much as possible from using the groups of muscles which have lost their coordinating power, and requiring him, when he walks, to employ crutches to assist him, By systematically carrying out this plan the nervous force of the pa- tient is not wasted, and a diseased organ, such as is his spinal cord, is not overtasked. Lately I have employed, and thus far -with apparently good re- sults, the actual cautery to the spinal column. I have used it in a great number of cases. The effect ‘has been to lessen, and in many cases entirely to abolish, the electric pains and the feeling of con- striction around the body. In one fully-developed case wdiich I had before the medical class of the University of New York, the pains, which were of great intensity, ceased within a few hours after the first cauterization. Ten days subsequently I repeated the oper- ation, the pains in the legs having returned, and again the relief was complete. Nerve-stretching is a therapeutical measure of some importance. PROGRESSIVE LOCOMOTOR ATAXIA. 595 Langenbeck1 was the first to perform this operation for locomotor ataxia, and the results, not only in relieving the electric-like pains for which the operation was performed, but in curing the ataxia, were such as to astonish the operator. For a short time afterward the reports of cases cured by this means were numerous. Certainly noth- ing in the whole range of neuro-therapy is so contrary to our precon- ceived opinions as to suppose for one instant that stretching the sci- atic nerves will have any influence in restoring sclerosed nerve-tissue to a normal condition. In time nerve-stretching was relegated to its proper place as a therapeutic measure. Sometimes the pains in the affected limbs are so severe that the ordinary forms of treatment are not adequate for their relief, and the patient gradually becomes ex- hausted from suffering and from loss of sleep. In such a case stretch- ing the sciatic nerves invariably puts an end to the suffering, some- times for several weeks and again for several months, and when the pain does return it is frequently of a more subdued character. The operation is simple, and free from danger. An incision should be made in the mesial line of the integument on the posterior surface of the thigh just above the popliteal space. On separating the biceps from the semitendinosus, the sciatic nerve will be readily discovered. If the little finger is then passed under the nerve, the latter can be stretched to the desired extent. The treatment of ataxia by suspension has recently attracted con- siderable attention. It was first practiced by Dr. Motchoukowski, of Odessa, Russia, as far back as 1883, but attracted no attention from the medical profession until Charcot2 published his article attesting to its efficiency as a therapeutic agent. Since then numerous cases of ataxia have been reported to have been cured by this means ; but, though my experience with this method of treatment has been exten- sive, I cannot say that I have ever seen a single case of genuine tabes in which suspension alone has arrested the progress of the disease. That it is of material assistance in relieving some of the symptoms of tabes in the majority of cases is beyond the shadow of a doubt; but it has also been shown that in a small proportion of cases the symp- toms are aggravated with each successive suspension. The modifications most liable to occur from suspension are : an improvement in the coordinating powers, thereby enabling the patient to stand and to walk better; an amelioration in the sharp, shooting pains in the affected extremities; and an abatement of the gastric crises. The difficulty of retaining or of passing the urine often ceases, and the sexual power, which is frequently weakened, is sometimes restored. Improvement from suspension is not apparent from the first. Usually from ten to fifteen or more suspensions are necessary before decided benefit is manifested. 1 Berlmer klin. Wochenschrift, No. 48, 1879. 2 Le prog. rned., Jan. 19, 1889. 596 DISEASES OF THE SPINAL CORD. The best suspension apparatus, to my mind, is one by which the traction is borne by the occiput and chin, the axillary supports not being used at all. The apparatus should be hung on a weight scales, so that the exact amount of traction exerted can be known and noted. The accompanying illustration (Fig. 81), made from a photograph, Fig. 81. gives an excellent representation of the apparatus as I first used it. Since then, however, the interposition of a weight-scales between the head-gear and the pulley-ropes, and the abolition of the axillary sup- ports, make the instrument much more scientific and exact. At first the traction should not exceed seventy-five pounds, and should be gradually increased with each suspension, until the limit of one hun- dred and twenty or one hundred and thirty pounds is reached. In the INFLAMMATION OF THE COLUMNS OF GOLL. 597 beginning the suspensions should not last longer than half a minute, but should be extended gradually up to two minutes. Judging from my own experience, and considering the experience of others who have used suspension properly, I cannot help being satisfied with the results obtained. Beneficial effects are more likely to follow in cases of incipient tabes than in those of longer duration, in which destruction of the nerve-fibres has taken place to a consider- able extent. In three cases of functional impotence decided evidence of amelioration was shown after three suspensions. Suspension is contra-indicated where tabes coexists with valvular cardiac disease, phthisis, and extreme anaemia. IX. We have seen that the columns of Goll or posterior median fasciculi are generally the seat of a lesion simultaneously with, or more probably secondarily to, that which, existing in the posterior root-zones, causes the group of symptoms wTe call locomotor ataxia. There is, however, no doubt that they may be the seat of primary disease, and, though the data are not yet sufficient to enable us to give the clinical history of the affection as fully as is desirable, we are not altogether without information on the subject. Our definite knowledge rests upon one case reported in full by Pierret,1 and which I quote, greatly condensed as follows : Catherine Magnaigat, when thirty years of age (1855), experienced numbness, “ pins and needles,” sensations of heat, and deep-seated pains in the extremities, especially the upper. There were also pains in the loins, obstinate headache, and a sense of tightness around the chest. In 1860, vertigo and weakness of the lower extremities super- vened. She did not distinctly feel the ground with her feet, and she was obliged to walk with a cane. In 1863 she entered the Salpetri6re, and came under M. Charcot’s care. Her condition was then as follows : Tactile sensibility was diminished in the soles of the feet, the left especially. She could not walk without a crutch, which she used under her right arm. When she wished to go forward she experienced an impulse to spring or leap, and finally she advanced by a series of short steps, and felt as if impelled by a force she could not resist. When she closed her eyes while standing alone she maintained the erect position for a while, but would eventually have fallen unless supported. She was easily fatigued, and walking caused pains which compelled her soon to stop. Her feet seemed to stick to the ground when she made volun- INFLAMMATION—SCLEROSIS—OF THE COLUMNS OF GOLL. 1 “ Notes sur un cas de sclerose primitive du faisceau median des cordons postd- rieurs,” Archives de vhysiologie, 1873, p. 74. 598 DISEASES OF THE SPINAL CORD. tary efforts to lift them. Sometimes, when she attempted to advance, she felt herself irresistibly drawn toward the left side. When after having taken a few steps she wished to go back, she turned round suddenly, as if moved by a spring. In 1806 she for the first time ex- perienced constricting pains around the body low down, and electric- like in character. Soon afterward she felt similar pains in the anterior part of the thighs. Cutaneous sensibility was then diminished in the lower extremities. The idea of the exact position of’ the limbs was not in the least impaired, and there was no incoordination. Such was her condition when in 1871 she died of pneumonia. The post-moi’tem examination showed that the columns of Goll were throughout their whole extent in a state of sclerosis. It was most manifest in the dorsal region, where it to a slight extent invaded the posterior root-zones, to which circumstance, doubtless, the electric- like pains experienced by the patient were due. The case would appear to show that sclerosis of the columns of Goll gives rise to certain symptoms in the lower extremities, however much the superior may retain their normal condition. In some cases of locomotor ataxia there has been noticed an unusual feeling of heaviness in the lower extremities, or a marked tendency to go back- ward, or a great feeling of fatigue after slight exertion, a marked incertitude in standing erect, or even an irresistible feel- ing of propulsion. In such instances, there- fore, the columns of Goll were affected at the same time with the posterior root-zones. M. Pierret holds the opinion that these col- umns, to some extent, preside over motion. Figs. 82, 83, 84, and 85 represent scle- rosis limited to the columns of Goll, and are taken from M. Pierret’s memoir. Fig. Fig. 82. Fig. 83. Fig. 84. Fig. 85. 82 refers to the cervical region, Fig. 83 to the dorsal. Fig. 84 shows the appearance of a section made at the level of the second dorsal vertebra, and Fig. 85 one taken from the upper part of the lumbar enlargement. The sclerosed portion is represented at a in each figure. DISSEMINATED INFLAMMATION OF THE SPINAL CORD. 599 In the present state of our knowledge, all that we can do is to await further developments relative to the interesting points raised by the case which M. Pierret has so well studied. X. DISSEMINATED INFLAMMATION OF THE SPINAL COED—MULTIPLE SPINAL SCLEEOSIS SCLEKOSIS IN PLATES INSULAR SCLEROSIS. Thus far we have considered the inflammatory affections of the spinal cord as they appear in one or another of the anatomical divisions which make up that nerve-centre. But we have now to engage our- selves with a lesion which has no fixed habitation, which is met with in the gray and white matter indiscriminately, and which occurs in distinct foci, patches, plates, or islets, in various parts at the same time or con- secutively. This is what is known as multiple spinal sclerosis or sclerosis in disseminated plates—the sclerose en plaques disskminees of Charcot. Symptoms.—Multiple spinal sclerosis generally first manifests its presence by more or less weakness in one or the other lower extremity. Before long the corresponding limb becomes involved; and, eventually, if the disorder continues to form additional centres of morbid action, the upper extremities are successively attacked. At other times the first symptoms are connected with sensibility, and consist of the various sensations of numbness, tingling, “pins and needles,” formication, and the like. Or these phenomena may make their appearance simultaneously with the paresis. The gait of a person affected with multiple spinal sclerosis is uncertain and titubating—like that of an individual slightly intoxicated. Although there is defective coordination, the patient stands as well with the eyes shut as open, and has no additional difficulty in walking in the dark or with the eyes closed. The paralysis advances, but there are no marked disturbances of sensibility, and the numbness which may have been present to some extent in the early stage usually disappears. The patient is, therefore, sensitive to changes of temperature, to pain, and to pressure. Pains are very uncommon. Occasionally, there are slight painful sensations in the paralyzed parts, but they are temporary. The general health usually remains good, and the mind is unaf- fected. Later, in the course of the disease, rigidity or contraction makes its appearance in the paralyzed limbs, or both these conditions may co- exist in the same extremity, some of the joints being contracted, and others rigidly extended. The tendency is for these conditions to be- come permanent. Again, there are violent tonic convulsions in the paralyzed limbs which may be spontaneous, but which are readily ex- 600 DISEASES OF THE SPINAL CORD. cited by impressions made upon the skin of the affected extremities, or even sometimes by mental emotions. They may precede, or coexist with, or follow the permanent contractions. In some instances these phenomena are not met with. They were absent in the case of Dr. Pennock, reported by Drs. Morris and Mitchell; in a case under my own charge, and in which I made an examination of the cord soon after death ; and in a case reported by Friedreich,1 in which multiple spinal sclerosis existed in conjunction with the lesions of locomotor ataxia. When present, as they generally are, these permanant contractions of the muscles exhibit different phases in the upper and lower extremi- ties. In the former the flexors predominate over the extensors, while in the latter the extensors prevail. The spasmodic tonic convulsive move- ments of the limbs are especially met with in the lower extremities, the upper being rarely their seat. After a time, which may vary from three or four to fifteen or twenty or even more years, the limbs become almost entirely paralyzed, and the contraction and rigidity are still more strongly marked. Whatever voluntary movements the patient is capable of executing now cause pains in the parts. The sensibility usually, however, even at this period remains but little affected. Reflex excitability generally exists though perhaps slightly impaired ; sometimes it is altogether lost, and again it may be greatly exaggerated. The bladder and the sphincter ani retain their power to the last. Bed-sores form on the parts subjected to pressure as the patient lies in bed, and death eventually ensues, either from exhaustion or from some intercurrent affection. Such is a description of multiple spinal sclerosis as it is ordinarily en- countered—and it must be confessed that the clinical features are not very striking or peculiar. But even this type, imperfect as it is, is sub- ject to great diversities. Sometimes there are violent pains of an elec- tric-like character simulating those which are so prominent a feature of locomotor ataxia and like them resulting from the implication of the posterior root-zones in the lesion. Sometimes the superior extremities are attacked first. Again, anassthesia constitutes a prominent feature, and the phenomena ordinarily present may be more or less modified in extent and intensity in different cases. In their very excellent monograph on the subject, MM. Bourneville and Guerard,11 in detailing the symptomatology of the spinal form of disseminated sclerosis, say: “ After a variable time the superior and inferior extremities become the seat of rhythmical agitations, which are only present, however, 1 “Ueber degenerative Atrophie der spinalen Hinterstrange,” Archiv fiir pathologischi Anatomic und Physiologic, 1863, p. 433. 8 “ T)e la scl6rose en plaques diss6mindes,” Paris, 1869, p. 61. DISSEMINATED INFLAMMATION OF THE SPINAL CORD. 601 when spontaneous or voluntary movements are made. In the state of repose the members are not affected with any tremor.” In this connection I desire to repeat what I wrote five years ago,1 that “ tremor is never observed in spinal sclerosis of any form, diffused, multiple, or cortical, unless the pons Varolii or superior ganglia of the brain are implicated. In the only case of this latter form published— that of Yulpian 2—the sclerosis extended throughout the whole length of the cord, and likewise involved the pons Varolii, cerebellar peduncles, and other intra-cranial organs, besides being accompanied with well- marked spinal meningitis. The tremor observed at a late period of the disease cannot, therefore, be ascribed to the lesion of the cord below the medulla oblongata.” Of the cases cited by Bourneville and in which post-mortem examinations were made, one from Yulpian and one from Morris and Mitchell, in which the lesions were restricted to the cord, there was no tremor at any time in the course of the disease; and in a case of my own already cited, and which will be still more specifically referred to here- after, in which the cord was the seat of several islets of sclerosed tissue, tremor had never been a feature of the symptomatology. As we shall see hereafter, when we come to the consideration of the cerebro-spinal form of the disease—multiple cerebro-spinal sclerosis— tremor constitutes one of the most prominent phenomena of the affec- tion. We have already seen that it is a marked symptom of the purely cerebral type of the affection. I am quite sure, however, that in the disease we are now considering, restricted as its lesions are to the spinal cord, rhythmical tremor is not encountered. Causes.—The causes of multiple spinal sclerosis are not well under- stood. In a case fully reported by Yulpian,3 the affection appeared to have been induced by a sprain of the left ankle. The extremity re- mained weak, and three years afterward the patient had a fall, and then the right lower extremity became weak and subsequently the right upper extremity. The left upper extremity was not affected for several years. In the case of Dr. Pennock, reported by Drs. Morris and Mitchell, the disease began while the patient was busily engaged in professional studies. In the case in which I verified the existence of the disease by post- mortem examination, it was apparently caused by exposure to cold and dampness. It is probable that blows on the spine, concussions—such as are pro- duced by railway accidents—and the gouty and syphilitic diatheses— 1 First and subsequent editions of this work, p. 473. * Op. cit., p. 64, et seq. 3 “Note sur la sclerose en plaques de la moelle epiniere,” Union medicate, 1866, Juin 7, 9, 14, et 19, obs. i. DISEASES OF THE SPINAL COED. may induce multiple spinal sclerosis. There is in reality no reason, to my mind, why all the influences which are capable of causing the dif- fused forms of sclerosis which have been considered, may not also cause the disseminated variety. But it is difficult to arrive at any definite information relative to this matter, so long as the clinical features of the disease are so little characteristic. Diagnosis.—There is very little in multiple spinal sclerosis sufficient- ly pathognomonic to aid us in our diagnosis of the affection. The symptoms in some cases are identical with those of spastic spinal paral- ysis ; in others they resemble those of locomotor ataxia, as in the two cases reported by Friedreich, to one of which allusion has already been made. In the present state of our knowledge, therefore, I am afraid we must wait for the scalpel and the microscope to determine with any degree of accuracy the diagnosis of multiple spinal sclerosis. Prognosis.—The disease is not one which is directly calculated to cause death. All the patients known to have died while subject to it, succumbed to some intercurrent affection, such as bronchitis, dysentery, typhoid fever, and pneumonia. It undoubtedly tends to weaken the vital powers, and hence is indirectly the cause of a fatal result. So far as any prospect of arresting, by therapeutic means, the tendency to the formation of other islets of inflammation and sclerosis, or of restoring the integrity of the cord is concerned, there does not appear to be much hope. For, though its progress is in many cases slow, and in others seems, at times, to be self-limited, it pursues its course unamenable, so far as we know, to medical treatment. In the diffused forms of spinal sclerosis there is but one centre of morbid action ; in the disseminated there are several, Avhich, if not coexistent, tend, through an inherent proclivity, to be produced indefinitely. To this circumstance is due the fact that the prognosis of the disease under consideration is more un- favorable than that of sclerosis of the posterior root-zones or even sym- metrical lateral sclerosis. Morbid Anatomy and Pathology.—Multiple spinal sclerosis consists in the dissemination through the cord of masses of sclerosed tissue, which have resulted from the proliferation of the neuroglia and the consequent atrophy and disappearance of the proper nerve-elements. They are of a gray color, of increased consistence, of irregular size and form, and may exist in any part of either the gray or white tissue of the cord ; often, however, manifesting a tendency to involve the two lateral halves of the cord symmetrically. In the case reported by Vulpian, the volume of the cord was evi- dently diminished, and on different points of its surface exhibited an ashy-gray coloration. The antero-posterior diameter of the cord was markedly lessened at those places where the islets of sclerosed tissue oxisted. In this case there had been progressive paresis, rigidity, and con DISSEMINATED INFLAMMATION OF TIIE SPINAL CORD. 603 traction, with extension of all four limbs, without tremor of any kind, The alterations were found in the anterior, lateral, and posterior col- umns, and in the anterior and posterior horns of gray matter. In the case of Dr. Pennock, reported by Drs. Morris and S. Weir Mitchell,1 the sclerosed tissue was confined mainly to the lateral col- umns. The posterior were involved to a very small extent. In this case there were partial anaesthesia, gradually-advancing paralysis im- plicating all four extremities, and paralysis of the bladder. The intel- lectual faculties were never affected in the least. The course of the disease was progressively onward, and, though there was toward the last a total loss of voluntary power below the neck, reflex action re- mained unaffected. There were no tremors with or without voluntary movements. In regard to this case, Dr. Mitchell, who made the micro- scopical examination, remarks that there were : “ 1. Integrity of mental and moral manifestations. “ 2. Absolute loss of voluntary motive power below the head, or rather below the neck. “ 3. Sensation nearly perfect. “ 4. Respiration good ; reflex motion preserved and exhibited in the form of spasm or irritation of certain parts of the skin.” All of which are what we should expect to find in sclerosis almost entirely confined to the lateral pyramidal tract. In the case which I have mentioned as coming under my own obser- vation, the patient, J. H., consulted me in the winter of 1869-’70. He was then unable to walk without a cane and the assistance of an attend- ant. He had previously been treated at a water-cure establishment, and more recently by the Swedish movement-cure, and of course with- out benefit. The symptoms were mainly connected with motility. Both lower extremities were paralyzed ; the bladder was inactive, but not the sphincter, and there wras obstinate constipation. There were occasional fibrillary contractions of the paralyzed muscles, and at times pain in the back and limbs—never, however, of any great degree of severity. There were no tremors, either with or without voluntary motions. The patient obtained very little benefit from the treatment to which I subjected him, and I advised him to return to his home in Ohio. A few months afterward, he died. The dorsal, lumbar, and sacral regions of the cord were sent to me for examination by his physicians, Drs. Ramsey and Bishop, of Delhi, Ohio. In a letter, the latter informed me that the vessels of the pia mater were injected. The cord arrived in good condition, having been carefully preserved in strong alcohol. Upon inspection, the antero-lateral columns in the 1 American Journal of the Medical Sciences, July, 1868. DISEASES OF THE SFINAL CORD. middle and lower dorsal regions to the extent of three and a half inches were seen to be of a grayish tint, which became deeper in shade from above downward. Below this, at the junction of the dorsal with the lumbar portion, was another patch two and a half inches in length, and also involving the whole superficies of the antero-lateral columns ; and, separated from this by a portion of apparently healthy tissue, was another discolored, irregular patch, an inch and a half in length, along the left antero-lateral column ; and, below this, a similar tract, two inches and an eighth long, involving the right antero-lateral column. The difference in consistence between these patches and the other parts of the cord was very decided, and the white stride were well marked. The sacral portion of the cord presented no abnormal appearance to the naked eye. Sections of the cord were then made through the sclerosed portions; and it was seen that the gray matter was only involved where the horns approached the surface ; and that, wherever a lesion existed, the normal contour of the sections was altered so as to make them sub- ovoidal, and thus to lessen the circumference. The greatest depth of any part of a sclerosed region was two-twelfths of an inch, and this was in the superior patch. The average thickness was about the one- twelfth of an inch. The whole cord in my possession was then immersed in a solution of chromic acid in water, and left there for a month to harden. Immedi- ately previous to examining with the microscope, the sections were col- ored by an ammoniacal solution of carmine. Under a twelfth-inch ob- jective, it was seen that, throughout the whole extent of the sclerosed portion of any section, the nerve-tubes had entirely disappeared ; and, wherever the gray substance was affected, the nerve-cells were dimin- ished in number. In the place of these elements wrere connective tis- sue, a large quantity of molecules, and connective-tissue cells in great abundance. In several sections taken from the dorsal, lumbar, and sacral re- gions, and which wrere apparently normal wdien viewed with the naked eye, the neuroglia was found to be in excess, and the nerve-tubes in a state of disintegration. The gray matter, except in those sections made through the part where the sclerosed portion extended from the white matter to it, was uniformly healthy, and in no part were the posterior columns in- volved. In this case there no tremor, although it was clearly one of multiple sclerosis, probably entirely confined to the spinal cord. At no time had there been head-symptoms of any kind. Histologically, therefore, we see that the sclerosed tissue consists mainly of an exces- sive amount of connective tissue—the neuroglia of Virchow. The cells are increased in size, and the nuclei are larger and much more numerous SECONDARY INFLAMMATION AND DEGENERATION. than in the normal condition. The capillaries are thickened, from the deposition on their walls of several layers of rounded cells. The effect of this morbid process is to compress the nervous fila- ments and to cause their atrophy. The fluid portion undergoes fatty degeneration, and the axis cylinders become disintegrated. Still, how- ever, they present somewhat of their characteristic color and consist- ency, and appear as white stri® traversing the morbid tissue. The membranes often exhibit evidences of inflammation, and are thickened, opaque in spots, or red in some cases, while in others they are adherent to each other and to the cord. Treatment.—Something can be done to mitigate the violence of the symptoms. Hypodermic injections of atropia have often a happy effect in diminishing the force and frequency of the tonic contractions. The nitrate of silver has been used by M. Piorry with temporary good re- sults. The primary or galvanic current has, in my hands, been of like effi- cacy in lessening the contractions or spasmodic rigidity, but with this agent, as well as with the others mentioned, there can be no great cer- tainty that we are dealing with a case of multiple spinal sclerosis. We are, therefore, forced to treat symptoms instead of lesions. Still, for the cure of the disease we may attempt the measures recommended for symmetrical lateral sclerosis, but with even less prospect of success. I should be disposed to use, with thoroughness and persistency, the actual cautery in the manner recommended when discussing the treatment of locomotor ataxia. XI. SECONDARY INFLAMMATION AND DEGENERATION OF THE SPINAL CORD. It is a well-recognized fact that disuse of an organ promotes its atrophy and degeneration. A muscle, which from any cause is ren- dered incapable of contracting, becomes smaller, and its fibrill® under- go conversion into fat. The same law applies to other organs, and among them the spinal cord. Whatever interrupts the passage of the normal excitations through its columns causes degeneration. Thus, if there be a cerebral haemorrhage, preventing the action of the brain on the muscles, the lateral pyramidal tract on the opposite side and the anterior pyramidal tract on the same side of the cord, not being stim- ulated by their accustomed excitation, undergo the change mentioned. If the cord itself be the seat of a lesion, or the posterior nerve-roots, and perhaps even the nerves or muscles, the posterior columns above, no longer being required to convey impressions to the brain, suffer atrophy and degeneration. To this alteration, which is not itself a primary disease, but which is always, in its very nature, consecutive 606 DISEASES OF THE SPINAL CORD. to lesions in superior or inferior parts of the nervous system, the term secondary degeneration has been applied. The fact that the spinal cord is affected by lesions of the brain was observed by Cruveilhier,1 who, however, failed to notice any consecutive change in the cord below the decussation of the pyramids. L. Tiirck2 was the first specially to inquire into this important subject, and, in a series of memoirs extending through the years from 1851 to 1855, he showed that the cord underwent secondary degener- tion, both from lesions of the brain and of its own substance. Since these memoirs, other pathologists, among whom MM. Charcot, Turner, Rokitansky, Vulpian, Cornil, and Lancereaux, may be mentioned, re- ported cases, but no one has investigated the subject with so much thoroughness as M. Bouchard.3 Symptoms.—The most important symptoms referable to second- ary degeneration of the cord from cerebral lesions are muscular con- tractions, exaggerated tendon reflexes, and the ankle clonus. These are not the contractions which sometimes exist from the very in- ception of a haemorrhage, for instance, but those which come on at a later period of the disease, and which, like the first, have generally been thought the consequence of irritation existing about the cicatrix. Bou- chard, however, shows very clearly that they are the result of changes taking place in the spinal cord, and the clinical history of which has not hitherto been carefully studied. They are very frequent. Of thirty-two cases of old hemiplegia analyzed by Bouchard, they were present in all but one. From my own experience I think it is safe to say that it is very rare to meet with a case of hemiplegia of over a year’s duration in which they do not exist. In examining a patient suffering from an old hemiplegia, it is com- mon to find the forearm of the paralyzed side flexed on the arm. Fre- quently, also, the fingers are bent into the palm of the hand, the hand flexed on the forearm, and the whole member carried across the front of the body, and held firmly against it by the contraction of the pecto- ralis major muscle. In such a case we find the muscles atrophied, hard, and stretched to an extreme degree of tension. Rectification of the position is, to a great extent, impossible by the voluntary efforts of the patient. He may be able to accomplish a little motion, and to do still more by using the sound hand to extend the affected arm ; but, if the hemiplegia has been of considerable duration, the range of his motility, with or without assistance, is very small, and is sometimes nothing. I 1 “ Anatomie Pathologique,” liv. xxxii., p. 15. 2 “ Ueber secondare Erkrankung einzelner Riickenmarksstrange und ihrer Forsetzun- gen zum Gehirne,” “ Sitzungsberichte der Kaiserlichen Wiener Academie,” 1851. * “Des degenerations secondaires de la moelle 6pinRre,” Archives generates df mid., 1866. SECONDARY INFLAMMATION AND DEGENERATION. 607 have found that the electric contractility of such muscles is diminished in some of their fibres, unaffected in others, and exalted in others, so that, when the electrical stimulus is applied, a hard, irregular, and knotty contraction is obtained. Polar degenerative reactions are not observed. The leg is usually stiff, and flexion of the knee-joint is performed with difficulty. The foot is generally flexed till it is brought into a position of talipes equinus. This gives a marked peculiarity to the gait. The flexion of the foot prevents the toes from being drawn upward when the leg is thrown forward, as in the act of walking. This, in addition to the rigidity of the knee-joint, makes it necessary for the leg to be thrown outward from the body while the foot de- scribes the arc of a circle. This condition of contracture only affects those muscles which have previously been paralyzed. The knee-jerk, and the tendon reflexes generally, are exaggerated, Fig. 86. Diagrammatic representation of the connections of the motor nerve-cells of the anterior horn. (Modified from Bramwell.) IP t"> Lateral pyramidal tract, a p t, Anterior pyramidal tract, or column of Tiirck. p m c, Posterior median column, or column of Goll. pec, Posterior external column, or column of Burdacb. dtc, Direct cerebellar tract, a-l at, Antero-lateral ascend- ing tract, or column of Gowers. M, a muscle. R, a deep reflex fibre passing through the posterior external column and joining the motor nerve-cell at 3. S, superficial reflex fibre passing through the posterior horn of gray matter and joining the motor cell at 2. 1, Fibre connecting the lateral pyramidal tract with a motor cell. 4, Motor nerve-fibre from motor cell to muscle. 5, Motor nerve-fibre from the anterior pyram- idal tract to motor nerve-cell. and the ankle clonus can readily be obtained. In fact, the symptoms are nearly identical with those described under the heading of Pri- 608 DISEASES OF THE SPINAL CORD. mary Sclerosis of the Lateral Pyramidal Tracts, on page 549, with the exception that in that disease, where the lesion begins primarily in the spinal cord, both legs are affected, while in the disease under consideration the degeneration of the motor tract is mainly limited to the entire lateral pyramidal tract of one side, so that the symptoms are manifested in the arm and leg of that side only. As a cerebral haemorrhage usually takes place in the motor tract above the decussa- tion in the pons, the descending degeneration will not be entirely •limited to the lateral pyramidal tract. A portion of the cerebral motor fibres do not decussate, but continue downward in the same side of the cord in what is known as the columns of Tiirck, or the anterior pyramidal tract (Fig. 70, page 554). This column probably connects with the cells in the anterior horn of gray matter of the same side. Usually the anterior pyramidal tract contains but a small proportion of the cerebral motor fibres, hence the three cardinal symptoms of inflammation of the spinal motor tract—that is, stiffness, exaggerated tendon reflexes, and the ankle clonus—will be very slightly defined on what is usually termed the sound side. Most frequently stiffness is not appreciated on that side at all, the knee-jerk is found to be slightly exaggerated, and there may be a tendency to the ankle clonus, which, however, is sel- dom well marked. Atrophy of the paralyzed muscles may be one of the secondary results of brain-disease; as we have seen, it is of a primary spinal affection. When the cord itself is the seat of primary disease, the lateral col- umns below undergo degeneration, and the muscles become perma- nently contracted. Many cases of distortion which ensue on sclerosis, tumors, and other lesions, are the result of this secondary degenera- tion. M. Charcot is of the opinion that the epileptiform attacks sometimes met with in hemiplegics may result from these secondary descending degenerations affecting the peduncles, the pons, and the medulla oblongata. No symptoms referable to ascending secondary degenerations— those of the posterior columns—have been recognized except in a few instances, and then the symptoms diff^*- 4»*it little from those previ- ously described under the heading of Locomotor Ataxia. Causes.—Secondary descending degeneration of the spinal cord may result from primary lesions of the cerebral motor cortex, of the motor fibres of the internal capsule, of the pons Varolii, of the me- dulla oblongata, and of the spinal cord itself. Secondary ascending degeneration of the posterior columns is caused by disease of the posterior roots of the spinal nerves, and from lesions originating in some other part of the cord gradually extending in area until the pos- terior columns become involved. The immediate causes are the loss SECONDARY INFLAMMATION AND DEGENERATION. 609 of the due supply of arterial blood, and the arrest of nutritive action from deficient nervous influence. The Diagnosis calls for no special consideration. Prognosis.—This is very unfavorable. Cerebral motor nerve-fibres whose continuity is inter.upted by any lesion which separates them from the cortical nerve-cells which supply them with their nutrition, invariably degenerate. This degeneration consists of an inflamma- tory destruction of the nerve-fibres, with a consequent proliferation of new connective tissue, and is termed sclerosis. Unless it is pos- sible to restore the destroyed nerve-fibres, and to resolve the hard- ened and increased quantity of connective tissue to its normal con- dition—which it is very evident we cannot do—it can be seen at a glance how utterly hopeless is the prospect of even an amelioration of the symptoms. Morbid Anatomy and Pathology.—Secondary degeneration is gen- erally found in the white substance, the gray being seldom affected. This might certainly have been expected, owing to the fact that it is the conducting power of the cord only that is lessened, and, as this power resides almost entirely in the fasciculi of the white substance in the lateral pyramidal tract and posterior columns, it is here that we ordinarily find the lesions. When a fibre belonging to the wThite sub- stance is injured, either in the cord or in its intra-cranial prolonga- tions, the secondary degeneration ensues either above or below the seat of the primary lesion, but it extends through the entire length of this portion to its central or peripheral extremity, according as it in- volves sensory or motor filaments. To these two varieties the terms ascending and descending degeneration are applied. The affected fibres alone are changed, and the alteration extends throughout their whole length. But, as the white fibres are constantly receiving other fibres which have had no initial injury, the secondary degeneration becomes relatively less the greater the distance is from the seat of the primary lesion. The morbid condition depends upon three processes: atheroma of the capillaries and the formation of granular corpuscles in the degen- erated tissue ; the degeneration and atrophy of a greater or less num- ber of nervous filaments ; the proliferation of connective tissue which takes the place of the nerve-tubes. These changes are similar to those which occur in the several forms of sclerosis, to which attention has already been directed, and are essentially inflammatory in character. The explanation of the rigidity of the muscles, the presence of contractures, of exaggerated tendon-reflexes, and of the ankle clo- nus, is identical with that which has been given for this same group of symptoms described under the heading of Morbid Anatomy and Pathology, in the chapter on Primary Sclerosis of the Lateral Pyram- idal Tract. 610 DISEASES OF TIIE SPINAL CORD. When there is atrophy of the paralyzed and contracted muscles as a result of secondary degeneration of the cord, we may be vei'y sure that the anterior horns of gray matter are involved. Charcot1 cites a case which he reported to the Societe de Biologie, in which a woman aged seventy was suddenly struck with left hemiplegia, occasioned, as the post-mortem examination showed, by a cerebral haemorrhage seat- ed in the centrum ovale of the right hemisphere. Contraction of the paralyzed muscles supervened very soon, and, two months after the attack, the muscles of the inferior as wrell as of the superior extrem- ity began to atrophy at the same time that their electric contractil- ity was notably diminished. The muscular atrophy advanced with great rapidity, and simultaneously the skin on the paralyzed parts, when submitted to pressure, was the seat of numex’ous bullae and even erosions. The examination of the spinal cord revealed the existence of a descending sclerosis, occupying the left side, and presenting its ordi- nary features. But in addition, at several points of the cervical and lumbar enlargements, the anterior horn of gray matter of the same side exhibited evidences of an inflammatory process, and at these points the large nerve-cells had undergone a marked degree of atrophy. Similar cases have been reported by Hallopeau. Treatment.—The best results in my experience have been obtained from the use of the primary galvanic current to the cord, the same or the induced current to the muscles, forcible extension and flexion of the contracted limbs, and the internal administration of nitrate of sil- ver and cod-liver oil. It will generally be found that the opposing muscles are more or less paralyzed, and that great good may be effect- ed by stimulating them with the primary or induced currents. The division of tendons is never necessary, unless for the rectification of distortions of the toes or fingers. Sometimes the toes are strongly flexed against the sole of the foot, rendering it almost impossible to walk, from the pain produced by the dorsal surface being brought in contact with the ground, and hence obliged to bear the weight of the body. In such cases the tendons may with propriety be divided, un- less the toes can be kept extended by some convenient prothetic appa- ratus, or, as in the case under my care, to wThich reference has been made, the toe may, if necessary, be amputated.— exercise of the affected muscles will do much to restore them. 1 “ Le9ons sur les maladies du systemc nerveux,” 1874, p. 245. NON-INFLAMMATORY SOFTENING OF THE SPINAL CORD. 611 CHAPTER YI. A7 ON-INF LAMM A TOR Y SOFTENING OF THE SPINAL CORD. Softeking of the spinal cord is, as we have seen, the common termination of acute myelitis, in which connection it has been suf- ficiently considered ; but it may originate primarily, and in that event possesses a clinical history very distinct from that of acute inflammatory softening. Symptoms.—The first symptom usually noticed in softening of the spinal cord is numbness in those parts of the body below the seat of the lesion. Soon after the occurrence of this symptom there is weakness of the same parts, and then the deficiency of sensation and the feebleness of motor power advance together, both gradually becoming more and more strongly marked. There are no muscular twitchings, no contrac- tions of the limbs, no pains either at the seat of the disease or in the paralyzed limbs. The bladder very soon becomes involved, and the patient finds that, when he attempts to urinate, the stream is not so strong as it once was, and that he is obliged at times to use the expulsive force of the abdomi- nal muscles in order to complete the evacuation of the bladder. Gradu- ally the contractile power of this viscus becomes less, and finally is altogether lost. The sphincter generally participates. The desire to urinate becomes more frequent, and when the inclination is felt the patient must at once yield to it. Eventually the bladder likewise becomes entirely paralyzed, and then there is neither the ability to expel the urine nor to retain it, and consequently it dribbles away constantly. Sometimes the first evidence of softening of the cord is perceived either in the bladder or its sphincter, and it may be restricted to these parts for a considerable period. I have a patient at the present time under treatment for what I have no doubt is softening of the cord, and in whom the bladder-troubles were the only notable symptoms for over two years. The intestines are similarly affected, and the bowels are either ob- stinately constipated or the sphincter ani is relaxed, leading to fecal evacuations as soon as the contents reach the rectum. Reflex excitability is weakened from the first, and gradually disappears, unless, as is rarely the case, the gray matter be un- affected. The progressive advance of the disease reduces the patient to a condition of utter helplessness. He is unable to walk, sensation is abolished in the paralyzed limbs, his urine and faeces are passed in- 612 DISEASES OF THE SPINAL CORD. voluntarily, bed-sores occur, the venereal appetite is extinct, or, if it should remain, erections are impossible, and the parts of the body below the seat of the disease are to all intents and purposes cut off from communication with the parts above. This condition may last for years without a fatal termination ensuing, but intercurrent affec- tions, especially resulting from the bladder troubles, may eventually cause death. Such is the course of spinal softening when the lesion is low down and involves both antero-lateral and posterior columns. When it is higher up, the symptoms are also referable to the thoracic extremities, and to the muscles concerned in deglutition and respiration. There are likewise visceral disturbances. When the lesion mainly affects or is confined to the lateral pyram- idal tract, the symptoms manifested are in intimate relation with the known physiological functions of the region in question. Thus the power of motion in the limbs below the softened portion of the cord gradually becomes less, the gait is from the first staggering, and, though even at a late stage the patient may be able to move his limbs while lying down or sitting, he cannot support the weight of his body upon them. When he tries to stand without extraneous aid, it is seen that he is especially weak in the knees and ankles. There is no more diffi- culty in standing or walking with the eyes shut than when they are open. This paralysis of motion, in which the bladder generally participates, may be of the most profound degree, and yet sensibility be perfect. A gentleman was under my care in whom I diagnosticated softening of the cord in that part extending on the right side from the second dorsal vertebra downward probably as far as the fourth sacral, while on the left side it began at about the fourth lumbar and extended downward probably as low as the fourth sacral. I gave the lesion these topo- graphical limits for the reason that on the right side the muscles sup- plied by the crural and sciatic nerves had lost their electro-muscular contractility, while it certainly did not extend above the origin of the ilio-hypogastric nerve, as the lower part of the rectus abdominis, which receives its motor power through this nerve, retained its contractile power. On the left side the muscles supplied by the crural nerve were possessed of their normal motor power, wnile those supplied by the sciatic had lost their contractility. It was, therefore, very certain that on this side the lesion did not extend above the fourth lumbar, the lowest spinal nerve contributing to the formation of the crural. I was able also to restrict the morbid process entirely to the antero- lateral columns, for in no part of the skin below the upper supposed limit of the lesion was there any loss of sensibility. The least impres- sion made upon the skin was felt. Tickling the sole of the foot excited laughter, but no reflex movements. I was therefore able to determine NON-INFLAMMATORY SOFTENING OF THE SPINAL CORD. 613 that the gray matter was involved. The bladder was paralyzed, and its sphincter likewise. The sphincter ani was also deprived of its con- tractile power to a great extent. The patient died at Cape May, and I had no opportunity of making a post-mortem examination. Probably, however, the lesion was essen- tially that which I have described. In all cases of spinal softening in- volving the antero-lateral columns, the electro-muscular contractility is soon lost, so that even the strongest induced or primary currents fail to cause contractions. As regards the implication of the posterior columns, there is an equal facility for determining the fact from a consideration of the symp- toms. The functions of these columns are intimately connected with sensation, and when such a morbid process as softening is set up in them the symptoms are those which indicate impairment of the cutane- ous and muscular sensibility. Thus, in a gentleman formerly under my charge, there had been going on for several months a morbid action in the spinal cord unattended by any prominent symptoms except anaes- thesia. There had never been pain or any derangement of motility, but simply a gradually-increasing loss of sensibility in both lower ex- tremities and in all the other parts of the body below the upper limit of the seat of the lesion. He was unable to walk in the dark or with his eyes shut, or to stand alone with his eyes closed and his feet close together, for he obtained no idea of his position unless he could have the aid of his eyes or hands. He had full power over the bladder and voluntary control over its sphincter and that of the rectum, but he never experienced the desire to urinate, did not feel the flow of urine through the urethra, nor the passage of the faeces through the anus, and evacuated his bladder and bowels at stated periods merely from the knowledge acquired by ex- perience that it was time to do so. Examination with the aesthesiometer showed that the upper limit of the lesion on both sides was in that part of the cord from which the second lumbar nerves are derived, for the loss of sensibility was appar- ent in all those parts supplied by the crural and sciatic nerves, both as regarded the skin and the muscles. Very weak faradaic currents caused muscular contractions, but the strongest which it was possible to ob- tain from a powerful machine produced no pain. There was no muscular incoordination, neither had there ever been electric-like pains in any part of the body. The patient died in 1873. For a year previously he had exhibited indications of insanity, and finally committed suicide by hanging himself to his bedpost. A post- mortem examination was made of his brain, but the physician who then had charge of the case thought it too great a trouble to examine the cord, and thus an opportunity for studying what must necessarily have been important lesions was lost. 614 DISEASES OF THE SPINAL CORD. In this case there was, I think, ample reason to diagnosticate a lesion of the posterior columns without any implication of the antero- lateral. The reasons for believing this lesion to have been softening will be indicated under the head of diagnosis. Causes.—The causes of spinal softening are not very clearly under- stood. Doubtless it arises as a consequence of acute myelitis, but it is often an independent and apparently a primary affection, being unpre- ceded by any obvious symptoms indicative of spinal derangement. Such influences as give rise to cerebral softening will, in all probability, cause spinal softening, and among them must be placed obliteration of blood-vessels from embolism and thrombosis. The actual occurrence of occlusion of spinal vessels from either of these causes has not, however, so far as I am aware, been demonstrated. The further etiology of spi- nal softening is not as yet a matter of any certainty, though I think several cases that have been under my observation could reasonably have their cause laid to excessive sexual indulgence. Diagnosis.—The diagnostic marks of most value in cases of sup- posed spinal softening are the absence of sensory and motor excite- ment. Thus there are no pains referable to the back or other parts of the body, no hypermsthesia, no twitchings, no spasms, no contractions, no exalted reflex actions. And this is the case in that form of the dis- ease involving the whole thickness of the cord, or in either of those limited to the anterior or posterior columns. There is no other affec- tion of the spinal cord which is not characterized, at some time or other of its progress, by irritation either of the sensory or motor nerves, or of both, excepting some cases of spinal anaamia giving rise to the cate- gories of symptoms previously considered. The clinical history of such cases, and the comparatively light character of the phenomena, will serve to distinguish them from those in which the lesion is softening. Prognosis.—The prognosis is always unfavorable as regards recov- ery and complete restoration, but spinal softening is not necessarily a fatal disease. At least, I have seen cases which had existed for many years, and which apparently had no elements of a fatal termination about them. But they were instances in which the seat of the disease was in the lower dorsal, or lumbar or sacral region of the cord. When it is higher up, the prospect of death ensuing is more probable. The restoration of the cord to its normal structure is impossible, and the patient lies paralyzed either in sensation or motion, or both, according to the situation and extent of the lesion, in a condition similar to that of a person who has received a wound inflicting irreparable injury on the cord. Such persons, as is well known, frequently live for many years afterward—then die of some entirely different disease. There is nothing about spinal softening calculated to produce exhaustion, un- less it be the tendency which exists to cystitis from paralysis of the bladder, and the consequent inflammation liable to be set up from the NON-INFLAMHATORY SOFTENING OF THE SPINAL CORD. 615 action of the retained urine. Care, however, will very greatly diminish the danger from this source. I have had a number of patients under my charge who had not, for many years, had a passage of urine from the bladder which was not effected with the catheter, and they had, in all that time, suffered no marked inconvenience. Morbid Anatomy and Pathology.—The appearance of a softened portion of the spinal cord to the naked eye has nothing very peculiar about it. When examined as to its consistence, it is seen to be some- times as soft as cream, at others scarcely altered in the resistance which it offers to the touch. In the first instance, when the lesion involves the gray and white matter together, section does not show the peculiar double crescentic arrangement of the former tissue, but it appears to be blended homogeneously with the white substance which surrounds it. Microscopically it is seen that the nervous tubules constituting the essential anatomical elements of the white substance are broken up, and no vestige of them remains in extreme cases—oil-globules and bodies called granule-masses, the constituent of which is fat, having taken their place. In the gray substance the nervous cells are de- stroyed, and oil and fat have made their appearance in large amount. Even the neuroglia or connective tissue of the cord exhibits a similar disintegration and regressive metamorphosis. These changes impair the functions of the cord, both as a nervous centre and as a structure serving for the transmission of sensory impressions to the brain, and of nervous force from it. When the disintegration is complete, the effect is the same as if the cord had been entirely divided by a cutting in- strument. Treatment.—There is nothing to be done which can by any possi- bility restore the integrity of the spinal cord after the process of soft- ening has fairly entered upon its course. In the very early stages, if patients apply for treatment at these times, something may perhaps be sccomplished by the use of phosphorus and strychnia, but the symp- toms come on so insidiously and gradually that the subject of them rarely has his apprehensions excited till it is too late to do any thing toward arresting the disease. And even when we do see cases which in appearance exhibit the symptoms met with in spinal softening in its initial stage, and which recover under treatment, there must always be a doubt in regard to the accuracy of the diagnosis—for many cases of temporary anaesthesia and impairment of motility are due to anaemia of the cord, the result of the causes set forth in a previous chapter. The patient, however, may be made comfortable to such an extent as to materially prolong his life. Care should to this end be taken that he does not sustain a fall or suffer an injury whereby the diffluent portion of the cord would be disturbed in its anatomical relations, and the danger of an attack of acute meningitis or of myelitis incurred. Bed-sores should be prevented, or, if they occur, treated according to 616 DISEASES OE THE SPINAL COED. the methods previously mentioned, and full instructions should be given in regard to emptying the bladder with the catheter at regular times, and of going to stool at the same hour every day. Locomotion may be provided for by some one of the chairs devised for the use of paraplegics. As there is little, in softening of the cord situated below the origin of the phrenic nerves, which is directly calculated to de- stroy life, there is no reason why, with the adoption of proper meas- ures, the patient should not enjoy a measurable degree of comfort for many years. Probably the event most apt to occur is acute or chronic cystitis from paralysis of the bladder, but attention to the injunction above given will do much toward lessening the liability to this affec- tion. CHAPTER YU. TUMORS OF THE SPINAL CORD. Following the example of Jaccoud, I shall consider under one head, tumors of the cord, of the membranes, and those which, growing from the interior surfaces of the vertebrae, may compress the cord, and thus interfere with its functions by deranging its structure. In the present state of our knowledge, we have not many exact data by which to dis- criminate between these several growths. Symptoms.—The phenomena which result from intra-spinal tumors, like those due to congestion, are of two categories, resulting as they do either from irritation or compression. Under the first head are em- braced pain in the back, in the limbs, and in the viscera, if the poste- rior columns are mainly the seat of the lesion or subjected to the press- ure of a vertebral tumor, and twitchings of the muscles, and contrac- tions of the limbs, if the antero-lateral columns are principally involved. When both sets of columns—as is generally the case—are affected, the troubles of sensibility and of motility are both present. If the tumor is situated in the cervical or upper dorsal region, there is generally tonic contraction of the muscles of the neck by which the head is thrown backward, causing the p«,dent to present the appear- ance of a person affected with the opisthotonos of tetanus. There are in such a case usually ocular troubles, such as those previously men- tioned, and more or less gastric derangement. The symptoms, so far as the limbs and viscera are concerned, vary in their extent according to the situation of the morbid growth. The symptoms of strong compression are anaesthesia and motor pa- ralysis. These may or may not be accompanied with muscular atrophy. Reflex excitability and electro-muscular contractility are generally at first increased, or at least not lessened, but, as the pressure augments TUMORS OF THE SPINAL CORD. 617 and the structure of the cord becomes more disorganized, they are less- ened. The bladder generally retains its power, but if the tumor be situated so as to compress the middle of the dorsal region there will be more or less difficulty in passing the urine which is retained through spasm of the sphincter. If the lesion exists at the upper part of the lumbar re- gion, or at about that part, the bladder and sphincter will be paralyzed, and the urine will dribble continuously.1 Many cases, of what may with Drs. Charcot and Brown-S6quard be called hemi-paraplegia, are due to spinal tumors. It often happens that these are small and compress a lateral half of the cord, leaving the other affected only by the transmitted pressure. A very remarkable case has been reported by Charcot,a in which the left inferior extremity was completely paralyzed, while the right was simply weak without having lost the power of contraction in any of its muscles. On the other hand, sensibility was greatly lessened in the right limb, while it was exalted in the left. There was paralysis of the bladder, but no at- rophy of either limb. Finally, anasarca and bed-sores appeared, and the patient gradually sank. On post-mortem examination, a tumor was found growing from the dura mater on the anterior face of the cord and compressing its left lateral half. The accompanying wood- cuts (Figs. 87 and 88), reduced from Charcot’s lithographic repre- sentations, show the situation and relations of this tumor. Fig. 87 shows the growth in sitv, and Fig. 88 the parts as they appeared when the tumor was pushed aside so as to allow the cavity to be seen in which it was lodged.3 Recollecting the facts that the fibres of the anterior or motor col- umns of the cord decussate at the medulla oblongata, while those of the posterior or sensory columns cross over soon after they enter the cord from the posterior roots of the spinal nerves, we can understand why, when the paralysis of motion is confined to one side, or is greater on that side, the lesion is on the corresponding side of the cord, and this loss of motility should be accompanied with anaesthesia of the opposite side of the body. Under the name of painful paraplegia (paraplkgie douloureuse), Cruveilhier referred to a form of spinal disease which has been subse- quently described more fully by Charcot. This latter author has ob- served six cases, in all of which there was cancer of the mammary gland. In three of these he had the opportunity of making post-mortem ex- 1 Charcot, “Lecjons sur les maladies du syst&me nerveux; seconde fascicule. De la com- pression lente de la moelle epiniere,” Paris, 1873, p. 114. a Archives de physiologic, No. 2, p. 291. 3 This case is quoted at length by Dr. Brown-Sequard in the Lancet of September 25, 1869, p. 429. In previous and subsequent numbers of this journal Brown-Sequard has contributed much valuable information on the subject of hemi-paraplegia. 618 DISEASES OF THE SPINAL CORD. animations, and discovered carcinoma of a lumbar vertebra in each, to which the irritation and compression of the cord were due. According to him, “the skin, especially during the paroxysms of pain, is often Fig. 87. Fig. 88. very sensitive to the touch. At the same time walking becomes trouble- some, and later the patient cannot walk without help; finally, muscular atrophy ensues, and the patient loses the power to stand.” Simon, from whom I quote these details, under the head of “ para- plegia dolorosa,” describes a case which came under his own observa- tion, in which, during life, symptoms similar to those mentioned bv Charcot were noticed, and in which, after death, a cancerous tumor was found growing from the first lumbar vertebra and compressing the posterior columns of the cord. Other lesions were present in the pos- terior columns both above and below the tumor ; they were appar- ently of the nature of sclerosis. Similar cases have been described by other authors. Although it is rendered certain that cancerous tumors of the verte- brae may give rise to paraplegia characterized by great pain, it must be borne in mind that these symptoms are not a necessary accompaniment of the lesion, and that they are met with in other affections of the cord. TUMORS OF THE SPINAL CORD. 619 A tumor situated in the cervical or upper dorsal region of the cord sometimes gives rise to characteristic symptoms. Thus there may be dilatation or contraction of the pupil on one or both sides, or one may be contracted and the other dilated. Cough and dyspnoea, vomiting, difficulty of swallowing, epileptiform convulsions, and a remarkable slowness of the pulse, are sometimes among the phenomena. But such symptoms are by no means invariable. Many years ago Yelpeau 1 re- ported a case of tumor of the cervical region of the cord in which none of these symptoms were present. The patient, a woman at thirty-four years of age, after having experienced mental troubles and been ex- posed to bad hygienic influences, suffered from convulsive movements of the limbs which were not of long continuance. Shortly afterward the left arm became the seat of a severe pain, and she had pains in the head. The pain in the arm increased, and little by little she lost the use of the limb. Renewed convulsive movements occurred in the in- ferior extremities, and were followed by complete paralysis. When she presented herself at the hospital she had no pain in the left arm, which was, however, entirely paralyzed, but which, nevertheless, retained its sensibility almost unaltered. Motion of the right arm, though difficult, was still possible, but it was the seat of very severe pain. Respiration was normal but a little weak; the pulse was frequent, sometimes strong, but generally small and regular. There was a large and deep ulcera- tion on the sacrum; the lower extremities were anasarcous and were de- prived of all sensation and power of motion. The fecal matters and the urine were passed involuntarily and unconsciously. Gradually she lost the ability to move the right upper extremity. She sank almost im- perceptibly without apparent cause,, and died after having been two months and a half in the hospital. On post-mortem examination numerous whitish opaline plates were found scattered over the arachnoid, but the principal lesion consisted of a tumor, which was situated between the arachnoid and the cord, and covered the entire anterior surface of the latter from the sixth cervical pair of nerves to the third dorsal. This growth appeared to have its origin in the left antero-lateral furrow. The anterior roots of the left spinal nerves within its area were so compressed that they were shrunk to mere threads, and the posterior roots of the same side were also sub- jected to pressure. The right posterior roots were in a normal condi- tion. The whole body of the cord was flattened by this tumor, but the left side was especially in this condition. The growth was cerebriform in appearance, and was thought to be cancerous. As an example of the symptoms resulting from a tumor occupying the dorsal region of the cord, the following, from Ollivier,8 is cited: 1 “ Observation sur une maladie de la moelle epiniere tendant & demontrer l’isolement desfonctions des racines sensitives et motrices des nerfs,” Journal de physiologie de Ma tome vi., 1826, p. 138. 2 “Trait6 des maladies de la moelle epiniere,” Paris, 1837, tome ii., p. 477. 620 DISEASES OF THE SPINAL CORD. A woman, aged fifty-two, had enjoyed good health till in 1819 she began to experience lancinating pains in the abdomen and breast. Af- ter several months these pains shifted their situation to the pelvis and the lower extremities, especially the left. These limbs then became the seat of varied phenomena, sometimes being cold, at others hot, and again numb ; they were also subject to the most intolerable itching. Then they became by turns immovable, and were agitated by convulsive movements. Although she could stand, walking was impossible. Fi- nally, in February, 1821, they began to atrophy, and at once lost all sensibility and power of motion. Then these symptoms disappeared, and there only remained numbness and pains apparently starting from the pelvis and traversing the nerves. In May, 1821, she entered the hospital. At this time the inferior extremities were rigid, and could not be flexed without causing pain of a very atrocious character. They were insensible to all external excitations, but were constantly the seat of severe and lancinating pains. There was, however, no pain along the vertebral column, and the general health of the patient was excel- lent. All these symptoms persisted till in January, 1823, the legs began to be flexed on the thighs, and these latter on the pelvis, to such an ex- tent that the heels pressed against the buttocks, and the knees touched the chest. Forced extension of the limbs was exceedingly painful, and when they were by main strength extended they at once returned to their former position as soon as the traction was discontinued. Two months before her death the left wrist and right knee became inflamed; the former suppurated, and the patient died six weeks afterward. Strychnia had been administered, but always aggravated the symp- toms. Morphia gave no relief. Examination after death showed the brain to be healthy. There was a band of sclerosed tissue on each side of the cerebellum. The spinal cord was healthy as far down as the tenth dorsal verte- bra. Here a tumor existed between the two layers of the arachnoid. The growth was oblong, and about two inches in length. It was simi- lar in appearance to brain-tissue, but firmer. It was not adherent to the cord, but throughout its whole extent pressed on the organ, which was softened throughout to the consistence of a thin jelly. At the most voluminous part of the tumor the cord was so much compressed that it was almost cut in two, so that there was the appearance of two cones with their apices together. A careful examination showed that in the softened part no trace of nerve-structure remained. Leyden,1 among other interesting cases, gives the following, of tu- mor occupying the lower dorsal region of the cord : The patient, a woman twenty-nine years old, after being delivered 1 “Klinik der Ruckenmarkskrankheiten,” erster Band, Berlin, 1874, p. 454. TUMORS OF THE SPINAL CORD. 621 of a dead child, became affected with a pain in the right leg, which, starting from the foot, reached the knee, and finally settled in the calf. She noticed at the same time a weakness of this leg, which prevented her walking well, and eventually confined her to bed. These symptoms disappeared, and she remained well for over three years, when the right leg again became weak, and was the seat of constant lancinating pains, which were aggravated by muscular exercise. In April, 1872, the left leg was also affected with similar pains. It soon became impossible for her to bend the knee or to move the limb. All these symptoms in- creased until, in February, 1872, she was unable to walk, and there was complete anaesthesia in both extremities as high as the hips. A painful sensation of constriction was felt around the body at the umbilicus. The electric excitability of the right lower extremity was lessened, of the left was normal. The reflex excitability of both lower extremities was increased ; the nutrition was good. At times they were the seat of strong contractions. By August, 1873, the patient wras entirely confined to bed on her back, and deprived of all voluntary move- ment of her lower extremities. There were, however, often paroxysms of tremor in both feet so strong as to shake the whole body, and at times powerful contrac- tions of the muscles, drawing the thighs against the ab- domen, while the knees were flexed to their utmost ex- tent. The constricting pain around the body was still present. In the beginning of October the patient was seized with typhus fever and died. On examining the spinal cord it was found that a tumor existed on the right side, reaching from the seventh to the tenth dorsal ver- tebra, and firmly attached to the dura mater. The en- tire length of this growth was eighty millimetres (a lit- tle over three inches). (Fig. 89.) Causes.—Nothing is known relative to the etiology of intra-spinal tumors beyond the fact that they may result from the syphilitic, scrofulous, and cancerous dia- theses, and from wounds and injuries. Diagnosis.—There are no certain marks by which we can determine with any great degree of certainty that a tumor is compressing the spinal cord. We may suspect such to be the case when the motor paralysis is more marked on one side of the body than the other, and the anaesthesia exists to a greater extent on the opposite side. The existence of either syphilis, scrofula, or cancer, in connection with spinal troubles not clearly referable to some other dis- ease, may likewise excite the suspicion that a tumor exists. But the Fig. 89. 622 DISEASES OF THE SPINAL CORD. symptoms—paralysis, hyperaesthesia, anaesthesia, contractions, rigid- ity, and spinal convulsions—are met with in other spinal disorders, notably in symmetrical lateral sclerosis. The unilateral predominance of the phenomena is probably, on the whole, most to be relied upon as a diagnostic mark. Prognosis.—This is always unfavorable. It is less so when a syphilitic origin can be made out, and when the tumor is situated in the posterior or lateral portion of the membranes it may be removed. No others recover. Morbid Anatomy and Pathology.—The most common intra-spinal morbid growths are those which are developed from the vertebrae, and they include many syphilitic, scrofulous, and cancerous tumors. They originate either from the bones or from the periosteum. Formations resulting from either of these diatheses may also grow from the menin- ges or the substance of the cord. Parasitic tumors due to either the echinococcus or the cysticercus, may also be developed within the spinal canal. Their usual seat is in the membranes ; and, according to Ollivier,1 the echinococcus is found in the spinal cavity of women only. Aneurismal tumors occasionally form in the intra-spinal arteries, and may compress the cord. Aneurisms of the thoracic or abdominal aorta may, by pressure, cause absorption of the vertebrae, and may thus eventually subject the cord to their influence. Among the other intra-spinal tumors are the glioma—a growth, the seat of which is especially in the brain and spinal cord, and whose struct- ure is very similar to that of sclerosed nerve-tissue—the sarcoma, the psammoma, the neuroma, fibroma, and myxoma, and tumors, generally syphilitic, developed from the vertebrae. Treatment.—The attempt should always be made, whenever the ex- istence of a tumor of the spinal cord is suspected, to effect its removal by anti-syphilitic treatment, with iodide of potassium and mercury. The following case will show the advantages of following this course: In the summer of 1869 I was requested to visit a gentleman who, I was informed, was paraplegic and subject to paroxysms of great suffer- ing. On making my examination, I found his limbs contracted, his re- flex excitability augmented, and motor paralysis and anaesthesia of both lower extremities. There were intense pain in the lower dorsal region, and violent spasms of the sphincter vesicas, alternating with paralysis of it and the bladder. There were also paroxysms of severe pain in the head, and occasional attacks of delirium. He denied any syphilitic infec- tion, but, on examining his head with my hands, I found a gummy tumor of the scalp over the right occipital region. Further inquiry and ex- amination revealed the existence of a similar tumor over the leftiaaius. I inferred that there might be one or more like growths within the : “ Trait6 des maladies de la moelle dpiniere,” Paris, 1837, tome ii., p. 549. SYPHILIS OF THE SPINAL CORD AND ITS MEMBRANES. 623 spinal canal, and I administered the iodide of potassium in gradually- increasing doses, with the bichloride of mercury in doses of the six- teenth of a grain three times a day. In less than two months every symptom of disease, except a general weakness, had disappeared. The tumor of the scalp wrnnt during the first month ; that of the arm a week later. The iodide of potassium was carried up to fifty grains three times a day. This patient continues in good health up to the present time. Even if there was not sufficient reason to diagnosticate the existence of an intra-spinal syphilitic tumor, the success of the treatment can scarcely leave a doubt on the subject. If this treatment fail, there is little else left. When the symp- toms point to compression of the cord by a tumor situated either in the membranes or in the spinal canal, the growth may be removed by operative procedure. This operation was first successfully performed by Horsley on a patient of Gowers’s.1 Since then, numerous opera- tions have shown that, under proper antiseptic precautions, the arches of several vertebrae may be removed, the membranes opened, and the cord searched for a space of several inches with comparative safety. In this manner tumors have been removed in several instances. As means of mitigating the pain and spinal convulsions, hypoder- mic injections of morphia or atropia, or of both combined, may be employed. CHAPTER VITI. SYPHILIS OF THE SPINAL CORD AND ITS MEMBRANES. When compared with like affections of the brain and its mem- branes, syphilitic accidents of the cord and its envelopes are certainly rare. Of coarse, this statement has reference only to new forma- tions. As a cause of many of the affections described in the fore- going chapters, syphilis occupies, if not the first place, at least one very near the front rank. Locomotor ataxia, for instance, is proba- bly in the majority of instances of syphilitic origin ; and Dr. Gow- ers has recently gone so far as to declare that in his opinion syphilis is its only cause. As in the brain, neoplasms of syphilitic origin are known to be developed on the periphery of the cord rather than in its substance, in the subarachnoid space and on the internal face of the dura mater. Adhesions of the membranes to each other and to the substance of the cord are thus induced, while this latter is little by little invaded by the new formation. Generally the neoplasm does not appear as a 1 British Medical Journal, January 28, 1888. 624 DISEASES OF THE SPINAL COED. well-defined tumor, but as a substance analogous to that of gummata diffused through the tissues. The histological and macroscopic characters are like those which are met with in like formations of the encephalon. Instead of a dif- fused infiltration, little miliary nodosities may be met with, dissemi- nated in the meninges. Engelstedt1 has reported a case of this kind. Sometimes there is found at the post-mortem examination of syphi- litic patients, who had during life presented evidences of spinal trou- bles, a kind of deposit replacing to a certain extent the cellulo-adipose tissue which lines the internal face of the spinal canal. From this there results an intimate adherence of the dura mater with the walls of this canal. Virchow has reported a similar case observed in an indi- vidual who had had multiple syphilitic accidents, and in the last pe- riod of his existence a painful rigidity of the neck and arms, which supervened on paralysis of the upper extremities. At the autopsy the dura mater wTas found considerably thickened at the height of the fifth and sixth cervical vertebrae, and adherent to the wrall of the canal by a great quantity of tough connective tissue. At other times the exudation occupies the internal face of the dura mater, and this results in adhesions of the membranes to each other. At the same time the adjacent part of the cord is the seat of a hyper- plasia of the neuroglia with distention of the nerve-structures. Hue- ter reports a case of this kind. In cases of syphilitic patients wdio have died after having pre- sented symptoms of a spinal affection, a simple softening of the cord has been discovered. On the other hand, there have never been any absolute proofs that pure myelitis has ever been developed through the influence of syphilis. And in a certain number of cases the autopsy has never revealed the slightest appreciable lesion of the cord (Zambaco, Kussmaul, Leon, Gros, and Lancereaux). Spinal affections are generally exhibited at an advanced period of syphilis, and in individuals who present unde- niable traces of the diathesis with all the accompaniments of a more or less advanced cachexia. They are characterized by pains localized in the spine or radiating to the limbs, with various derangements of sensibility (formication, numbness, anaesthesia, etc.). Little by little rigidity of the muscles supervenes, and this is succeeded by temporary contractions and movements which gradually lose their energy, and are accompanied with painful cramps. All these symptoms, which tre generally regarded as being due to meningitis, are subject to alter 1a- tions of amelioration and aggravation, and eventually all phenomena of excitation give place to paralysis. This generally first shows itself in one of the lower extremities, and advances with great rapidity. Yery soon the opposite limb is attacked, and the paraplegia becomes 1 Archiv der Heilkunde, Band iv., 1863, p. 139. SYPHILIS OF THE SPINAL CORD AND ITS MEMBRANES 625 complete. Often the sphincters alone are involved. It is to be noticed that the paralysis of sensibility does not keep pace with that of motion, which, after existing for a long time, is supplement- ed by phenomena of anaesthesia or parsesthesia. Then there is often a period of repose. At this period proper treatment may procure for the patient a gradual but nevertheless satisfactory cure. This termination is, above all, to be looked for when the lesion remains confined to the inferior part of the cord. The prognosis is much less favorable when the genito-urinary functions are involved. In such cases we ordinarily find that sooner or later cutaneous trophic troubles are developed over the sacrum—purulent cystitis, etc.—with all their consequences. Hectic fever is excited, and the patient dies greatly emaciated. When syphilitic lesions affect the upper part of the cervical region of the cord, patients are exposed to still greater dangers. In such cases the symptoms are very rapidly developed, for the paralysis involves all the muscles of the trunk, including the respiratory appa- ratus. The disease, in fact, follows a course analogous to that of acute ascending paralysis. In such instances a specific treatment instituted opportunely may still be sufficient to save the life of the patient, but cannot effect a complete cure. The tissues which have been infiltrated with the syphilitic exudations undergo a veritable inodular retraction and alteration, to which there are sometimes add- ed secondary ascending and descending degenerations. When the secondary degeneration affects the posterior columns, the paralysis may be replaced by certain manifestations of tabes dorsalis, but this syphilitic ataxia is not to be confounded with ordinary locomotor ataxia. In the cases of those patients in whom at the autopsy appreciable alterations of the marrow are not found, the spinal affection has generally followed a subacute course. It then greatly resembles the acute ascending paralysis of Landry. Sometimes its real charac- ter is recognized as being like that which is exhibited at an early period of syphilis, in the course of the first year after contamina- tion. Ordinarily it is not preceded by any prodromatic symptoms, but it is sometimes the case that a very short time after the devel- opment of the paralysis the affected limbs are the seat of vague pains. The paralysis begins in the lower extremities, and is com- plete after a few days. It is accompanied by a certain degree of weakness of the bladder, which is manifested either by incontinence or retention of urine. After the second week the patient is confined to his bed, and in a period relatively short he succumbs to septic infection. Therapeutics can avail nothing against this form of syphi- litic myelitis. 626 DISEASES OF THE SPINAL CORD. CHAPTER IX. SYRINGOMYELIA. It is only within the past few years that the attention of neurolo- gists has been drawn to the study of the symptoms produced by the formation of abnormal cavities within the spinal cord. That such cavities were of frequent occurrence has been known for many years, but recently the researches of Schultze in 1882,1 and again in 1885,2 on the pathology of the disease, and further contributions to the clinical study of the disease by Baumler,3 Buhl,4 Starr,6 Van Giesen,6 Jeffries,7 and others, show that, at least in many instances, this dis- ease may be diagnosticated with accuracy. Symptoms.—As the disease usually begins in the cervical or upper dorsal regions of the cord, the first symptoms, under those circum- stances, will be observed in the upper extremities. The motor symptoms are progressive paralysis followed by atro- phy of the affected muscles. Sometimes whole groups of muscles supplied by one nerve are paralyzed simultaneously ; again one muscle after another may become affected. Fibrillary muscular twitchings are frequently observed, not only in the paralyzed muscles, but also in those muscles which are about to become paralyzed. Contractions of the unaffected muscles often follow, thus producing various deformi- ties, the most common of which is the main en grijfe. The electrical reactions show a quantitative decline consequent upon the diminished volume of muscular tissue, and the polar degenerative reactions may or may not be present. If the motor cells in the anterior horn of gray matter are involved in the destructive process, the polar degenerative reactions can readily be obtained ; otherwise they can not be. The superficial reflexes are generally abolished ;. the knee-jerk is either normal or else slightly exaggerated. As far as the motor symptoms are concerned up to this point, they differ but little from those previously described under the heading of progressive muscular atrophy. In time, however, as the disease ex- tends so as to destroy a greater area of the cord, and more pressure is exerted on the surrounding tracts by the fluid within the cavity, the motor phenomena invade the lower extremities. These become we ik ; 1 Virchow’s “ Archives,” vol. lxxxvii. 2 Ibid., vol. cii. 3 Deutsche Archiv fur him. Med., Bd. xl, 1886. 4 Archiv fur gen. Mecl., July, 1889. 5 Am. Journ. Med. Sciences, May, 1888. 6 Journ. Nerv. and Ment. Dis., July, 1889. 1 Ibid., September, 1890. SYRINGOMYELIA. 627 stiffness of the muscles supervenes ; the patellar tendon reflex is exag- gerated ; and the ankle clonus can frequently be obtained. Romberg’s symptom, or the inability to stand upright with the feet close together and with the eyes closed, is sometimes observed. These symptoms, with the exception of the last one, are identical with those produced by inflammation of the lateral pyramidal tracts, and their presence in syringomyelia indicates that that tract has become implicated either from pressure or else from being involved in the diseased process. The sensory symptoms are not confined to the regions in which the muscular paralysis exists. The sensations of pain and temperature are abolished, while the sense of touch is preserved. There will be absolute anaesthesia for heat and cold, for pricking the skin and irritating it by strong electrical currents over the affected areas, and yet the individual can distinctly feel that the parts are touched, and can usually locate with considerable accuracy the spot where the touch was felt. Jacquet1 reports one case in which the tactile sense was destroyed together with the senses of pain and temperature. Pricking, stinging, and burning sensations are frequently complained of. The trophic and vaso-motor symptoms are not always well marked. Usually the affected limbs are cold and blue, and generally the secre- tion of sweat is diminished or abolished. Cuts and abrasions of the skin heal with difficulty, and ulcers and bed-sores which sometimes ap- pear are not amenable to the usual forms of treatment. The finger nails become brittle, and occasionally dislocations of joints and fract- ures of bones have occurred similar to those observed in locomotor ataxia. Causes.—Little is known in regard to the etiology of this disease. In some cases it seems to follow from injuries of the spinal cord, in others it develops in apparently healthy subjects who are not suffering from any congenital taint or predisposition. Diagnosis.—Syringomyelia may be confounded with hysteria, mul- tiple neuritis, progressive muscular atrophy, pachymeningitis, and pos- sibly with anesthetic leprosy. From hysteria, syringomyelia can usually be differentiated by the history of the case, the presence in the latter disease of the reactions of degeneration, of fibrillary twitcbings, and by the early appearance of muscular atrophy and the well-marked trophic and vaso-motor changes. In multiple neuritis the nerves are tender and are painful under pressure, the tactile sense is abolished with the other varieties of sen- sation, the disturbances of sensibility correspond in location with the disorders of motility, and there is usually a great deal of pain in the affected members which is augmented both by active and passive motion. 1 Compt. rend, hcbdom. soc. dc bioL, Paris, tome ii, No. 3, 1890. DISEASES OF THE SPINAL CORD. In progressive muscular atrophy there are no- abnormities of sen- sibility, no tendency to the formation of ulcers and bed-sores, and no diminution in the excretion of sweat. Cervical pachymeningitis can be distinguished by the severe ten- derness and pain over the region of the inflammation, and by the absence of the symptoms of disease of the central gray matter of the cord. Anaesthetic leprosy, though of very rare occurrence, at least in this country, bears some resemblance to syringomyelia. In one variety of the former affection—-that is, the lepra nervorum—the senses of pain and temperature may be abolished while the sense of touch remains intact. If there are no accompanying shin lesions the differential diagnosis may be difficult or impossible. Prognosis.—iNo case of a cure has yet been recorded. The patient either dies from exhaustion or else the disease in its progress involves the upper regions of the cord, the perfect integrity of which is essen- tial to life. Morbid Anatomy and Pathology.—The formation of abnormal cavities within the spinal cord may depend upon any one of sev- eral morbid conditions. In childhood, hydromyelia, or the disten- tion of the central canal by fluid, sometimes occurs. Gowers 1 is in- clined to regard this condition as similar in nature to syringomyelia, and believes that both conditions are congenital. Schultze,2 on the contrary, while admitting that a congenital defect is responsible for hydromyelia, considers that syringomyelia may develop in a healthy cord free from any hereditary predisposition. I have seen specimens of the former disease in which the tissues surrounding the dilated canal were healthy, the epithelial lining being plainly visible under the microscope. Syringomyelia may develop from haemorrhage into the cord, from softening of the cord followed by absorption, from sar- coma, and from gliomatous tumors. The latter is by far the most common. According to Schultze, it begins with an infiltration of gliomatous cells, usually in the neighborhood of the central canal, and confines itself almost entirely to the gray matter. The pressure thus brought to bear upon the surrounding tissues gradually destroys them. The gliomatous mass thus formed eventually breaks down and be- comes absorbed, leaving a cavity the walls of which are lined with connective tissue. The accompanying illustrations, Fig. 90 and Fig. 91 (after Van Gieson), show the position of the cavity in the cord in his case, and also sections of the cord made at different levels. The infiltration is not always of a gliomatous nature. Berkley3 reports a case in which there was a dense hyaline infiltration which 1 “ Diseases of the Nervous System,” p. 422. 2 Zeitschrift fur klin. Med., No. 13, 1887. 3 Brain, London, 1889-1890, vol. xlviii. .Fig. 90.—Syringomyelia. (Van Giesen.) Fig. 91.—Syringomyelia. (Van Gieeen.) PSEUDO-HYPERTROPHIC PARALYSIS. 629 seemed to exude from the blood-vessels, which after absorbing, and to a great extent destroying, the surrounding tissue, broke down itself and was absorbed, leaving a cavity. Chemical tests showed that the exudation was hyaline. He refers to Huten, Steudener, and Langhaus as having observed similar pathological changes. In some instances the cavity in the cord is undoubtedly a congeni- tal defect. Van Gieson 1 reports a case of this kind. But I am in- clined to the opinion that the majority of .eases develop in subjects whose spinal cords were previously normal. Treatment.—There is very little to be said on this subject. The very nature of the disease precludes the possibility of a cure being effected. The most that can be done is to relieve the symptoms of the disease and to make the patient as comfortable as possible. Electrization of the paralyzed muscles, rest, and a general tonic treatment, together with a full nourishing diet, will prove of some service, and may retard the progress of the disease. CHAPTER X. PSEUDO-HYPERTROPHIC PARALYSIS. In the early editions of this work I considered this disease under the head of hypertrophy of muscular connective tissue, although treat- ing of it as one of the affections of the motor and trophic cells of the cord. But this view must now be abandoned, since the evidence of later years practically points to this disease as being essentially a myosis. The clinical similarity of this affection with diseases depend- ent upon lesions of the central nervous system is so obvious that no apology is necessary for inserting it in its present position. Although previously noticed, the first to thoroughly investigate the condition was Duchenne,2 who described it under the name of parapl'egie hypertrophique de Venfcince de cause cerebrate. lie has since designated it paralysie pseudo-hypertrophique, ou myo-sclerosique.3 Jaccoud4 calls it sclerose mnsculaire progressive (progressive muscular sclero- sis). Dr. Foster5 terms it paralysis with apparent muscular hypertro- phy, and Barth6 fatty muscular atrophy. 1 Journ. Nerv. and Ment. Dis., July, 1S89. 2 “De l’electrisation localisee,” etc., Paris, 1861, p. 353. 3 Archives Generates, etc., 1868. 4 Op. cit., p. 365. 6 Lancet, May 8, 1869. 6 “ Beitrage zur Kenntniss der atrophia musculorem lipomatosa,” Archiv der Hcil- kundc, 1871, p. 120. 630 DISEASES OF TIIE SPINAL CORD. Symptoms.—The first symptom observed is weakness in the lower extremities, which causes an inability to stand steadily, or to walk without stumbling or falling. The legs are separated widely in stand- ing or walking, and thus a peculiar character is given to the gait, which somewhat resembles that of a duck. Very soon an enlargement of the calf of one of the legs is perceived, the other before long is affected, and then the muscles of the thighs and gluteal region become involved. As the child stands or walks, a remarkable incurvation of the spine in the lumbo-sacral region is perceived, so that if, as Duchenne remarks, a plumb-line be allowed to fall from the most posterior part of the spinous process of a vertebra, it passes far behind the sacrum. lie considers this phenomenon to be due to weakness of the erector muscles of the spine. The muscles of the trunk may become involved, as may also those of the upper extremities—the deltoids being the first affected in the majority of cases, and the progress being much slower than in the low'd* extremities. With the advance of the hypertrophy the paralysis becomes more strongly marked, and finally the child is confined to the recumbent posture. Distortions from disturbance of muscular equilibrium may take place, and the attempt at flexion or extension becomes painful. Occasionally the skin over the affected parts presents a peculiar mottled appearance, such as would be produced in the healthy skin by exposure to cold. After a period which varies in duration from two to five or six years, the hypertrophied limbs may begin to diminish in size, and eventually they put on very much the appearance exhibited in infantile spinal paralysis. This does not appear to be a constant occurrence, but is markedly exhibited in a case now under my care. Sometimes the muscles which are attacked, as the disease advances from the low*er extremities, do not become hypertrophied, but on the contrary diminish in volume as in infantile spinal paralysis. We thus have in the same individual some muscles paralyzed with coexistent hypertrophy, while others are paralyzed and atrophied. Electric contractility is ahvays lessened, both to the induced and to the primary currents, but the polar degenerative reactions are never observed. The knee-jerk, from primary changes in the muscles, is gradually diminished and is finally abolished. The course of the disease is slow*, its average duration being about five or six years. As it advances, there are symptoms indicating loss of mental power, and cerebral disturbance is sometimes also indicated by ocular troubles and pain in the head. Death takes place by the respiratory muscles becoming implicated, by exhaustion, or by some intercurrent affection. Weir Mitchell, in the Philadelphia Photographic Review, for 1871, PSEUDO-HYPERTROPHIC PARALYSIS. 631 reported a case which has recently been reexamined by Dr. George S. Gerhard.1 The most remarkable feature of the case, that of a boy now thirteen years old, is that the tongue and all the facial mus- cles, but particularly the temporals, are hypertrophied. His speech is altered from the enlargement of the tongue, and he has some difficulty in taking his food. There is also a somewhat more than normal car- diac impulse. As regards the hypertrophy of the facial muscles this case is remarkable, and would be unique, hut for the occurrence of a like condition in a case of my own, in which the left side of the face is hypertrophied. In the case which came under my notice March 7, 1871, the patient, a boy seven years old, exhibited a great disinclination to learn to walk. At three years of age he could not stand longer than a few seconds, and even for this time he was obliged to spread the legs apart and to hold on to some article of furniture. It was not noticed till he was five years old that his legs wTere larger than was natural. The hypertrophy began in the right calf, then attacked the left, and then the glutei mus- cles, before affecting the muscles of the thighs. The upper extremi- ties are as yet unaffected, but the spinal curve is very evident. The accompanying woodcuts (Figs. 92 and 93) give a posterior and profile view of this boy, from photographs. He was unable to stand alone while the photographs were being taken, hut the spinal curve is well shown, and the positions are those he spontaneously assumed. He died in the spring of 1875, with pneumonia, having been for the previous three years unable to stand or even sit. The muscles of the upper ex- tremities were paralyzed for two years before his death, but under- went rapid atrophy instead of enlargement. Another case, that of a bright, intelligent boy, six years of age, was brought to me May 3, 1871, at the suggestion of my friend I)r. Trask, of Astoria, who accompanied the patient. Several months pre- vious the child had been noticed to fall frequently while at play in the house, and to show weakness in the legs when ascending a stair- case. The parents were unable to account for this debility, for, as the father assured me, the legs were exceedingly well developed. As the boy stood in my consulting-room, I observed that he separated his legs to a greater than usual distance, and that as he walked he also kept them far apart, and that his gait was staggering. As soon as his trousers were removed I at once perceived the nature of his disease, for the calves of both legs were hypertrophied to an enormous extent, and the incurvation of the spine was well marked. The electro-mus- cular contractility was almost entirely abolished in the gastrocnemii and solei muscles, and notably lessened in the muscles of the thighs, the gluteal region, and the back. These latter were not hypertrophied. On the contrary, they appeared to be rather under than above the 1 “ Pseudo-hypertrophic Paralysis,” Philadelphia Medical Times, Oct. 16, 1875, p. 31. 632 DISEASES OF THE SPINAL CORD. normal size, and they were in a very decided paretic condition. Thus, when I requested him to cross one leg over the other as he sat on a chair, he was unable to do so without seizing hold of the leg with his Fig. 92. Fig. 93. hands and thus assisting with their strength, and, as he lay at full length on his back on the floor, he could not draw up his legs without great trouble, though he could flex the thighs with readiness. On measuring the calves at their greatest dimensions, I found the right to have a circumference of twelve and a quarter inches, and the left of eleven and a half inches. The right thigh, at its point of greatest circumference, measui’ed but eleven and a quarter inches, and the left ten and three-quarters inches. I saw this patient again in the course of two months. The paralysis of the lower extremities had in- PSEUDO-HYPERTROPHIC PARALYSIS. 633 creased to such an extent as to cause walking to be very difficult. At every step he lifted the thigh almost to the line of a right angle with the body, for he had no power to raise the foot. The flexors of the thigh, upon the pelvis, did not therefore appear to be much weakened. The calves were of about the same size as before. The upper extremi- ties were still unaffected. I did not see this case again for nearly two years. The paralysis had then so far extended as to render walking impossible, but the arms were still strong, and bv their means the patient dragged himself along over the floor. The calves had diminished in size, and the extensor muscles of the foot had become atrophied to such an extent as to allow of the permanent elevation of the heels by the uncompensated action of the still incompletely-paralyzed gastrocnemii and solei. The thighs were now hypertrophied, as were also the glutei muscles. Accurately measured, the circumference of the calves was, for the right, eight and a half inches, a loss of three and three-quarters inches ; and for the left, eight and a quarter inches, a loss of three and a quarter inches. On the other hand, the right thigh measured, at its largest part, fifteen inches, an increase of three and three-quarters inches; and the left fourteen and three-quarters inches, an increase of four inches. I saw this patient again in the summer of 1874, a year after the last visit, when, in order to allow of his wearing a shoe, I divided the right tendo-achillis, with the result of bringing down the heel and perma- nently relieving the extreme condition of talipes equinus which existed. The calves had undergone still further atrophy, and the thighs were likewise beginning to shrink. There was a slight disposition to a con- traction of the flexors of the thighs, and the upper extremities were be- coming paretic. A year subsequently (July, 1875) I again saw this patient. He had then been using a steel apparatus, which enabled him to stand, or rather the apparatus stood, and, being strong, supported the completely-para- lyzed patient. The calves now measured, the right eight inches, and the left eight and a quarter inches in circumference—a loss from the first measurements of four and a quarter inches and three and a quarter inches respectively. The thighs had also lost greatly from their hyper- trophied condition of two years before. The right now measured, at its largest part, ten and a half inches, a loss of five inches, and the left ten inches, a loss of four and three-quarters inches. The upper extremities were decidedly weaker than they were a year ago, but there was as yet no hypertrophy. The patient could not even sit without support, and there was notable weakness of the muscles which maintain the erect position of the head. Throughout the whole of the period during which this patient has been under my observation, the mind has remained clear, and the gen- eral health has been excellent, circulation, respiration, digestion, and DISEASES OF THE SPINAL CORD. urination, all being well performed. The cutaneous tactile sensibility and the sensibility to pain have not been in the least weakened. While these pages are going through the press, I have again (De- cember 2, 1875) examined this patient, whose general health began to show signs of giving way. To my astonishment, a feature presented itself which thus far is entirely exceptional. A second stage of hyper- trophy is going on ; the calves now measure, the right ten inches, and the left ten and a quarter. The thighs were not measured, but were considerably larger than Avhen I last saw them ; and the father, a very intelligent gentleman, said that the enlargement in the lower extremities had been going on for tAvo or three months. The left side of the face was decidedly larger than the right. The patient was still unable to walk, stand, or sit alone, but was comparatively strong in the arms, and in good gen- eral health. His mind was remark- ably bright. At all my examinations except the last two, I removed, by means of Du- chenne’s trocar, portions of the hy- pertrophied and atrophied muscles, the results of the examination of which will be given under the head of the morbid anatomy. Quite recently Dr. E. B. Richard- son, of Mount Sterling, Kentucky, has given me the details, with photo- graphs, of an interesting case of the disease under notice. The patient, a boy, is eight years of age, of average intelligence, though not capable of prolonged mental exertion. The dis- ease is of several years’ duration, and he is slowly getting worse. His loco- motion is peculiar ; usually he walks Avith his hands grasping the front of the thighs, and his legs are drawn up suddenly, as if with strings fastened to his back. In ascending a stair- case, he does so with his hands on his thighs, and the same foot is always advanced first, and not each alter- nately. If sitting doAvn, he raises himself by clasping the thighs strongly ; otherwise he cannot get up at all. The boy’s father is a strong and robust man ; his mother is delicate, Fig. 94. PSEUDO-HYPERTROPHIC PARALYSIS. 635 and has had seven children, of whom three are younger than the pa- tient. In two, at least, of the other children there is some enlargement of the gastrocnemii mus- cles and a general ema- ciated appearance of the upper extremities. With the birth of the last child the mother had puerperal mania, and, June 23d, had not fully recovered. She had a sister and a brother who were insane, and there is incurable insanity in collateral branches of her family. Fig. 94, from a photo- graph, shows well the atro- phy of the trunk and up- per extremities, the spinal curve, and the hypertro- phy of the gastrocnemii muscles. Fig. 95 exhib- its the remarkable position assumed by the patient Fig. 95. Fie. 96. Fie. 97. just as he is about to rise from the sitting posture. The atrophy of the muscles of the chest and abdomen is also shown. The postures assumed when an attempt is made to change from a DISEASES OF TIIE SPINAL CORD. horizontal to a vertical position are characteristic. The movements are slow and labored, and are performed with difficulty. When the patient is extended at full length upon his back and is then told to arise, he slowly gets upon his hands and knees, then—still keeping his hands upon the floor—he gradually brings his legs into a vertical posi- tion (Fig. 96). The hands are then placed, one after the other, upon the knees, when, by “ climbing up the thighs,” as it is termed, the trunk is slowly raised to an upright position (Fig. 97). Causes.—The disease is one which is almost entirely confined to children, and boys are more liable than girls. Nevertheless, it is not a disease peculiar to very early infancy. Of thirteen cases observed by Duchenne, six are stated to have begun in first infancy, while in seven the inception occurred at from two to ten years. Cases have also been reported as occurring in adults. From a table containing an analysis of forty-one cases given by Dr. Webber, in his paper already cited, it appears that in one case the patient was twenty-six when the disease began, in one a few years under forty, and in one about twenty- eight. Duclienne expresses the opinion that a hereditary tendency some- times exists, and this appears to be the fact. Of the cases analyzed by Poore, in two, a maternal uncle and aunt had the disease ; in one, three maternal uncles and aunts were affected ; in one, one maternal uncle and one half-uncle ; in one, three maternal half-brothers ; and in one, a maternal half-brother, three maternal uncles, and other members on the mother’s side. The disease does not appear, therefore, to be transmitted directly from parent to offspring, but is a marked example of atavism. The descent is always from the mother’s side. As to exciting causes, little or nothing is known. In none of my cases could any reasonable explanation of its etiology be given. There is some reason for ascribing it occasionally to exposure to cold and dampness, and to antecedent febrile diseases. Diagnosis.—The only affection at all resembling that under consid- eration is simple muscular hypertrophy due to an excessive supply of blood being sent to a part of the body. The histories and phenomena of the two disorders are, however, so very different, that I do not see how any error can arise in making a diagnosis between them. Never- theless, it is tolerably certain that mistakes on this point have been made. Thus, such cases as the one reported by Mr. Maunder,’ which was clearly one of muscular hypertrophy possessing no analogies with the disease under consideration, have to my knowdedge been regarded as instances of the disease under notice. Duchenne,2 under this head, gives very elaborate directions for the 1 Medical Times and Gazette, March 27, 1869. 2 Op. cit., and “ Do 1’electrisation loealis6e,” troisieme Edition, Paris, 1872, p. 608. PSEUDO-IIYPERTROPIIIC PARALYSIS. 637 discrimination of cases of pseudo-hypertrophic paralysis from those of progressive muscular atrophy occurring in infants, infantile paralysis, and the tardy development of the coordinative and motor functions in young children. But it appears to me that very slight inquiry and examination will suffice to make errors in regard to any of these con- ditions almost impossible on the part of any one capable of distinguish- ing one disease from another. Prognosis.—The prognosis is unfavorable. Two cases of recovery are related by Duchenne, and other observers have reported improve- ments, but the tendency is to death, though life may be prolonged many years notwithstanding the gradual advance of the disease. And yet the fatal result is rarely directly due to the disease itself. Some intercurrent affection ensues, and the vital power, being enfeebled, cannot resist effectually the newr disorder. Thus death occurred in my first case by pneumonia ; and of thirteen cases referred to by Poore, in which the termination is given, not one died directly of the disease. Morbid Anatomy and Pathology.—When the study of this affection was in its infancy, certain changes discovered in the spinal cord, and particularly in the cells of the anterior horns, were regarded as the primary lesions of this disease. Reports of cases in which autopsies were obtained by Barth,1 Muller,2 and Clark,3 in earlier years, and even in later years by Gibney and Amidor.,4 seemed to confirm this view of the case ; but since then more careful investigation of the subject by Middleton 5 and Schultze,6 and still more recently by Sachs,7 shows almost conclusively that the primary pathological change occurs in the muscles, and that in the majority of instances the spinal cord is free from any semblance of disease. Sachs,8 in his interesting paper on this subject, collected seventeen cases of this disease, in all of which scientific examinations of the cord were properly conducted. In eleven of these “the spinal cord and anterior nerve-roots were found abso- lutely normal” ; in the other six cases “the changes that were found could not be held responsible for the changes in the muscles.” Ilandford9 contributes another case, the study of which confirms 1 “ Beitrage zur Kenntniss der atrophia musculorum lipomatosa,” Archiv der Heil- kunde, Leipzig, 1871, p. 120. 2 “Beitrage zur path. Anat. und Physiol, des menschlichen Riickenmarks, Heft ii., Leipzig, 1870. 3 Journal of Mental Sciences, April, 1870, p. 41. 4 Transactions of the American Neurological Association, 1886. 5 Glasgow Medical Journal, 1884, No. 22, p. 81. 6 “ Heber den mit ilypertrophie verbundenen progressiven Muskelschwund,” Wies- baden, 1886. 7 Transactions of the American Neurological Association, 1886. 8 Ibid. 9 Transactions of the Pathological Society, London, 1888-89, xl., p. 24. 638 DISEASES OF THE SPINAL CORD. the view, already expressed, of the myotic origin of the disease. The autopsy demonstrated the unusual extent to which the disease had advanced. In addition to the atrophy of the extremities, the muscles of the trunk were greatly affected. The pectoral muscles had disap- peared entirely, and the heart and diaphragm were both degenerated. Sections of the cord at all levels showed that the cells in the anterior horn were mainly in good condition, and seemed to be in their usual numbers. In most sections cells could be seen here and there pig- mented, or that did not stain well, or that had lost their processes, or in some way appeared degenerated. Such cells were, however, on the whole very few, and were not, in the author’s opinion, sufficiently degenerated to account for such universal and extensive muscular degeneration. In the upper lumbar enlargement an area of softening was discovered situated in the gray substance of one lateral half, inter- mediate between the anterior and posterior horns. It seemed to be the result of a comparatively recent haemorrhage. It cannot be entertained for a moment that the area of softening was in any manner related to the symptoms of pseudo-hypertrophic paralysis. Its situation in one half of the cord and in the lumbar region, and the fact that it did not involve any of the multipolar cells, precludes the possibility of its affecting muscles, especially those sup- plied from regions of the cord above the seat of the softening. The slightly degenerated appearance of some of the cells in the anterior horn probably ensued because they were useless, the muscular fibres which they supplied having disappeared. The nerve-roots were healthy. Thus it would seem that the weight of evidence tends to prove that pseudo-hypertrophic paralysis is not a disease of the central nervous system. The majority of observers agree upon the morbid changes which occur in the muscles. In the first stage there may be —as Pepper has shown, as my second case likewise exhibits, and as occurred in Therese’s1 case—atrophy of the muscular fibres instead of hypertrophy. A microscopical examination shows the transverse strife to be in process of disappearing, and in some of the fibrillae to have altogether gone. The connective tissue already shows a tendency to proliferation, but there is as yet no trace of that fatty degeneration and deposit which afterward becomes the most striking patho-anatomical feature of the disease. In the case which I have detailed, a portion of the primarily-atrophied left rectus femoris muscle was removed by Du- chenne’s trocar, and, examined with a fourth-inch objective, presented the appearance above described. In Pepper’s case not a single fibril of the deltoid muscle which he examined exhibited evidence of fatty degeneration, though the connective tissue was very greatly in excess 1 France Med., Paris, 1889, i., p. 814. PSEUDO-HYPERTROPHIC PARALYSIS. 639 of the normal proportion, and in places there were small collections of minute fat-globules or refracting granules. But in the form in which hypertrophy is a prominent feature there may or may not be hypertrophy of the muscular fibres. Virchow claims that hypertrophy of the muscular fibres is pathognomonic of the disease, but in Jacoby’s1 case there was a distinct diminution in the number of muscular fibres, some of which were small and some were normal, but none of them were hypertrophied. Middleton2 noted variations in thickness of the muscular fibres. In some instances they appeared hypertrophied, in others they did not. All observers agree that there is a notably-increased development of the connective tissue, with fatty infiltration, and fatty degeneration of the muscular fibres. As the process advances, the fibrillse in great part disappear, fat and connective tissue crowding them out, as it were, and eventually even this latter is in a great measure replaced by fat-vesicles. The muscle is now at its most advanced stage of hypertrophy. But the process is not yet complete, for a stage of secondary atrophy begins, the fat is absorbed, and finally nothing is left but a few degenerated muscular fibrillee and a mass of connective tissue. There is thus in the first place simply a change in the muscular fibrillae characterized by a disappearance of the transverse striaB. This is probably the first stage of the fatty degeneration, which is afterward manifested unmistakably. At the same time the connective tissue between the bundles of fibrillse and the fibrillse themselves is increased in amount. Then the disintegration of the muscular fibrillse becomes more evident, the connective tissue is still more increased, and fat- vesicles make their appearance between the fibrillse and the bundles of fibres. Finally, the muscular tissue mostly disappears, the fat is ab- sorbed, and connective tissue, with perhaps a few fibrillse, in a more or less advanced stage of degeneration, is all that remains. It is therefore evident, from what has been said, that pseudo-hyper- trophic paralysis is primarily a muscular dystrophy, beginning as an inflammation of the muscular tissue and connective tissue, and ending with a more or less complete degeneration. Treatment.—Duchenne, as we have seen, succeeded in curing two cases in their incipiency, with the faradaic current. Authors are agreed that, if anything is likely to prove successful, it is electricity in some one of its forms, and all cases have been treated with this agent. Thus far, however, not only is there no record of another cure, but there is scarcely the mention of even slight improvement. The disease has gone on slowly but certainly in its progress, unchecked by therapeuti- cal measures. Still we are not, on that account, to despair. I would recommend faradization and galvanization of the affected muscles, the application 1 Journal of Nervous and Mental Diseases, 1887. 2 Op. cit. 640 DISEASES OF THE SPINAL CORD. of heat, kneading the muscles, massage, and rest. Of these remedies I consider faradization the most important. It should be applied once or twice a day to all the implicated muscles. Internally, strychnia, iron, and phosphorus may be used, and bene- fit may be derived from their tonic virtues. This concludes what I have to say relative to the diseases of the spinal cord. I have endeavored to make the subject as plain as possi- ble, but, in the study of a class of diseases still to a great extent ob- scure in their medical relations, there must necessarily be defects in the description. In order to a better understanding of the normal and morbid anat- omy of the cord, as established by the most recent investigations, I have enlarged and modified from Flechsig and from Gowers a diagram of a transverse section, which will be found to give, on examination, very exact information. In it are clearly indicated the several divisions of the cord with the study of which we have been engaged. A. Anterior Median Fissure. B. Posterior Median Fissure. C. Intermediate Fissure. D. Anterior Gray Cornu. E. Posterior Gray Cornu. F. Gray Commissure, with Central Canal. G. Anterior Pyramidal Tract, or Uncrossed Pyramidal Tract, or Column of Tttrck. I. Anterior Root-Zones. K. Lateral Pyramidal Tract, or Crossed Pyramidal Tract. L. Direct Cerebellar Tract. M. Posterior External Column, or Column of Burdach. N. Posterior Median Column, or Column of Goll. P. Antero-Lateral Ascending Tract, or Column of Gowers. SECTION III. CEREBRO-SPINAL DISEASES. CHAPTER I. Although there are objections to the name employed to designate the terrible disease I now propose to consider, the same is true of all other terms which have been applied to it, and the present has the ad- vantage of being well known. So long as we are obliged, through ig- norance of pathology and morbid anatomy, to use a nomenclature based on symptoms, we must expect to be inexact. The name hydrophobia is as old as Galen, and still retains its preeminence, notwithstanding the fact that the symptom on which it is based is sometimes absent. Symptoms.—Beginning with the reception of the injury by which the body has been inoculated, we find that it heals in the ordinary way, and that there are no immediate signs of infection. At a period which varies greatly in different cases, pain or a sensation of uneasiness is usually experienced at the seat of the wound. This, however, is rarely of such intensity as to cause suffering, and probably would generally be overlooked or disregarded but for the apprehension which the pa- tient has, and which directs his attention to every sensation which can be attributed to the wound. But there may be absolutely no pain or uneasiness other than such as are met with in all wounds till the phe- nomena of the affection are manifested. The period between the re- ception of the injury and the beginning of the symptoms of hydropho- bia is known as the stage of incubation. The duration of this stage is variable. It is rarely shorter than a month, and probably never longer than two years. Instances are on record, however, in which the disease has been developed within ten days, and others, about which, however, there is much doubt, in which the latent period has reached to ten years and longer. The vast raa- HYDROPHOBIA. 644 CEREBRO-SPINAL DISEASES. Thus far the mental symptoms have scarcely been considered, but they are present almost from the first. Indeed, they may be among the very first indications of disorder. They consist of emotional disturb- ances of various kinds, and sometimes radical changes of character and disposition. It has been alleged by some authors that the dreams, at a very early period after inoculation, are connected with the animal giving the the wound. I have never met with this symptom, but in the case pre- viously cited, and which I saw twice in consultation, a circumstance still more remarkable is related by Dr. Cook. The patient, a child three years old, was bitten by a bitch in heat on or about August 20, 1870. On November 15th the mother noticed that he slept badly ; on the 16th, among other manifestations, he “ was cranky all day.” On the 17th he was seen by Dr. Cook.1 “ On entering the room,” the doctor, in his report of the case, “ and seeing several children, and not noticing any thing wrong with any of them, I very naturally inquired which was the patient. I was pointed to a little boy sitting at a table in a high chair. On approach- ing him, he turned his face toward me, revealing the most peculiar-look- ing eyes I have ever seen. They were not like those seen in persons suffering from delirium in prolonged fevers, nor yet like those we see in the second stage of cerebral meningitis, although somewhat resem- bling both of these conditions, but more like the eyes of a person in a fit of violent anger, slightly combined with a feeling of fear. “ When I reached out my hand to touch his, he shrank from me as from a blow, at the same time making a desperate effort to catch his breath, precisely as a naked person might if a pail of cold water was unexpectedly poured over him. This I understood to be a laryngeal spasm. It was very brief, lasting but the fraction of a minute, prob- ably not more than ten seconds. I took a seat a little distance from him, where I could see his every motion, and regarded him attentively for a long time. “ He seemed an unusually intelligent child, for one of his age, speak- ing very distinctly with a clear, ringing voice, which his parents in- formed me was a little unnatural, as it ‘ seemed strained.’ He had at times a disposition to stammer, which was also unnatural. For one hour after my observation commenced, he talked almost incessantly of dogs, and repeated very few sentences a second time. He seemed familiar with all the most common breeds, relating some anecdote of the bull-dog, the mastiff, the bird-dog, the spaniel, the coach-dog. and the poodle. “ Connected with all his naratives was a tragic or gloomy termina- tion. The mastiff, after carrying him an incredible distance about the city, finally disappeared through a bottomless hole in the street, he only 1 Op. cit., p. 81. HYDROPHOBIA. 645 escaping a similar fate by suddenly dismounting. The bull-dog, after bringing for his admiration and pleasure a great variety of puppies, sud- denly turned cannibal, and swallowed the whole lot. The spaniel, after having been his playmate for a very long time, finally took it into his head one day to get on to a coffin that was being carried through the streets, and ride away to reappear no more.” There were no other evidences of disordered mental action in this child, and he died, perfectly conscious to the last. Usually, however, this is not the case, and various morbid desires are entertained by the patient. Thus, in a case which I saw in this city in 1865, there was an impulse to strike those near, and an intense dislike of certain persons who had always been intimate friends of the patient. In both the other cases there were paroxysms of previous delirium, during which the sufferers bit and struck at all within their reach, and of which hallucinations and delusions constituted marked features. In the case of the boy just cited, the stories of dogs which he related were evidently delusions which he accepted as realities. The temperature is always elevated from the very beginning of the disease. It is rarely below 105° Fahr., and may rise as high as 110° during the height of a paroxysm or immediately after its cessation. Death usually takes place on the third day after the accession of the symptoms indicating the full development of the disease. The chief of these is laryngeal spasm. A fatal termination is rarely delayed till after the third day, though cases are not uncommon in which it has en- sued on the first or second day. In all the cases, except two, which have been under my observation, the third was the fatal day. In Dr. Cook’s the disease may be considered as having been fairly developed on the 17th of November, the first day in which any spasm of the throat was witnessed. Death resulted on the evening of the 18th. In June, 1874, I attended, in consultation with Dr. Alexander Hadden, my sixth case of hydrophobia. The patient, a man about twenty-five years of age, had been bitten about three weeks before by a dog not clearly identified. When Dr. Hadden first saw him on the 24th of June, at 8.30 p. m., the man was in bed, complaining of nervousness, soreness in his neck and throat, and a strange feeling of tightness around the chest. His countenance was anxious, his pupils were di- lated, and his general appearance was that of a person facing some im- pending danger, and not in extreme pain. He said his throat was sore, and that he could not swallow any thing, not even water. Examination showed that there was no congestion or inflammation of his throat. His pulse, respiration, and temperature, were normal, excepting that he occasionally sighed. There was also a little disposition to hack and spit. He complained of thirst, but said he knew he could not drink, for the very sight of water made him shudder. He was told to try, and some water was brought, but the sight of it caused a violent spasm. He CEREBRO-SPINAL DISEASES. 646 threw himself around in the bed backward and forward, and ordered the water to be taken away. He immediately afterward called for the goblet, said he was thirsty and must drink, seized it, and with a violent effort succeeded in taking a single swallow, which was followed by a severe convulsive shudder and contraction of the muscles of the neck and chest. Dr. Hadden, recognizing the symptoms of hydrophobia, asked if he had been recently injured by any animal. At first he replied in the negative, but on the doctor’s sajdng, “ Not by a dog ? ” he answered, “ Only slightly on the knuckle of the right hand by a little black dog belonging to a baker around the corner on the avenue.” He further stated that there was nothing the matter with the dog, for he had seen it afterward, and only about a week since it had been taken to the pound and the bite was inflicted three or four weeks before. For two days previously he had felt badly, was thirsty, and had drunk a good deal of water; and the evening before had gone out, but soon returned, saying he felt chilly. While taking a cup of tea at 6 p. m. that day (the 23d), he had experienced the first difficulty in swallowing. Shortly afterward, while going to the kitchen, a cool draught of air blew on him and caused him to stagger so that he nearly fell. The next morning Dr. Hadden saw him with Dr. Leavitt. “We found him in a frightful state of excitement; had broken down the bed, and was struggling with his attendants to get at liberty. He was shouting and cryipg out to them to let him go, and called for water, which, when brought, he could not drink. His mind was clear, and he knew all those around him; was spitting a viscid saliva, and was careful not to spit on any one, not even on his clothes. It was so abundant that his attendants were obliged to wipe it from his lips. Dr. Leavitt and myself, after viewing the case in all its aspects, concluded to inject in the tissue of the leg one-half a grain of morphine and one sixty-fourth of a grain of atropine in solution, which was done at 3 A. m. by Dr. Leavitt. We carefully watched the effect till 3.30 A. m., when his violence having in no way abated, another injection was given in the same part, of three-eighths of a grain of morphine and one-eighth of a grain of atropine, which in some degree produced the character- istic effect of morphine, and very clearly the appearances of the atro- pine; for, notwithstanding he was struggling violently, the saliva, which had been very troublesome, was completely dried up, so much so that the patient himself remarked that he was very thirsty, and his mouth felt as if he had been chewing a brick. Fifteen drops of chloroform were then injected, with no effects whatever, unless to weaken his al- ready weak and frequent pulse. At 4.15 A. m., three-eighths of a grain of morphine were again introduced under the skin, without atropine. This quieted the patient so that he was easily restrained, and he re- mained in this condition from 4.30 A. M. till 10 A. M., when the effects HYDROPHOBIA. 647 had so far passed off that the attendants were alarmed at his violence, and che abundance of saliva he was spitting from his mouth. Dr. Wil- liam A. Hammond saw him with me at this time. He supported the diagnosis and thought well of the treatment; he saw that it subdued vio- lence and suppressed the flow of saliva—the two most important feat- ures of this hopeless disease. At 10.15 A. m., by his order, three- eighths of a grain of morphia in solution were injected into the tissue of the thigh, which served to temper down the increasing violence of the spasms, but did not stop the flow of saliva. I accordingly, at 10.45 A. H., injected three-eighths of a grain of morphia and one-fortieth of a grain of atropia, which had the desired effect of producing the quieting effect of the morphia as well as the specific effect of the atropia on the salivary glands. The poisonous effects of the morphia and atropia were at no time apparent. He died at 4.15 p. m., June 26,1874, about twenty- four hours after the first spasm.” 1 As stated by Dr. Hadden, I was called to see the patient at about ten o’clock on the morning of June 26th. When I went into the room he was lying upon the floor pinioned, to a certain extent, and surround- ed with pillows to prevent him injuring himself. He was then spitting continually ; in fact, every expiration was accompanied by an effort to spit out the thick, tenacious mucus so characteristic of hydrophobia. His pupils were largely dilated, but, as Dr. Hadden stated, not more so than before the atropia was given. He was able to converse with tolerable fluency, and, when I put two or three questions to him, he an- swered, but not very directly. So far as I could make out, both from his answers and appearance, he was not suffering from acute pain. There was a good deal of movement of his limbs, not apparently spas- modic, for there seemed to be the element of volition in the actions he made with his arms and legs. He could not swallow fluids, and even a piece of ice given to him was ejected with force from his throat. His pulse was too rapid to be counted, and his respiration was hurried and irregular. I fully concurred in the suggestion to give him morphia for the pur- pose of moderating the intensity of his symptoms. A hypodermic in- jection was administered, and a sedative effect was produced. After I left, his paroxysms returned with great violence, and he died that after- noon. Generally death occurs during a spasm. This was the result in four of the six cases I have witnessed. In the others the patients died quietly, a consequence probably of the sedative medicines administered. When death takes place during the former condition it is probably due to apnoea ; in the latter, to exhaustion. In all cases the powers of life, 1 “ Report of a Case of Hydrophobia,” by Alexander Hadden, M. D., “ Proceedings of the New York Neurological Society,” Psychological and Medico-Legal Journal, Sep- tember, 1874, p. 166. 648 CEREBRO-SPINAL DISEASES. from the violent convulsions, the loss of sleep, and the deprivation of food, are drained away to their utmost. The most recent case of hydrophobia coming under my observation was that of a gentleman whom I saw at Haverstraw, New York, in consultation writh Dr. W. B. Bailey, of that place, on May 25, 1887. The patient was bitten on the thumb by a small pet dog which had been bitten some time before by a strange cur. On a previous occasion the patient had found a bone lodged in the dog’s throat, and, from the symptoms exhibited, thinking that something of this kind ailed the dog again, the owner put his hand down the animal’s throat, and the thumb, coming in contact with one of the sharp teeth, was slightly cut. A short time afterward the dog died. Little was thought of the wound at the time ; but in a few days afterward the thumb became painful and began to swell, and Dr. Bailey cauterized the wound. The swell- ing gradually advanced up the arm, and became so painful that he was unable to sleep. All this subsided, however, until almost exactly a month subsequent to the infliction of the wound the first manifesta- tions of hydrophobia made their appearance. I saw him on the fourth day, about six o’clock in the evening, and he was then in bed sleeping quietly, under the influence of morphia. When he awoke he was per- fectly rational, shook hands with me, and talked quite cheerfully. He said he was feeling better, and, to try him, I asked him in an off-hand manner if he would like a drink of w7ater. He answered “ No,” in a voice which showed great fear, and I noticed a twitching in the muscles of his throat that I had previously seen in hydrophobic patients. In order to satisfy myself completely in regard to the character of his disease, I told him that he would have to get up and take a drink. He replied that he would try, and I handed him a glass filled with water. As he took the tumbler in his hand he trembled violently from head to foot, and the muscles of his throat were again thrown into violent spasms. He made several unsuccessful attempts to raise the glass to his lips, but finally, with an almost superhuman effort, he succeeded. He managed to gulp down three swallows of the water, wdiich caused such violent convulsions of the throat, and seemed to put him in so much agony, that I took it from him. lie then got into bed and a hypodermic injection of morphia was given him and he sank into a peaceful slumber. Previous to my arrival he had had many severe spasms, but they had been quieted by morphia, and I advised that the administration of this drug should be continued. He died the day after I saw him. Causes.—It has generally been supposed that hydrophobia has but one source in the human subject, and that is inoculation by the saliva of an animal affected with rabies ; that it cannot be communicated to one individual of the human species by the saliva of another affected with hydrophobia ; and that neither dogs nor other animals can be in- HYDROPIIOBLi. 649 fected by inoculation with the saliva of a hydrophobic man. Magen- die’s experiment as to the latter point is considered by many to be of exceedingly doubtful value, as hydrophobia was, it is said, prevailing among dogs at the time, and that hence the animal may have been bitten. As we shall see hereafter, these suppositions are all more or less ill-founded. Thus it is very probable that the saliva of healthy animals, the dog especially, is, under certain circumstances, capable of producing hydro- phobia in man and other animals. A case of the kind is recorded in Sufeland’s Journal of December, 1839, and similar ones are frequently met with. In none of the cases I have witnessed was the dog which had inflicted the wound supposed to have been rabid. In one case which I saw in this city, with a physician whose name I cannot recall, the patient, a stableman, was bitten by a dog that was to all appear- ance in perfect health. In the case reported by Dr. Cook, the animal, a bitch, was being led quietly through the passage-way of the house, when the child became entangled in the chain, fell against the dog, and was bitten apparently in anger. The animal was well known, and was not even suspected of being hydrophobic. She was in heat ; and Dr. Cook raises, for the first time to my knowledge, the question whether this circumstance renders the saliva of the animal capable of inducing hydrophobia in the human subject. With a view of throwing as much light as possible on the subject, he consulted the records of Bellevue Hospital, in order to ascertain the facts in relation to a man who died of what was supposed to be hydrophobia from the bite of a bitch in heat. The result of his inquiries was to show very certainly that the man did die of hydrophobia ; that the animal was not rabid, and that she was in heat. In the case, the details of which have just been given, there was a good deal of doubt in regard to the identification of the dog which in- flicted the bite. The patient said he had been bitten “ by a little black dog belonging to a baker around the corner on the avenue.” But no such dog was known, and there was no baker “ around the corner,” on either Second or Third Avenue. The only dog that was known to have bitten the man was alive and well on the 7th of July, two weeks after- ward. In the present state of our knowledge it is useless to pursue this point of the inquiry further. It is one in regard to which certainty appears to be impossible of attainment. Fleming,2 however, seems to admit the possibility of an animal under strong sexual excite- ment being able to communicate hydrophobia to a healthy animal, when he says : 1 “ Dictionnaire des sciences medicales,” article “ Rage,” tome xlvii., p. 46. Also Journal de physiologie, tome i., p. 47. 2 “ Rabies and Hydrophobia,” London, 1872, p. 124. CEFvEBRO-SPINAL DISEASES. 650 “The hypothesis that certain ferments—an improper term—may be developed in great abundance in the saliva under the influence of psychical disturbance, would account for those instances in which rabies shows itself in dogs bitten by others which are excited or furious by sexual desire, though themselves healthy.” It would appear from certain experiments that the saliva is the only means of communication. Thus Dupuytren, Breschet, and Magendie endeavored to convey the disease by injecting the blood of dogs suf- fering from rabies into the veins of healthy dogs, but always unsuc- cessfully. The flesh, milk, semen, and abdominal secretions were like- wise found not to be media for transmission. On the other hand, Eckel, of Vienna, after several failures, inocu- lated a dog with the blood of a man who was affected with hydropho- bia. On the sixty-second day thereafter the animal was seized with unmistakable rabies and died. Fleming, however, from whom I quote this statement, says that it must not be forgotten that, at the time of these experiments, rabies was raging as an epizootic. But Bouley,1 who has investigated the whole subject of hydrophobia with great abil- ity, declares that it can be transmitted only by inoculation, and the only agent wdffch has the power of communicating it is the saliva, in which alone the virus exists. Any other liquid taken from a rabid ani- mal is ineffective. Inoculation by blood, even its transfusion, has failed to produce any results. He also says that all living beings affected with hydrophobia are capable of transmitting it ; that is, the saliva of all rabid animals is virulent, it matters not to what species they belong. Whether or not it originates spontaneously in the lower animals, it is very certain that it has no other origin in man than inoculation. Although there is no sure evidence on the point, there appears to be no room to doubt that hydrophobia may be communicated by inocu- lation from a person affected with the disease to an unaffected indi- vidual. Aurelianus, Enaux, and Chaussier, and others cited by Flem- ing, mention instances in which it has been induced in persons who have accidentally had the saliva of hydrophobic patients applied to their lips. Fleming2 states that in 1871 a girl named Bence died in Liverpool from hydrophobia. It was believed she had not been bitten, but the death of her little brother, from the disease, occurred about three weeks previously, and the supposition was that the virus had been communicated in some way to the girl through a wound in her foot. The fact that hydrophobia can be communicated from man to the lower animals is sufficiently well established by the experiments of Magendie, Breschet, Earle, and Renault. 1 “ Hydrophobia,” by H. Bouley, translated from the French by A. Liautaud, M. D., V. S., New York, 1874, p. 6. 2 Op. cit., p. 141. HYDROPHOBIA. 651 The wolf is said to be the most dangerous of all animals when rabid, for the reason probably that it seizes the neck or face, parts not fully protected by clothing, and thus the saliva is not so apt to be rubbed off as when the leg, for instance, is the part attacked. The slightest abrasion of the skin coming in contact with the saliva may be sufficient for inoculation. Cases are recorded in which the dis- ease has resulted from dogs licking the hand or face on which there were pimples or sores. Diagnosis.—That protean disease, hysteria, occasionally puts on the semblance of hydrophobia. Several cases of the kind have occurred to me, and, in all, the symptoms were in general character very much like those which are exhibited by genuine hydrophobia, though in some re- spects, perhaps, a little exaggerated. It will in these and similar cases —the result of fright and imagination—often be found that the patient has been bitten by a dog not long before. There is a want of consist- ency about the symptoms which of itself is sufficient to excite suspicion as to the real character of the phenomena. Thus, although at times the attempt to swallow will excite laryngeal and other spasms, these do not always occur under similar circumstances, and are not induced by those secondary and more refined influences, such as the sound of fall- ing water, bright lights in the face, excitations applied to the skin, see- ing others drink, etc., which so generally cause them in the real dis- ease. There are not the same anxiety and depression in the simulated disease as in the real, though the apparent emotional disturbance is much greater. The hysterical patient is loud in the expression of ap- prehensions, while the real hydrophobic one, though intensely anxious and terrified, endeavors to prevent others perceiving the state of his mind. The history of the case, the existence of the hysterical diathesis, and the fact that the symptoms come on soon after the bite without any period of incubation, will further aid in establishing the diagnosis be- tween the false and the real disease. The last case of the simulated disease which has come under my ob- servation was that of a policeman whom I saw in consultation with Dr. S. G. Cook i,n the summer of 1874. The man was then in the Park Hospital, held down on a bed, and snapping like a dog at every person who came in his way. At the sight of water he became intensely ex- cited, foamed at the mouth, and went through a series of fearful con- tortions of his limbs. But, when I took a glass of water in my hand and told him in a commanding voice to drink immediately, he swallowed the liquid without the slightest difficulty. The bromide of potassium in large doses was prescribed, and the next day all his symptoms had disappeared. On inquiry it was ascertained that he had been bitten by a dog several days before, and that his comrades had frightened him by their inquiries and sug- gestions. CEREBRO-SPINAL DISEASES. The fact that a disease resembling hydrophobia may be induced by physical derangement and by mental disturbance especially of the im- agination, and that death may be the consequence, is very well estab- lished, and may account for the apparently spontaneous instances, and for those cases of long incubation which are cited by authors. Thus M. Labadie Lagrave 1 quotes from Raymond (de Marseille) the case of a child twelve years old who became hydrophobic without known cause and died at the end of ten days. Also a case from Rouppe of a sailor who had convulsions and died hydrophobic without known cause, and another from Pouteau of a man who died in fifteen hours with symptoms of hydrophobia which had ensued on a violent paroxysm of anger. Berthier a refers to several similar cases occurring as the result of menstrual derangement. Fleming8 cites the instance of a woman who had been bitten in the face and who was admitted to the H6tel-Dieu in Paris. After a few days she was cured of her wounds and discharged. Going about her usual avocations one day she heard a man exclaim, “She has not gone mad, then ! ” From that time she could not swallow liquids, and on the same day was readmitted to the HOtel-Dieu, and this time to die of hydrophobia. The following case is also given by Fleming: “A woman in the clinic of Dr. Maisonneuve had been bitten by a dog, which was supposed not to be rabid, and the injury Cad healed; when two months after the accident she was me.t by two students, who had been with the doctor at the time, and who asked her if she was not yet mad. Immediately she was seized with nervous symptoms, became intensely anxious and un- easy, and went into the hospital in the belief that she was hydrophobic; She was put under the care of M. Laugier and the following day was evidently affected with the disease; hemiplegia appeared, with a vio- lent delirium, accompanied by an irrepressible amount of fear, and she died asphyxiated in forty-eight hours.” The temperature in all cases of pseudo-hydrophobia that I have wit- nessed was not above the normal standard. Hydrophobia has been confounded with tetanus, and some writers have regarded it as a modified form of this affection. The distinction is, however, so well marked that it scarcely seems necessary to dwell upon it. The facts that in tetanus the spasms are tonic, while in hydrophobia they are clonic ; that in the first-named they are mainly shown as regards the jaws and back, while in the latter they radiate from the throat; that in tetanus the mind is clear throughout, wdiile 1 Article “ Hydrophobie,” in “ Nouveau dictionnaire de medecine et de chirurgie pra- tiques,” tome xviii., Paris, 1874, p. 17. 8 “Des nevroses menstruelles,” Paris, 1874, p. 169. 3 Op. cil., p. 176. HYDROPHOBIA. 653 in hydrophobia more or less mental implication is always present, will suffice to render any mistake in the diagnosis of the two diseases impossible. From epilepsy the distinction is so obvious as not to require further mention. Prognosis.—There is no authentic instance on record of a cure of hydrophobia. Several such have been reported, but inquiry has always shown misstatement or error somewhere. The fact that the hysterical counterpart has several times been regarded as the real disease, is the main support for the opinion of some authors that the affection is curable. Several years ago Dr. Ligget,1 of Maryland, reported a case of hy- drophobia cured by calomel. A careful examination of the details of this case excites very grave doubts in my mind in regard to its really being an instance of the disease in question. The subject was a negro-woman who had been bitten about two weeks before any symptoms were manifested. The dog was lying quietly in the yard, and bit her in the great-toe as she was teasing him with her foot. The animal was at once chained up, and died in two or three days with “ all the symptoms of rabies canina in its most virulent form.” It does not appear that the doctor saw the dog, and it is very probable that the rigid confinement would have caused the animal to exhibit symptoms which would easily be mistaken by laymen for those of hydrophobia. Again, the period of incubation was unusually short, and the symp- toms, as detailed by Dr. Ligget, are clearly not those of hydrophobia. Thus, although he repeatedly states that there was inability to swallow liquids, there is no distinct mention made of the pathognomonic laryn- geal and pharyngeal spasms which occur in hydrophobia, and which are so frightful in character. The convulsions all appear to have been gen- eral, and there was a “ horror ” of water, wffiich is not a phenomenon of the true disease. For these reasons I am constrained to believe that the disease treated by drachm-doses of calomel was in reality one of hys- teria which assumed the form of hydrophobia. In this opinion I am sustained by an eminent medical gentleman residing in Dr. Ligget’s neighborhood, who, as the latter admits, declared the affection to be “ a case of that protean disease, hysteria, simulating hydrophobia.” Calomel has been repeatedly tried before and since Dr. Ligget’s case, but without effect. But, although the prognosis is so hopeless in the developed dis- ease, it is much more favorable as regards the probability of the supervention of hydrophobia from the bites of rabid animals ; for, of 1 “ Case of Hydrophobia successfully treated with Drachm-Doses of Calomel,” Amer- ican Journal of Medical Science, January, 1860, p. 96. 654 CEREBRO-SPINAL DISEASES. those bitten by dogs unmistakably affected with the disease, not more than one in fifteen becomes successfully inoculated. This liability differs greatly according to the circumstance of the part being cov- ered or not. The wounds of the face, neck, or hands, are much more likely to be followed by hydrophobia than those inflicted on the legs or feet, where the virus is rubbed off by the clothing before the teeth reach the flesh. The bite of a rabid wolf is more apt to be followed by the dis- ease than the bite of a dog, for the reason that the first-named gen- erally seizes the throat or face. Thus, Trolliet states that at Brives, in France, seventeen persons were bitten by a rabid wolf, of whom ten died of hydrophobia ; and, of twenty-three bitten by another, thirteen died. On the other hand, Hunter states that on one occasion a dog bit twenty persons, of whom only one was inoculated. Those first bitten by a rabid animal are more liable to have hydrophobia than those bit- ten subsequently, when the poison is in a measure exhausted. Proba- bly the most dangerous wounds are those which barely penetrate the epidermis, and in which, therefore, the venom is not washed away by any flow of blood. Morbid Anatomy.—Within the last few years the study of the mor- bid anatomy of hydrophobia has led to results which may be considered, at least for the present, as determining, with some degree of exactness, the situation and character of the essential lesions of this terrible dis- ease. In 1869 Meynert examined microscopically the spinal cords of a boy and girl, patients at Oppolzer’s clinic, who died of hydrophobia. In the first case, he found thickening of the walls of the spinal ves- sels, amyloid degeneration and nuclear proliferation of the cells of the neuroglia. In the second case, the neuroglia of the posterior columns of the cord was hypertrophied, through swelling of the stellate bodies. In the antero-lateral columns there were granular and amyloid degenera- tion, and numerous distended blood-vessels. The cortical substance of the brain exhibited the presence of a large number of lacunae with colloid masses. The nerve-cells of this part were the seat partly of molecular disintegration, and partly of sclerotic enlargement. Next are the observations of Dr. Clifford Allbutt,1 who examined the nerve-centres in two patients, who died of hydrophobia while in- mates of the Leeds General Infirmary. Throughout the brain and spinal cord there were evidences of great vascular congestion with transudation into the surrounding tissue. In several places the walls of the vessels 1 “ Specimens illustrating the Pathological Anatomy of Hydrophobia,” “ Transactions of the Pathological Society of London,” vol. xxiii., p. 16, 1872. HYDROPHOBIA. 655 were thickened and there were here and there patches of incipient nuclear proliferation. There were also haemorrhages into the mednlla oblongata. In many places there was a refracting material to be seen outside of the vessels, which probably was of the nature of a coagulated fibrinous exudation. Finally, Dr. Allbutt found in the encephalon occa- sionally, and in both spinal cords, and especially in both medullas, little gaps caused by the disappearance of nerve-strands which had passed through the granular degeneration of Clarke. These phenomena, adds Dr. Allbutt, point to the action of an animal poison acting primarily on the cerebro-spinal nervous system. Then in July, 1S74, were my own researches,1 made at Dr. Hadden’s request, in the case, the details of which, as observed during life, have just been given. As preliminary to the description of the microscopical appearances, it may be stated that, on removing the calvarium, the membranes of the brain were found to be congested, but there was no appearance of serous effusion to an abnormal extent either in the sub-arachnoidal space or in the ventricles. The substance of the brain was only slight- ly congested, but the consistence, especially of the cortical tissue, was somewhat less than normal. The cerebellum appeared to be healthy, as did also the pons Varolii, the corpus striatum, the optic thalamus, and other ganglia, with the exception of the medulla oblongata, which seemed to be slightly softened. The membranes covering it and the upper part of the spinal cord were congested. I took for examination (1) portions of the cortical substance of the brain ; (2) sections of the corpus striatum ; (3) sections of the optio thalamus ; (4) sections of the cerebellum ; (5) the pons Varolii ; (6) the medulla oblongata ; (7) a section of the spinal cord at the level of the second pair of cervical nerves ; (8) a portion of the pneumogastric nerve from the neck: 1. Cortical substance of the brain. My examinations of this tissue were made upon specimens which had been kept in absolute alcohol eighteen hours, in glass tubes sur- rounded with ice. I experienced no difficulty in cutting sufficiently thin sections. In all the sections the following conditions existed (ob- ject-glass one-fourth inch): a. The blood-vessels were increased in size and number, and their walls appeared to be thickened. b. There were minute extravasations of blood throughout, in some of which the blood-disks could still be distinguished, but in most of them they were broken down. c. The external layer of nerve-cells had almost entirely been re- placed by fatty matter in the form of oil-globules. The cells that re* 1 “Proceedings of the New York Neurological Society,” July 7, 1874, in Psychological and Medico-Legal Journal, September, 1874, p. 169. 656 CEREBRO-SPINAL DISEASES. mained were filled with a highly-refracting granular material, which was also oil in very minute particles. None of these cells were bi-nu- clear. Amyloid corpuscles were discovered generally at the junction of this with the next stratum. d. The second layer of cells had also to a great degree been re- placed by fat, but not to the same extent as the outer layer. It is well known that -this layer is composed of more numerous and larger cells than the outer ; but there was no doubt of their atrophy or dis- appearance. e. The third layer, composed of large cells, was scarcely affected. A few oil-globules were seen, and occasionally an amyloid corpuscle. The remaining strata were not involved, so far as I could see, to the slighest extent. In Fig. 98 a vertical section of the cortical substance is seen: 1, the Fig. 98. outer or peripheral stratum ; 2, the second layer ; 3, the third layer or large cells. 2. The corpus striatum, the optic thalamus, and the cerebellum were in an apparently normal condition, though there was some evidence of arterial injection. 3. The pons Yarolii was not examined in the fresh state, but was placed entire in a solution of bichromate of potash to harden. Subse- quently examined, it was found to be the seat of extravasation of blood, and the vessels were enlarged and their walls thickened. 4. The greater portion of the medulla oblongata was also placed in HYDROPHOBIA. 657 the bichromate of potash solution, but several sections were made after the part had been in absolute alcohol surrounded by ice for twenty- four hours. a. The first of these was made through the olivary bodies, at the level of the floor of the fourth ventricle, so as to include the nuclei of the pneumogastric and hypoglossal nerves. Numerous extravasations of blood could be seen with the naked eye, but with an inch objective they were more clearly made out. The ves- sels were then seen to be enlarged and more numerous than in the nor- mal condition. The gray matter forming the nuclei of the pneumogas- tric and hypoglossal nerves was observed to be of a distinctly granular appearance, and the roots of the nerves presented a like characteristic. In other respects the section exhibited nothing abnormal. b. Examined with a fourth-inch objective, this granular matter of the nuclei was seen to consist of oil-globules and amyloid corpuscles. The cells were ascertained to be atrophied both in size and numbers. Indeed, they had almost entirely disappeared. Of course it was not pos- sible, in a fresh and unprepared preparation, to form any definite idea of the relative proportion of nerve to neuroglia cells, but the deficiency of all cell-structure was very remarkable. (Fig. 99, a, oil-globules; b, amyloid bodies ; c, nerve-cells ; d, blood-vessels.) Fig. 100. Pig. 99. c. The nerve-roots, when examined in like manner, were seen to have undergone a similar change, the granular matter consisting en- tirely of fat, mainly in the form of oil-globules (Fig. 100). 658 CEREBRO-SPINAL DISEASES. Sections made immediately below the level of the point of the calamus scriptorius, so as to include the main root of the spinal ac- cessory nerve and its nucleus, exhibited almost exactly the same appearances. 5. The Spinal Cord.—The section of the cord was made at a point about midway between the first and second cervical nerves. The gray matter of the anterior and posterior horns was found in a state of granu- lar and fatty degeneration, the cells atrophied, and the nerve-roots in Fig. 101. a similar condition. In the white matter, both of the anterior and posterior columns, there was nuclear proliferation of the neuroglia- cells (Fig. 101). 6. The peripheral portion of the pneumogastric nerve, carefully removed by my assistant and placed in strong alcohol, exhibited a red appearance, but this may have been due to imbibition. Benedict,1 about the time of my own observations, made a series of researches into the morbid anatomy of hydrophobia as met with in dogs. His results were— 1. The vessels situated between the cerebral convolutions were distended with blood, and their external walls were coated with an exudation of a highly refractive material consisting of granules. 2. Numerous cavities were found to exist in the gray matter of the brain, and these were filled with a like granular, highly refracting ma- terial similar to that found in the walls of the vessels. 1 “ Die anatomisehen Yeranderungen bei der Lyssa des Hundes,” Wiener medicinische Presse, July 5, 1874. HYDROPHOBIA. 659 3. Masses of myeline, indicative of softening, and chemical changes of the nerve-tissue, were also discovered. Benedict regards the appearances as identical with those which Lockhart Clarke has considered as indicating granular degeneration. From the foregoing data it will be perceived that at last something definite has been ascertained relative to the morbid anatomy of hydro- phobia. Whether we regard the condition, according to Benedict, as an acute exudative inflammation, or as a granular degeneration, is of no con- sequence so far as the facts are concerned. Whether on the one hand the granular matter is an exudation, or whether it results from degenera- tion of the nerve-tissue, are points which will probably ere long be cleared up. My own view is in accordance with that of Lockhart Clarke, who, detecting a like change in other affections of the nerve-centres, views it not as an exudation but as a degeneration. As to the gross lesions, congestion of the brain and spinal cord has been found by many observers. Sometimes the nerves at the wound are inflamed, but this is not a uniform occurrence. The eighth pair has been found to present a pink- ish appearance in some cases. In four cases in which the blood was examined by Schivardi,1 infusoria of the genera bacterium, monas, vibrio, and torula, existed. The fauces, pharynx, larynx, trachea, and lungs, are generally found reddened and congested, as much from the asphyxia as from any spe- cific influence of the disease. Pathology.—Even if we had no information relative to the morbid anatomy of hydrophobia, no one who has ever witnessed a case could fail to perceive the implication of the hemispheres, the medulla oblon- gata, and the spinal cord. The hallucinations and other mental phe- nomena point to the hemispheres ; the irregular action of the respira- tory muscles and the heart, together with the gastric derangement and pharyngeal convulsions, indicates the implication of the pneumogastric nerves ; and the spasms of the larynx point to the origins of the spinal accessory nerves in the spinal cord. Since we have arrived at some degree of exactness relative to the lesions in the disease, we cannot fail to have our conviction on these points strengthened. The nature of the virus is unknown. It is probably of the nature of a ferment, but this cannot be regarded as satisfactorily proved. In 1820, Dr. Marochetti observed, in the Ukraine, that during the formative period of hydrophobia small vesicles or pustules formed un- der the tongue, and that, if these were opened and cauterized, the fur- ther development of the disease was prevented. I have never been able to find these formations, but they were recognized, two years after Marochetti published his account, by Magistral, in France. This latter opened and cauterized them in the manner recommended by Marochetti 1 “ Observations nouvelles sur la rage,” Besan9on, 1868, p. 22. 660 CEREBRO-SPINAL DISEASES. in ten cases, in five of which, nevertheless, the affection went on to full development, and the patients died. I am not aware that any one else has discovered these pustules. For full details relative to hydrophobia as it appears in dogs, I must refer the reader to the late Mr. Youatt’s excellent book on canine madness, and to the more recent and thorough treatise of Fleming. I may state that it is very clearly established that canine rabies is not so frequent in very hot as it is in temperate or cold weather; that it is not induced by thirst or improper food, or by preventing copulation. Is hydrophobia primarily a disease of the nerve-centres or a blood- disease ? I suppose it is utterly impossible, in the present state of our knowledge, to answer such a question. It may start as a blood-disease and end as a nerve-disease. Blood-diseases lead to structural changes of various organs of the body, and the nerve-centres are likewise in- volved to a considerable extent. Is it not worth while to call attention to the numerous instances of blood-diseases which produce structural changes ? Hydrophobia may be a blood-disease, and yet afterward be succeeded by changes in the nerve-centres. It is not necessary to suppose that hydrophobia is a nerve-disease from the beginning. It is perfectly possible, however, that it may be, and there are a great many instances which can readily be adduced in proof of this assertion. Take tetanus for example. Very few pathologists pretend to say that tetanus is a blood-disease. It is a disease propagated through the nerve-tissue starting from injury of a peripheral nerve, and inducing structural changes in the spinal cord. Dr. Lockhart Clarke, as we have seen, has ascertained in a number of cases that the essential condition of tetanus is a granular degeneration of the cord, and that is, probably, only the beginning of the fatty degeneration I find in hydrophobia, and yet there is no suspicion of blood-poisoning in tetanus. Hydro- phobia presents many analogies to tetanus, not only in its morbid anat- omy but in its natural history. Epilepsy can be caused by injuries to peripheral nerves. I had a case some years ago of a lady who wounded her thumb, and six months afterward she had epileptic paroxysms, which were preceded by an aura originating in the cicatrix. And if epilepsy—which is another one of the spasmodic diseases—can be induced by a simple wound, why not hydrophobia ? So that we have examples of analogous diseases caused by wounds of nerves, without the necessity of supposing the blood to be primarily affected. Still, there cannot be much doubt that the poison in the saliva, and not the wound made by the animal’s teeth, is the essential influence producing hydrophobia. It is not at all certain, however, that the lat- ter may not in some cases produce a modification of the characteristics of the disease, perhaps causing those tetanoid phenomena which are oc- casionally present. HYDROPHOBIA. 661 Treatment.—The measures of treatment relate to those proper im- mediately after the infliction of the wound, with the view of preventing the development of the disease, and those advisable after the affection is unmistakably manifested. Under the first category comes excision, which should be performed as soon as possible, and which is probably the best of all prophylactics. The operation should not be done with a niggardly hand, but every part with which the teeth of the animal have come in contact should be re- moved, as well as the tissue into which the poison may have become infiltrated. Previous to the operation, in fact as soon as the wound has been received, a tight ligature should be bound around the limb immediately above the injury, and, after the knife has done its work, cupping-glasses should be applied over the spot, till the tissues in the vicinity are thoroughly drained of blood. I have performed excision, for the wounds received from dogs certainly rabid, eleven times, and always with the effect of preventing hydrophobia. Cauterization may be performed instead of excision, and is preferred by some practitioners. Mr. Youatt used it with over four hundred per- sons bitten by rabid animals, and never unsuccessfully. Four times he employed it on himself, but there is a strong probability that the prac- tice at last failed with Mr. Youatt himself, for he committed suicide while supposed to be suffering from the initial symptoms of hydropho- bia. He preferred the nitrate of silver as an escharotic. Others have made use of the actual cautery, caustic alkalies, the mineral acids, arsenic, chloride of zinc, and carbolic acid. I have employed cauteriza- tion seven times—four with the nitrate of silver and three with the actual cautery—upon persons bitten by rabid dogs, and always with success. Mr. Youatt at one time had faith that the Scutellaria lateriflora, or scullcap, was a preventive. He moistened three pieces of tape with the saliva of a rabid dog, and inserted them as rowels into the skin of three dogs. To two of these he gave Scutellaria combined with bella- donna, while the third was left to itself. On the twenty-ninth day after the inoculation this latter became rabid, while the others, several months afterward, were alive and well. Notwithstanding this experience, it would not be justifiable in the physician to neglect performing either excision or cauterization as soon as possible after the reception of the bite. Even if several weeks or months have elapsed, one or the other—preferably excision—should be performed. The researches of Pasteur relative to the production and prevention of hydrophobia have not yet, in my opinion, led to any definite results. It would appear, from accounts that have reached us from France, that many persons inoculated after Pasteur’s method have subsequently CEREBRO-SPINAL DISEASES. died of hydrophobia, while it is very certain that many who have been inoculated in Pasteur’s Institute in Paris had not previously been bitten by rabid animals. In this country such statistics as have been published are to the like effect.1 It would certainly, therefore, be pre- mature, in the present state of our knowledge, to give an adhesion to the Pasteur method. On the contrary, after due consideration, I am inclined to express the opinion that it is not so sure a preventive of hydrophobia as is early excision or cauterization. Were I myself so unfortunate as to be bitten by a hydrophobic animal, I would not sub- ject myself to inoculation after the process in question. As to the treatment of the fully-developed disease, there is noth- ing, in my opinion, which has hitherto succeeded in arresting its onward course. Cases of cure have been reported, but, as already stated, they are open to the suspicion of not being true instances of the disease. Excessive bloodletting has been reported as a successful remedy ; injection of warm water into the veins dissipated the paroxysms in a case reported by Magendie, the patient, however, dying ; and nearly every stimulant, narcotic and sedative, in the materia medica has been used. In the case which I saw with Dr. Cook, and which has already been cited, the hydrate of chloral was administered. The effect certainly was to mitigate the severity and frequency of the spasms, but it was, as Dr. Cook states, given too late in the course of the disease to pro- duce any permanently curative result. In the present state of our knowledge I should be more disposed to rely on the hot-air bath at a temperature of about 200° Fahr., and the administration of hydrate of chloral in large doses frequently repeated, than on any other plan of treatment. In Dr. Cook’s case the Turkish bath was proposed, but the parents of the child would not consent to its use. Hypodermic injections of morphia and atropia may be used with some advantage to mitigate the force of the paroxysms. Before concluding my remarks on hydrophobia, it is proper to allude to the attempts of Dr. Schivardi,® of Milan, to cure the disease by the primary galvanic current. In one case the current was feeble, and was continued for nineteen hours. Great improvement ensued ; the oppression disappeared, and the dysphagia was entirely relieved. Through some misunderstanding, advantage was not taken of these ameliorations, and the patient was allowed to die. In the other case, which was one of undoubted hydrophobia, oc- curring in a girl nine years old, the current from twenty-two Daniell’s cells was employed. The current was passed from the soles of the feet to the forehead for fifty-eight hours almost continuously, and the duration of the disease prolonged to seven days and seven hours, when 1 See Medical and Surgical Reporter, July 5 and October 25, 1890. 2 “ Observations nouvelles sur la rage.” EPILEPSY. 663 the patient died. During the last two days there were no hydrophobic symptoms. Further trials are necessary before the therapeutical value of gal- vanism in hydrophobia can be ascertained. CHAPTER II. EPILEPSY. Epilepsy, although only a symptom of a morbid condition, must for the present be considered as a disease, for the reason that we are not able to designate with certainty its exact seat, or the nature of the lesion which exists. It is characterized by paroxysms of more or less frequency and severity, during which consciousness is lost, and which may or may not be marked by slight spasm, or partial or general con- vulsions, or mental aberration, or by all of these circumstances collec- tively. The essential element of the epileptic paroxysm is loss of con- sciousness. Without that there is no true, fully-formed epileptic par- oxysm. Symptoms.—Although in many cases there are no precursory phe- nomena, it often happens that there are indications of an approaching attack. These are exceedingly variable in character and situation. They may consist of pain in the head, a sensation of constriction or fullness, vertigo, noises in the ears, a feeling as if the ears are stopped with cotton or water, flashes of light, or sudden blindness, illusions or hallucinations of any of the senses—irritability of temper, extraordinary cheerfulness, difficulties of speech, pains in various parts of the body, especially in the stomach, bowels, or ovaries, sensations of numbness or of tingling, or of an indescribable character, which begin in an ex- tremity or in some other region, and appear to pass rapidly to the head —a feeling of constriction in the throat, vomiting, sudden evacuation of the bladder or rectum, erections of the penis, with or without the sexual orgasm, and discharge of semen, with many others of almost every pos- sible description. The prodromata may precede the attack by a considerable period, but usually are only a few moments in advance of it. Indeed, often the interval is so short that they may be regarded as a part of the paroxysm. The sensations of numbness or tingling, or of an electric shock, as a sharp stab, or blow, or pain, which precede the attack and which origi- nate in different parts of the body, and in some cases seem to run rap- idly toward the head, are called auras. Sometimes this aura is fixed, and may consist of various derangements of sensation besides those above 664 CEREBRO-SPINAL DISEASES. mentioned. In a number of my patients it has been a sensation at the pit of the stomach, such as that produced by a slight feeling of hunger or of anxiety. Again, it has consisted of a sharp impression on the tongue; at others of a subjective sense of smell, and again colored visions, or hallucinations of sight. In regard to these aurae of colors, Dr. Hughlings Jackson1 has made some interesting observations. He finds that red is the color which is usually seen first, though the others may follow in such rapid succession as to present an image of all the primary colors. Loss of the power to see colors (color-blindness) is generally first shown as regards red; and if this affection advances, the insensibility is progressively shown tow- ard the violet end of the spectrum. So in the epileptic chromatic hyperesthesia, the formation of colors is in the same direction, and hence red is first perceived and violet last—theoretically, at least, for there are not yet sufficient data collected to enable us to speak with any degree of certainty on the subject. There are exceptions, how- ever, for Dr. Jackson cites the case of one of his patients who always saw blue just before an attack. In my own experience, red has been invariably the predominating color, and in most cases the only one. The case of the gentleman who, just before his paroxysm of epilepsy, saw an old woman clothed in red approach him, with a stick raised in a threatening manner, and the fit coming on as soon as the blow fell on his head, is well known. Two similar instances have come under my own notice. Other derangements of sight may coexist with the chromatism as epileptic aurae. Thus, Sauvages2 mentions the fact that a woman sub- ject to epilepsy saw during the paroxysm dreadful spectres, and that real objects appeared magnified to an extraordinary degree ; a fly seemed as large as a fowl, and a fowl appeared equal in size to an ox. In colored objects, green predominated with her, a fact which Ferrier states he has met with in other convulsive diseases. He also states that a very intelligent boy, who was under his care for convulsions of the voluntary muscles, when he looked at some large caricatures, glar- ingly colored with red and yellow, insisted on it that they were covered with green, till his paroxysm abated, “ during which his intellects had not been at all affected.” A young lady, who had overtasked her mind at school, was thrown thereby into what I regarded as a more or less hysterical condition, but which some authorities would probably consider epileptic. She saw spectres of various kinds all day, but every real object at which she looked appeared to be of an enormous size: a head, for instance, seemed to be several feet in diameter, and little children looked like giants. 1 British Medical Journal, February 7, 1874. 2 Reported by Ferrier, in “An Essay toward a Theory of Apparitions,” London, 1813, p. 86. EPILEPSY. 665 When I took out my watch, while examining her pulse, she remarked that it was* as large as the wheel of a carriage. In the case of a young gentleman, now under my care for epilepsy, the attacks are invariably preceded by a period which lasts several hours and sometimes a whole day, during which he “sees small.” Every thing appears to be of infinitesimal size. This phenomenon I have never seen noted by any other writer on epilepsy. Aurce connected with the sense of hearing are uncommon, except such as merely consist of tinnitus—roaring, buzzing, singing, etc.— these are often met with. But in one case there were distinct hallu- cinations of hearing preceding the attack, the patient always fancying that he heard his name repeatedly called. An aura may be entirely manifested by dreams or delusions. As an instance of the first I quote the following remarkable case from my trea- tise on “ Sleep and its Derangements.” The patient occasionally visits me for medical advice, but has had no epileptic paroxysm for over four years. “ A lady of decided good sense had an epileptic seizure, which was preceded by a singular dream. She had gone to bed feeling somewhat fatigued with the labors of the day, which had consisted in attending three or four morning receptions, winding up with a dinner-party. She had scarcely fallen asleep when she dreamed that an old man clothed in black approached her, holding an iron crown of great weight in his hands. As he came nearer she perceived that it was her father, who had been dead several years, but whose features she distinctly recollected. Holding the crown at arm’s length, he said: ‘ My daughter, during my life- time I was forced to wear this crown; death relieved me of the burden, but it now descends to you.’ Saying which, he placed the crown on her head and disappeared gradually from her sight. Immediately she felt a great weight and an intense feeling of constriction in her head. To add to her distress she imagined that the rim of the crown was stud- ded on the inside with sharp points which wounded her forehead so that the blood streamed down her face. She awoke with agitation, excited, but felt nothing uncomfortable. Looking at the clock on the mantel- piece, she found that she had been in bed exactly thirty-five minutes. She returned to bed and soon fell asleep, but was again awakened by a similar dream. This time the apparition reproached her for not being willing to wear the crown. She had been in bed this last time over three hours before awakening. Again she fell asleep, and again, at broad daylight, was awakened by a like dream. “ She now got up, took a bath, and proceeded to dress herself, with her maid’s assistance. Recalling the particulars of her dream, she rec- ollected that she had heard her father say one day that in his youth, while in England, his native country, he had been subject to epileptic convulsions, consequent on a fall from a tree, and that he had been CEREBRO SPINAL DISEASES. 666 cured by having the operation of trephining performed by a distin* guished London surgeon. “ Though by no means superstitious, the dreams made a deep im- pression upon her, and, her sister entering the room at the time, she proceeded to detail them to her. While thus engaged she suddenly gave a loud scream, became unconscious, and fell upon the floor, in a true epileptic convulsion. This paroxysm was not a very severe one. It was followed in about a week by another, and, strange to say, this was preceded as the first by a dream of her father placing an iron crown on her head, and of pain being thereby produced.” Subsequently this lady had two other attacks, at intervals of several months, and both were preceded by the dream of the iron crown. In the case of a gentleman formerly under my treatment for epi- lepsy, the fits were invariably preceded by dreams of troubles of the head, such as decapitation, hanging, perforation with an auger, etc. It is probable that in such cases as the foregoing, the dream is ex- cited, as dreams often are, by derangements of sensibility, which are themselves the auras. In some cases the aurae are entirely psychical, consisting of illusions, hallucinations, or delusions. Delusions are not common as aurae. I have, however, had one case in a lady, who had an epileptic seizure immediately after hearing of the death of a gentleman to whom she was engaged to be married, and whose subsequent paroxysms were almost always preceded by the delusion that she was going to be killed. There was no exaggeration of motility, but the delusion was firmly held and acted upon, to the extent that she would give away her effects, and make other preparations for her death. The following day the fit usually occurred, although sometimes it was delayed for two days. Delasiauve,1 of two hundred and sixty-four cases, found the parox- ysms unannounced in one hundred and one, and with precursory phe- nomena in one hundred and eighty-three. The prodromata were im- mediate in one hundred and fifty cases. These he divides into seven categories, as follows. It is to be recollected that cases may appear un- der one or more categories, according as the prodromata, as is often the case, are met with simultaneously in different pa.rts of the body : First Series.—Precursory Signs in the Head.—Seventy-five cases. Vertigo, flashes of light 33 Headache, weight in the head 15 Heat of face 3 Various localized sensations 13 Indefinite sensations 1 Illusions, hallucinations, and other sensorial aberrations 9 Rotation of the head or of the eyes 5 Grinding of the teeth, derangement of the motility of the tongue 2 Tendency to sleep 1 Constriction of the throat 3 1 “ Trait6 de l’epilepsie—histoire—traitement—medecine legale,” Paris, 1854, p. 47. EPILEPSY. 667 Second Series.—Precursory Signs in the Throat.—Twenty-two cases. Oppression of the chest and sense of suffocation 9 Sensation of a ball or of motion in the pectoral region 2 Shivering sensation of cold or of an aura 5 Pain or heat 4 Palpitations, spasms 2 Third Series.—Precursory Signs in the Abdomen.—Thirty-two cases. Pain with or without oppression, eructations, vomiting 13 Intestinal or uterine colic 3 Sensation of a ball 3 Sensation of cold, of a vapor, etc 6 Stomachal heat 1 Undefinable sensations 6 Fourth Series.—Precursory Signs in the Extremities.—Ninety four cases. Numbness, contractions, jerkings, retractions, cramps, formications, etc.. 36 Pain with or without spasms. 13 Tremblings 10 Aura or phenomena approaching thereto 20 Undefinable sensations 15 Fifth Series.—Precursory Signs, consisting of General and Tim definable Sensations.—Twenty-two cases. General agitation or rotation of the body 8 Condition of discomfort, fainting, etc ! 6 Yague sensations 7 Moroseness 1 Sixth Series.—Precursory Signs situated in the Genital Organs. —Five cases, such as retraction of the testicles, aura starting from the testicles and spermatic cords, sensations located in the uterus, etc. Seventh Series.—Exceptional Cases.—Desire to defecate, to uri- nate, profuse perspiration, etc. The Paroxysm.—Great differences are observed in the character and severity of the paroxysm. Ordinarily two varieties are recognized, the petit mcil or slight attack, and the grand mal or severe seizure. The first is unattended by marked spasm or agitation ; the latter is characterized by more or less violent tonic and clonic convulsions. These divisions are, however, not regarded as sufficiently precise by those who have studied the disease in question with care and precision, and more minute classifications of the phenomena of the epileptic par- oxysm have accordingly been made. The one which I have used in my lectures at the University Medical College for several years past is less 668 CEREBRO-SRINAL DISEASES. complex than some others, and embraces all the known varieties. It is as follows: 1. Momentary unconsciousness without marked spasm. 2. Unconsciousness with evident though local spasm. 3. Unconsciousness with general tonic and clonic convulsions. 4. Irregular or aborted paroxysms. 5. Recent investigations have led me to the recognition of a dis- tinct form of epilepsy characterized by hallucinations, and to which I have ventured to propose the name Thalamic Epilepsy. Besides these several varieties, there are certain accompaniments, such as hysteria, mania, and paralysis, which will require consideration. 1. Momentary Unconsciousness without Evident Spasm.—The pa- tient is perhaps standing, engaged in conversation, when a momentary blank in his mental processes occurs. It probably does not attract attention ; it is instantaneous, disappears, leaving no feeling of dis- comfort after it, and there is an almost immediate continuance of his thoughts and speech. Or he may be walking in the street when the accession occurs. lie loses himself for an instant, but he continues to walk, and does not even stagger. ' In somewhat more severe seizures, if conversing, he stops sudden- ly, stares vacantly but fixedly for a moment, and may drop anything which he has in his hand. ’ If walking, his steps are arrested for an instant, he staggers, and would fall but for the quick return of consciousness. Such is the general character of these absences, faints, spells, etc., as they are popularly called ; varying, however, according to the cir- cumstances of the moment and the condition of the patient. They fre- quently exist for a long time without the patient paying much atten- tion to th6m. In a gentleman now under my charge they occurred several times in the course of the day when walking, riding on horse- back, sitting quietly in his library, engaged in conversation, or eating. The continuity of his acts was scarcely interrupted, and those about him never noticed that anything was wrong. In the case of a young lady they occur generally at the dinner- table. She drops her knife and fork, looks steadily to the front, ceases to eat, and in about two seconds resumes her occupation with a long- drawn inspiration. Those near her observe that her countenance be- comes very pale, and that she does not hear or see. Sometimes these attacks, slight as they are, are followed by pain in the head, vertigo, confusion of ideas, numbness, and other evidences of nervous derangement, which may last for several hours, and which be- come more pronounced as the epileptic condition becomes more con- firmed. 2. Unconsciousness, with Evident though Local Spasm.—Iri this variety the loss of consciousness is of longer duration than in the pre- EPILEPSY. 669 ceding’, and is attended with convulsions light in character, but yet ap- parent to those around. The eyes are fixed, as in the first variety, the mind becomes a blank, and there is a sensation of vertigo immediately before the loss of consciousness, and at the time of its restoration. The face usually becomes pale first and then red, or either of these con- ditions may occur without the other being observed. The spasms may be very slight. Sometimes there is momentary strabismus, at others retraction of the angles of the mouth on one or both sides, rotation of the head or a sudden drawing of it backward, or the tongue is thrust forward and the jaws close on it, inflicting slight injury. Again, the chair in which the patient may be sitting is pushed back with some force, and the body is bent forward, or the muscles of the neck may be affected, and the circulation thus interrupted in the veins of the neck, causing a dark hue of the complexion. Sometimes the spasms have an appearance of being volitional. A patient under my charge tugs violently at his hand ; another walks about the room, but without taking any determinate course ; a young lady leaves her chair and stands upon another one at some distance from her, and another talks all kinds of gibberish. My experience of such cases is in accordance with that of Reynolds,1 to the effect that there is no recollection of these acts. These attacks are often preceded by prodromata of various kinds. The duration rarely exceeds a minute, and is generally much less. 3. Unconsciousness, with General Tonic and Clonic Convulsions. —Prodromata may or may not be present. In any event the paroxysm occurs suddenly. The first circumstance may be a cry of a very peculiar character, somewhat resembling the bleating of a young lamb. The eyes become fixed, and the patient falls to the ground, usually with a bound, as if he is shot. The loss of consciousness occurs with the cry, or with the fixedness of the gaze. The muscles are now thrown into a state of tonic contraction ; the respiration is impeded, or altogether arrested ; the face, if at first pale, becomes dark ; the pupils are dilated, and sensibility is entirely abol- ished. Careful examination of a patient in this stage of the paroxysm re- veals some important features : the body is rigid, but is usually inclined more to one side than the other, in the position of a tetanic patient with pleurosthotonos ; the eyes are open, and are twisted to one side ; the face is likewise more retracted on one side than the other ; the sterno-cleido-mastoid muscles, and others of the neck, stand out like thick cords ; the carotids throb with force ; the veins of the head and neck are turgid with black blood, and the pulse is usually weak and fluttering. After this stage has lasted for a period varying from two or three 1 “System of Medicine,” vol. ii., p. 261, article “Epilepsy.” 670 CEREBRO-SPJNAL DISEASES. seconds to half a minute, a great change ensues. The unconsciousness continues, but the general tonic spasm relaxes, and clonic convulsions take its place. These are general, but are ordinarily more strongly marked on one side of the body than on the other. The muscles of the face are alternately contracted and relaxed ; the tongue is often thrust between the teeth, and, the jaws being closed upon it, it is terribly in- jured ; the upper and lower extremities are in a state of continued agi- tation, and the contents of the bladder, rectum, and vesiculae seminales, may be evacuated. The respiration is forced and irregular, froth issues from the mouth, and, if the tongue has been bitten, it is colored with blood. The muscles of the neck do not relax to any considerable extent; consequently the veins remain distended, and the face continues to bo livid. The pupils oscillate, sometimes being dilated and then contract ed, or one may be contracted and the other dilated. The heart beats with great irregularity, both as to force and frequency. This stage may last from a few seconds to five minutes. Cases of longer duration are on record, but they are exceedingly rare. The third stage of the paroxysm is characterized by the gradual return of consciousness. The patient, though still somewhat convulsed, looks around him, and gives evidence of returning sensibility in other ways. The pupils cease their disorderly movements, and are contracted; the respiration and pulse become more regular, and he may even attempt to speak. It often happens that little spots of extravasated blood make their appearance under the skin of the forehead, eyelids, cheeks, and sometimes on the neck and breast. These disappear in a few days. The duration of this stage is from a few seconds to four or five minutes, and it is often so slightly marked as to escape observation. With the cessation of the convulsive movements the stage of stupor usually supervenes, though it may be entirely absent, especially in old cases of epilepsy. During this stage there are sometimes clonic spasms of no great degree of severity. It may last a few minutes or several hours. When the patient arouses from it, he generally has headache, and a feeling of lassitude and soreness of the muscles, from the violent contractions they have undergone. 4. Irregular or Aborted Paroxysms.—In these it may happen that the loss of consciousness is not complete, or that the patient has con- vulsive movements partial in character and accompanied simply by ver- tigo, or he may have unconsciousness lasting for an hour or more, during which he performs automatic acts, of which he has no recollec- tion, but which are not accompanied by any movements that can prop- erly be called spasmodic. In his interesting lecture on “ Apoplectiform Cerebral Congestion,” Trousseau 1 cites a number of cases which were clearly instances of 1 Op. cit., Bazire’s translation, pp. 19, et scq. EPILEPSY. 671 irregular or abortive epileptic paroxysms. Among them is that of a magistrate whose sister was an inmate of a lunatic asylum. He was president of a provincial tribunal. One day he got up all of a sudden, muttered a few unintelligible words, and went to the deliberating-room. The usher followed him, and saw him make water in a comer. A few minutes afterward he returned to his seat, and again listened with in- telligence and attention to the pleadings momentarily interrupted. He had no recollection of the incredibly incongruous act he had committed. This gentleman belonged to a literary society, which held its meetings at the H6tel-de-Ville, of Paris. At one of these, during the discussion of an important historical point, he was seized with vertigo. He ran quickly down to the Place de Hotel-de-Yille, and walked about for a few minutes on the quays, avoiding with success both carriages and the passers-by. On recovering himself he perceived that he had come out without his great-coat and his hat. He therefore returned to the meet- ing, and resumed with a perfectly lucid mind the historical discussion in which he had already taken a very active part. He retained no recol- lection whatever of what had occurred between the beginning of the attack and the moment he recovered himself. Many cases similar to these might be cited from other authors. From a number w'hich have happened in my own experience I adduce the following: J. H. consulted me for epilepsy in the summer of 1869. His ordi- nary attacks were of the fully-developed form; but upon two occasions they were different from any with which he had previously been af- fected. On one of these, while overlooking some workmen, he was observed to put his hand to his head, and then sudddenly to run toward a fence, which he speedily climbed. Jumping down into the back-yard of the adjoining house, he seized a stick of wood near by, and made a furious onslaught on the door and windows. While thus engaged he was seized by several men, and forcibly held, notwithstanding his strug- gles. While thus being restrained he recovered his consciousness, but had no recollection of any thing which had taken place after he had put his hand to his head, which action he said was due to severe pain with vertigo. The duration of the attack was not over three minutes. On the other occasion he was seized with pain and vertigo while engaged in paying a bill at a coal-yard. He rushed into the street, and began to turn rapidly round. He was seized and held till he re- covered his consciousness. This attack lasted about four minutes. Subsequently he had a similar paroxysm in my consulting-room. His face suddenly became very pale, his eyes were fixed, and his pupils oscillated. Suddenly he rose from the chair, grasped the mantel-piece for an instant, and then rushed violently around the room, throwing his arms about, and uttering a peculiar inarticulate cry. I made no at- tempt to restrain him, and in about two minutes he became calm. 672 CEREBRO-SPINAL DISEASES. During the whole paroxysm his face was pale, and at its close the pu* pils were dilated. He had no recollection of any thing which had oc- curred after he rose from the chair, but was conscious then of vertigo. Another case is that of a girl brought to my clinic at the Bellevue Hospital Medical College during the summer of 1869. She had been severely injured in the skull by a fall against a mass of old iron. Ne- crosis subsequently ensued, and several large pieces of the external table were exfoliated. While before the class, she started to her feet, and walked several times around the closed area. She was unconscious, and to all appearance insensible. When the paroxysm was over she returned to her seat. The duration did not exceed a minute, and there was no excitement or delirium. Another patient, a partner in an extensive mercantile establish- ment, who was subject to attacks of both the grand, and petit mal, left his office at about eleven o’clock for the purpose of getting a signature to a paper of some kind from a gentleman whose place of business was a few minutes’ walk distant. Not returning by three o’clock, inquiry was made, and it was ascertained that he had visited the office, obtained the signature, and had left in apparently good health before half-past eleven. Since then nothing had been heard of him. He did not make his appearance at his own office till nearly five o’clock. The last thing he recollected was passing St. Paul’s Church at the corner of Broadway and Yesey Street, just as the congregation was coming out after morning service. It was subsequently ascertained that he had gone to Brooklyn after getting the signature he wanted, had visited a newspaper-office and purchased a paper ; had returned to New York, entered an omnibus at the Fulton Ferry, left it at the corner of Twenty-third Street and Fifth Avenue, entered the Fifth Avenue Hotel, and while there recovered his recollection. But none of these cases, nor any of which I have seen any report, are equal in interest to one which occurred in my practice during the autumn of 1875. The patient, who was engaged in active business as a manufacturer, left his office at about 9 A. M., saying he was going to a florist’s to purchase some bulbs. He remained absent eight days. He was tracked all over the city, but the detectives and friends were always an hour or more behind him. It was ascertained that he had been to theatres, to hotels, where he slept, to shops where he had made pur- chases, and that he had made a journey of a hundred miles from New York, and, losing his ticket and not being able to give a satisfactory account of himself, was put off of the train at a way-station. He had then returned to New York, passed the night at an hotel, and on the eighth day, at about ten o’clock, made his appearance at his office. He had no recollection of any one event which had taken place after leav- ing his place of business, eight days previously, till he awoke on the morning after his return to the city, and found himself in an hotel at EPILEPSY. 673 which he was a stranger. It was ascertained beyond question that in all this time his actions had been entirely correct to all appearance, that his speech was coherent, and that he had acted entirely in all respects as any man in the full possession of his mental faculties wmuld have acted. He had drunk nothing but a glass of ale, which he took with some oysters at a restaurant in Sixth Avenue. It could not be ascertained that this patient had ever had an epilep- tic paroxysm ; but he had a year previously been under my charge for cerebral symptoms, indicating the existence of chronic basilar menin- gitis, and only a week before his disappearance I had discharged him cured, after a month’s treatment for severe pain in the head, dizziness, paralysis of the third nerve on the right side, and extreme insomnia. There were all the indications of specific cause, and I had treated him with large doses of the iodide of potassium, as on the former occasion. Most, if not all, of the cases of “ double consciousness ” that have been reported are doubtless epileptic in character. An interesting case of the kind has been related by M. Azam.1 It is that of a young woman who, after having suffered from hysteria and convulsions, had two dis- tinct phases of existence, living, in fact, two separate and different lives, and exhibiting different likes and dislikes and mental characteristics. Another case was that of a sergeant, reported by Dr. Mesnet,3 wTho, after receiving a severe wound of the skull, had paroxysms charac- terized by total change in his mentality, and obliviousness of all acts performed in his normal state. During these periods he was con- scious, and acted in a logical and coherent manner. 5. Unconsciousness with Hallucinations.—In this form of epilepsy, which I described in a paper read before the American Neurological As- sociation, June 18,1880,3 the characteristics are conscious hallucinations, followed by unconsciousness but unattended by muscular spasm. I have had the opportunity of seeing two cases (one since the reading of the paper) while the paroxysms were present, and in neither was there the least spasmodic action. I quote part of the description of one of the cases, that of a young woman on which the memoir in question is based : “ I had the opportunity of witnessing seventeen paroxysms. Some- times they were preceded by a well-marked aura, and this was always a sensation apparently somewhere within the cranium, but not capable of being exactly localized or described. This was never felt until within the last two years. It lasted only a second or two, and was im- mediately followed by the ‘ vision.’ 1 “ Amnesie periodique, ou dedoublement de la vie,” Annales Medico-psychologiques, July, 1876. 2 Union Medicate, July 21 and 23, 1874. Translated in 7 he Chicago Journal for Nervous and Mental Disease, January, 1875. 3 “ On Thalamic Epilepsy,” Archives of Scientific Medicine, August, 1880. Also, Neuro- logical Contributions, No. Ill, 1881. 674 CEREBRO-SPINAL DISEASES. “ The first paroxysm of this series which I witnessed was ushered in by the aura. She had hardly time to say, ‘ It’s coming,’ when the hallucination began. She described it as consisting of a large white bear in motion before her on the carpet. It seemed to be walking slowly to and fro, its head bent toward the floor as if scenting some- thing. I closely watched her, and could detect no spasm anywhere. She spoke clearly, without hesitation, and with entire distinctness. The pupils were normal. “I had taken out my watch to time the duration of the attack. Thirty-five seconds elapsed, and then her pupils suddenly dilated, her head fell forward, and her left hand, which was at this instant pointing in the direction of the visional bear, dropped to her side. I pinched the skin of her face, then of each hand, without eliciting any evidence of cutaneous sensibility. I took up a fold of skin on each forearm just above the wrist and stuck a cataract-needle, which was at hand, through it, with a like result. Her pulse—I had not felt it during the existence of the hallucination—was beating at the rate of about sixty a minute, and was full. Her face had not altered in color, nor was there any other change in it except such as was due to relaxation of the muscles—such as is present in sleep. The eyelids were closed, but not spasmodically. She remained in this state exactly twenty-eight seconds, breathing perhaps a little more slowly and deeply than before the accession of the paroxysm. Suddenly she raised her head, looked inquiringly around her for a moment, and then, as if becoming aware of a sensation, looked at both her arms where I had pricked them. A drop of blood was oozing from each puncture. She asked what it was, and then, without waiting for an answer, exclaimed, ‘You have bled me ! ’ She was then entirely herself, and talked coherently, and without the least excitement, about the hallucination. “ While making memoranda of the phenomena I had observed, and while she was walking up and down the floor, she said that she was going to have another attack, as she felt the peculiar sensation again in her head. She had no sooner uttered the words than the vision came. ‘ It’s a girl this time ! ’ she exclaimed—‘ a girl with long auburn hair, and a cap on her head ; she looks like a French nurse. I think I will sit down, for if I do not I shall fall as soon as I become insen- sible ; ’ saying which, she quietly sat down in a large arm-chair. “I pinched the skin of her right hand. ‘Oh !’ she exclaimed, ‘I feel that; I am not insensible yet; I see everything in the room as well as I do the girl who is not here. I can feel the least touch, and my hearing is as good as ever.’ “ I asked her what ‘ the girl ’ was doing. ‘ Oh, nothing,’ she replied ; ‘ she is only standing there in front of the fireplace, looking at me.’ “ I told her to shut her eyes, and then to tell me if she still saw ‘ the girl.’ EPILEPSY. 675 “‘Yes,’ she answered, ‘just as distinctly as I did when they were open.’ “At forty-one seconds she became unconscious, and remained in this state for one minute and five seconds, awaking—I say awak- ing, for her appearance was like that of a person asleep—sudden- ly, and apparently in a normal condition of mental and physical health.” Subsequently, from inattention to treatment on the part of the pa- tient, the paroxysms passed into others with strong muscular contrac- tions, and she exhibited indications of a tendency to the perpetration of acts of violence. In all, six cases of this interesting form of epilepsy have come under my observation ; and I have learned of others being recognized by several physicians of competent powers of observation. Relative to the mental disturbance which sometimes ensues upon epi- leptic paroxysms, Dr. Hughlings Jackson1 has recently given some inter- esting details relative to acts performed by epileptics during periods of unconsciousness. In his opinion such acts are automatic, not—to speak exactly—epileptic, but post-epileptic. “ The condition after the parox- ysm is duplex : (1) there is loss or defect of consciousness, and there is (.2) mental automatism. In other words, there is (1) loss of control, ■permitting (2) increased automatic action.” The epileptic seizure may be so slight and transitory as to escape observation, but the slighter it is the more apt is the resulting automatism to be complex and elab- orate. Dr. Jackson gives a number of exceedingly interesting cases in illus- tration of his views, which in addition are enforced with much cogent reasoning. But, while in the main agreeing with him, I am scarcely prepared to deny that such unconscious attacks may not be substituted for the more fully-developed paroxysm instead of, as in his opinion, always following a seizure. Epileptic fits may take place at night during sleep, and the patient be unaware of their existence, unless he inflicts some injury on himself, such as biting his tongue, or is told of their occurrence by persons who may be in the same room with him. In two hundred and six of my cases the period of access is noted, and, of these, forty-seven were noc- turnal, and one hundred and fifty-nine diurnal. In the intervals between the paroxysms epileptics often exhibit cer- tain evidences of disordered mental, sensorial, and motor functions. Thus, as regards the first category, the memory may be impaired, and there may be diminished mental power. There are, however, many exceptions to this rule; and, even where there have been a great many attacks, the mind may preserve its normal degree of integrity. As 1“0n Temporary Mental Disorders after Epileptic Paroxysms,” “ West Riding Lu- natic Asylum Medical Reports,” vol. v., p. 105. 676 CEREBRO-SPINAL DISEASES. Reynolds remarks, in regard to this point: “ A patient may be epileptic and a lunatic; he may be epileptic and asthmatic, but there are some epileptics whose minds are as healthy as their lungs; and, so far as the natural history of epilepsy is concerned, it is a mistake to derive it from complicated cases.” Still, in the majority of cases, it will be found that the mind sooner or later becomes involved, and it sometimes happens that a single attack causes marked intellectual deterioration. Derangements of sensibility are common from the beginning. Headache, a feeling of constriction around the forehead, and occasion- ally a pain at the back of the head, are noticed. Vertigo is also fre- quently present, as are also sensations of numbness'in different parts of the body. The pupils are almost invariably dilated. The motor power of the patient is generally weakened without there being any decided paralysis. Twitchings of the muscles are not un- common, and there is often a general excitability of the reflex faculty of the spinal cord, by which jerkings of the limbs are produced by slight excitations. The circulation is generally sluggish, the extremities are cold, and the capillaries are turgid and inactive, so that, if the finger be pressed firmly upon the skin, a considerable period elapses before the white spot disappears by the refilling of the vessels. In examining with the ophthalmoscope the fundus of the eye in epileptics, we can often detect evidences either of cerebral congestion or of ansemia, and thus obtain valuable indications for treatment. For several years, in my lectures, I have constantly insisted on this point, and in my cliniques have exhibited several cases in which I had been guided to successful treatment by the ophthalmoscope. Drs. Kostle and Niemetshek,1 of Prague, consider that the brain in epileptics is always aneemic, and that this condition is invariably found by ophthalmoscopic examination. According to these observers, the venous pulse is pro- duced when the eye is made anaemic, and they assert that the retina is anaemic, and that there is consequently venous pulsation in every case of epilepsy. That this opinion is erroneous, both as to the facts and inferences, I am very sure. Venous pulsation, so far from being indica- tive of anaemia, really shows the existence of the very opposite con- dition. My observations are, however, to the effect that venous pul- sation is present in many cases of epilepsy, and that it accompanies dilatation of the veins. There is no invariable rule relative to the occurrence of any par- ticular form of epilepsy in the same person. It thus often happens that all the varieties of paroxysm mentioned, except the irregular or aborted form, which is more rare, are met with in one individual. The more severe forms may occur at longer intervals, and the milder forms 1 Prayer Vierteljahrschrift, H. 106, 107, 1870, and Quarterly Journal of Psychological Medicine, January, 1871, p. 128. EPILEPSY. 677 more frequently. As regards frequency, there are great variations. Some patients go a year or more without attacks, while others have several every day. It generally happens that the intervals become progressively shorter. As a rule, attacks of the milder forms are more frequent than the fully-developed paroxysm, and attacks of the latter are milder, as they are more frequent. Mania is sometimes a consequence of epilepsy. It comes on after the attack, and is rarely of more than a few minutes’ duration. Those cases in which it precedes the paroxysm, and lasts several hours or days, are cases of mania conjoined with epilepsy—a combination which, as every insane asylum shows, is not uncommon. The mania of epi- lepsy is usually of a very exalted character, and during its existence the subject may commit homicide or other crimes. The mental state of epilepsy has been well studied by Falret,1 and a very interesting case has been recently reported by Dr. Thorne,2 in a paper entitled “ Masked Epilepsy.” In this instance the patient often returned to his home without being able to give any account of what he had been doing or where he had been. During these attacks he was frequently the subject of that form of mental derangement called klep- tomania. Generally they ensued on paroxysms either of the grand or petit mal, but sometimes they were substituted for the regular seiz- ures. He had no recollection of what occurred during the attacks. Sometimes he was furiously excited in them, and would endeavor to injure himself and others in his blind rage. Relative to the diagnosis of the remarkable paroxysms, the main feature of which is unconsciousness, or rather non-recollection of consciousness, in which the individual acts apparently automatically, great difficulties exist. Probably nothing short of a full history of the case, from infancy up, will suffice for the recognition of the real nature of the phenomena. There appears to be an idea in the minds of some physicians, that every outrageous criminal act is the result of epilepsy, and so wide-spread is this notion, that now the first plea of the murderer is, that he “ knew nothing about it ; ” and the fact that an individual who has perpetrated a murderous outrage is the subject from time to time of epileptic seizures, is regarded as sufficient to absolve him from all responsibility for his actions. The fact of a discolored spot on his pillow, or of an infantile convulsion, is seized upon as a valid reason for acquittal, or even for setting aside a verdict found after a full and fair trial. In the first place, it must be understood that an undoubted epileptic is just as capable of murdering for revenge or gain as is a healthy person, and that he is just as accountable, and should accord- ingly suffer the full penalty of the law for his conduct. At the same 1 “ De l’etat mental des 6pileptiques,” Archives generates de m’edecine, Decembre, I860, et Avril et Octobre, 1861. 8 “St. Bartholomew’s Hospital Reports,” 1870. 678 CEREBRO SPINAL DISEASES. time, it is not to be questioned that acts of violence may be perpetrated during seizures which are either epileptic or the direct consequence of an epileptic paroxysm. It is only by the most thorough and careful inquiry into all the motives for and circumstances attending upon the act, as well as all the antecedents of the individual, that a proper discrimination can be made. Each case must be determined for itself ; there are no rules applicable invariably to all. The medico-legal relations of epilepsy do not, however, come with- in the scope of the present treatise. Paralysis may follow epilepsy, but, unless the case is complicated with some organic disease of the brain or spinal cord, the loss of power is temporary. Causes.—Among the predisposing causes of epilepsy, hereditary tendency stands first. Reynolds 1 states that, in about one-third of the cases under his observation, hereditary taint existed. He does not, by this statement, however, mean to assert that epilepsy existed in one- third of the parents, but that some disease of the nervous system, more or less closely allied to epilepsy, was present in either the parents, the grandparents, the aunts, uncles, brothers, or sisters. Only twelve per cent, of his cases gave a distinct history of epilepsy in either branch of their families. Herpin,5 of sixty-eight cases, found that ten were descended from epileptic ancestors. Delasiauve,3 of three hundred cases, found decided evidence of hereditary tendency in thirty-three. In one hundred and sixty-seven there were no data, and in one hundred and twenty hereditary taint was denied. Of the thirty-three cases, five were descended from epi- leptic ancestors. Sieveking 4 found that hereditary influence was present in 11.1 per cent, of his cases. In my own experience I have notes in regard to this point in three hundred and ninety-six cases. Of these, sixty-four had epileptic fa- thers, mothers, grandparents, uncles, aunts, brothers, or sisters, and forty-eight had relatives insane, hysterical, cataleptic, affected with severe neuralgia, or of remarkably irritable nervous systems. Sex does not appear to exercise any appreciable influence as a pre- disposing cause. Of five hundred and seventy-two cases noted by my- self, two hundred and ninety-eight were in males and two hundred and seventy-four in females. Other authors have, however, had directly opposite experience. Age has a very decided influence. Reynolds gives the following table of one hundred and seventy-two cases collected by himself : 1 Op. cit., p. 253. 8 “ Du pronostic et du traitement curatif de 1’epilepsie,” Paris, 1852, p. 325. 3 Op. cit., p. 189. * “ On Epilepsy,” etc., London, 1858, p. '74. EPILEPSY. 679 Age at Commencement. Males. Females. Total 10 9 19 Between 10 and 20 years 66 40 106 26 20 46 1 1 2 Total 102 TO 172 My own cases were as follows : Age at Commencement. Males. Females. Total, i Under 10 years 31 178 72 17 29 151 71 23 60 329 143 40 Between 10 and 20 years Between 20 and 45 years Over 45 years Total 298 274 572 It is thus seen that the period of life between ten and twenty years is that at which epilepsy is most apt to occur. The experience of oth- ers is to the same effect. The influence of temperament has been thought important by some writers. But, aside from the different opinions entertained relative to the characteristics of the temperaments, it is by no means established that, even when strictly defined, tempera- ment exercises any effect as a predisposing cause. I have no accurate records on this point, though so far as my memory serves me I have observed no marked predominance of epileptics with any temperament. The exciting causes may very properly be classified as psychical, eccentric, general organic changes, and physical influences. Relative to the influences of these causes, Reynolds gives the following table : Nature of Cause. No. of Cases. I. Psychical—such as fright, grief, worry, overwork 29 II. Eccentric irritation—dentition, indigestion, venereal excesses, dys- entery, etc 16 III. General organic changes—fatigue, pregnancy, miscarriages, rheu- matic fever, scarlet fever, diphtheria, pneumonia 9 IY. Physical influences—blows on head, falls, insolation, cuts 9 In my own cases no exciting cause could be assigned in one hun- dred and seventy-seven. The remaining three hundred and ninety-five cases were, according to the evidence received, caused as follows : Fright 35 Anxiety 17 Grief 30 Over mental exertion 48 Dentition 21 Indigestion 33 Carried forward 184 680 CEREBRO -SPINAL DISEASES. Brought forward 184 Venereal and sexual excesses 60 Menstrual derangement 66 Blows on the head ......... 24 Peripheral wounds and injuries 4 Palls 13 Sunstroke., * 11 Scarlet fever 3 Measles 3 Diphtheria 9 Pregnancy 3 Syphilis 13 Malaria ...» 6 396 Diagnosis.—The diagnosis of epilepsy presents no difficulties to the careful observer. It may, however, be confounded with several condi- tions, the principal of which are cerebral congestion, cerebral haemor- rhage, hysteria, the convulsions of infancy and of Bright’s disease, poisoning by opium and alcohol, syncope, and with the convulsions of epileptiform character which occur in the course of certain organic dis- eases of the brain. The diagnosis from cerebral congestion and cerebral haemorrhage has already been given in the chapters treating of those affections. In hysteria, the convulsions, which are sometimes epileptiform in charac- ter, are preceded or accompanied by other evidences of the hysterical state. Consciousness is rarely entirely lost, the tongue is not bitten, and there is no subsequent stage of stupor. The convulsions of infancy not epileptic are not repeated but from a readily-ascertained exciting cause, such as dentition, indigestion, falls, etc. So far as the paroxysm is concerned, I know of no specific points of difference; but it must be recollected that the paroxysm is not the only feature of epilepsy, and that it is the only feature of infantile con- vulsions. These latter may pass into epilepsy; but, if they do not, I have never been able to find a single case in my experience rn which epilepsy ensuing in adult life has been preceded by the ordinary infan- tile convulsions. In Blight’s disease, though the convulsions may be epileptiform in character, coma is the principal feature, and the history of the case will further serve to render the diagnosis exact. The same remarks are applicable to poisoning by opium and alcohol. From syncope epilepsy is distinguished by the facts that the loss of consciousness is sudden and complete, that the pulse is not feeble, and that recovery is rapid. These remarks apply to the milder attacks with- out convulsions. From the more severe forms of the paroxysm the dis- tinction is too obvious to require amplification. In organic diseases of the brain, such as tumors, softening, sclerosis, etc., the accompanying symptoms, pain, paralysis, tremor, imbecility, EPILEPSY. 681 difficulties of speech, and derangements of the special senses, will serve to distinguish them from epilepsy. Epilepsy is often assumed by designing persons for purposes of fraud. In such cases the pretender usually overacts his part ; hia sensibility is not abolished, as may readily be ascertained by putting the end of the finger on the conjunctiva, and the size of the pupils is not altered. Prognosis.—The prognosis depends to a great extent on the dura- tion of the disease. Recent cases can often be cured, but those which have lasted for several years are rarely brought to a favorable termina- tion. Among the other unfavorable elements are the existence of hereditary influence, the beginning of the disease late in life, the pres- ence of material mental weakness, and the existence of long intervals between the attacks. As regards the probability of the supervention of any form of in- tellectual derangement or debility, the most important ascertained point is that the mild paroxysms unattended by convulsions are more productive of mental decay than the severe form of seizure. The oc- currence of the first attack late in life is likewise a predisponent to dementia. I have never, in my own experience, known death to take place dur- ing a paroxysm of true epilepsy ; such cases, however, do occur. Usu- ally, some intercurrent affection carries the patient off, though even with this liability life is sometimes astonishingly prolonged. I am acquainted with the case of a lady who is now sixty-five years of age, and who, since her tenth year, has averaged six paroxysms daily, all of the severest character. Her mind is almost entirely gone, but physi- cally her health is excellent, and to all appearance she may live twenty years longer. I am not aware of any exact observations tending to show the rela- tive danger to life of attacks of the milder and severer forms ; though it is reasonable to suppose that, so far as regards the occurrence of death during the paroxysm, the convulsive form is more fatal. Morbid Anatomy.—In post-mortem examinations of persons dying epileptic, abnormal conditions are found in every part of the brain and spinal cord. Some of these lesions are undoubtedly secondary, others unessential, while those which may be considered primary vary in their seat and character. In a great many cases, perhaps the majority, no lesions are discoverable. No one has been more thorough in the search for the essential cause of epilepsy than Schroeder van der Kolk ;1 though his observations can scarcely be regarded as yielding conclusive results, they serve to show, 1 “ On the Minute Structure and Functions of the Medulla Oblongata, and on the Proxi- mate Causes and Rational Treatment of Epilepsy,” “ New Sydenham Society Transla- tions,” London, 1859. 682 CEREBRO-SPINAL DISEASES. when taken in connection with the pathology of the disease in ques- tion, that its seat is mainly in the medulla oblongata, with second- ary implication of other parts of the cerebro-spinal nervous system. Oftentimes, in accordance with other pathologists, he found noth- ing to account for the affection, but at others he found hardening and contraction of the medulla oblongata, and again degeneration of the brain either as a consequence or cause of the disease. Mi- croscopical examination sometimes showed him the medulla indu- rated, sometimes softened, and, as a constant phenomenon, “whether the patient died in or out of the fit, great redness and vascular ten- sion in the fourth ventricle, penetrating into the medulla oblongata sometimes to a considerable depth.” These appearances were due to enlargement of the blood-vessels, as was shown by microscopical measurements. It is probable, however, as Scliroeder van der Kolk asserts, that the lesions in question are the results, and not the causes, of the paroxysms. Other observers have not so uniformly found this enlargement of the blood-vessels of the medulla. In three cases of death occurring in epileptics, in which I have had the opportunity of making post-mortem examinations, they certainly did not exist, nor was there any other le- sion detected by the most careful microscopical exploration. In one other case the vessels of the medulla oblongata were enlarged, and there was amyloid degeneration of the pituitary body. Fox1 gives the following list of the post-mortem appearances : Foreign bodies developed on the meninges, in the ventricles, in the cortical substance ; increase of subarachnoid fluid or distention of the ventricles by serum, induration, softening, and general swelling of the cerebral mass ; general or pai’tial hyperaemia, cysts, tubercles, cancers, exostoses, periosteal growths, thickening, or some change of the arach- noid or the pia mater ; abnormal thickness or abnormal thinness of the cranial bones ; excessive size of head, increase of the volume of the cranial cavity, deformities or abnormality in the conformation of this cavity ; caries of the cranial bones ; pus between the bone and the dura mater ; acute or chronic hydrocephalus, hydatids, ossification of the dura mater, tubercle of the dura mater or pachymeningitis, abscess in the cerebral tissue, spots or regions of haemorrhage ; various traumatic lesions ; alterations of the pineal gland ; inequality of weight and size of the cerebral hemisphere ; various lesions connected with blood-ves- sels—aneurism, embolism, atheroma, increase in size of the capillaries in the medulla oblongata, fatty degeneration of some portion of the medulla oblongata ; capillary dilatation in the pons and cerebellum ; haemorrhage of pons; anaemia of brain, either from disease of vessels or dependent upon general anaemia, etc., etc. 1 “ The Pathological Anatomy of the Nervous Centres,” London, 1874, p. 805. EPILEPSY. 683 Indeed, no point is more thoroughly established than that epilepsy results from very different morbid conditions, and that they are simply the starting-points in the majority of cases. The true lesion has not yet been detected, and in fact, as we shall presently see when discuss- ing the pathology of the disease, there may be no necessary anatomical lesion whatever. Pathology.—The points which may be considered as to some extent established relative to the pathology of epilepsy are briefly summarized as follows by Reynolds :1 “ 1. That the seat of primary derangement is the medulla oblongata and upper portion of the spinal cord. “ 2. That the derangement consists in an increased and perverted readiness of action in these organs, the result of such action being the induction of spasm in the contractile fibres of the vessels supplying the brain, and in those of the muscles of the face, pharynx, larynx, respira- tory apparatus, and limbs generally. “ By contraction of the vessels the brain is deprived of blood, and consciousness is arrested; the face is or may be deprived of blood, and there is pallor; by contraction of the vessels which have been men- tioned, there is arrest of respiration, the chest-walls are fixed, and the other phenomena of the first stage of the attack are brought about. “ 3. That the arrest of breathing leads to the special convulsions of asphyxia, and that the amount of these is in direct proportion to the perfection and continuance of the asphyxia. “ 4. That the subsequent phenomena are those of poisoned blood, i. e., of blood poisoned by the retention of carbonic acid, and altered by the absence of a due amount of oxygen. “ 5. That the primary nutrition-change, which is the starting-point of epilepsy, may exist alone, and epilepsy be an idiopathic disease, i. e., a morbus per se. “ 6. That this change may be transmitted hereditarily. “ 7. That it may be induced by conditions acting upon the nervous centres directly, such as mechanical injuries, overwork, insolation, emo- tional disturbances, excessive venery, etc. “ 8. That the nutrition-changes of epilepsy may be a part of some general metamorphosis, such as that present in the several cachexias— rheumatism, gout, syphilis, scrofula, and the like. “ 9. That it may be induced by some unknown circumstances deter- mining a relative excess of change in the medulla during the general excess and perversion of organic change occurring at the periods of puberty, of pregnancy, and of dentition. 1 Op. cit.y p. 275, and more fully stated in his “ Treatise on Epilepsy, its Symptoms, Treatment, and Relations to other Chronic Convulsive Diseases,” London, 1861, chapter v., p. 238. CEIIEBRO-SPINAL DISEASES. 684 “ 10. That it may be due to diseased action, extending from con- tiguous portions of the nervous centres or their appendages. “ 11. That the so-called epileptic aura is a condition of sensation or of motion, dependent upon some change in the central nervous system, and is, like the paroxysm, a peripheral expression of the disease, and not its cause.” While admitting the correctness of these conclusions, they do not, in my opinion, tell the whole story of the theory of epilepsy. In very many memoirs Dr. Brown-Sequard has pointed out the dependence of the affection upon injuries of the upper part of the spinal cord, and upon irritations existing in various parts of the body. His researches, and facts observed every day by physicians who see many cases of epi- lepsy, show very conclusively that the starting-point is often in the sympathetic nerve—the nerve by which the calibre of the blood-vessels is regulated. Neither can I accept the view that the first intra-cranial condition producing a paroxysm is in all cases spasm of the blood-vessels and the consequent deprivation of the blood-supply to the brain. On the con- trary, I am very sure that the primary state is often paralysis of the cerebral blood-vessels and resulting hyperasmia. By this condition the medulla oblongata is thrown into a state of over-excitation, giving rise to convulsions, and consciousness is lost from the fact that the hemi- spheres participate. That convulsions, epileptiform in character, may be produced both by cerebral anaemia and cerebral hyperaemia, when either condition involves the medulla oblongata, is a fact which experiment has abundantly established, and that loss of consciousness follows either condition involving the hemispheres is equally certain. We have, con- sequently, two kinds of epilepsy—the one due to anaemia, the other to congestion—and it is to this fact that is due the circumstance that sometimes the paroxysms are prevented by measures which tend to in- crease the amount of blood in the brain, and at others by remedies which exercise a contrary influence. The existence of the two species of epilepsy is likewise shown by ophthalmoscopic examination—a point upon which I have already insisted. During natural sleep the amount of blood is, as I have elsewhere shown, decreased from the quantity which circulates in the cerebral blood-vessels during wakefulness. Epilepsy occurring during sleep is therefore of the angemic variety. But it often happens that sleep passes gradually into stupor, from the fact that causes tending to in- crease the flow of blood to the brain, or to arrest its passage from this organ, are in operation. In such cases epilepsy of the congestive va- riety may be induced. In those cases in which the tongue is bitten, the medulla oblongata is probably always in a condition of hyperaemia ; and this state, as Schroeder van der Kolk has very conclusively shown, is mainly in the EPILEPSY. 685 course of the roots of the hypoglossal nerve. The intermissions between the attacks are ingeniously explained by the same able observer, by likening the cells of the medulla oblongata to Leyden jars charged with electricity, or to the electrical organs of the conger- eel and torpedo. After being discharged, time is necessary for the reaccumulation of sufficient electricity to discharge them again ; and, when the cells of the medulla have once discharged themselves in an epileptic convulsion, a period must elapse before another access can take place. Nothnagel1 believes that the pons Yarolii and the medulla ob- longata are the seat of epilepsy, and that it is in these centres that we are to look for the anatomical changes. Although, as his own experiments as well as those of Hitzig show that epilepsy may be produced by irritation of the cortical substance of the brain, the fact only proves that such irritation is an exciting cause, and is no more to be regarded as indicating the cortex as the seat of the disease than the fact that irritation of the sciatic nerve, followed by epi- lepsy, indicates that part of the nervous system as containing the essential lesion. Operations for the removal of cortical tumors for the cure of epi- lepsy, and excision of portions of the cortex in which the motor cen- tres have been located, have rarely been folio-wed by anything more than temporary relief. The foregoing remarks apply in the main to that form of epileptic seizure characterized by convulsion. In the imperfectly-developed at- tacks the implication of the medulla oblongata must be very slight, the hemispheres being the organs mainly affected, and the condition being sometimes anaemic, at others hyperaemic. It must not be supposed, from what has been said, that simple cere- bral anaemia and simple cerebral congestion, attended with epileptiform convulsions, are identical with the anaemia and congestion of epilepsy. This disease is cerebral anaemia or congestion with another element, the exact nature of which we do not understand, but which is certainly of such a character as to constitute the main differential point between epilepsy and any other affection. A chapter on epilepsy would be manifestly incomplete without a statement of the views held by Dr. Hughlings Jackson 2 relative to its pathology and natural history. According to this eminent authority those parts of the body suffer first and most, from convulsions or other manifestations of the disease, which are most frequently brought into volitional action, and those parts least which are most automatic in 1 “ Epilepsie,” in Ziemssen’s “ Handbuch der speciellen Pathologie und Therapie,” iwolfter Band, “ Krankheiten des Nervensystems,” ii., zweiter Halfte, pp. 250, el seq. 2 “ On the Anatomical, Physiological and Pathological Investigation of Epileptics,” “West Riding Lunatic Asylum Medical Reports,” vol. iii., 1813, p. 315. 686 CEE EBRO-SPINAL DISEASES. their operation. Thus he says, in a paper published in the Lancet, February 1, 1873 : “ There are three parts where fits of this group mostly begin : (1) in the hand ; (2) in the face, or tongue, or both ; (3) in the foot. In other words, they usually begin in those parts of one side of the body which have the most voluntary use. The order of frequency in which parts suffer illustrates the same law. I mean that fits beginning in the hand are commonest ; next in frequency are those which begin in the face or tongue, and rarest are those which begin in the foot. The law is seen in details. When the fit begins in the hand, the index-finger and thumb are usually the digits first seized ; when in the face, the side of the cheek is first in spasm ; when in the foot, almost invariably the great-toe.” As Dr. Jackson says, the spasm “ prefers,” so to speak, to begin in those parts which have the most voluntary uses ; in other words, in those parts which have the more leading, independent, separate and varied movements ; in other words still, in those parts the movements of which are last acquired—“ educated.” Physiologically, a voluntary part, the hand, for instance, is one which has the greater number of different movements at the greater number of different intervals ; that is, the more “ varied ” uses. An automatic part, the chest, for exam- ple, is one which has the greater number of similar movements at the greater number of equal intervals; shortly, the more “ similar ” uses. Hence, convulsions which begin in the hand usually begin in the thumb and index-finger—in the most voluntary parts of the body. An epileptic paroxysm is a sudden, excessive, and rapid discharge of gray matter of some part of the brain. Instead of working off its force gradually and regularly, it explodes it, as it were. The gray mat- ter which is the seat of a “ discharging lesion ” is in a permanently ab- normal state of nutrition, and hence is permanently abnormal in func- tion. Thus a first fit is a discharge of a part which has for some time before been in a state of mal-nutrition. And a still further inference is that such “ causes ” of epilepsy as fright are only determining causes of the first explosion. In regard to this latter point, I am entirely in accord with Dr. Jack- son. We frequently see cases of epilepsy which, we are told, were ori- ginally caused by a mental shock of some kind. But if the shock were in reality the primary cause there should be no subsequent epileptic seizures. With the cessation of the cause the effect should cease. On the contrary, we find that after some time, generally quite long, which of itself is sufficient to show that the continuance is not due to the initial convulsion, a second occurs, and then, after a shorter in- terval, a third, and so on. It is very evident that if the fright were the cause the fits would be more frequent at first, and less so subse- quently. EPILEPSY. 687 But to return to Dr. Jackson’s views : “ Epilepsy is not a particular grouping of symptoms occurring occasionally ; it is a name for any sort of nervous symptom or group of symptoms occurring occasionally from local discharge, whether the discharge puts muscles in movement or not—that is, whether there be a convulsion or not matters nothing for the definition. A paroxysm of subjective sensation of smell is an epilepsy as much as is a paroxysm of convulsion ; each is the result of sudden local dis- charge of gray matter. “ It does not matter for the definition whether there be loss of con- sciousness or not; loss of consciousness is a fundamental thing in most of the accepted definitions. If there be no loss of consciousness there is, according to most physicians, not epilepsy, and the term ‘epilepti- form ’ is used. But, even when using the term epilepsy in the ordinary sense of the word, the separation into cases where there is, and where there is not loss of consciousness, has no physiological warrant. It is an arbitrary distinction of psychological parentage. Loss of conscious- ness is not an utterly different thing from other symptoms. It is not to be spoken of as an epiphenomenon or as a complication. Conscious- ness has of course anatomical substrata as speaking has. The sensori-motor processes concerned in consciousness are only in degree different from others. They are the most special of all special nervous processes, the series evolved out of all other (lower) series. “ To lose consciousness is to lose the use of the most special of aU nervous processes whatsoever. If those parts of the brain be first af- fected by strong discharge where the most special of all nervous pro- cesses lie, there will be loss of consciousness at the outset. If processes of subordinate series be discharged, loss of consciousness, of course, occurs later. For example, in cases of convulsions beginning in the hand, consciousness is in most cases lost as soon as or just before the leg is reached by the spasm. In these cases the internal process will be that consciousness is lost as soon as the most special of all processes are reached by the internal discharge (or since the sensori-motor pro- cesses underlying consciousness are evolved out of lower series), when as large a quantity of a subordinate yet important series is put hors de combat. But, of course, one does not locate consciousness so geograph- ically as the mere words we must use seem to imply. If a patient sud- denly loses, by any process, the use of any large part of either of the two highest divisions of the nervous system, he will lose consciousness. “ The following are epilepsies : “ (1) A sudden and temporary stench in the nose, with transient unconsciousness ; (2) a sudden and temporary development of blue vision ; (3) spasm of the right side of the face with stoppage of speech ; (4) tingling of the index-finger and thumb, followed by spasm of the hand and forearm ; (5) a convulsion almost immediately 688 CEREBRO-SPINAL DISEASES. universal, with immediate loss of consciousness ; (6) certain vertigi- nous attacks. “All these six seizures are alike, in that each results from an occasional and excessive discharge of unstable gray matter. This is the one functional alteration of nerve-tissue underlying the different phenomena.” Dr. Jackson then goes on to state that though these six kinds of seizures are alike physiologically, they are very unlike anatomically. That is, that the seat of the discharging lesion is different for each, and he urges that the efforts of physicians should be directed to the discovery of this seat from a consideration of the character and locali- zation of the manifestation. In a “ destroying lesion,” such, for in- stance, as is produced by cerebral haemorrhage, the scientific physician endeavors, by a careful study of the phenomena, to determine the situa- tion of the injury, but in cases of spasm the inquiries rarely relate to anything more than an attempt to ascertain the character of the con- vulsion. That this is true is not to be doubted. Further, Dr. Jackson asserts that by comparing the phenomena produced by a “ destroying lesion ” with those which result from a “ discharging lesion ” we may obtain very important data for further comparison. The experiments of Ferrier, Hitzig and Fritsche, and others, have proved conclusively that destruction of certain cortical areas is invari- ably followed by paralysis of certain muscles. Irritation of the same cortical areas, on the other hand, just as invariably produces spas- modic movements in the same muscles which were previously paralyzed by a destructive lesion. It is thus definitely proved that certain mus- cles, or groups of muscles, are in intimate relation with certain groups of cortical cells. The precise situation of these various groups of cells, or “ centres,” as they are termed, has been definitely located (see p. 337). Thus we are enabled, in cases of epilepsy in which the spasms are unilateral, or confined to. one limb, or to a part of one limb, to locate with precision that part of the cerebral motor cortex which is the seat of irritation, and which gives rise to the “ discharges of motor force.” Perhaps it would be too much to say that Dr. Jackson’s views should be adopted in their entirety, but that they are in great part cor- rect every physician who has seen much of the very important disease to which they relate will readily admit. The point in regard to which I should be most disposed to differ with him is that in which he too sweepingly, in my opinion, classes all “occasional, sudden, excessive, rapid and local, sensorial or motor phenomena ” as epileptic. Thus, I am quite sure I have repeatedly witnessed “tingling of the index-fin- ger and thumb, followed by spasm of the hand and forearm,” result from injury of the eccentric nervous system, from pressure on, or other injury of, the brachial plexus, for instance. Now, although such lesion EPILEPSY. 689 may, under certain circumstances, produce such intra-eranial disorder as eventually to cause epilepsy, knowing what we do of the functions of the nerves and the effects of injuries to their trunks, we need not go so far as the gray matter for an explanation of the phenomena. Ex- periments on animals—and indeed as I have repeatedly witnessed in the human subject—show us that, even when a nerve-trunk is divided, irri- tation of its peripheral extremity will give rise to just such phenomena as Dr. Jackson calls epileptic, except in the one point—not an essential one—of “ tingling.” In a patient whom I saw in the Presbyterian Hospital a year or so ago, in the service of Dr. Post, the median nerve was exposed for the space of over two inches, and when it was touched with a probe or the finger, tingling in the skin below and spasm of the muscles of the forearm were at once produced. In the present state of our knowledge it appears to me better to regard no spasm as epileptic, which is not accompanied with loss, or at least disturbance of consciousness. The experiments of Hitzig, Per- rier, and others, certainly throw a great deal of light on the nature of the epileptic phenomena, and give great support to many of Dr. Jack- son’s arguments ; but they also show us that irritation of the gray matter of the brain will cause spasms, which, though partaking to a superficial examination of the character of epilepsy, are clearly not this disease, even as Dr. Jackson regards it. It is true that such irritation repeatedly made will in time so alter the properties of the gray matter as to lead to the production of spontaneous spasms, which may be epi- leptic, but that is quite a different thing. The experiments made by Dr. Roberts Bartholow 1 on a patient under his charge, in the Good Samaritan Hospital in Cincinnati, show that both disorders of sensibility and spasm are produced in the human subject by irritation of the gray matter of the cerebral convolutions ; but in this case the phenomena disappeared as soon as the irritation ceased. Such transient results, clearly and distinctly due to an irrita- tion of the gray matter, may be epileptiform, but to my mind they are not epileptic. But quite recently Hitzig 2 has succeeded in producing true epilepsy in animals by irritating the cortical centres ; after a shorter or longer period—a day to five or six weeks—spontaneous, well-characterized epileptic convulsions ensued. The importance of such observations as those of Bartholow and Hitzig can scarcely be over-estimated. Brown-Sequard has shown that epilepsy may be caused by irritation of the peripheral nervous system, and it is quite certain that the tin- gling and spasm of the hand, which are at first perhaps only due to ec- centric lesions or derangements, may result in epilepsy. A case is now under my charge—a young gentleman from North 1 American Journal of the Medical Sciences, April, 1874. 8 “ Untersuchungen ueber das Gehirn,” Berlin, 1874, p. 271. 690 CER EBRO-SPINAL DISEASES. Carolina, whom I saw first over two years since. At that time it was only necessary to touch the left side of his neck, over the middle third of the sterno-mastoid muscle, to induce spasm of the muscles of the neck, shoulder, and face, on the same side, unaccompanied by loss of consciousness. This condition had apparently been induced in the first instance by his wearing a high shirt-collar, and in the beginning con- sisted of nothing more than a slight twitching of the muscles at the left angle of the mouth. Probably, if he had then ceased wearing that kind of collar, the excessive hyperaesthesia of the eccentric nerves would have spontaneously ceased. As it was, an increase of all the phenomena took place; and finally, the least touch, even that of a camel’s-hair pencil or a current of air, was sufficient to induce a spasm. Blistering, cauterization, and all kinds of local anaesthetics, were tried in vain, but eventually they ceased under the use of large doses of the bromide of sodium. But during all this time, unless an irritation of some kind—the lighter the more powerful, for strong pressure was not an efficient agent—there were no spasms. That such a condition was evidence of a strong epileptoid tendency I did not doubt, and mjr fore- bodings of the ultimate result were fulfilled, for after the lapse of about two years he returned to me with no hyperaesthsia of the skin of his neck, but with occasional fully-developed epileptic paroxysms, for which he is now under treatment. Inquiry, however, showed that they were the result of late hours and indiscretions in diet, and that apparently they had no connection with the former series of attacks. Relative to this subject of convulsion without loss of consciousness but appearing paroxysmally, I shall have some remarks to make in the next chapter, under the head of “ Convulsive Tremor.” It has been urged by some writers that migraine is a modified epi- lepsy. Dr. Hughlings Jackson would certainly regard such cases as those of Sir John Herschel, the astronomer-royal, the late Sir C. Wheat- stone, Dr. Hubert Airy, and, going farther back, those of Dr. Parry and Dr. Wollaston, as genuine epilepsy. Dr. Latham,1 in his very in- structive little book, from which I cite these examples, quotes as fol- lows Sir John Herschel’s account of the phenomena observed in his own case, in which there were present in his field of vision irregular fortification-like figures, the margins of which were colored: “ In one attack in myself, which occurred while I was conversing with an acquaintance, I soon became painfully sensible that I had not the usual command of speech ; that my memory failed so much that I did not know what I had said or had attempted to say, and that I might be talking to another.” Dr. Airy, who has also described his own case, says : “ Sometimes the speech is affected, and the memory at the same 1 “ On Nervous or Sick Headache,” Cambridge (England), 1 p. 10; also, Philo- sophical Magazine, vol. xxx., p. 21. EPILEPSY. 691 lime. On one occasion the mouth was seen to be drawn to one side.” In a young female who came under Dr. Latham’s observation, and who had colored spectra, there was a tingling of the arm and the side of the tongue, and on the same side with the spectra. Her sister and father were affected in precisely the same way. In another case the patient complained of a feeling of pinching and scratching on that side of the face corresponding with the glimmering. In most of these cases these spectra and sensations were followed by headache of severe character, attended with nausea and vomiting. But, notwithstanding the resemblance to epilepsy which all these phenomena of migraine suggest, Dr. Latham asserts that it differs widely from that terrible disorder in that it never threatens life, is never associated with unconsciousness, and that he has never known it to pass into epilepsy. On the contrary, with advancing age the at- tacks, as a rule, become much less frequent. They cease generally after fifty or sixty, and in women, not uncommonly, at the change of life. Dr. Latham holds the view that migraine is an affection of the sym- pathetic system; that the ocular spectra are the result of an ansemic condition of the brain due to a tonic contraction of the arteries; and that the pain which subsequently appears is the result of arterial relax- ation and consequent cerebral congestion. In his most thorough and valuable work Dr. Liveing1 discusses the whole subject of migraine in all its relations; and, while admitting with Marshall Hall, Sieveking and others that very intimate relations exist between sick-headache and epilepsy, and adducing several examples in which epilepsy has occurred to persons who were in previous years sub- ject to the former affection, nevertheless regards such occurrences as quite exceptional, and as instances only of that occasional metamor- phosis of neuroses so often witnessed. That migraine is an affection of the vaso-motor system is rendered very probable by the observations of Mollendorff,2 who reaches the con- clusion that it is the consequence of arterial hyperoemia. He found that ophthalmoscopic examination of the eye of the affected side re- vealed the existence of dilatation of the arteria centralis retinas as well as of the choroidal vessels and of a bright-scarlet color of the fundus, while on the other side the vessels were normal, and the fundus, of its usual dark-red color. This theory is adopted by Dr. Bergens in a recent elaborate paper. It is the very opposite to that proposed by Dr. Bois-Reymond, accord- 1 “ On Megrim, Sick-headache, and some Allied Disorders, a Contribution to the Pa- thology of Nerve-Storms,” London, 1873. 2 “Ueber Hemicrania,” Archiv. fur palhologische Anatomie, Band xl., p. 385. 8 “ On the Pathogenesis of Hemicrania,” translation from the German by Dr, H. Gradle, in the Chicago Journal of Nervous and Mental Diseases, vol. i., 1874, p. 296. 692 CEREBRO-SPINAL DISEASES. ing to which migraine is due to a tetanic contraction of the cerebral arteries. Neither of these authors regards migraine as a form of epi- lepsy. My experience with sick-headache has been quite extensive. I have frequently witnessed cases in which there were chromatic ocular spectra such as those described by Latham, Sieveking, and others, but I have never perceived anything more in the most marked forms of the affec- tion than a resemblance to some of the phenomena of the epileptic attack. One very noticeable difference is as regards the effect upon the mind. In epilepsy the slightest and most transient seizures gener- ally impair, after a time, the mental faculties, especially the memory, while in migraine, no matter how severe or how frequent may be the attacks, the mind in all its parts retains its full vigor. There seems to be little or no doubt, therefore, that epilepsy is the result of cerebral irritation, which finally culminates in a sudden discharge of nerve-force. The seat of the discharge may be either in the cortex or in the medulla oblongata. There is some evidence, how- ever, which tends to show that even where the primary irritation is cortical the spasms are the result of the reflection of this irritation to the “ epileptic centre ” in the medulla. Treatment.—The treatment of epilepsy rests almost solely on ex- perience. To attempt the consideration of all the means which have been employed would be a fruitless task, even though it were possible. I shall therefore content myself with detailing the measures which I have found most useful. Among medical remedies the bromides stand preeminent, and should be thoroughly tried first in every case. The bromide of potassium, sodium, or calcium may be used. Of these, the bromide of sodium is the most advantageous in the majority of cases. Its taste—that of common salt—is not unpleasant, and it agrees better with the digestive system than the potassium compound. The bromide of calcium de- ranges the system still less, but its taste is not so pleasant, and it is much more expensive. Whichever one is preferred, the dose for an adult in ordinary cases and in the beginning of the treatment is fifteen grains three times a day in solution. It must be clearly understood that the bromide, if successful in arresting the convulsions, must be taken for a long time, in order to increase the probability of a cure. I never discontinue it under two years, and sometimes persevere with it still longer, if in the mean time there have been attacks of vertigo, aurre, or other epileptoid manifesta- tions. After the initial doses have been given for about two months, if there are no symptoms indicating extreme bromism, or if there has been no paroxysm, I increase the doses by one-half. If there have been paroxysms in the mean time, I increase one-half after each paroxysm, EPILEPSY. 693 until they are arrested, or until I am satisfied that the bromide is ineffi- cacious or injurious. I have sometimes been compelled to carry it to the extent of nearly two hundred grains a day, and to continue it at that quantity for eight or ten days. When the system is thoroughly under the influence of the remedy and the convulsions have ceased, the doses may be reduced; but they should not be discontinued. The bromides are less efficacious in the nocturnal variety of epilep- tic seizures, and in those which consist mainly of loss of consciousness, than in the diurnal and strongly convulsive kinds. In the former, sometimes, they increase the number and severity of the attacks, and in such cases should of course be at once discontinued. A point connected with their action must not be overlooked, and that is, the cachexia which so generally attends their administration in large doses. In a memoir,1 published over six years ago, and which has been cited in another connection, I brought forward several cases in which this cachexia had been produced. Greatly-increased experience has convinced me that, though in general it never causes any perma- nently ill effects, frequently great constitutional disturbance is in- duced. In three cases large carbuncles were caused, in a few I have been obliged to suspend for a time the administration of the medicink, and in two cases death resulted, in one from the patient taking larger doses than were prescribed, and continuing them while not under my immediate care, and in the other from the supervention of pneumonia while under the full influence of the remedy. But, I am very sure that the bromic cachexia is favorable to the eradi- cation of the epileptic tendency, and I therefore endeavor to produce it as soon as possible. It appears in many cases to alter the whole organ- ism of the patient to such an extent as to leave him, when it disap- pears, with his nutritive processes and his proclivities so modified that epilepsy is no longer possible. The physician will require all his firm- ness and courage to persevere in those cases in which the bromism is extreme, but he should not yield unless the phenomena are so intense and the strength of the patient so greatly reduced as to excite his gravest apprehensions. The phenomena indicative of bromism will be given further on under the head of toxic affections of the nervous system. It may be, however, mentioned here that in the peculiar faculty possessed by the bromides of lessening the reflex excitability of the pharynx we have a ready means of ascertaining the extent to which the system is under the ac- tion of the remedy. If the handle of a spoon be pressed gently against the posterior wall of the pharynx of a healthy person, slight nausea and efforts to vomit are at once excited ; but, if such a person be subse- quently brought fully under the influence of any one of the bromides, 1 “ On some of the Effects of the Bromide of Potassium when administered in Large Doses,” Journal of Psychological Medicine, January, 1869, p. 46. 694 CEREBRO-SPINAL DISEASES. the irritability of that part is destroyed, so that nausea or vomiting is no longer excited by pressure. Herpin 1 several years ago called attention to the Salts of zinc in the treatment of epilepsy. He preferred the oxide, and for a long time I made extensive use of this preparation in the treatment of the disease in question. Latterly, however, I have used the lactate, and still more recently the bromide, with very definitely beneficial results. It is best administered in the form of a sirup—my formula is : IJ. Zinci bromidi, 3 j ; syrupus simplicis, § j. M. ft. sol.—which may be given in doses of ten drops gradually increased to thirty or more three times a day. It should be given largely diluted, as being the less apt to excite nausea. In several cases the bromide of zinc has proved exceedingly effica- cious thus far in arresting the paroxysms where other bromides had failed. Bromism is not an attendant on its administration, and yet it is quite probable that the bromine of the compound exercises consid- erable curative influence. I have given it as long a time as six months consecutively without producing cachexia, and to the extent in some cases of forty grains a day. A troublesome feature which often attends the administration of the bromides—except the zinc compound—is the cutaneous eruption. Arsenic has been said to obviate the tendency to this complication, and to cure it where already present. In a few cases I have seen the use of the drug—four or five drops of Fowler’s solution with each dose of the bromide—prove serviceable ; but in the majority of cases it has ap- peared to be inefficacious. Owing to the supervention of carbuncles with a strong predisposition to gangrene of the skin, I have been obliged in several cases to discontinue the bromide of potassium. The calcium compound is, I think, not so liable as those of potassium, sodium, or ammonium, to cause this trouble. In the nocturnal form of epilepsy strychnia is sometimes remarkably efficacious. It may be given in the beginning in the dose of the thir- tieth of a grain three times a day gradually increased. A good for- mula for its administration is : $ Strychnia sulph., gr. ij ; aqua dest., § j. M. ft. sol. Dose, eight drops three times a day for the first two weeks, then nine drops for the next two weeks, increasing a drop every two weeks for a year, and perhaps longer. Strychnia is also said to be useful in epilepsy of stomachal origin— that is, cases produced by gastric derangement. The nitrite of amyl, first proposed and used in epilepsy by Dr. Weir Mitchell, is certainly beneficial in arresting the paroxysm, when there is an aura sufficiently pronounced and slow to give the patient the time to employ it. Five to ten drops may be inhaled from a handkerchief with safety, and generally with success. As there is generally not time to pour it out, this quantity should always be kept on the person in a 1 “Du pronostic et du traitement curatif de l’epilepsie,” Paris, 1852. EPILEPSY. 695 glass-stoppered vial ready for use at a moment’s notice. Dr. McBride, of this city, has had made little hollow thin glass beads containing the proper quantity of the nitrite of amyl, and when the patient experi- ences the warning, one of these is crushed in a handkerchief and the vapor inhaled through the mouth. Dr. Crichton Browne 1 has not only used the nitrite of amyl in pre- senting individual paroxysms, but has given it with advantage with the view of breaking up the status epilepticus—a condition in which the fits succeed each other with scarcely an intermission, the patient being unconscious during such intervals as occur. The results of his expe- rience are such as to convince him that it will be found invaluable in many cases, not only in postponing the paroxysm, but altogether pre- venting epileptic seizures. It may be stated that the effect of the nitrite when inhaled is to ac- celerate the action of the heart, to make the face red, and to cause a feeling of fullness in the head, and a sensation as if pins and needles were sticking into the skin of the face, neck, and chest. These phe- nomena disappear in a few moments, Within the last few years I have used the nitrite of amyl internally with, in some cases, decided benefit. It may be given in doses of from half a drop up to three or four, gradually increased, if necessary, and should be continued for a long time. A good formula is : . Amyl nit., Tij x ; alcoholis, n# xc. M. ft. sol. Dose, from five to twenty or thirty drops a day. I usually begin with five drops on a lump of sugar, morning, afternoon, and bedtime, increasing the doses one drop every week so long as it continues to control the disease. Several cases of epileptiform seizures clearly due to syphilitic infec- tion have been under my charge, and have been treated with benefit by the bromides in conjunction with the iodide of potassium. In five of these, cures are known to have been effected. As regards other medicinal remedies for epilepsy, I have but little to say. Belladonna has never in my hands produced the least good effect, neither has the nitrate of silver, nor indigo, nor cotyledon um- bilicus, nor digitalis, nor any of the salts of copper. The same may be said of a hundred other substances less favorably known. Hydrate of chloral in three cases mitigated the frequency of the paroxysms, but only for a short time. Calabar bean was slightly beneficial in one case. Borax, after a very full trial, absolutely failed. But the whole treatment of epilepsy is not confined to drugs. Sur- gical and hygienic measures are often in the highest degree beneficial, and the latter should be brought into action in every case. Of the surgical means the excision of any cicatrix which, by entan- gling a nerve, may be a source of reflex irritation, is occasionally a 1 “ Nitrite of Amyl in Epilepsy,” “ West Riding Lunatic Asylum Medical Reports,” vol. iii., 1873, p. 151. 696 CEREBRO-SPINAL DISEASES. useful measure. This point has been brought forward in an inter- esting memoir by Dr. F. D. Lente,1 in connection with cicatrices of the scalp, but the like reasoning and action are applicable to cica- trices existing in any other part of the body from which an aura appears to start. In injuries of the skull, followed by epilepsy, trephining may be of great service. It has been aptly said that no blow upon the head is slight enough to be despised, and, so far as epilepsy is concerned, this is preeminently true. I have, during the past five years, trephined twenty-three times for epilepsy which was apparently due to cranial injuries. In seven of these the fits ceased, and in two of the seven cases there was neither fracture nor depression. Of the remaining sixteen cases there was no cranial injury to be found in three ; and in thirteen, though there was sucb injury, the operation proved unsuc- cessful, though beneficial results in lessening the frequency of the attacks were obtained in the majority. In one of them the fits did not recur for over a year. The fact that in two of the successful cases no fracture or depression was found is a strong point in favor of Dr. Lente’s view that epilepsy is sometimes the result of a cicatrix of the scalp, for, in both, the incisions in the scalp, as in all the others, were made so as to include the scalp-wound. In those cases in which the spasms are confined to one side of the body, to one leg, to one arm, or to one side of the face, trephining over the motor centre involved, and the removal of the tumor or the excision of the diseased area of cortex, should be insisted upon as soon as the precise character of the disease can be ascertained. As the result of my experience, I am decidedly of the opinion that, in all cases of epilepsy in which there is injury of the skull or scalp, trephining or excision of the cicatrix should be performed, as may be proper. In some cases counter-irritation to the nape of the neck is decidedly beneficial. It may consist either of a seton, which may be left in for several months, or the repeated application of the actual cautery. Counter-irritation is especially indicated in those cases in which the tongue is bitten, and instances in which internal remedies have failed till they were supplemented by this means are not uncommon. The hygienic management of the patient is important. A large por- tion of the day should be passed in the open air ; bodily exercise should be regular, but not excessive ; the food should be nutritious, but neither exciting nor indigestible. The importance of avoiding every aliment- ary substance calculated to cause gastric or intestinal irritation cannot be over-estimated. I have frequently seen paroxysms directly caused 1 “Neuralgia and other Neuroses arising from Cicatrices of the Scalp, and their Surgical Treatment,” “ Transactions of the American Neurological Association,” vol. i., New York, 1875, p. 157. EPILEPSY. 697 by nuts, dried fruits, pastry, heavy and badly-baked bread, excess in the use of alcoholic liquors, confectionery, and the like. And a diet consisting mainly of farinaceous substances is certainly preferable to one in which meat forms the larger part. I have in three cases effected entire cures by confining the patients for several months to a diet con- sisting at first of skim-milk, to which after a time a little bread was added. The bowels must be kept regular. Baths should be frequently taken, but should not be so cold as to cause severe shock or physical depression. Turkish baths, I am inclined to think, are useful in many cases, particularly in those occurring in persons of full and gross habit of body. Overheated and ill-ventilated apartments should be avoided. The clothing should be warm in winter and cool in summer. The mind should not be overtasked, and the emotions must not be unduly excited. Individual attacks may sometimes be prevented by other means than the nitrite of amyl. One gentleman under my charge assures me that he can often dissipate the premonitary symptoms, and thus stop the development of the paroxysm, by a strong exertion of the will. Another can arrest them sometimes by changing the position of his body. If standing, he lies down ; if lying down, he rises suddenly and paces the room violently. Another stops them by putting salt in his mouth, and two can frequently prevent them by tightening straps which I have instructed them to keep constantly around the wrist. In all these cases there is an aura, and in the two latter it appears to start from the hand. But, before resorting to any specific treatment for epilepsy, diligent search should be made for the cause, and this should be removed, if possible, without the least delay. Often an eccentric irritation, such as worms in the intestinal canal, implication of a nerve in an injury, disorders of menstruation, etc., can be discovered, without the removal of which a permanent cure is impossible. In several of the cases cited, success in the treatment was in a great measure due to acting on this principle. The treatment during the paroxysm remains to be considered. It is simple, and, beyond a few obvious measures, consists in letting the patient alone. The head should be elevated, the collar and cravat loosened, a piece of soft wood put between the teeth so as to prevent injury to the tongue, and the patient so placed that he cannot fall or otherwise injure himself in his struggles. During the subsequent stupor he should be kept quiet. Bloodletting is never necessary, although it is recommended as proper in certain cases by Jaccoud. 698 CEREBRO-SPINAL DISEASES. CHAPTER III. Under the designation of convulsive tremor, I propose to include all those cases of non-rhythmical tremor or clonic convulsive move- ments which are unattended with loss of consciousness, but which, nevertheless, are paroxysmal in character. As the affection has not yet found its way into the systematic trea- tises, I shall, as in the matter of spinal irritation, devote a few words to its history, and, in so doing, shall draw largely from a paper of my own on the subject, published over eight years ago,1 and from a clinical lecture* delivered to the class at the Bellevue Hospital Medical College in the winter of 1871-’72. A few years ago Friedreich3 reported a case of what he termed paramyoclonus multiplex, which differs in no essential particular from the cases described in this chapter. There is a tendency on the part of some observers to regard paramyoclonus multiplex and convulsive tremor as two distinct affections, without there being, in my opinion, any just grounds for so doing. History and Symptoms.—In the year 1822 Dr. Pritchard,4 under the name of convulsive tremor, gave an account of two cases, presenting somewhat similar features to the one before us. His attention was first directed to the subject by noticing that, in some epileptic patients who had come under his observation, fits of tremor occurred in the in- tervals between the paroxysms and even appeared to take the place of the ordinary seizure. He then noticed several cases in which there were no epileptic attacks, but in which there were violent clonic spasms of the muscles, accompanied with severe pain in the head and profuse perspiration. Dr. Pritchard states that, previous to his observations, the affection had not attracted much attention ; but he cites a case from Tulpius of a young unmarried woman, of a pale complexion and phlegmatic temperament, who was afflicted during three years with what was called the shaking-palsy, which did not affect her constantly, but came on in periodical fits; each paroxysm lasted nearly two hours, and was accompanied by hoarseness and loss of voice, the consciousness being unimpaired. He also refers to other cases quoted by Sauvages from Bonetus, in which the symptoms were very similar, consisting of convulsive tremor, attended with headache and vertigo. This disorder was fatal in a few days, and after death a parasite was found in the brain. In this con- CONVULSIVE TREMOR. 1 “On Convulsive Tremor,” New York Medical Journal, June, 1867, p. 185. 2 “Clinical Lectures on Diseases of the Nervous System,” New York, 1874, p. 164. 3 Virchow's Archives, Bd. lxxxvi., p. 421.' 4 “A Treatise on Diseases of the Nervous System,” London, 1822, p. S93. CONVULSIVE TREMOR. 699 nection it is interesting to recall the fact that the sheep is subject to a somewhat similar train of symptoms, due to the presence of an ento- zobn in the brain. Dr. Pritchard then relates his own cases, of which the following ac- count is an abstract: John Pugh, a carpenter, of meagre habit, low stature, and dark hair, aged fifty, was admitted into St. Peter’s Hospital March 1, 1820. About a month previously he had suffered from tonsillitis and subse- quently had some difficulty of breathing, which was supposed to be asthmatic. He had complained of headache for some time. On the 23d of February he was attacked with a violent tremor, which con- tinued for two or three hours, and then went off after he had taken an emetic. It recurred on the following day at the same time, and on every succeeding day about the same hour. At the time of his admis- sion he was laboring under a paroxysm. On first looking at the man, Dr. Pritchard supposed him to be in the cold stage of intermittent fever, but on closer and more careful ex- amination his affection was seen to be very different. All the muscles of the upper extremities, including those connected with the ribs, clav- icle, and scapula, were constantly agitated by a convulsive movement which was almost entirely confined to them. The lower extremities were quite free from disorder. The man was perfectly conscious, and able to answer any question distinctly. His pulse was quick and ap- parently irregular. Owing to the constant agitation of the tendons it was impossible to arrive at certainty on this latter point. The skin was warm, and there was no sensation of chilliness. The upper part of the body was in a state of profuse perspiration. He complained of ver- tigo and headache. Bloodletting was ordered; a large orifice was made, and the blood allowed to flow till thirty-eight ounces had escaped, when syncope en- sued. When half the above quantity had passed, the tremor became more general and severe. The gluteal muscles were so greatly con- vulsed that by their action the patient was thrown up from his seat with the motion of a man sitting on a trotting horse. When he became sick and faint, the arm was tied up and he was laid upon a bed. The tremor immediately ceased, except some slight and partial quivering. He was then strongly purged, and this operation was continued every night. On the 5th, at 11 A. M., the tremor returned. Cold effu- sion was directed ; as soon as the cold water was thrown over him the tremor ceased. On the 9th there had been no return of the tremor. Calomel and sulphate of magnesia were now prescribed and on the 11th the tremor returned, lasting, however, but about twenty minutes. From this time he was free from the affection, but, as might have been expected, when the character of the treatment is considered, he fell into a state of de- 700 CEREBRO-SPINAL DISEASES. bility. There were loss of appetite, cough, expectoration, and inflam- mation of the vein, ensuing from the bleeding. In the next case the paroxysms of tremor were the most remarkable feature, but there were also stupor and delirium. John Jones, a seafaring man, aged twenty-five, was brought to the hospital March 11, 1819, under a warrant of lunacy ; was in the habit of drinking spirituous liquors. Three weeks previously he was seized with rigors, attended with coldness, and followed by heat, headache, and wandering pains in the limbs. The symptoms ushered in a state of stupor and delirium, during which his countenance became distorted, the eyes rolled, the muscles of the face were slightly convulsed, and the body was generally agitated. After a time all these symptoms subsided and he became perfectly rational, but seemed a little stupid, as if roused from a sleep. The paroxysms returned at uncertain intervals and with the same succession of symptoms. He was bled and purged, and finally brought to the hospital. On admission he was in a state of delirium. He rolled his head about and was in constant motion. The temporal arteries beat rapidly and forcibly; the scalp was hot, the feet cold; face flushed and tongue a little furred. His head was shaved and covered with cold wet pads, his feet were immersed in hot water, twenty leeches were then applied to the head, and calomel and tartar-emetic with cathartic draught administered. The next day he was rational, but, as he complained of pain in the head and in the region of the liver, and as his pulse was 130, full and jerking, he was bled to the extent of eight ounces ; syncope followed. Twelve leeches and a blister were then applied to the right hypo- chondriac region, and calomel, cathartic draught, and low diet ordered. Notwithstanding the treatment, he continued to survive, and in the evening had two returns of the tremor followed by the usual symptoms. On the 14th had several paroxysms, and was again freely purged ; was occasionally bled from the temporal artery, and often leeched freely. Nitrate of silver wras subsequently administered, and on the 23d of June he was discharged cured. Dr. Pritchard states that he met with two other instances of parox- ysms of tremor unaccompanied with spasm, and occurring in persons who had suffered from an attack of paralysis. Evidently Dr. Pritchard has embraced two or three separate affec- tions under the designation of convulsive tremor. The first case I have quoted from him appears to be a distinct and not previously-described disorder; the second case was probably one of cerebral congestion or aborted epilepsy; and those which he states he had seen as the sequence of paralysis were doubtless to be classed under some one or other of the forms of sclerosis of the brain and spinal cord. The first case alone is to be regarded as one of convulsive tremor, as described in this chapter. CONVULSIVE TREMOR. 701 In his very excellent treatise on the shaking-palsy, Parkinson,1 in oalling attention to the fact that several diseases characterized by tre- mor have been confounded with paralysis agitans, quotes the following case from Dr. Kirkland : “ Mary Ford, of a sanguineous and robust constitution, had an invol- untary motion of her right arm, occasioned by a fright, which first brought on convulsion-fits and most excruciating pain in the stomach, which vanished on a sudden, and her right arm was instantaneously flung into an involuntary and perpetual motion like the swing of a pen- dulum, raising the hand at every vibration higher than the head ; but, if by any means whatever it was stopped, the pain in her stomach came on again, and convulsion-fits were the certain consequence, which went off when the vibration of her hand returned.” Parkinson also quotes another case from the same source, resulting apparently from worms, and which is thus described : “ A poor boy, about twelve or thirteen years of age, was seized with a shaking-palsy. His legs became useless, and, together with his head and hands, were in continual agitation ; after many weeks’ trial of va- rious remedies, my assistance was desired. His bowels being cleared, I ordered him a grain of opium a day in the gum-pill ; and in three or four days the shaking had nearly left him. By pursuing this plan, the medi- cine proving a vermifuge, he could soon walk, and was restored to per- fect health. Toulmouche,3 in a paper which is very suggestive in the light of re- cent contributions to neurological pathology, cites a case which was evidently one of convulsive tremor : “ A woman, whose respiration was convulsive, presented from time to time the following condition : Her nostrils were strongly dilated, the angles of the mouth drawn down, the shoulders and chest spasmodical- ly elevated, the inspiration strong and deep, the sterno-cleido-mastoid muscles were powerfully contracted. During these paroxysms, which lasted several minutes, the patient was deprived of the faculty of speech and threatened with suffocation. Nevertheless, she could, if so direct- ed, move the head, the shoulders, and the muscles of the face, although the spasm continued. ... In another case the affection was almost en- tirely confined to the sterno-cleido-mastoid muscle. The patient could turn the head in either direction, but gradually it moved from right to left, without her ability to control its action, so that the right ear al- most rested upon the sternum. The other muscles of the shoulder con- tracted at the same time. He likewise reports another case in which the head was almost continually in motion, the patient executing twen- 1 “Essay on the Shaking-Palsy,” London, lSlY, p. 29. 2 “ Observations de quelques fonctions involuntaires des appareils de la locomotion, et de la prehension,” “Memoires de l’academie royale de medecine,” tome Paris, 1833. 702 CEREBROSPINAL DISEASES. ty-two rotations in a minute ; the movement was due to the alternate contraction of the sterno-cleido-mastoid and splenius muscles of each side ; respiration was not obstructed. The movements diminished and finally ceased after two or three attacks of haemoptysis. “ The conclusions which the author draws from his own cases, and those which he cites from other authorities, are mainly interesting in relation to his theory of the pathology. They are— “ 1. That there exist, for the movements of the different groups of muscles, different central motor forces. “ 2. That the cerebellum only presides over the coordination of those complex movements wThich are necessary to the different acts of stand- ing and locomotion, and not at all over those that regulate the more sim- ple movements of the trunk and the members. “3. That this nerve-centre supplies to vertebrate animals the power to maintain themselves in equilibrium and to exercise locomotion. “ 4. That, if, in the species of neurosis I have described, the sensa- tion and the intellectual faculties experience no change, this fact is due to the circumstance that the lesions of the cerebellum have not yet in- volved the tubercula quadrigemina. That these last-named organs are in a state of dependence upon the brain ; since in the normal state ani- mals move through the impulsion of various motives of which the brain is the seat. “ 5. That finally a number of affections called nervous, consisting in the most erratic derangements of the muscular functions, such as an irresistible tendency to go backward or to advance without rational motive, to leap, to perform other disorderly movements, constitute only a species of insanity or aberration of the locomotor functions depend- ing on an affection either organic or functional of the cerebellum.” I have quoted the conclusions of Toulmouche in full more as evi- dence of the fact that he was disposed to locate the seat of these trou- bles in the cerebellum, than as intending to endorse his collateral hypotheses. At one time I also held the opinion that the seat of con- vulsive tremor was in the cerebellum, but I have for some time had a different idea on the subject. Up to the publication of my own paper, in 1867, there had been no attempt made to define accurately the features of the disease under no- tice. My description of the affection was based upon three cases. They were as follows : Case I.—J. S., a gentleman, aged thirty-five, single, and engaged in mercantile pursuits, consulted me on March, 14, 1867, for an affec- tion which, as he said, “was driving him mad.” Ordinarily he had nothing to complain of on the score of health. His appetite was good, and all his functions were performed with regularity ; but two or three times during the course of the day he would be seized with severe and uncontrollable muscular tremor, involving his head and all the muscles CONVULSIVE TREMOR. 703 of the trunk and arms. At the same time there would be Headache and an intense feeling of anxiety. There was no loss of consciousness, not even for an instant, or inability to walk or to direct any muscle, and no confusion of thought. After the paroxysm had lasted fifteen or twenty minutes it gradually passed oft’, leaving him in a profuse perspira- tion. While he was sitting in my library an attack came on. He was seized with as much suddenness as though he were struck with an epi- leptic fit. His head shook violently, the muscles of his face were con- vulsed, his arms and hands trembled, and his gluteal muscles contracted so powerfully as to cause him to move convulsively up and down on his chair. His lower extremities were altogether free from spasm or con- vulsion. Upon putting my hand on his wrist, I found that every ten- don was in action, and in the arm, hand, neck, and face, the vibration of the muscular fibres could be distinctly seen and felt. I thought the action was greater on the left than on the right side. The thermometer applied to the axilla marked 101° Fahr., and the assthesiometer showed an increased sensibility of the skin of the face, neck, hands, and all the upper parts of the body I examined. The res- piration was quickened, and the pulse was increased from 80 to 95 per minute. During the continuance of the paroxysm he conversed rationally but with some difficulty, owing to the action of the muscles of the neck, mouth, and chest. The pupils contracted briskly under the influence of light, and dilated when it was shut off. Several times he rose from his chair and paced the room; his movements were perfectly well made. There was a little headache, confined to the occipital region, and a slight but persistent vertigo. I desired him to perform a few movements with his hands, such as buttoning his waistcoat. He had no great difficulty in carrying his hands to the buttons, but it was impossible for him to seize them, and the more his efforts were directed to this end the more difficult it was for him to accomplish it. The trouble was not in loss of strength, for, when I asked him to grasp my hand, he did it with great force, but the tremor was so constant that he could not keep the ends of his fingers at any one point. After the paroxysm had lasted about fifteen minutes it began to subside, and in ten minutes more had entirely passed away. The ther- mometer in the axilla now marked but 98° Fahr., and the hypertesthesia had entirely disappeared, leaving the sensibility of the skin natural. The respiration and pulse became normal in frequency. Upon questioning this gentleman, I ascertained that he had in- dulged to excess in venereal pleasures, and that the first attack of tremor had begun during sexual intercourse. He said that, just as the orgasm was approaching its height, he had experienced a severe pain 704 CEREBRO-SPINAL DISEASES. in the back of his head, accompanied with tremor. That, notwith- standing, he had completed the act, but felt very greatly debilitated after it; the tremor continued for a few minutes, and then passed off. This was about four months before I saw him. Since the beginning of his disease he had entirely abstained from all sexual indulgence, but his tremors had not left him for a night or day. In consequence he was low-spirited, and apprehensive of losing his reason. Case II.—The second case was that of a young lady, aged twenty- one, who was sent to me March 21, 1867, by Dr. C. F. Taylor, to whom she had gone to be treated for lateral curvature of the spine. In addition to this trouble she had for four years been afflicted with a disorder, cer- tainly very singular in its characteristics, and for which she had been treated by many physicians of many systems of practice. The chief and most distressing feature was a spasmodic action of the diaphragm coming on every ten or fifteen minutes, producing convulsive respira- tion, a feeling of impending suffocation, and great mental anxiety. The paroxysms lasted four or five minutes, and then passed off with a long, deep-drawn sigh. None of the respiratory muscles but the dia- phragm were convulsed. By placing the hands over the abdomen this muscle could be distinctly felt in a state of rapid and irregular action. In the intervals of the diaphragmatic paroxysms, there were frequent tremors of the arms, legs, and head. There was almost constant head- ache extending across the crown to the cerebellar region. There was no fever or increased temperature, but great hyperesthesia of the whole surface of the body. The menstrual function was normal in every respect, and there was no evidence of hysteria. Her appetite was bad, and what she did eat was not of a very nutritious character. Occasionally she was subject to fits of great mental and muscular ex- citement, during which she fought and bit all who came near her, but there was no mental aberration. She had never been subject to inter- mittent fever. In this case the convulsive tremor, though more prominently mani- fested in the diaphragm, was not confined to this muscle, for, as I have stated, when it was quiet the muscles of other parts of the body were in irregular but rapid action. There was not the entire cessation of tremor as exhibited in the first case, and the paroxysms were much less uniform and much less extensive in their character. In both cases the tremor was absent during sleep. Case III.—In a third case the patient was a young man aged twenty- five, and a clerk by occupation. He came under my care April 2,1867, to be treated for obstinate headaches, with which he had been affected for several years. On an average he had an attack twice a week of so severe a character as to unfit him for all occupation and to confine him to bed. The pain was limited to the back part of the head, and was exceedingly sharp and lancinating; vertigo and an indescribable twist- CONVULSIVE TREMOR. 705 ing sensation within the cranium accompanied the attack. In addition there was convulsive tremor of the muscles of the head, face, and neck, occurring in paroxysms at intervals while the headache lasted. There was no loss of consciousness and no confusion of thought. There were, however, great physical prostration, and an indisposition to make any mental exertion. In his youth he had, as he informed me, practised masturbation to excess, and since attaining to manhood had indulged freely with women. He was also addicted to the abuse of alcoholic liquors. He was thin, pale, and of deficient vital power. His digestive system was deranged, his appetite bad, his pulse weak and frequent. There was no disease of the lungs or heart. He had had gonorrhoea and stricture, but had never contracted a chancre. He had been under the charge of several physicians, but had never been able to subject himself to the regimen and restrictions in his habits of life which they recommended. Latterly he had undertaken to treat himself, and had done so mainly by inhalation of chloroform. This patient would not abstain from debauchery of all kinds, and 1 dismissed him. Case IV.—A fourth case formed the subject of a clinical lecture which I delivered three years since before the class of the Bellevue Hospital Medical College. The patient, a young man, aged about twen- ty-one, was well nourished, of general healthy appearance, and by oc- cupation a farmer. At periods varying from a few weeks to several months, he was sub- ject to violent convulsive movements in almost all the muscles of the body, and unattended, except in one instance, by loss of consciousness. The paroxysms lasted several hours, and during their continuance the patient, owing to the violent jactitations into which his limbs were thrown, was totally unable to execute voluntary movements. He was even unable to stand without support, and could not guide either his hands or feet. The muscles of speech were likewise affected, and he was consequently unable to articulate distinctly the words he might attempt to utter. While all this was going on, his body was bathed in cold perspiration, and the circulation was accelerated. The respiration was increased in frequency, and there was well-marked and persistent pain in the back of the head and nape of the neck. He was very posi- tive that, except in the one instance to which reference has been made, he had never lost consciousness during a paroxysm, but had always been possessed of his full reasoning faculties. On the occasion of loss of consciousness the paroxysm had lasted several hours ; he was in consequence very much exhausted, and there- fore he may have been suffering from simple syncope, still it is possible the attack in question was epileptic. When he came under my notice, he had been affected for about six years. 706 CEREBRO-SPINAL DISEASES. As he described his paroxysms, the muscles were affected very much as are those of a person suffering from chorea of very violent charac- ter. Case V.—A fifth case was that of a man thirty years of age, who, in November, 1875, came to my clinic for diseases of the nervous sys- tem at the University Medical College. At intervals through the day, as often as twenty or more times, he was seized with violent convulsive movements, tremulous in character, and mainly confined to the muscles of the trunk, neck, and upper extremities. As in the other cases, there was no loss of consciousness, nor was there any other mental disturb- ance. He had no power of control over these paroxysms and no warn- ing of their approach. They were unattended with disturbances of the respiration, circulation, or sensibility. The duration rarely exceeded ten seconds, and was generally shorter than this. It was impossible to say where the convulsive movements originated. They came more as an explosion than as a gradually-developed action. While the convulsion was at its height, he could always cut it short and prevent others for a time by smoking a pipe of tobacco, the requi- sites for which he kept constantly ready. He had been affected for seven years, but had in that time experienced an intermission of about six months. He had never had a paroxysm while asleep. Case VI.—This case was that of a lady from Ohio, who consulted me for paroxysms of convulsive tremor, coming on several times in the course of the week, and involving the upper and lower extremities and neck. There were also marked disturbances of the respiration and cir- culation, and pain in the nape of the neck. The movements consisted of rapid but limited flexions and extensions of the limbs and rotatory movements of the head. The duration of a paroxysm was rarely less than ten minutes, and sometimes was several hours. There was no mental disturbance or impairment of consciousness. The disease had existed for several years, and had proved unamenable to all medical treatment. After each seizure there was a very intense feeling of fa- tigue, but no tendency to sleep or stupor. No paroxysm had ever oc- curred during sleep. The general health was excellent, and the mind was active and strong. Several other cases similar in general features to the foregoing have been under my charge. From this history and description it will be seen that convulsive tremor is an affection characterized by paroxysms of clonic convulsions affecting the voluntary muscles and unattended by loss of conscious- ness or by mental aberration, though sometimes there is emotional dis- turbance. Vertigo and pain in the head are also occasional accompani- ments. Causes.—Nothing very definite is known relative to the etiology of the disease. In one of my cases it began during sexual intercourse ; CONVULSIVE TREMOR. 707 fn another (Case V.) it ensued immediately after a sunstroke, the first paroxysm occurring while the patient was still in a comatose condition; in another (Case III.), sexual and alcoholic excesses appeared to be the cause. In none of the others could any approach to a relation of cause and effect be established. Diagnosis.—From epilepsy, convulsive tremor is distinguished by the absence of loss of consciousness. Many of the cases which Dr. Hughlings Jackson considers epileptic are, in my opinion, more prop- erly embraced under the present category. From chorea it differs in the facts that the muscular action is paroxysmal and not continuous, and that the movements are different in character, those of convulsive tremor being rapid and tremulous, while those of chorea are slower and more systematic. The paroxysmal nature of the actions serves to dis- tinguish it from athetosis, multiple cerebral sclerosis, multiple cerebro- spinal sclerosis, and paralysis agitans. From hysteria it is in uncom- plicated cases diagnosticated by the absence of other symptoms of the hysterical condition, by the fact that the convulsions are not marked by tonic spasms, and the circumstance that they have for each individual case a definite character. Prognosis.—The prognosis is generally favorable, the disease, in my experience, being quite amenable to medical treatment. All the cases under my care recovered except one in which the patient refused to submit to proper hygienic restraints, and in whom treatment was not therefore systematically pursued. Morbid Anatomy and Pathology.—In former papers I have stated my belief that convulsive tremor was an affection of the cerebellum, but in the light of the investigations of Fritsch and Hitzig, Nothnagel, Ferrier, and Bartholow, I am now disposed to consider it due to irrita- tion of nerve-centres in the cortical substance of the cerebrum, con- joined with a hypersesthetic condition of the medulla oblongata and upper part of the spinal cord. And I am the more confirmed in this opinion by some recent experiments by which I have ascertained that a very similar disorder can be induced in dogs by the faradization of the parts mentioned. Ferrier1 produced epileptiform convulsions in rabbits by faradizing the greater part of a hemisphere. In one of my own experiments I exposed both hemispheres and applied to each a piece of chamois-skin thoroughly moistened with water, and cut to fit the surface. The electrodes—metallic buttons—were, then placed one on each piece of cha- mois-skin, and moved lightly over the surfaces for a few seconds. The animal was then allowed to emerge from the anaesthetic condition, and immediately general convulsive movements ensued without loss of consciousness. The result was, therefore, similar to that obtained by 1 “Experimental Researches in Cerebral Physiology and Pathology,” “West Riding Lunatic Asylum Medical Reports,” vol. iii., 1873, p. 30. 708 CEREBRO-SPINAL DISEASES. Ferrier, but so far as I can judge the convulsive movements were more general, and there was no pleurothotonos as in his cases. The parox- ysm lasted about ten seconds, and was repeated, though m >t to the same degree of intensity, after an interval of three minutes. During the next half-hour there were repeated localized convulsive movements in various parts of the body. In another dog I exposed both hemispheres, and also the upper part of the spinal cord, as far down as the fourth cervical vertebra. A piece of wet chamois-skin was then laid upon the brain, and one electrode—a thin plate of copper—placed in contact with it, while the other—a thin copper wire doubled upon itself—was moved up and down upon the exposed spinal cord. During this operation the animal was in a state of general convulsion, the respiratory muscles, especially the dia- phragm, being involved. The current was passed in this manner for ten seconds. The animal was then allowed to recover consciousness. As soon as the effects of ether had measurably passed off, convulsive movements ensued throughout the body, the diaphragm being marked- ly affected with the other respiratory muscles, and the heart beating with great irregularity, both in regard to force and rhythm. In these experiments a Gaiffe’s faradaic machine was employed, and the current was so feeble as barely to move the hammer and to be felt when the electrodes were applied to the tongue. I think with Dr. Hughlings Jackson that such convulsive movements are the result of “ discharging lesions ” of nerve-centres. The case of the patient to which I have referred under the head of epilepsy, in whom there was convulsive tremor of one side of the neck and face, induced by irritation applied to the skin of that side, shows, as well as others on record, that such instances may be developed into epilepsy under adequate circumstances, but, as there said, I cannot regard them as primarily epileptic. In another case—that of a young lady who has come under my care since the chapter on epilepsy was written, who is very excitable, has had two choreic periods, and once, certainly, an epileptic seizure—there are daily several attacks of convulsive tremor, in which the action starts from the right side of the neck, gradually invades the right side of the face, and eventually the muscles of the corresponding upper extremity. There is not for a moment the slightest impairment of con- sciousness. The face, however, is at first deathly pale, but soon be- comes flushed. There is no stupor, no mental confusion before, during, or after the attack. She laughs and talks during its continuance, and has a perfect recollection of every thing that takes place during the paroxysm. That such a case is very near to epilepsy is undoubted, but then congestion is very near to inflammation, and may exist for years without advancing to full development. There are certain morbid conditions usually classed as choreic, CONVULSIVE TREMOR. 709 which have more affinity with convulsive tremor than with chorea, though, perhaps, they are, with even greater propriety, placed under the head of hysteria. These are the turnings, salaam-convulsions, jump- ings, etc. It is quite probable that the lesion causing those disorders is similar to that producing convulsive tremor. The morbid anatomy of the affection under notice is entirely a matter of supposition, and indeed there are not many data for forming an opinion relative to the essential nature of the structural alteration. So far as we can judge from a consideration of the phenomena, the seat is in the cortical substance of the brain, and in the medulla oblongata and upper part of the spinal cord. The disturbances of the respiration and circulation point to these latter organs as a part of the anatomical substratum. In those cases in which there are spasms localized in various parts of the face, neck, or extremities, it is probable that the lesion exists entirely in a limited part of the cortical substance constituting the motor centre for the region involved. Treatment.—In the first cases that came under my observation, I employed counter-irritation in the form of a seton inserted into the nape of the neck, large doses of the bromide of potassium, and the primary galvanic current. Iron and quinine were given in two cases to relieve the general anaemic condition which existed. These measures were entirely successful, except in the third case, in which the bromide of potassium produced no perceptible effect. The tincture of hyoscya- mus was substituted for it with good results, but all treatment wras subsequently abandoned as stated. In the fourth case the patient was treated with gradually-increasing doses of strychnia, with the effect of causing a complete cure. A solu- tion of the sulphate of strychnia, consisting of two grains to the ounce of water, was administered in doses of ten drops three times a day, the doses being increased by one drop every day, till the physiological effects of the drug were obtained. A return to the original dose of ten drops was then directed, and an increase as before. From thirty to thirty-five drops were generally necessary to cause slight rigidity of the muscles of the legs and neck. The patient continued treatment for several months, and had no further spasms. In the fifth, sixth, and other cases, I have relied for internal treat- ment entirely on the bromide of zinc given in solution in gradually- increasing doses. In all of these the result has been entirely satisfac- tory. In the fifth case, no paroxysm ensued after the first day of treat- ment. Four weeks afterward, the patient presented himself at my clinic, and announced the complete cessation of all convulsive move- ments, and that he had resumed his work, which had been interrupted for several years. In the sixth case I administered the zinc, and in addition applied 710 CEREBRO-SPINAL DISEASES. the actual cautery repeatedly to the nape of the neck. Only one paroxysm occurred after the treatment was begun, and that was in- duced by the excitement and irritation caused by the primary galvanic current applied to the spine. The patient, two months afterward, re- mained entirely well, though still continuing to take the zinc. In all the other cases, five in number, the bromide of zinc has suf- ficed to effect the cure. I have uniformly given it in solution, either in w7ater or simple syrup, in the proportion of one drachm to the ounce. Of this mixture, ten drops were given three times a day for the first two weeks, then fif- teen drops three times a day for the next fortnight, and so on, increas- ing five drops for the doses of each subsequent two weeks. This course has been continued for from three to six months, and then the doses are gradually reduced, except in Cases V. and VI., in which I shall continue them for a much longer period, and in two others which have been but for a short time under treatment. CHAPTER IV. CHOREA. Although it is quite certain that several distinct affections are in* eluded under the term “ chorea,” these are analogous to each other, and, as we know little about the essential anatomical features of these disorders, and as they are allied by their symptoms, it will be advisable, for the present, to consider them together. Symptoms.—Even in simple, typical, and uncomplicated cases of chorea, the symptoms exhibit great variety. They are connected mainly with the mind, with motility, and with sensibility, though, at the same time, the functions of organic life are generally more or less deranged. Among the earliest symptoms of chorea are those referable to dis- ordered brain-action. The character and disposition of the patient undergo a marked change, and there is, besides, from the first, a very decided impairment of mental vigor. The emotions are easily excited, and the temper becomes fretful and irritable. Hallucinations are not uncommon, and these are generally connected either with the sight or hearing. Sometimes both these senses are involved. The sleep is generally disturbed by disagreeable dreams, sometimes reaching to the intensity of nightmare, and these are so vivid that the patient often considers them realities. In a few cases there is decided mania, but this is not of a very aggravated form, and is of temporary duration. Three such instances CHOREA. 711 have recently been under my care, all occurring in young girls of about the age of puberty, and exhibiting in all other respects the typical characteristics of chorea. In two cases under my observation, the first notable event in the course of the disease was an epileptic paroxysm, which, however, was not repeated in either case. The most prominent symptoms of the disease are, in the great ma- jority of cases, exhibited in the irregular and disorderly muscular con- tractions which make their appearance at a very early period, and which have given it a name in nearly every language of the civilized world. Thus, we have the terms chorea (%opem, a dance), St. Vitus’s dance, St. Guy’s dance, etc. In the beginning the foot of one side drags a little, and soon after- ward the corresponding upper extremity becomes affected with the choreic movements. These are manifested in the fingers, in the flexion, extension, and rotation of the wrist, and in the movements of the elbow and shoulder. No matter where the hand be placed, it cannot be kept steady, but it and the whole extremity are in a constant state of agita- tion. Before long the muscles of the neck and face participate, the head is jerked from side to side, and a continual series of grimaces is the result of the actions in the facial muscles. In some cases the involuntary movements are confined to one lat- eral half of the body, constituting the form known as hemichorea. This is the case in about one-fourth of the instances. Thus, of two hun- dred and thirty-five cases cited by See,1 the phenomena in sixty-four were limited to one side. This limitation has not, as was formerly supposed, any relation with hemiplegia, but is solely the result of the suspension of the progress of the disease. At first the movements are moderate, but they go on, becoming more and more severe, until, in extreme cases, the condition of the pa- tient becomes exceedingly pitiable; The arms, the legs, the face, and head, are in almost constant action. Every attempt to perform a vol- untary movement excites still more the disorderly actions, and thus the patient is unable to feed or dress himself, and sometimes even walking becomes impossible. In one type of cases the convulsive movements come on paroxys- mally, and are often of the most astonishing character. The patient is, perhaps, lying quietly on the bed, when suddenly the head is thrown backward, the limbs set in involuntary motion, and the muscles of the trunk contract so violently as to throw the sufferer forcibly to the floor. Again, a series of gyratory motions ensues, and the patient turns round on one foot until complete exhaustion follows ; or there may be 1 “ De la choree et des affections nerveuses en general, avec leurs rapports avec les diatheses, et principalement avec le rlieumatisme,’* “ Mem. de l’academie de medecine,” 1850, tome xiv., p. 343, et seq. 712 CEREBRO-SPINAL DISEASES. leaps and contortions of various kinds. Sometimes the movements are rhythmical. A lady, who was under my charge, was suddenly seized with an irresistible impulse to bend the left elbow. The arm con- tinued in motion for half an hour, and then the right arm began a like movement. In a few minutes the head began to nod, then the left knee was alternately flexed and extended, and finally the right knee became similarly affected. For over an hour these movements con- tinued, and then a regular alternation ensued—first the left arm, then the right, then the head, next the left leg, and finally the right leg. These actions were perfectly timed, and were all performed in exactly ten seconds, as I ascertained by determinations made on several occa- sions. As she sat in a chair, or lay on a bed, she was a curious sight. Though she was good-tempered with it all, her emotional system was in a state of great exaltation. She recovered in a few weeks. Chorea of rhythmical or uniform character has often prevailed epi- demically. The most authentic recorded visitation of the kind was one which occurred at Aix-la-Chapelle in 1374. This was in the form of a dancing mania, and is fully described by Hecker1 under the name of St. John’s dance. The men and women subject to it met in the streets and churches, where “ they formed circles hand-in-hand, and, appearing to have lost all control over their senses, continued dancing, regardless of the by-standers, for hours together in wild delirium, until at length thejT fell to the ground in a state of exhaustion. They then complained of extreme oppression, and groaned as if in the agonies of death, until they were swathed in cloths bound tightly around their waists, upon which they again recovered, and remained free from complaint until the next attack. This practice of swathing was resorted to on account of the tympany which followed these spasmodic ravings, but the by- standers frequently relieved patients in a less artificial manner, by thumping and trampling upon the parts affected. While dancing they neither saw nor heard, being insensible to external impressions through the senses, but were haunted by visions—their fancies conjuring up spirits, whose names they shrieked out; and some of them afterward asserted that they felt as if they had been immersed in a stream of blood, which obliged them to leap so high. Others, during the parox- ysm, saw the heavens open and the Saviour enthroned with the Virgin Mary, according as the religious notions of the age were strangely and variously reflected in their imaginations. In the most fully-developed and best-marked instances of the dis- ease, it was often ushered in by an attack of epileptic convulsions. Such were probably cases of hystero-epilepsy, an affection to be pres- ently considered at greater length. The affection spread like wild-fire—being fed by that principle of imitation which appears to be so powerful an influence in causing the 1 “Epidemics of the Middle Ages,” “Sydenham Society Translation,” 1844, p, 87. CHOREA. 713 propagation of this and analogous disorders of the nervous system. Those affected were generally regarded as being possessed by evil de- mons, and consequently only to be cured by the exorcisms of the clergy. In 1418 it broke out in Strasbourg, and there received the name of St. Vitus’s dance, from the fact that the most efficacious means of cure was thought to consist in the intercession of this saint. Similar attacks of dancing mania had occurred before that of St. John, but the details are more or less obscure, and several have occurred since. Among these latter must be placed the tarentism which overran Italy, and various more restricted epidemics of like disorders. In our own country we have had the Jumpers, and we still have the Shakers. In addition to these are many of the manifestations of witchcraft, which were choreic, and of which this country has had its full share, and of spiritualism, which it enjoys the doubtful honor of having initiated.1 Huntington has described a form of chorea which occurs in families, and seems to be influenced by heredity. Several instances of the dis- ease occurring in one family have come under my observation. It differs materially from ordinary chorea in that it does not make its appear- ance until adult life, that there is every evidence of mental deteriora- tion, and that the disease is progressive, and usually terminates fatally. In chorea, even of the ordinary simple kind, the speech is imperfect, owing to the incoordination of the muscles directly concerned in articu- lation, and those which affect respiration. There are, therefore, stutter- ing and stammering, and at times a peculiar difficulty of speaking, ow- ing to the attempt being made when the chest is empty ; that is, when expiration has just been accomplished. The vocal cords are sometimes affected, causing the individual to utter peculiar sounds, such as bark- ing, grunting, and sighing, both on inspiration and on expiration. The tongue and lips rarely escape being involved to a considerable extent. The muscles of mastication and deglutition are generally affected, and hence the food is imperfectly chewed, and often causes choking from difficulty of swallowing it. In some cases chorea is accompanied with paralysis—the chorea paralytica of authors. This loss of the power of voluntary motion is usually hemiplegic, and involves the same muscles, which are the seat of the irregular movements. Occasionally there are contractions of the limbs, but not to any great degree. Dr. Weir Mitchell2 has also called attention to disorderly move- ments supervening after paralysis, to which he applies the term of post-paralytic chorea. The propositions which he enunciates are : 1. That adults who have had hemiplegia, and who have entirely recovered, are often the subjects of choreal disorder. 1 See the author’s “ On Certain Causes of Nervous Derangement,” for more complete details on this and analogous subjects, and for accounts of other examples. 2 “Post-Paralytic Chorea,” American Journal of the Medical Sciences, October, 1874. 714 CEREBRO-SPINAL DISEASES. 2. That the younger the patient the more apt these choreal devel- opments are to ensue. Dr. Mitchell adduces several interesting cases in support of these propositions, and quite a large number have come under my own obser- vation. But the condition in question is an entirely different affection from athetosis, with which it has been frequently confounded. Chorea is sometimes of very limited extent. It may be only shown in the hand or foot, but more frequently, when restricted in its topog- raphy, it is manifested in the head or face. There may be only a little twitching of the muscles at the angles of the mouth, or of those which raise the upper lip, or of the orbicularis palpebrarum, by which the eyelids are closed, or of the levator palpebrse superioris, or of the corrugator supercilii, or occipito-frontalis. Sometimes the head is ro- tated suddenly, or twitched to one side, or there is a shrugging of the shoulders. In several cases that have been under my care, the abnormal mani- festations were entirely confined to the organs of voice or speech. In one instance—that of a young girl from Illinois—while there was a general hypersesthesia of the whole nervous system, there wTere no choreic movements except of the respiratory and laryngeal muscles. The respiration was therefore exceedingly irregular, and at times inar- ticulate sounds were made, which were involuntary. Articulate speech was lost from inability to coordinate the muscles, but there was no paralysis, for the tongue could be moved freely in all directions, and the lips were as mobile as ever, except when the patient made an effort to speak. After a few weeks the sound from the larynx was made regularly at each expiration. There were no sounds during sleep. In this case there was a strong hysterical element present. The affection resisted all treatment, and finally I sent the patient home, scarcely improved except in her general health. One morning she awoke, began to speak, and there was no resumption of the laryngeal sounds. She has continued well ever since, now over two years. Again, there may be an irregular action of the muscles of speech, and in consequence words are uttered against the will of the patient, and often without any previous knowledge of what is going to be said. The language used is often of a profane or indecent character. This condition has been termed “ coprolalia.” Several such cases have been under my observation, and I have alluded to twro of them in a recent lecture1 on chorea. Since then another remarkable case of the kind has come under my care. In this instance there is scarcely a minute during the day that the speech is not going on, and this without the least power on the part of the patient to arrest or direct it. If he is asked a question, he can only use a few apposite words, the others being alto- gether without relation to the subject about which he wishes to speak. 1 Journal of Psychological Medicine, January, 1871, p. 51. CHOREA. 715 The convulsive movements in chorea almost invariably stop during sleep. They are also sometimes temporarily arrested by intense men- tal occupation, but are always rendered worse by emotional disturbance or physical fatigue. On the contrary, they are diminished by mental and emotional quietude. Strange as it may appear, the sensation of being tired is scarcely ever experienced by choreic patients. Generally there are wandering pains in the limbs, headache, and pain in the back. The cutaneous sensibility is usually increased, but in some cases it is greatly lessened, and may be abolished altogether in some parts of the body. The functions of the several viscera are ordinarily more or less de- ranged. There are paroxysms of palpitation of the heart, and the action of this organ is to some extent irregular during the whole course of the disease. Endocardial murmurs are often present, either systolic or diastolic, but are the result of the anaemia which is so prominent a feature of chorea. Respiration is imperfect; the stomach does not digest well ; and there are nausea and vomiting. The bowels are con- stipated ; the urine is loaded with phosphates, and is of diminished quantity ; and the menstrual function in girls is imperfectly performed, either as regards quantity or quality. The skin is dry and harsh, the hair loses its gloss, the complexion is pale, the lips bloodless, the pupils dilated, and the sclerotic coat of the eye of more than normal whiteness. The tendency of chorea is to increase to a certain point, and then to gradually diminish. In favorable cases occurring in children, it runs its course in about three months. This period can be materially short- ened by appropriate treatment. Sometimes it ceases very suddenly, and in others passes into a chronic condition, which may last for years or during the life of the patient. Occasionally it terminates in death, either directly or in consequence of the supervention of some inter- current affection. Three fatal cases have come under my observation. One of these I saw several times in consultation with my friend Dr. T. G. Thomas. The patient was a young lady about twenty years of age, and her paroxysms were of the most violent character, sometimes being so strong as to cause her to throw herself off the bed, or to dash about the room with great force. No treatment appeared to exercise any re- straining effect, and, after about two years, she died of an abdominal affection. There was no post-mortem examination. In the other two cases, death ensued from exhaustion. Relapses are common in chorea, especially in children, and some- times as many as half a dozen attacks occur. Subsequent seizures are usually less severe than the first. Chorea is often complicated with hysteria—a combination which will be described hereafter. It may also exist in conjunction with rheumatism and malarial fevers, and the exanthemata. CEREBRO-SPINAL DISEASES. In an interesting monograph, Dr. Gowers1 gives the results of his studies and investigations relative to certain features of the choreic condition. He found that the electric excitability of both nerves and muscles on the affected side in cases of hemichorea is increased in most cases after the lapse of a few weeks ; that there is no necessary rela- tion between the spontaneous spasmodic movements of the affected muscles and the incoordination which takes place when voluntary movements are attempted ; that there is no regularity about the dis- tribution of the disorderly movements in cases of hemichorea, and that there appears to be a relation in some cases of chorea with other con- vulsive affections, such as hysterical and epileptoid seizures of various kinds, and even true epilepsy. As Dr. Gowers observes, this relation, the existence of which is unquestionable, points in some cases to a com- mon origin ; in others, to a predisposition excited by the one disease. Causes.—Chief among the predisposing causes of chorea is age. It is more frequent during the period extending from six to fifteen years than during all the rest of life. See, of five hundred and thii*ty-one cases, found four hundred and fifty-three of ages ranging from six to fifteen years. During the last ten years, in my hospital and private practice and at my clinics, many cases of chorea have come under my observation and treatment, but I have kept no systematic account of them since the first edition of this work was published (1871). At that time I had full notes of eighty-two cases ; of these, sixty-seven were of ages between six and fifteen years. Under the age of six, the disease is less frequent as we go toward birth. Cases have been met with in infants at the breast of six months old. The youngest case I have had was a girl of eighteen months. After fifteen, the disease, unless it occurs as an epidemic, is not very common. Cases are, however, met with in adults, and even in very old persons. I have seen four cases in individuals over thirty, and three in persons between the ages of twenty and thirty. Of course, I refer to the origination of the disease at these ages : instances of its beginning in childhood, becoming chronic, and lasting through life, are not so rare. In those cases reported by authors of the affection origi- nating very late in life, we have every reason to conclude that they were instances of organic lesions of the brain or spinal cord—pi'obably sclerosis—giving rise to rhythmical movements or paralytic tremor. The female sex is much more liable to chorea than the male. Of See’s five hundred and thirty-one cases, three hundred and ninety-three were girls and one hundred and thirty-eight boys. Of the eighty-two cases of which I have full records, seventy were females and twelve males. Rheumatism has been supposed to be a 1 “ On some Points in the Clinical History of Chorea.” Reprinted from the British Medical Journal, London, 1878. CHOREA. 717 predisposing cause of chorea. Of one hundred and twenty-eight cases, See found sixty-one in association with rheumatism ; but when we come to inquire further, we find that only thirty-two of these were articular rheumatism, while the rest were cases in which there were wandering pains which may have been, and probably were, without the least affin- ity with true rheumatism. While it is certainly the case that chorea sometimes follows or exists coincidentally with rheumatism, I doubt if its influence is any more than that of a depressing agent to the organism. Of the eighty- two cases observed by myself, only sixteen were connected with rheu- matism, while eighteen were just as intimately related to other dis- eases. The affection appears to be more common in winter than in sum- mer. Of my cases, fifty-four occurred in the six months from October to March, and twenty-eight in the other six months of the year. Among the exciting causes, those connected with the emotions occupy the first place. Twenty-seven of my cases were directly the result of fright, apprehension, anxiety, mental excitement, or some other cause of the kind. In eight it was induced by intense study at school, and in four from imitating others similarly affected. This lat- ter factor is not of so general application as in former times, when social life was different. To it is, doubtless, to be ascribed the spread of choreiform movements through certain localities, and especially convents, such as occurred in the thirteenth, fourteenth, and fifteenth centuries, to some of which reference has already been made. Recently the theory has been advanced that eye-strain is a frequent cause of chorea. It is possible that such a condition in a few instances may be a contributing cause in a person predisposed to chorea, but in the main I am inclined to consider such influence as exceedingly slight. Among other causes, bad hygienic influences and exhausting dis- eases generally are to be mentioned. Pregnancy is also asserted to be a cause, and cases are on record in which the foetus has been born choreic of a choreic mother. Diagnosis.—There is not much danger at the present day that chorea will be confounded with many of the diseases from which, not long ago, it was not clearly disassociated. Thus, from paralysis agitans, epilepsy, locomotor ataxia, multiple cerebral and cerebro-spinal scle- rosis, the fuller acquaintance which we have in recent years acquired of these maladies prevents the necessity of dwelling on their character- istics as distinguished from those of chorea. The course of the latter disease, and the symptoms, other than those connected with motility, are in the others so different that no one who has studied their phe- nomena could fail in making a correct diagnosis. With hysteria, some of the forms of chorea may be confounded, and the two affections are not infrequently blended in the same person. 718 CEREBRO-SPINAL DISEASES. It must be confessed, too, that there are cases in which the diagnosis cannot be clearly made out. So far as the patient is concerned, the difficulty of forming a correct opinion in such cases is not a matter of much moment. The great majority of cases of chorea, such as are met with in chil- dren, are readily distinguished from hysteria. The facts of the disease occurring before puberty in so large a proportion of instances, that the emotional system is rarely disturbed as in hysteria, that the affection is not so paroxysmal, and that the accessions of hysteria are more sud- den, will be sufficient to render the diagnosis accurate. From convulsive tremor—with which in some of its forms it is closely analogous—ordinary chorea is diagnosticated by the facts that it is not paroxysmal, but continues while the patient is awake, that the movements are more disorderly, while at the same time more purposive, that the natural tendency is toward spontaneous recovery, and that it usually occurs in children. But it must be admitted that it is difficult to determine to which disease certain rhythmical and paroxysmal dis- orders are to be ascribed. It would perhaps be more correct to place all such under the head of convulsive tremor or hysteria, with which affections they are certainly closely allied. Prognosis.—This is usually favorable in those cases which occur before puberty. The chorea of adults is, however, in most instances, a very unmanageable affection, and generally either terminates in death or becomes permanent. Cases in which death has ensued have been reported by various authors—among them, Dr. John W. Ogle,1 Dr. J. Ilugldings Jackson,2 and Dr. G. See.3 As already stated, three fatal cases have occurred in my own experience. The tendency, however, in the chorea of young persons is decidedly toward recovery, even under unfavorable circumstances as regards hygiene or medical treat- ment. Morbid Anatomy and Pathology.—In many cases of persons dying, either from chorea or from intercurrent affection, no changes have been found which could, with probability, be regarded as constituting the disease. In other cases, morbid alterations from the healthy state have been found. The idea has therefore prevailed that there are two kinds of chorea—one wrhich is entirely functional, belonging to the so- called neuroses, the other the result of organic disease of the brain or spinal cord, or both. In Ogle’s sixteen fatal cases, congestion of the brain and its membranes was found in some, while in others the dis- ease existed in the spinal cord. 1 “ Remarks on Chorea Sancti Viti, including the History, Course, and Termination of Sixteen Fatal Cases,” etc., British and Foreign Medico- Chirurgical Review, January, 1868, p. 208. 2 “ The Physiology and Pathology of Hemi-Chorea,” Edinburgh Medical Journal, Oc- tober, 1868. 3 Op. cil. CHOREA. 719 In an analysis of one hundred cases of chorea, Dr. Hughes1 cites fourteen fatal cases. In all but four of these there was intra-cranial congestion with other structural changes, such as softening, opacities, and adhesions. The spinal cord was not examined in six cases. Of the remaining eight, it was healthy in three, and congested, softened, or with adhesions or opacities of the membranes in the remaining five. In seven fatal cases, collected by Romberg,1 there was softening and degeneration of different parts of the brain and of the spinal cord. Other similar cases have been reported, and in the majority there were fibrinous concretions on some portion of the heart’s valves or lining membrane. In 1850 and 1863, Dr. Senhouse Kirkes3 published the details of a number of cases which went to show the association between chorea and rheumatism, and he made the prediction that “future experience will still more positively demonstrate that an affection of the left valves of the heart, with the presence of granular degeneration upon them, is an almost invariable attendant upon chorea, under whatever circum- stances the chorea may be developed.” The relation is also insisted upon by See and other authors, and such cases as those of Ogle are cited in its support. But the doctrine is only applicable, with any probability, to the fatal cases, and, in those of Ogle, rheumatism was not always an antecedent. In regard to this point, I am entirely in accord with the views expressed by Dr. Ogle in the following extract, which I make from his valuable paper : “ Again it might be asked, if there was merely a mechanical cause (which, of course, would be constant in operation), such as embolism, why should the movements be so decidedly and universally interrupted during quiet sleep ? Or, why should certain peculiarities as to age or sex be considered as predisposing influences ? Recognizing the fre- quent existence of these fibrinous deposits, or granulations, on the heart’s valves in chorea, I should be much inclined to look upon these post-mortem appearances rather as results of some antecedent condition of the blood, common also to the choreic condition. It is very freely recognized that this affection is frequently in some way or other con- nected with that condition of blood which obtains in what we call anaemia, or that existing in rheumatic constitutions. In both of these states we know that the fibrine of the blood is much in excess (as also it is in pregnancy and other conditions looked upon as obnoxious to chorea), and in these states we know that the fibrine (with which the blood is surcharged) is very prone to be readily precipitated, either owing to its superabundance or from other obscure and acquired prop- 1 “Digest of One Hundred Cases of Chorea,” “Guy’s Hospital Reports,” vol. iv., 1846, p. 360. 4 “ Lehrbuch der Nervenlcrankheitcn,” Band ii. 3 London Medical Gazette, 1850, and Medical Times and Gazette, 1863. 720 CEREBRO-SPINAL DISEASES. erties (possibly also from some interference with the relation of the fibrine and the other constituents of the blood), upon the heart’s walls or valves. May not this hyperinosis be the explanation of the coinci- dence alluded to ? In most cases, the deposit is probably very slight, and, in many cases, so slight as to require search for it. May it not infrequently be that it is often only found in quite the dying state ? Speculation might suggest that the fibrinous deposits arise from some interference with the degree of solubility of the fibrine, induced by the presence of some ununited elements within the blood (some result of tissue-metamorphosis) produced by the excessive muscular action and other functional disturbance which exist in the choreic state, thus being not in any way related to this state as a cause, but as a conse- quence.” In the paper to which reference has already been made, Dr. Hugh- lings Jackson associates hemichorea with the plugging by emboli of the vessels of the corpus striatum of one side, and, in a recent valuable paper, Dr. Charlton Bastian1 says : “ I need only hint at the important bearing which the possibility of the occurrence of minute embolisms of this kind may have in the eluci- dation of previously-obscure forms of so-called functional disease of the nervous system, as I hope shortly to publish the details of a fatal case of chorea, in which such embolisms led to ruptures and obliterations of small vessels throughout the corpora striata and in the course of the middle cerebral arteries generally—this being a case of bilateral chorea in -which delirium was also present.” As the result of our present knowledge of the morbid anatomy of chorea, while it cannot be said that we are always able to define its seat with accuracy, we have strong evidence to support the view that it is caused by either functional or by organic irritation of motor cells in the cerebro-spinal system. In this respect it differs but little, if any, from the morbid anatomy of the other forms of mobile spasm. Irritation of the motor cells of the cortex, the corpus striatum, the pons, and probably the spinal cord, is responsible, in my opinion, for the manifestations of chorea. As previously stated, I am inclined to think that there are at least two distinct diseases—one due to spinal and the other to cerebral lesion, the latter probably consisting of sev- eral forms—but that it is advisable to consider them as one disease of various types, until further investigation enables us to speak with cer- tainty on the subject, and to classify them according to the morbid anatomical condition of each. The investigations of Chauveau,® Le Gros and Onimus,8 and others, upon choreaic dogs ; the lesions discovered in the spinal cord in fatal 1 “ On the Plugging of Minute Vessels in the Gray Matter of the Brain,” etc., British Medical Journal, January 30, 1869, p. 96. 2 Archiv. generates de med., 1866. 3 Comptes rendus, 1870. CHOREA. 721 cases of chorea by Hughes,1 Romberg,* Ellischer,3 and Bastian ;4 and cases such as those reported by Weir Mitchell and Burr,5 show the probability, at least, of the spinal cord being the seat of the primary morbid changes in some instances. In the paper already cited, Dr. Hughlings Jackson says of the cho- reic phenomena : “ They are not mere spasms and cramps, but an aim- less progression of movements of considerable complexity, much nearer the purposive movements of health. They are not so much incoher- ences of muscles (like the ‘ fist ’ we see in a partial fit of those convul- sions, which begin unilaterally where all the muscles of the hand are in action at once) as incoherences of movements of muscles. There is some method in their madness. They are not analogous to playing at once many keys of a piano in mere order of continuity, but to a random playing of harmonious chords. Again, they are successions of movements ; moreover, they are successions of different move- ments.”. Dr. Jackson’s theory of chorea is, that it is, like epilepsy, the result of “ discharging lesions ” of the cortical matter of the cerebrum ; and the experiments of Fritsch and Hitzig, Nothnagel, Ferrier, and others, go very far to confirm his views. Two essential points of difference from epilepsy must, however, be noted : the facts that in chorea there is no loss of consciousness, and that the discharges are successive, not paroxysmal, and less automatic. Moreover, his hypothesis leaves out of consideration the spinal element of the disease. That there are dis- charging and inhibitory centres in the spinal cord is supported by many artificial and natural experiments. The “ spinal epilepsy ” of Brown- Sequard is doubtless often a chorea of spinal origin ; and my own experiments, cited under the head of convulsive tremor, also show that there are motorial centres in the spinal cord. Treatment.—Diseases which are almost certain to terminate fatally, and those which ordinarily recover without medical treatment, are very sure to have a great many medicines used in their therapeutics; Chorea belonging, as it does, to this latter category, has a medical armamentarium almost equaling that of hydrophobia. I shall, of course, not even pretend to mention all these measures, but will merely cite those which the weight of evidence, and especially that derived from my own experience, indicates as the most effectual. Of the benefit to be derived from proper medical treatment in shortening the duration of the disease, and preventing chronicity, I have no doubt. Bromide, in some one of its forms, is a favorite remedy for chorea. I have employed it in many cases, and sometimes with good results. My preference is for the bromide of sodium, in doses of from ten to fifteen grains, three times a day, dissolved in a sufficient quantity of 1 Op. cit. 3 Op. cit. 3 Archiv fur path. Anal., Berlin, 18*74. 4 Op. cit. 6 “Trans. Amer. Neurol. Assoc.,” 1890, 722 CEREBRO-SPINAL DISEASES. water to prevent gastric irritation. In the majority of instances, how- ever, I am opposed to its use. While admitting that the preparations of bromide diminish nerve-cell irritability, it is also well established that they depress the system, weaken the muscular power, and, by con- tracting the arterioles, prevent the proper nutrition of the brain and spinal cord. I have therefore confined their administration to those cases in which the chorea coexists with maniacal symptoms, insomnia, or other symptoms of a hyperaemic condition of the brain. Iron is also frequently administered as a sole remedy, and still more generally as an adjuvant. Indeed, no matter what special treatment may be adopted, iron is generally indicated to improve the quality of the blood. I rarely use it unless for this latter purpose. Tartarized antimony, copper, sulphate of aniline, Calabar bean, and various other substances have been employed with more or less suc- cess, according to reports, but I have little personal experience of their value, except as regards the Calabar bean, which I have several times employed as an adjuvant, but with doubtful results. I have used both the primary galvanic and induced currents in many cases. In my opinion they are inefficacious except in that form in which there is distinct paralysis. Arsenic enjoys a high reputation in the treatment of chorea, and, if properly administered, may be regarded as almost a specific. It should be given in gradually-increasing doses up to the point of induc- ing evidence of its toxic influence, such as nausea and vomiting and puffiness of the face, especially under the eyes. For a child of five or six years the initial doses may be four drops of Fowler’s solution three times a day for the first day ; for the next day, five drops are given at a dose ; for the next, six, and so on till the phenomena mentioned appear. Then the doses should be set back to four or five drops, and again increased as before. Of the benefits of this treatment no one who has tried it can have any doubt. Its advantages have been shown in a report of cases from the clinique of the University Medical Col- lege, made by Dr. Morton.1 But the gastric method of administering arsenic is not so efficacious in the treatment of chorea as the hypoder- mic, and in a recent paper3 I called attention to this point, following Radcliffe, who over ten years ago introduced the practice : In this country hypodermic injections of arsenic in the treatment of chorea appear to have been first used by Dr. J. Lewis Smith,3 but since that time the measure does not seem to have attracted any at- tention. For the last ten years I have, in obstinate cases of chorea, em- 1 “Treatment of Chorea by Arsenic,” Neurological Contributions, No. II., p. 79. 2 “ On the Treatment of Chorea with Hypodermic Injections of Arsenic,” St. Louis Clinical Record, October, 1879. 3 Medical Record. CHOREA. 723 ployed hypodermic injections of Fowler’s solution with marked suc- cess. In recent or slight cases they do not appear to be necessary, these yielding readily to the use of arsenic by the stomach, or very often getting well of themselves ; but in instances of long standing, which are generally classed as incurable, I am quite sure that we have, in the means referred to, a valuable therapeutic measure, which ought not to be disregarded. In administering arsenic by this method a few points of manipula- tion are to be considered, for there is a decided tendency to the causa- tion of cellulitis and consequent abscess, and also of painful cutaneous inflammation. A point for the injection should be chosen in some part of the body where the skin is loosely attached to the subjacent tissues. The skin near the insertion of the deltoid is not a suitable place for the hypodermic injection of arsenic, however well adapted for injections of other substances. I very soon found out that, when inserted there, erythema or abscess, or both, were the invariable sequences. More- over, the mere act of injecting arsenic in those situations where the skin is tight and the tissues dense is accompanied with very consider- able pain. The best point is on the front of the forearm about midway between the wrist and the bend of the elbow. Here the skin is loose, and can be easily lifted up by the thumb and finger from the tissues below. In the next place the arsenic should be deposited just under the skin in the cellular tissues, and not in the substance of the skin or muscles. Neglect of this point will almost invariably lead to the formation of abscess. The point of the syringe should therefore be just carried through tli£ skin and then for about half an inch parallel to the face of the arm. The injection should then be made slowly, and it is well to lift up the skin over the place where the injection has been made, so as further to facilitate its absorption. And, lastly, it will not do to inject the undiluted Fowler’s solution, for if this provision be not followed, cellulitis, erythema, and intense pain, will certainly be produced. The dose which it is deemed proper to inject should be diluted with at least an equal quantity of water, or, preferably, of glycerine. The latter substance seems to be more readily absorbed and to produce less irritation than water. All these precautions are for the purpose of preventing local troubles. There is certainly a strong disposition on the part of arsenic to produce them. If, however, attention be paid to the rules I have laid down, there will rarely, if ever, be any local disturbance. The dose of arsenic administered by hypodermic injection may be very considerably larger than that which the stomach will ordinarily tolerate, and it is just here that the superior advantages of the method are most clearly shown. It is in chronic cases of chorea and certain CEREBRO-SPINAL DISEASES. choreiform affections that large doses of arsenic are especially re- quired, and the effect of such doses in curing the disease is not only generally prompt, but is unassociated with any toxic phenomena. I have frequently given as high as thirty-five drops of Fowler’s solution by hypodermic injection as an initial dose. It is very certain that the stomach would not tolerate this quantity. Again, I have often car- ried the amount taken by the stomach to the utmost bounds of pru- dence—till the eyes were puffed, and vomiting was almost incessant— and then have continued the arsenic in larger doses by hypodermic injection, with the result of the cessation of all gastric symptoms and the rapid cure of the disorder. With these introductory remarks I pass to the description of two or three cases in wdiich the beneficial effects of the arsenic adminis- tered hypodermically were unquestionable : Case I.—Mrs. A. C., of Jersey City, consulted me, not for chorea, but for a spasmodic affection of the muscles of the neck attended with great pain. On examination, I found that the left sterno-cleido- mastoid was the subject of clonic spasm, and that the left trapezius was also similarly involved. As a consequence the head was, every few seconds, jerked round toward the right shoulder, at the same time being drawn backward. It was possible, by a strong effort of the will, to arrest these movements for a half a minute, and at times, when alone and undisturbed, they wei’e less strong and frequent. During sleep they entirely ceased. The affection had come on suddenly some five years previously, apparently as the result of exposure to cold. No therapeutic measures (among which had been electricity, water- cure, and braces of various kinds) had produced the slightest bene- ficial effect. In the beginning I administered Fowler’s solution in doses of eight drops three times a day, increasing the doses a drop every day. When sixteen drops were reached, the skin around the eyes became puffed, and each dose excited nausea and vomiting. Up to this time there had been a very slight degree of improvement, but I found it was im- possible to carry the arsenic far enough wThen administered by the stomach to get the full effect of the drug. I therefore, on the 20th, administered hypodermically one injection of twenty-five drops diluted with a like quantity of glycerine. On the 21st she received thirty drops, and now there were decided evidences of improvement—the pain was greatly mitigated, and the spasmodic movements were less extensive and less frequent. On the 21st thirty-two drops were given, and on the 22d thirty-five. The amelioration was now still more strongly marked, and by continuing the doses of thirty-five drops till the 25th the pain and the movements were caused to cease entirely. The medicine was now stopped, and the patient has remained to this day free from any spasm. There is still (October 6th) a slight ten- CHOREA. 725 dency for the head to turn to the right, hut this is being gradually overcome, and the power over the formerly alfected muscles is com- plete. Case II.—Miss II., aged twelve, a young lady from Texas, was brought to me by her mother to be treated for chorea, with which she had been alfected for several months. The muscles chiefly affected were those of the face, both shoulders, and both upper extremities, but at times there was a curious protrusion of the abdomen from the spas- modic action of the erector spinae muscle. I at once began the treatment with arsenic and the application of pulverized ether to the spine, the former in doses of five drops of Fowler’s solution three times a day, increased a drop every alternate day, and the latter once daily. By the time ten drops of the arsenical solution was reached (which was in ten days), there was decided im- provement. The eyes were slightly puffed, but the stomach bore the remedy exceedingly well. I continued the medicine up to fourteen drops without exciting gastric disturbance, and then, as the choreic movements had ceased, I refrained from further increase, but kept on with the doses of fourteen drops for three or four days longer. She then went home cured. But in six months she returned to me, with all the choreic symp- toms as bad as ever, and her mother informed me they had made their appearance a couple of weeks before without apparent cause. I again tried the arsenical treatment with ether to the spine, which had been so beneficial the year before, but it was now apparent that, from some cause or other, the stomach had become intolerant of the drug, for I found it impossible to administer with safety more than eight drops, and this quantity had no beneficial influence over the disease. I there- fore determined to use the hypodermic injections. Twelve drops were the initial dose, the next day thirteen were given, the next fourteen, and the next fifteen. There were no choreic movements after this dose was attained. It was given daily for a week, and then the patient was discharged cured. In all this time there had been no toxic symptoms beyond slight puffing of the face. Case III.—I. H., a boy eight years of age, was brought to me affected with general chorea. The case was a chronic one, having lasted about a year, and had been treated by his physician with a single drop of Fowler’s solution administered once every alternate day, and with sulphate of zinc in about as efficacious doses. I be- gan the treatment in this case with hypodermic injections of five drops of Fowler’s solution given daily, and every alternate day in- creased a drop. In ten days thereafter the patient was taking ten drops daily. As by this time great amelioration had ensued, I did not carry the increase further, but, with the view of preventing a relapse, the doses were continued for several days. On the 28th all treat- 726 CEREBRO-SriNAL DISEASES. ment was suspended, the patient being entirely free from choreiform movements. In cases of acute chorea, a large number of which I have treated with hypodermic injections of arsenic, smaller doses may be given than when administered by the stomach, and they do not require to be so frequently repeated. Thus it often suffices, for the speedy cure of the disease, to give four drops of Fowler’s solution hypodermically every alternate day for a week or ten days, and then to increase the dose to five drops for a like period. I have compared the duration of acute chorea as treated by the gastric and hypodermic administration of arsenic, and have ascertained that the period is shortened one half by the latter method. While admitting that the tendency in such cases is, with hygienic measures, toward a cure, the beneficial effects of the arsenic are none the less evident. I have repeatedly seen the most marked improvement result from a single injection. In his excellent monograph Garin1 has insisted on the advantages of this method of treating chorea, and has adduced many instances of its good effects. As to the employment of strychnia, as detailed in former editions of this work, I am not disposed to recommend it, in view of the excel- lent results obtainable by the use of arsenic, except in special cases, in which, from some idiosyncrasy, the latter medium is not tolerated. It may also be of service as an adjunct in moderate doses. The ether-spray to the spine, as employed by Lubilski, Zimberlin, and others, is also an excellent adjuvant. Its effect is immediately quieting, and it may be used two or three times a day for five or six minutes along the whole length of the spine. In the paroxysmal forms of chorea, ether or chloroform by inhala- tion is often necessary to cut short or prevent an immediate seizure, but in other respects the treatment mentioned is entirely applicable. In all cases hygienic measures are of the utmost importance. Ex- ercise in the open air is indispensable ; the food should be of the most nutritious character ; the bedroom should be well ventilated ; bathing should be frequent; the bowels should be kept well regulated ; and the child, if at school, should be at once removed, and all study for the time be interdicted. Ridicule or threats, so often indulged in toward choreic children, generally do harm, but at the same time they should be encouraged to use all reasonable effort to prevent a bad habit being formed. In the epidemic variety of the disorder, threats, and even strong repressive measures, are, on the contrary, decidedly beneficial in curing and arresting the further progress of the disease. It is certainly advantageous to keep the patient mentally and phys- 1 “ Du traitement de la choree specialment par l’araenic et les injections du liqueur de Fowler,” Paris, 18'79. HYSTERIA. ically in a state of comparative repose, but I have never obtained any beneficial effect from confining him to bed in a dark room, as recom- mended by some writers. On the contrary, I have several times seen the disorder aggravated by this measure. It is one that is particularly distasteful to most children, and hence keeps them in a continual state of fretfulness and excitement. Moreover, it is a measure decidedly antagonistic to the general good health of the patient, who requires light and fresh air as influential hygienic factors in bringing about a favorable result. As regards mental occupation, hard study is of course to be avoided ; but I do not think it advisable to prohibit the reading of such books as amuse, without requiring any considerable degree of intellectual effort for their understanding. CHAPTER Y. HYSTERIA. A large volume might be written on hysteria—and many such have been published—and there would still be points in its clinical his- tory unconsidered. It is difficult, therefore, in a general treatise like the present, to give a full view of a disease which plays so important a part in nervous pathology, and which is so varied in its manifestations. The most that I can hope to do is to lay down certain broad principles and features, and leave the recognition of details to the intelligence and discrimination of those who read this work. Symptoms.—The phenomena of hysteria may be manifested, as re- gards the mind, sensibility, motility, and visceral action, separately or in any possible combination. Thus it is not uncommon to meet with cases in which the only evidence of the disease is seen in abnormal mental action ; others are characterized solely by derangements of sen- sibility, such as hyperaesthesia or anaesthesia ; others by aberration of the faculty of motion, such as paralysis, spasms, contractions. Again, all of these categories may be witnessed in the same person, giving rise, among other phenomena, to coma and convulsions ; and again, some one or more of the viscera may be deranged in their functions, and thus the appearance of organic disease be simulated. As there is such a marked want of uniformity in the character cf hysteria as it affects different persons, I will not endeavor to present a typical case of the disorder, but will consider separately the principal phenomena which may have an hysterical origin. But, in setting out to make the attempt, I am reminded of Dante’s despair at the thought of his inability to describe the horrors of the ninth gulf : 728 CEREBRO-SPINAL DISEASES. “ Chi poria mai pur con parole sciolte Dicer del sangue, e delle piaghe appieno, Ch’io ora vidi, per narrar piu volte? Ogni lingua per certo verria meno, Per lo nostro sermone, e per la mente, C’hanno a tanto comprender poco seno.” The Hysterical Diathesis.—Though it is very common to hear the hysterical diathesis or temperament mentioned by medical authors, I have never been able to recognize its existence by any external traits. The fact that it has been so very differently described by writers, from Hippocrates and Galen to our own day, is good evidence that it is not readily detected. Thus, Hippocrates and Galen recognized the existence of the hys- terical temperament, but each gave it different characteristics. Lou- yer-Villermy1 had very decided views of its features, and he described it as follows : “Every hysterical woman is stout, short, dark, plethoric, full of life and of health. The complexion is brunette and ruddy, the eyes black and sparkling, the mouth large, the teeth white, the lips of a carnation red, the hair luxuriant and of the color of jet, the sexual organs well developed, and the spermatic liquid abundant.” Aside from his physiological error relative to the spermatic liquid, these are the characteristics of the women of the south of Europe. If he had lived in the north, where hysteria is fully as common, he would have found that his description of the hysterical temperament would not have held good. Indeed, Sydenham, Whyte, Copland, and other English authors, represent the hysterical predisposition with almost the very opposite characteristics. As Briquet5 remarks, there is no hyster- ical constitution appreciable by the study of external appearances. The disease takes women as it finds them, blondes, brunettes, stout, thin, strong, weak, ruddy, or pale, there is no choice. Some hysterical women have delicate figures and intelligent minds, but there are others whose dull, stolid faces give evidence of their stupidity ; and others, again, whose thin, fleshless, and wan faces tell us that the Greek type of female beauty is not to be regarded as predisposing to the develop- ment of hysteria. While, therefore, admitting the existence of the hysterical diathesis, I know of no marks by which its presence can be determined, other than the acts of the patient, which go to make up the clinical history. Mental Symptoms.—These are very various, but generally consist in emotional disturbance, an inability or indisposition to exert the will, and in the existence of illusions, hallucinations, or delusions. Attacks 1 Quoted by Briquet, “ Traite clinique et therapeutique de l’hysterie,” Paris, 1859, p. 91. 2 Op. cii.t p 92. HYSTERIA. 729 are often characterized by no other prominent symptoms than those connected with mental action, and they may assume every possible character. At times, the patient is depressed in spirits, and sheds tears profusely ; a few minutes afterward, she has forgotten her grief, and laughs immoderately, without adequate cause. Sometimes she laughs and cries at the same time. Or, there may be a total insusceptibility to any emotion, a listless insouciance, which contrasts strongly with her natural disposition. Or, again, an emotion the exact opposite of the proper one is excited. This is quite a common form of manifestation. A mother, for instance, is informed that her daughter has contracted an improper marriage, and is immediately seized with immoderate laughter, and shows every ex- pression of pleasure, when the rest of the family are overwhelmed with grief and shame. Another draws the chief prize in a lottery, and be- gins at once to cry and wring her hands. A third, hearing that bur- glars have entered the house and have stolen all her jewelry and silver, sits stolidly in her chair, her hands folded in her lap, and her whole ex- pression indicating the most complete indifference. During either of these conditions, she may be entirely silent, or excessively voluble, or she may exhibit other hysterical phenomena. As regards the will, the manifestations of disorder are sometimes very remarkable. That the patient is, for the time being, unable to exert it, is evident, but, under the influence of some strong exciting cause, she frequently astonishes those about her by suddenly reacquir- ing her lost volitional power. A young lady came under my charge for what was supposed to be a disease of the spinal cord. She had taken to her bed suddenly, soon after striking her back rather gently against the edge of a table, declar- ing that she could not walk. On examination, I was convinced that there was no disease whatever of the spine, other than that of a purely hysterical character, and I so expressed myself to her. She, neverthe- less, insisted upon it that her spine was seriously injured, and she con- tinued to keep her bed, lamenting daily her sad fate at being compelled to pass so long a time shut out from the enjoyments of life. There was no paralysis or even simulation of it, for she moved her legs about freely enough in the bed. But, one evening, her brother, who had long been absent, returned home. She heard the bustle in the house attend- ant upon his arrival, but all were too busy to pay any attention to her in her chamber up-stairs. Suddenly exclaiming, “I can stand this no longer,” she sprang from her bed, rang for her maid, and, hurrying on her clothes, proceeded down-stairs and entered the drawing-room, to the great surprise of all the family. In another case, a lady closed her eyes, and declared that she could not open them. She was brought to me as a case of double ptosis. There was no spasm of the orbicularis palpebrarum on either side, and 730 CEREBRO-SPINAL DISEASES. I had no difficulty in opening the eyes by gently raising the lids. The pupils were normal; there was no diplopia, and there were no evidences of such cerebral lesions as are generally met with as causes of ptosis. Moreover, she was subject to paroxysms of hysterical syncope. Under the circumstances, I had no hesitation in expressing my opinion to her friends that the case was one of hysteria. I advised the use of the in- duced current to the eyes, and she found this so disagreeable, not to say painful, that two applications were sufficient to restore her volitional power, so that she opened her eyes without difficulty. In my remarks on aphasia, I have cited a case (p. 182) in which the power to speak suddenly returned under the influence of excitement, and was suddenly lost again, to be gradually recovered. Many cases of this loss of volition in hysteria have been under my care, and most physicians have witnessed similar instances. Illusions are very common phenomena of hysteria, and these may be connected with any or all of the senses. A ball rolling over the floor is taken for a rat; the sound of rain falling on the roof is mistaken for the noise of burglars in the next room; the knives used at table all “ smell fishy; ” every thing tastes sour or bitter or sweet, as the case may be, and a draught of cold air on the hand is supposed to be the touch of a person or a spirit. Hallucinations of various kinds are equally frequent. Images are seen where there is nothing; voices are heard where there is absolute silence; odors are smelt where there is nothing to smell; and strange tastes are perceived when the mouth is empty. Thus one patient sees angels, another demons, another animals of various kinds. One hears voices whispering to her, another musical sounds, and another noises like the breaking of glass or dishes. Another is constantly sensible of a smell as if something is burning, and another always has a taste of turpentine in her mouth. It is not often the case that these erroneous perceptions impose on the intellect, but sometimes they do, and then delusions are enter- tained, or these may, as in cases of absolute insanity, be formed with- out the intervention of the deranged perceptive faculties. They differ however, from the delusions of insanity, such as have been already described, in the facts that they do not last long and that they rarely exercise any powerful influence over the actions of the patients. Besides these mental phenomena indicative of cerebral disturbance, there are, sometimes, an extraordinary acuteness of understanding and readiness at reasoning and speech quite beyond the natural powers of the patient. At other times, on the contrary, the intellect is dulled, and the conversational power reduced to a low point. Sensibility.—This may be affected so as to result in the production either of hypercesthesia or anaesthesia. Hyperesthesia, caused by hysteria, is characterized by the facts that HYSTERIA. 731 it is never permanently fixed in one place, that it is generally exces- sively acute, and that it is unaccompanied by evidences of serious dis- ease of the nervous centres or the nerves. A common seat is the skin, and its favorite region is the trunk, especially the skin over the mam- mary glands, and that covering the labia majora. Another situation frequently affected is the skin of the face. Cutaneous hyperaesthesia may consist either of spontaneous pain or of tenderness to impressions made upon the surface of the body. Mus- cular hyperaesthesia, or myalgia, is likewise common. Dr. Inman1 has investigated this branch of the subject very carefully, and has ascer- tained that the painful spots correspond to the origins and insertions of the muscles. Muscular pains due to hysteria are often mistaken for pains of the viscera. Thus the headache which is so frequent a phenomenon of the hysterical condition is very seldom located within the cranium. It may be of very limited extent, constituting the form known as the clavus hystericus, or may be of rfiore extensive limits. Its ordinary situations are the frontal regions, occupying, in this case, the occipito-frontalis and corrugator supercilii muscles ; the temporal regions, being then located in the temporal muscles; the vertex, being then seated in the tendon of the occipito-frontalis muscle; and the occipital region, in the occipito-frontalis, trapezius, splenius, and complexus. Briquet states that, of three hundred and fifty-six hysterical patients whom he ques- tioned on the subject, three hundred were constantly subject to head- ache. I have very rarely met with a case of hysteria in which it was not almost constantly present, and never one in which it was not a symptom at some time or other. Pains are often felt in the muscles of the chest, abdomen, and back. This latter is a favorite situation, especially in the region between the shoulders, and in the muscles on each side of the vertebral column in the lumbar region. Pains in the joints are common manifestations of hysteria, and they are often mistaken for serious organic disease. When, as is sometimes the case, they are accompanied with contractions of the muscles, the liability to error on the part of the practitioner is increased. Sir Ben- jamin Brodie,2 several years ago, pointed out the true nature of certain affections of the joints occurring in hysterical women ; and, since his time, others, among whom Barlow3 and Skey4 are to be mentioned, have called special attention to the subject. The pain may be attended with swelling, but there is no accumulation of fluid in the cavity of the 1 “On Myalgia: its Nature, Causes, and Treatment, etc.,” London, 1860. 2 “Illustrations of Certain Local Nervous Affections,” London, 1837. 8 “A Treatise on Diseases of the Joints,” London. 4 “ Hysteria, etc. Six Lectures delivered to the Students of St. Bartholomew’s Hos- pital, 1866,” London, 1867. 732 CEREBRO-SPINAL DISEASES. synovial membrane. The knee is more frequently affected than any other joint. Quite recently a young lady has been under my charge whose knee had been for two years kept in a steel apparatus for the purpose of preventing motion. Careful examination convinced me that this was a case of hysterical joint. I therefore flexed and extended the limb several times to its utmost limits, told her to throw away the steel rods, and to walk on the leg as much as she pleased. Within six months she walked as well as she ever had, and was even able to waltz with ease, with no other treatment than daily passive movements of the joint. In regard to these neuroses Meyer 1 has lately communicated much interesting information, and has indicated the leading phenomena which suffice to distinguish them from organic diseases. Thus the pain ceases at night, light handling is more painful than severe pressure, transient swellings are apt to occur, the temperature of the part is subject to changes, there is no tendency to atrophy of tfte muscles in the vicinity, and they are often cured spontaneously, or by prayer, or by sudden movements of the joint, or by some powerful physical cause. Neuralgia often has a hysterical origin, and may be in the form of toothache, pleurodynia, sciatica, or pain in the course of any other nerve. The viscera are likewise frequently hyperaesthetic; the stomach, bowels, the kidneys, bladder, uterus, and ovaries, are the organs most frequently affected. And of these the most common seat of hyperaesthesia in hys- terical women is the ovary, and, according to Chairou/the left ovary more frequently than the right. I have several times succeeded in causing hysterical attacks by moderate pressure on the ovary, and have rarely failed to find one or both the seat of marked tenderness in cases of the affection. Indeed, so common is it to find ovarian tenderness in hys- terical women, that I am almost disposed with Chairou to regard this condition as a pathognomonic sign. Charcot 3 also lays great stress on the symptom. The organs of the special senses rarely escape having their sensi- bility exalted, and, consequently, there are increased power of vision, morbid acuteness of hearing, and an abnormal sensitiveness of the smell and taste. Sometimes with these hyperaesthetic conditions there is pain. Anaesthesia.—Though not so common as hyperaesthesia, anaesthesia is frequently a manifestation of hysteria. One of its most common seats is the skin. In the days of witchcraft, many a hysterical woman with anaesthetic spots on her skin, went to the gallows or the stake on sus- 1 Berliner klinische Wochenschrifl, No. 26, 1874. Also Psychological and Medico- Legal Journal, September, 1874. 2 “ Etude? cliniques sur la hysteric,” Paris, 1870, p. 7. 8 Op. cit. p. 283. HYSTERIA. 733 picion of being leagued with the devil. The belief was that, wherever the hand of the arch-fiend or his assistants touched the skin, the spot at once lost its sensibility. Two patients are now under my charge in whom there is hemi-antes- thesia, paroxysmal in its character. When it is at its height, no irri- tation applied to the skin is felt, not even the wire brush of a powerful induction-coil. In neither case are the attacks preceded or accompanied by numbness. Sometimes the location is very limited, and the loss of sensibility may be partial or complete. In the former case there is numbness, and the full extent can only be exactly ascertained by the aesthesi- ometer. The mucous membranes may become anaesthetic. One frequently affected is that which lines the genital canal. In such a case, the sexual passion is entirely extinguished, coition is unattended with pleasure, and may even excite disgust. The organs of the special senses may be the seat of anaesthesia, and thus blindness, deafness, loss of the senses of smell and of taste, may be caused, more or less complete in character, in different cases. Chairou 1 has, however, shown that in all cases of hysteria the reflex excitability of the larynx is abolished. If in a hysterical woman the finger be passed down the throat so as to be brought in contact with the epiglottis, it will be found that this part is absolutely insensible, and that it can be rubbed or even scraped with the nail without caus- ing irritation of any kind. Or the superior orifice of the larynx may be similarly treated with the finger or with a probang, a feather, a roll of paper, or any similar instrument, without exciting either cough or efforts to vomit. Since becoming acquainted with Chairou’s observations I have inva- riably made such an operation as that described a part of my examina- tion of hysterical persons male or female, and have never failed to verify his statements. It is somewhat astonishing that his observations have attracted so little attention. Anaesthesia of the muscles is occasionally met with, and has, at times, been the occasion of much discussion in medical and theological circles. Many of the phenomena observed in the Jansenist convulsion- naires were the result of muscular anaesthesia. In an essay2 recently published, I have called attention to the symptoms, and have adduced several cases from the records of my own experience. The extent of the anaesthesia is sometimes remarkable. In some of the cases that have been under my care, the most powerful induced currents which it was safe to use, failed to cause pain in the muscles to which they were applied. 1 Op. cit., p. 12. 2 “ On Certain Conditions of Nervous Derangement,” New York, 1881. 734 CEREBRO-SPINAL DISEASES. Alterations of Motility.—These may be evidenced in the way of paralysis or of clonic or tonic spasm. Hysterical paralysis has long been known, and is quite a common manifestation of the affection. It may appear in the character of hemi- plegia, paraplegia, or of much more restricted extent. I have a case, now under care, in which it is limited to the index-finger, and I have had several in which a single muscle of the eyeball, or in which the leva- tor palpebrae superioris, was alone affected. Hysterical aphonia is due to paralysis of one or more muscles of the larynx. Like the loss of power in other muscles from a similar cause, it often comes on very suddenly, and as suddenly disappears. Paraplegia, hysterical in its character, may be partial or complete as regards a muscle, group of muscles, or a limb. When incomplete, the patient, if it involves the lower extremities, drags her limbs slug- gishly along, or shuffles her foot over the floor, using a cane or crutches or holding on to articles of furniture that may be in the room. There is nothing about the gait like that of locomotor ataxia or, in fact, of any other of the diseases of the cord already considered ; and careful observation will generally reveal the fact that, during one interview and examination, the patient walks very unequally, according to the state of her mind at the time, or the influences which act upon her. Spasms may be either tonic or clonic, and may affect any muscle of the body. In the pharynx, tonic spasm causes the sensation to which the term globus hystericus is applied, and which gives rise to the sen- sation of a ball in the throat. In the oesophagus, spasm may continue for a long time, and may thus simulate stricture. It may also be seated in the stomach, intestines, or bladder. Pig. 102. In the limbs spasm of the tonic character causes contraction, and thus, especially when combined with paralysis, may give the appear- HYSTERIA. 735 ance of organic lesion. I have frequently known hysterical contrac- tions to last several months at a time, and have had many cases of the kind under my charge in which the actual cautery had been applied to the hack for supposed inflammation of the cord. In some cases the duration is even longer than this. Charcot cites an instance in which a woman, aged fifty-five, was seized, eight- een years previously, with a hysterical paroxysm followed by para- plegia and contraction. At first this latter phenomenon disappeared from time to time to reappear again and again, but for the past six- teen years there had been no change. The extensors and adductors, as will be seen from the accompanying woodcut (Fig. 102), are the muscles mainly affected. The muscles of the legs and thighs were notably atrophied, and the faradaic contractility was lessened. For several years this patient had ceased to exhibit hysterical phenomena. The subject of permanent hysterical contraction is well considered by MM. Bourneville and Voulet,1 and the foregoing case is detailed at length in their memoir. In such instances there is probably, as in Case XIII. of their work, in which there was a post-mortem examina- tion, and which has already been cited in this treatise (page 551), symmetrical lateral spinal sclerosis. Clonic spasms simulate chorea or epilepsy. They are especially common among the women who attend spiritualistic gatherings, and indeed I have seen several cases at such places among the weak-minded men who believe in the nonsense called spiritualism. The functional actions of the viscera are exceedingly liable to de- rangement in hysteria. Any organ of the body may be affected, but the stomach appears to be the favorite one. There may be obstinate vomiting, or persistent flatulence, or acidity, or indigestion in some other form ; or the bowels may be the seat, giving rise to intestinal in- digestion, diarrhoea, or obstinate costiveness ; or the kidneys may be involved, and there may be an enormous secretion of pale, limpid urine, or the quantity may be reduced to a minimum ; or the uterus or the ovaries may be the seat. Not infrequently organic disease of the heart is simulated, there being palpitation and general irregular action of this organ. Besides these several manifestations of hysteria, there are parox- ysms of the disease, characterized by emotional disturbance, spasm, convulsions, partial loss of consciousness, and sometimes coma. All these phenomena may be manifested during an attack, or a seizure may consist of any one or more of them. The convulsions sometimes bear a resemblance to epilepsy, sometimes to tetanus, sometimes to hydro- phobia, sometimes to catalepsy, sometimes to chorea. But, though simulating these diseases, the essentially hysterical paroxysm can be readily distinguished from either of them, mainly by the facts of its 1 “De la contraction hysterique permanents, ” Paris, 1872. 736 CEREBRO-SPINAL DISEASES. lack of consistency, the absence of the constitutional disturbance which attends the others, and by the presence of emotional excite- ment, and the consequent irrational laughing or crying. Attention will be again directed to some of these conditions in the ensuing chapter. Mania may be simulated, but the false can scarcely be mistaken for the real disease by any practitioner with his wits about him. Causes.—Of the predisposing causes, sex stands first. Of the many cases of hysteria which have been under my charge or seen by me in consultation, but four were in males. In one of these the affection was apparently induced by excessive study, and was characterized by frequent paroxysms of laughing and crying. One was a physician, and the disease took the form of coma; one was a lawyer in this city, the disease in him simulating epilepsy ; and the fourth was a shop- keeper from New Jersey, who had tetanoid paroxysms attended -with fits of sobbing, crying, and laughing, and in whom it was excited by masturbation. But, while there is this great predominance of females as the sub- jects of hysteria, I do not believe that the fact is always due to any particular influence of the uterus or other generative organs. It is probably the result in many instances of the delicacy of organization, and the greater development of the emotional system, acted upon by the exciting causes to be presently mentioned. Age is another predisposing cause. The period of life at which hysteria is most common is that extending from sixteen to twenty-five. After the latter age there is a gradual decline until the age is reached at which the menstrual function begins to become irregular, and then the number of cases increases. The civil condition, as regards marriage or celibacy, is to be taken into consideration among the predisposing causes. Undoubtedly the disease is much more frequent among the single than the married, but it is by no means confined to them. In my opinion the increased pro- clivity of single women to hysteria is not to be attributed to ungrati- fied sexual desires, or even to the non-fulfillment of the functions of the generative organs, but rather to that lack of aims in life, and the consequent reflection of the thoughts and emotions upon self, which are so inseparably connected with the present condition of single women. Certainly those celibates who have made for themselves objects in ex- istence are no more subject to hysteria, in my experience, than married women. Want of occupation is one of the powerful predisposing causes of hysteria, and it is to a great extent through the direct influence of this factor acting upon a more impressionable organization that, in my opinion, hysteria is more common in women than in men. In those savage and semi-savage countries where women work, hysteria is un- heard of. It used to be almost unknown among the negro women in HYSTERIA. 737 the South, hut since their emancipation, if my inquiries have ascertained the truth, it is becoming quite common among them. Hereditary influence is undoubtedly an important predisposing cause of hysteria. My own statistics are not complete on this point, but they are full enough to show that the majority had either hysterical mothers, aunts, or grandmothers, and many of the others had relatives affected with other nervous diseases. Briquet speaks very emphatically of tlie decided influence of hereditary tendency as deduced from his inquiries. The luxurious habits of life attendant upon refinement and educa- tion conduce to the development of hysteria. Attendance at theatres and operas, the cultivation of music, the reading of poetry and novels, the study of art, and any other influence capable of developing the emo- tional system at the expense of the purely physical or intellectual, fa- vor the growth of hysterical tendencies. Of exciting causes, sudden emotional disturbance ranks first. Anx- iety, grief, disappointment, the intense desire of self-gratification, a fit of ill-temper, with other similar factors, often induce paroxysms of the disease. Mental or physical fatigue, menstrual derangement, or uterine or ovarian disorders, may also act as exciting causes. But probably, above all these, is the contagion set in action by the contact with a hysterical person. I have seen a whole hospital ward of women thrown into paroxysms of hysteria by one patient suffering from an attack. Diagnosis.—To detail the diagnostic marks which distinguish hys- teria from other diseases would require more space than is proper in a work like the present, and would, moreover, be rather a work of super- erogation. The physician has simply to recollect that all hysterical affections have a family resemblance, and that, although almost every known disease may be simulated, yet that the counterfeit is never a good one. Attention to the symptoms of the several diseases already, and to be described, with a careful observation of the case, and due inquiry into the antecedents of the patient, will prevent a mistake be- ing made. He must also recollect that the hysterical patient always tries to impress others with the belief that she is very ill. She craves sym- pathy, and feeds on it with the effect of nourishing her disease. If she can cajole her medical attendant by appealing to his kindly emotions, she will do it, but failing in this she will try her power over his fears, and will leave no stone unturned to deceive him. Careful watching, with thorough skepticism, will either result in her detection, or in her defeat from sheer weariness. Prognosis.—As regards the prospect of recover}' from any particular manifestation of hysteria, or from a paroxysm of any kind, the prog- nosis is favorable, provided proper treatment be employed, but, as re- gards the liability to further attacks, much depends on the circum* 738 CEREBRO-SPINAL DISEASES. stances which surround the patient and the time during which she has been subject to the affection. If she can be submitted to proper treat- ment, without the interference of herself or her friends, the prospect of recovery, even in bad cases, is good ; but if she is to be allowed to do as she pleases, or if injudicious friends are constantly lavishing the sym- pathy and mistaken kindness which keep her disease alive, there is not much use in medicine or hygiene, and, as Reynolds says, the “ case is hopeless, and might as well be left alone.” Morbid Anatomy and Pathology.—Hysteria contributes absolutely nothing to the science of morbid anatomy. The brain, the spinal cord, the sympathetic nerve, give no evidence of its former presence. It is true, hysteria very rarely causes death, but hysterical patients have died of intercurrent affections, and post-mortem examinations have been made, and nothing which could reasonably be regarded as the essential cause of the disease has been found. Several of the older writers im- agined that they had discovered the lesion in the genital organs, in the stomach and intestines, in the brain, and even in the spleen ; but mod- ern research teaches us differently. At present, then, we are in total ignorance of the character of the lesion. From the symptoms, which are so obviously indicative of disordered brain and spinal cord, I have felt myself justified in classing it, provisionally at least, among the cere- bro-spinal diseases. The pathology or morbid physiology of hysteria is beginning to be better understood as our knowledge of the cerebral and spinal actions becomes more complete. Looking at the brain as a complex organ evolv- ing a complex force—the mind—we can understand the possibility of certain parts of it becoming disordered, as regards excess, diminution, or quality, in the results of their actions. We have seen, under the head of insanity, that the mind is made up of certain sub-forces—the perception, the intellect, the emotions, and the will—and that these, when disordered, constitute varieties of insanity, which are easily recog- nized. , Hysteria essentially consists in the predominance of the emotions over the intellect, and especially over the will, and this exaltation may be so intense as to interfere with the sensibility of various parts of the body, or to derange the contractility of muscles. At the same time, in the paroxysms of the disease, the reflex and automatic functions of the spinal cord are involved to a great extent. We daily witness examples of the influence of emotions on sensi- bility and motility. Fear renders the sensibility more acute and pro- duces trembling, which is simply clonic spasm ; grief causes tonic con- tractions of the muscles ; surprise, terror, or horror, paralyzes them ; joy or anger destroys sensibility to pain, and so on. At the same time that there is this exaltation of emotional power in hysteria, the power of the will is not only relatively but is absolutely diminished. The two factors, acting together steadily and persistently, HYSTERIA. 739 induce many of the manifestations of hysteria. The disease is, there- fore, a partial insanity—an insanity, however, in which the patient does not entirely lose the power of control, and which is capable of being overcome by the voluntary effort of the patient, provided a sufficient stimulus to normal volition be brought to bear. It thus happens that, through the influence of such stimulus, every symptom of hysteria dis- appears as if by magic. The spinal cord is often secondarily affected, and it is likewise fre- quently primarily involved. The gray or the white substance, the pos- terior or the antero-lateral columns may be implicated, the symptoms varying accordingly. Through the spinal cord, in its abnormal condi- tion, we have the convulsions of various kinds, the spasms, contrac- tions, and the paraplegic and hemiplegic phenomena connected with motion and sensation. As to the influence of the vaso-motor system, though I admit its existence, I am convinced that it is simply a link in the chain, and is secondary to the emotional disturbance already mentioned. Treatment.—No cases are so well calculated to test the patience and tact of the physician as those of hysteria. For he has an affection to deal with, which not only requires proper medical treatment, but in which he must often exert the highest mental qualities, in order to cure the disease. A great deal, therefore depends on the knowledge of hu- man nature and the force of character of the physician ; and it is doubt- less owing to this fact that some physicians, with all their medical knowledge, fail in curing hysterical affections, while others, with no superior science, succeed at once. The first thing to be done is to gain the confidence and, what is of still greater importance, the respect of the patient. Having done this, any treatment, moral or medical, calculated to relieve her, will be much more apt to produce the desired effect. During the period between the paroxysms, the treatment must be directed mainly against symptoms. If the patient can be made to be- lieve that her case is thoroughly understood, and that she is not sus- pected of shamming, and that, with her assistance, the hyperesthesia, or anesthesia, or paralysis, will be removed, the effect which is desired will probably be produced. For putting a hysterical patient into a proper frame of mind, I know of nothing equal to the bromides, of either potassium, sodium, calcium, or zinc, given in large doses, repeated three or four times a day, till the full effect is obtained. This will generally relieve hyperaesthesia wherever it may be seated, and the influence over the mental phenomena of the disease is usually very decidedly shown. If anaesthesia be the prominent condition, electricity is to be used, and it is almost a specific. I have never seen a case of hysterical an- aesthesia resist it. A few days ago, I was consulted by a young lady who was entirely anaesthetic over the whole of the surface of one side of the body, and who had suffered for several weeks. Three applica- 740 CEREBRO-SPINAL DISEASES. tions of the induced current through the wire brush, which was passed, at each seance, over the whole anaesthetic region, entirely cured her. For hysterical paralysis, strychnia and phosphorus are the best in- ternal remedies. They may be taken together in the form recommended on page 68, and rarely fail to produce a cure. Their effect is, how- ever, greatly increased by the use of electricity, both of the primary and induced forms—the first being applied to the spine, and the latter to the paralyzed muscles. In cases of spasm, I prefer the bromides, internally, and the primary galvanic current, applied to the contracted muscles. Visceral derangements are best treated by strychnia and phospho- rus, as recommended for paralysis. Counter-irritation, in the form of blisters, is almost always of service. For gastric troubles, the subcar- bonate of bismuth, in doses of fifteen or twenty grains, after each meal, will generally prove of service. In a very obstinate case of hysterical vomiting under my charge, everything failed but hydrocyanic acid. Recently, in several extreme cases of hysterical vomiting, and nota- bly in one I saw in consultation with Dr. C. T. Whybrew, I have ob- tained very prompt results from the valerianate of caffeine in doses of three grains repeated in a half-hour if necessary. Paret1 adduces sev- eral examples of its beneficial effects in like cases. In other cases I have arrested hysterical vomiting by giving four or five pills of hydrochlorate of cocaine, each pill containing the one twentieth of a grain of the drug. Hysterical paroxysms are best treated with ether or chloroform, ad- ministered by inhalation. I have repeatedly used the hydrate of chlo- ral, but it has not in my hands been as speedy or as effectual in it3 action as either of the other agents. I give them to the extent of pro- ducing complete insensibility, and repeat them again and again, if there are any evidences of a return of the seizure. Whether in the purely emotional paroxysms or those characterized by muscular spasms of various kinds, or any possible combination, nothing is equal, according to my experience, to ether or chloroform by inhalation. I have tried every other known means, from cold water, dashed in the face, to moral suasion, and none of them are comparable to ether or chloroform. I have also found decided benefit from the mono-bromide of cam- phor in breaking up what may be called the status hystericus. In a recent communication2 I called attention to its good effects in such cases. It may be given in pill or emulsion in doses of from three to five grains every hour or two, as may be required. In those cases in which ether or chloroform is contraindicated the mono-bromide of cam- phor is particularly valuable. 1 “ De l’emploi de valerianate de cafeine,” Paris, 1875. 2 “Note relative to the Mono-Bromide of Camphor,” New York Medical Journal, vol xiii., 1871. HYSTERIA. 741 But, for the dissipation of the hysterical tendency, long-continued treatment is necessary. Medicines which are ordinarily regarded as antispasrnodics, such as valerian, asafoetida, musk, and the like, I have never seen produce any benefit in any form of hysteria, and, for the purpose of causing any radical change in the organism, they are worse than useless. As medicines for this object, I know of nothing superior to phosphorus, in some one of its forms, and strychnia. They should be taken for months in small doses, and should be supported by all hy- gienic measures calculated to improve the tone of the system. Travel is of inestimable advantage, and, above all, association with persons of both sexes, whose intellects control their emotions, and who are en- dowed with sound common-sense and that tact and knowledge of human nature which, for the purposes of every-dav life, are of more value than many other qualities often ranked above them. It is very certain that in most cases of hysteria the exhibition of sympathy is exceedingly injudicious and is generally taken advantage of by the patient to impose still further on those around her. Thus a lady to whom I was called had gotten into a morbid condition attended with frequent paroxysms of weeping, because, as she said, she no longer cared for her husband or children, and that she wished they were dead, etc. All the arguments of her friends failed to convince her that she was a good wife and mother, but, on my telling her husband in her pres- ence that I was afraid it would be necessary to send her to a lunatic asylum, her interest was at once awakened, and the next morning she was entirely free from all hysterical phenomena. She subsequently told me that nothing had roused her but the fear of being put in a hospital for the insane. In another case a lady had terrified her friends and excited the greatest commotion by threatening to put an end to her life by jump- ing out of the window. When I saw her she was strapped down to a bed and was being supplicated by half a dozen people in the room not to kill herself, to which she was energetically replying that she would. I loosened the straps, opened the window, and told her to jump out. She walked to the window, looked out for a moment, and then, apply- ing no very polite epithet to me, went back to bed, and I heard no more of her suicidal desires. A still more remarkable case is given by M. Charcot.1 The pa- tient, a woman, had been for at least four years the subject of con- traction of one of the lower extremities, as shown in the woodcut (Fig. 103). In consequence of her insubordination on one occasion, he spoke to her very sharply, and threatened to send her out of the hos- pital. The next morning the contraction had entirely disappeared. In the face of facts like these it appears absurd to invoke supernatural agencies. 1 “ Legons sur les maladies du systeme nerveux,” Paris, 1872—’73, p. 31S. 742 CEREBRO-SPINAL DISEASES. It is, perhaps, scarcely necessary to state that the society of other hysterical persons must be rigidly eschewed, and that even the casual meeting with such individuals is dangerous. Fig. 103. CHAPTER VI 11YSTEROID AFFECTIONS—CATALEPSY, ECSTASY, HYSTERO-EPILEPSY. There are certain disorders so very like hysteria in some of its manifestations, and often existing with it in the same individual, that they might with propriety have been considered in the last chapter, es- pecially as by some high authorities the scope of hysteria is so enlarged as to be made to embrace them within its limits. But, though they may owe their existence to the same peculiar condition of the nervous system, to which the ordinary phenomena of hysteria are due, there is sufficient individuality about them to warrant their being studied separateljT. At the same time there will be no difficulty in our bearing in mind that they are decidedly of such general and special character- istics as to impress us very forcibly with the idea that they are essen- tially hysterical. We may, therefore, with propriety, class them to- gether in the present chapter as hysteroid. I. Although there are no post-mortem appearances characteristic of catalepsy, the phenomena of the disease observed during life point to CATALEPSY. CATALEPSY. 743 its seat in the brain and spinal cord. Like epilepsy, therefore, it is a symptom representing an unknown morbid change in the nervous centres. Symptoms.—Catalepsy is an affection marked by the occurrence of peculiar paroxysms at regular or irregular periods. The seizures usu- ally come on with suddenness, and are characterized by more or less complete suspension of mental action and of sensibility, and by the supervention of muscular rigidity, causing the limbs to retain, for a long time, any position in which they may be placed. The phenomena, therefore, relate to the mind, to sensation, and to motion. The suspension of mental action is, in general, complete, but in some cases there are an imperfect consciousness and an ability to appreciate strong sensorial impressions. Thus, in a case quoted by Dr. Chambers from Dr. Jebb—which, however, was clearly a case of catalepsy compli- cated with hysteria—the patient, before emerging from the paroxysm, sang “ three plaintive songs in a tone of voice so elegantly expressive, and with such affecting modulation, as evidently pointed out how much the most powerful passion of the mind wTas concerned in the production of her disorder, as indeed her history confirmed.” 1 The aspect of a cataleptic patient is very striking. The eyelids are sometimes wide open, at others gently closed ; the pupils are dilated, and do not respond to strong light; the respiration is slow, regular, but generally so feeble as to be perceived with difficulty; the pulse is usu- ally almost imperceptible, but is rhythmical and sluggish ; the face is pale, the mouth is half open, and the rigidity of the body and the cold- ness of the extremities add to the death-like appearance which im- presses all beholders. The cutaneous sensibility is ordinarily completely abolished. Pins may be stuck into the skin, and they are not felt ; but, owing to the abolition of the power of motion and of reflex action, it is possible that in some cases, at least, the patients would give evidence of sensation if they could. Cases are on record in which tears have been caused by excessive emotional disturbance excited by the words or actions of per- sons surrounding the patients, thus showing that the senses of sight and hearing were capable of being exercised. Such instances are, however, rare, and are probably imperfectly-developed paroxysms, or those com- plicated with hysteria or ecstasy. The symptoms relating to the muscles are very remarkable. Com- ing on, as the paroxysm usually does, without \varning of any kind, the patient is at once arrested in any act which is being performed, and the whole body assumes a condition of extreme rigidity. The power of the will over the muscles is lost, and the limbs preserve any position in which they may be placed by the by-standers. Thus, if the arm be raised from the side, it remains extended, and may keep this position 1 Article “ Catalepsy,” in Reynolds’s “ System of Medicine,” vol. ii., p. 100. 744 CEREBRO-SPINAL DISEASES. for an hour or longer before it sinks slowly back to its original situ- ation. No matter how awkward or irksome the position may be, it is retained till the exalted irritability of the muscles becomes thorough- ly exhausted. The ability to swallow is not lost, and the electric contractility of the muscles is not perceptibly affected one way or the other. The paroxysm may last a few minutes or hours, or may be prolonged to several days. The temperature of the body, in all the cases that have come under my observation, was reduced from two to four degrees below the nor- mal standard, and in the extremities much more than this. The paroxysm generally disappears with as much abruptness as marked its accession. A few deep inspirations are taken, the eyes are opened, or lose their fixedness, the muscles relax, and consciousness is restored. In fully-developed seizures the patient has no knowledge of what has occurred during the attack. Ten cases of true catalepsy, uncomplicated either with hysteria or ecstasy, have been under my professional care. In two of these the seizures were more or less imperfectly developed, and strong sensorial excitations were, in a measure, perceived and recollected after emer- gence from the attack. But in every instance the character of the im- pression was misinterpreted. A bright light thrown upon the eyes with a mirror was spoken of as an “ angel’s wing which brushed across my face,” and the scratch of a pin was remembered as “ a piece of ice being drawn over the skin.” In these cases there was the consciousness of mental action during the paroxysm, but it was difficult for the patients to describe the thoughts which took place. They appeared to be somewhat of the nature of dreams. In both cases the muscular rigidity was well marked but was not excessive, and appeared to be mainly manifested in the ex- tensors. It was not difficult to extend the arm or the leg, but flexion required the exertion of a good deal of strength. In the other eight cases the paroxysms were completely formed. Consciousness was entirely abolished ; there was no sensibility any- where, and no reflex actions could be excited except those of degluti- tion. In one of these cases, seizures several times occurred in my con- sulting-room, and I had the opportunity of ascertaining the effect of electricity. If the arm was extended, the strongest induced current I could apply to the biceps, though causing contraction, failed to procure flexion, but relaxation of the extensors was at once produced by the application to them of the galvanic current. I likewise, in this case, repeatedly examined the fundus of the eye with the ophthalmoscope, and invariably found the choroids pale, and the retinal vessels straight and attenuated. In none of these cases was there any knowledge of what passed CATALEPSY. 745 during the paroxysms, and no consciousness of there having been any mental activity. Besides these, several instances have occurred in my experience in which cataleptic phenomena were exhibited in the course of other dis- eases. In one of them, a young man whom I saw in consultation with Dr. Max Herzog, of this city, there was well-marked mania—a second attack. On my entering the room in which he was seated I observed that he had a rapt expression of countenance, and that his limbs were quiet, and apparently rigid. In an undertone I remarked to Dr. Her- zog that the patient had a somewhat cataleptic appearance. Seizing his arm I raised it from the body and it remained extended; the other arm was also elevated and continued in that position. I then lifted the legs alternately from the floor, and they were kept in their appar- ently uncomfortable positions. During the consultation, probably a half-hour, the extremities remained as I had placed them. A few days afterward, he became so violent that it was necessary to send him to a lunatic asylum. In another case the patient, a young lady of this city, was brought to me by her father for examination and advice. As she entered my consulting-room, I saw that there was a high degree of mental exalta- tion present—her eyes were raised to the ceiling, her hands were clasped, and her lips were moving as if in prayer. I raised her left arm from the body, and then the right ; both remained extended, and con- tinued so till I changed the positions, which I did by bending the elbows, bringing them to the front, putting them behind her, and so on. I then again extended them, and she left the house with them in this position; but, on getting into the street, and feeling a cold wind that was blowing at the time, they fell to her side and she began to use them to draw her shawl around her. She had been subject to epi- lepsy for several months, but had never before exhibited cataleptic phenomena. In the former of these cases there was no possibility of ascertaining the mental associations of the patient with the muscular rigidity; in the latter the patient said that she had a very distinct recollection of my extending her arms, but why she had kept them so she did not know, and that she was not conscious of fatigue, or of any other sensation. It will have been noticed that in both these cases the paroxysms were not spontaneous, but were excited by outside interference. The particulars of a very interesting case of catalepsy have been recently given to me by Dr. M. B. Early, late house-physician to Belle- vue Hospital. The patient, a German, a cigar-maker, aged twenty-three, had served in the army, entered the hospital October 4, 1872. In the previous July he had been drunk, and, quarreling with some rough people, was severely beaten and kicked on the head and other parts of his body. 746 CEREBRO-SPINAL DISEASES. On the 27th of September he had an attack resembling a convul- sion. He was smoking at the time, and, while thus engaged, his mother noticed that the cigar began to shake, then his whole body quivered. She attempted to take the cigar from his mouth, but the jaws were tightly closed, and the cigar was bitten through. He swallowed the portion that was left in his mouth. He seemed to be conscious, for when requested by his mother to go to bed he shook his head. He did not sleep, but, when spoken to, nodded or shook his head in assent or dissent as the case might be. He did not foam at the mouth or bite his tongue. His feet were very cold. The attack lasted about five minutes. He then vomited the piece of cigar he had swallowed, and went to bed, sleeping all afternoon. The following day he had a similar attack, not so severe as the first. During the five following days he was free from paroxysms, but would not talk, although he ate and seemed to understand what was said to him, and would do any little thing his mother requested. On the sixth day, soon after breakfast, he had another paroxysm, but of a different character from the others. While the previous seizures were charac- terized by tremor, this was marked by a rigidity of all the voluntary muscles in the body. The attack lasted a few minutes, and the next day he was taken to the hospital, where he came under Dr. Early’s observation. On admission, October 4th, he lay in a stupid condition, his eyes sometimes open and sometimes closed. Occasionally he looked around, and appeared to understand what was said to him, but could neither speak nor move. The pupils were dilated. When his limbs were placed in any position they continued there for a considerable period. The muscles were rigid, temperature 100° Fahr. On being slapped smartly on the buttocks with a book, the patient got up, looked about him, and walked around the ward. He then drank a glass of milk and went back to bed. Just before getting up he smiled, and answered a question. During the night he went to the water-closet. In the morning he arose, looked around him, and drank some more milk. When slapped with a book shortly afterward, he did not move a muscle; seemed more stupid, did not swallow when food was placed in his mouth, and apparently did not feel the prick of a pin. The patient continued in this state for several days. On the 12th he was photographed. The accompanying woodcuts, Figs. 104 and 105, show the positions of his limbs at the time. Under the treatment the patient gradually improved, and on the 9th of November was discharged cured. An ophthalmoscopic examination, made November 3d, showed an anaemic condition of the disk. Cataleptic persons are usually of dull and sluggish mental and phys- ical organization. Such has certainly been the case in all the in- CATALEPSY. 747 stances that have come under my observation. The disease does not ordinarily show any decided tendency to become worse, either as regards the severity or frequency of the paroxysms, providing the ex- citing causes be avoided. On the contrary, there is often a well- Fig. 104. marked natural tendency to spontaneous cure, or at least to a cure through vhe influence of purely hygienic influences, moral as well as physical. In the majority of cases catalepsy is complicated with hysteria or Fig. 105. ecstasy, and sometimes with epilepsy. Of this latter combination I ha ve seen two cases, and in one of these ecstasy was also a feature. This case I have alluded to in another communication.1 The patient 1 “ The Physics and Physiology of Spiritualism,” New York, 1871, p. 55. 748 CEItEBRO-SPINAL DISEASES. was a young girl, was cataleptic on an average once a week, and epileptic twice or three times in the intervals. Five years previously she had spent six months in France, but had not acquired more than a very slight knowledge of the language—scarcely, in fact, suffi- cient to enable her to ask for what she wanted at her meals. Immedi- ately before her cataleptic seizures, she went into a state of ecstasy, during which she recited poetry in French, and delivered harangues about virtue and godliness in the same language. She pronounced at these times exceedingly well, and seemed never at a loss for a word. To all surrounding influences she was apparently dead; but she sat bolt upright in her chair, staring at vacancy, and her organs of speech in constant action. Gradually, she passed into the cataleptic paroxysm, in which she usually remained for from one to three hours. Many cases of the combination of catalepsy with hysteria and ecstasy have become celebrated in other relations than those of true science. Causes.—Among the predisposing causes, sex is, in my experience, the most efficient, though other writers have denied any influence due to sex. Of one hundred and forty-eight cases cited by Puel,1 sixty- eight were males and eighty females. Seven of my cases were in females. Hereditary influence is generally apparent. Of the ten un- complicated cases under my observation, all had relatives affected with some well-marked disease of the nervous system. In four cases, there were near relatives insane; in three, the mothers were hysterical; in one, a brother was epileptic; in one, the father was similarly affected; and, in one, a sister was cataleptic. It rarely begins after the age of twenty-five. Of exciting causes, emotional disturbance stands first. Four of my cases were directly the result—one of fright, one of anger, one of grief, and one of the shock caused by a boy starting out sud- denly from behind a door where he had been concealed. In one other case, the cause was worms in the intestinal canal; in two, business troubles; in one a severe fall; and, in the other two, I could not ascer- tain with certainty what the cause was, though I had strong reasons for suspecting it to be masturbation. The Diagnosis is not a matter of the least difficulty to any one who has even an imperfect knowledge of the phenomena, except, perhaps, as regards its discrimination from hysteria, that simulator of almost every nervous disease. In those cases complicated with hysteria, the distinction is of no importance; in others, the uniformity of the charac- teristics which indicate catalepsy, with a consideration of the general history of the case, will serve to make the diagnosis sufficiently precise. It must, however, be borne in mind that the two diseases are near of kin, and that the discrimination is important more as a matter of ab- stract science than as one of any bearing on the therapeutics. It is, however, sometimes a matter of moment to distinguish between the 1 “De la catalepsie,” “Memoires de l’Academie de Medecine,” tome xx , 1658, p. 409. CATALEPSY. 749 cataleptic paroxysm and death. In former times, instances were not uncommon in which the mistake was made, to be discovered after life had really become extinct in the coffin. Such fatal errors would prob- ably be impossible now with the stethoscope for examining the heart, the thermometer for determining the temperature, electricity for acting on the muscles, and, above all, the ability to place the limbs in posi- tions which they maintain against the laws of gravity. Moreover, our knowledge of diseases in general is such as to enable us to determine with great certainty the course they are liable to take, and the manner in which death occurs in each. Prognosis.—This is usually favorable, even in severe cases. All my patients recovered under the treatment to be presently mentioned. Morbid Anatomy and Pathology.—There is not much to say relative to the morbid anatomy of catalepsy. In some cases in which death has taken place, other diseases were present, and the lesions found were rather to be associated with them than with catalepsy. Puel,1 in his very elaborate treatise, says that the first report of a post-mortem examination of a patient dying while subject to the dis- ease in question is that of Hollerius, made in 1596. The patient, a man, had but one paroxysm, and died the same day. The lungs and liver were gangrenous, a collection of reddish serum was found in the posterior part of the brain, and sanguineous concretions (thrombi) in the superior longitudinal sinus. Deidier, in 1811, reported the case of an elderly man who had but one paroxysm, lasting a day, and who died eight days afterward. In this instance there were found, on each side of the longitudinal sinus, two little glandular bodies which were described perfectly, and to which the catalepsy was attributed. These were nothing more than the granu- lations of the dura mater, now known as the Pacchionian bodies. In a maniac who was subject to catalepsy and who died at Charen- ton, in 1834, the report by Georget and Calmeil states that the pia mater was found thickened and injected ; the cortical substance of the brain was reddened and softened, and the white substance contained enlarged vessels. In another case the same observers found the cortical substance discolored, and the white tissue injected. As they remark, however, these are the lesions of insanity Avith general paralysis. In other cases no alterations which could normally be associated with the cataleptic phenomena were discovered. The pathology of catalepsy is very imperfectly known. The symp- toms indicate that the brain and spinal cord are involved, and there is some evidence to show that they are in a state of ansemia. But there is a condition induced in these organs which is the essential feature of the disease, and of this we know nothing. There is a possibility that the affection may be a masked form of epilepsy, and this view is borne 1 Op. cit., p. 518. 750 CEREBRO-SPINAL DISEASES. out by the fact that the treatment which is most successful in this lat- ter disease is most efficacious in catalepsy. But recent researches have served to give us perhaps some inkling of the real nature of catalepsy, and to supply us with examples of arti- ficially-induced cataleptiform phenomena which are of great interest as analogical to instances of the natural disease. The investigations which have been made relative to motor centres in the brain lead us to sup- pose that there are likewise inhibitory centres in the cerebro-spinal sys- tem, probably both in the brain and spinal cord. We often meet with cases in which there is complete paralysis of one or more parts of the body, and which are suddenly caused by some strong impression pro- duced upon the emotions. Now, catalepsy is, for the time being, a pa- ralysis of the will, a condition in which, while the muscles have not lest their power to contract, there is a loss of volitional influence over them. They are still capable of responding to stimulation from without, but, in the absence of stimulation from within, they retain whatever degree of contraction may be given to them. Some of the results which follow experiments made to induce what is called the hypnotic state, are very suggestive of catalepsy. A era »v- fish, as Czermack 1 has shown, can be thrown into the cataleptic condi- tion, during which he is rigid and immovable. And I have repeatedly put frogs, lobsters, and hens, into a similar state. The full considera- tion of these interesting phenomena would be out of place in a practi- cal treatise on diseases of the nervous system.5 But I may at least state that I have recently developed the most intense cataleptoid phenomena in several subjects through the influ- ence of suggestion, while they were in the hypnotic, or, as I think it should more jxroperly be called, the syggignostic (ovyytyvwoKo), to agree with) condition. Among other exhibitions of the phenomena is one which is especially striking. By merely telling the subject that his body is so rigid that he cannot bend it, he at once becomes cata- leptic in every voluntary muscle, and may then be laid upon the backs of two chaii’s, as shown in the cut (Fig. 106), in which position he will remain for several minutes ; then the muscles gradually become unable longer to endure the strain, and the body sinks slowly to the floor. Very few trained gymnasts could perform this feat at all, and no one in his normal state could maintain the necessax-y muscular tension as long as the physically weak young man from whom the drawing is made. As is seen, the body rests only on the occiput and on one os calcis ; and I have known the position to be steadily kept for full five minutes. In these cases there is no excitation of muscular con- 1 “ On Hypnotism in Animals,” translated from the German by Clara Hammond, Popular Science Monthly, September and November, 1873. 2 For a more complete account of the phenomena and physiology of catalepsy, ecsta- sy, somnambulism, etc., the reader is referred to the author’s work “ On Certain Condi- tions of Nervous Derangement,” New York, G. P. Putnam’s Sons, 1881. CATALEPSY. 751 traction by reflex action, such as is supposed by Charcot and Hei- denhain to produce it, but it is induced solely by suggesting to the Fig. 106. subject that his body is in a rigid state. Immediately the muscles become tense, and he can be handled like a board. There may thus be in catalepsy inhibitory lesions, just as in epilepsy there are discharging lesions. But as in this latter disease there is something more than the convulsive movements, so in catalepsy there is a morbid element in addition to the muscular inhibition. And this appears to be an overwhelming inclination to agree with the sugges- tions received from other persons. Catalepsy is therefore hypnotism —or, as I prefer to call it, from its main characteristic, syggignoscism —with the addition of phenomena of muscular rigidity. Any syggi- gnostic subject can be thrown into a cataleptic condition, and the cata- leptic patient can readily be made to exhibit the ordinary manifesta- tions of syggignoscism. Treatment.—The bromide of potassium, or one of the other bro- mides previously mentioned under the head of epilepsy, is the most efficient agent in the treatment of catalepsy. I have never yet failed to cure the disease with this remedy, combined with the oxide of zinc, and with the simultaneous use of strychnia and other tonics. I have never, however, had occasion to give it in larger doses than twenty grains, three times a day, or to continue it beyond eight months. In no disease of the nervous system, not even excepting hysteria, is it more necessary that the mind should be brought under proper disci- pline, and kept as far as possible from the operation of all causes calcu- lated to promote emotional excitement. At the same time, a well- regulated system of hygiene, as regards all the physical requirements of the body, is indispensable. 752 CEREBRO-SPINAL DISEASES. II. ECSTASY. Though closelv allied to catalepsy, ecstasy differs from it in several important particulars. One of the main points of difference is, that the patient recollects the train of thought which has been going on during the seizure, and this of itself is sufficient to warrant their being sepa- rately considered. It often happens, however, that the two diseases alternate or coexist. Symptoms.—In ecstasy there is muscular immobility rather than rigidity, although the latter is sometimes present ; the eyes are open, the lips parted ; the face is turned upward, the hands are often out- stretched ; the body is erect and raised to its utmost height, or else is extended at full length in the recumbent posture. A peculiar radiant smile illumes the countenance, and the whole aspect and attitude is that of intense mental exaltation. The mind is so filled with some particular train of thought, that ex- citations of the senses, if of moderate intensity, are not perceived. We meet with this fact often in normal conditions, when the mind is deeply engaged in reflection, or when it is engrossed with some powerful emo- tion. Sometimes there is complete silence, the mind being apparently ab- sorbed with meditation or with the contemplation of some beatific vision. Again, there may be mystical speaking, prophesying, singing, or the lips may be in motion as if in speaking, but without any sound escap- ing. At times various attitudes are assumed which are in consonance with the ideas passing through the ecstatic’s mind. Again, stigmata or spots of blood appear in the hands or other parts of the body, and which are supposed to represent the wounds made by the nails in the hands and feet of Jesus, or the thrust of the spear in his side ; and, again, a real or assumed abstinence from food exists. Among the ecstatics of a former period, St. Francis of Assisi, St. Catherine of Sienna, St. Theresa, Joan of Arc, and Madame Guyon, are to be mentioned, and whole sects, both among Catholics and Protes- tants, exhibited all the manifestations of the disorder. Most of the religious impostors who have at various times made their appearance, and many very sincere and devout persons, have been ecstatics. In its combinations with catalepsy, chorea, and hysteria, ecstasy has frequently played an important part in the history of the civilized world —at one time, leading to a belief in witchcraft ; at another, to demoni- ac and angelic possession ; at another, to mesmerism and clairvoyance; and, in our day, tc spiritualism. The consideration of these follies, ECSTASY. 753 though interesting, scarcely comes within the scope of the present treatise. But within the last few years several very remarkable examples of ecstasy have been observed, and some references to two or three of them will probably not be out of place. First among them, as well on account of the interesting phenom- ena manifested as from the fact that the patient was regarded by a great many religious enthusiasts—physicians among them—as the sub- ject of miraculous interference, must be placed Louise Lateau.1 With- out going into the full details of the case, a short account will probably prove both interesting and instructive : Louise Lateau was born at Bois-d’Haine, a small village in Belgium, on the 30th of January, 1850. She was reared in the utmost poverty, was chlorotic, and did not menstruate till she was eighteen years old. She loved solitude and silence, and when not engaged in work—and 6he does not appear to have labored much—she spent her time in medi- tation and prayer. She was subject to paroxysms of ecstasy, during which, as many other ecstatics, she spoke very edifying things, of char- ity, poverty, and the priesthood. She saw St. Ursula, St. Roch, St. Theresa, and the Holy Virgin. Persons who saw her in these states declared that, while lying on the bed, her whole body was raised up more than a foot high, the heels alone being in contact with the bed. The stigmatization ensued very soon after these seizures. On a Fri- day she bled from the left side of her chest. On the following Friday this flow was renewed, and in addition blood escaped from the dorsal surface of both feet ; and on the third Friday not only did she bleed from the side and feet, but also from the dorsal and palmar surfaces of both hands. Every succeeding Friday the blood flowed from these places, and finally other points of exit were established on the forehead and between the shoulders. 1 For the theological view of this remarkable case the reader is referred to the follow- ing works, a part only of those written in support of her pretensions: “ Louise Lateau de Bois-d’Haine, sa vie, ses extases, ses stigmates; etude medicale,” par le Dr. F. Lefebvre, professeur de pathologie gen6rale et de therapeutique 5. la university catholique de Lou- vain, etc., Louvain, 1873; “ Les stigmatisees Louise Lateau de Bois-d’Haine, soeur Ber- nard de la Croix, etc.,” par le Dr. A. Imbert-Gourbeire, professeur l’dcole de medecine de Clermont Ferrand, Paris, 1873 ; “ Biographie de Louise Lateau, la stigmatisee de Bois- d’Haine,” par H. Yan Looy-Tournai, Paris and Leipzig, 1874 ; “ Louise Lateau la stigma- tisee de Bois-d’Haine d’apres des sources authentiques, m6dicales et theologiques,” par le professeur docteur A. Rohling, translated from the German by Dr. Arsene de None, Bruxelles et Paris, 1874; “Louise Lateau, ihr Wunderleben und ihre Bedutung im deutscher Kirchenconflicte,” von Paul Majuncke, Berlin, 1875. Among the treatises in which the miracle is denied, and the phenomena attributed to either disease or fraud, are : “ Louise Lateau, Rapport medicale sur la stigmatisee de Bois- d’Haine fait A l’academie rovale de medecine de Belgique,” par le Docteur Warlomont, Bruxelles and Paris, 1875 ; “ Science et miracle, Louise Lateau, ou la stigmatisde beige,” par le Dr. Bourneville, Paris, 1875 “Les miracles,” par M. Virchow, Revue des cours scientifiques, January 23, 1875. 754 CER EBRO-SPINAL DISEASES. At first these bleedings only took place at night, but after two or three months they occurred in the daytime, and were accompanied by paroxysms of ecstasy, during which she was insensible to all external impressions, and acted the passion of Jesus and the crucifixion. M. Warlomont, being commissioned by the Royal Academy of Medi- cine of Belgium to examine Louise Lateau, went to her house, accom- panied by several friends, and made a careful examination of her per- son. At that time, Friday morning at six o’clock, the blood was flow- ing freely from all the stigmata. In a few moments the sacrament would be brought to her, and then the second act of the drama would begin. The scene that followed can be best described in M. Warlo- mcfnt’s own words : “ It is a quarter-past six. ‘ Here comes the communion,’ said M. Niels [a priest], ‘kneel down.’ Louise fell on her knees on the floor, closed her eyes and crossed her hands, on which the communion-cloth was extended. A priest, followed by several acolytes, entered ; the penitent put out her tongue, received the holy wafer, and then re- mained immovable in the attitude of prayer. “We observed her with more care than seemed to have been hith- erto given to her at similar periods. Some thought that she was simply in a state of meditation, from which she would emerge in the course of half an hour or so. But it was a mistake. Having taken the commun- ion, the penitent went into a special state. Her immobility was that of a statue, her eyes were closed ; on raising the ej'elids the pupils were seen to be largely dilated, immovable, and apparently insensible to light. Strong pressure made upon the parts in the vicinity of the stigmata caused no sensation of pain, although a few moments before they were exquisitely tender. Pricking the skin gave no evidence of the slightest sensibility. A limb, on being raised, offered no resistance, and sank slowly back to its former position. Anaesthesia was complete, unless the cornea remained still impressionable. The pulse had fallen from 120 to 100 pulsations. At a given moment I raised one of the eyelids, and M. Yerriest quickly touched the cornea. Louise at once seemed to recover herself from a sound sleep, arose and walked to a chair, upon which she seated herself. ‘This time,’ I said, ‘we have wakened her.’ ‘ No,’ said M. Niels, looking at his watch, ‘ it was time for her to awake.’ ” She remained conscious ; the blood still continued to flow ; the an- aesthesia had ceased, her pulse rose to 120, and at the end of half an hour she was herself. “ Our first visit ended here. At half-past eleven we made another. The poor child had resumed her attitude of extreme suffering, against which she contended with all the energy that re- mained to her. The wounds in the hands still continued to bleed. M. Verriest auscultated with care the lungs, heart, and great vessels, and found the bruit de souffle which he had detected in the morning at the ECSTASY. 755 apex of the heart and over the carotids. The handle of a spoon piessed against the velum, the base of the tongue, and the pharynx, provoked no effort at vomiting. The glasses of our spectacles, as they came in contact with the air expired, were covered with vapor. As the patient appeared to suffer from our presence, we went away. “We made our third visit at two o’clock. There were still fifteen minutes before the beginning of the ecstatic crisis, which always took place punctually at a quarter-past two and ended at about half-past four. The pupils at this time were slightly contracted, the eyelids were almost entirely closed; the eyes, looking at nothing, were veiled from our view. We tried in vain to attract her attention ; her mind was otherwise engaged, and her pains were evidently becoming more in- tense. At exactly a quarter-past two her eyes became fixed in a direc- tion above and to the right. The ecstasy had begun. “ The time had now come to introduce those who were prompted by curiosity. This could now be done without inconvenience, for the ec- static, for the ensuing two hours, would be lost to the appreciation of what might be passing around her. The room crowded could hold about ten persons, but enough were allowed to enter to make the total twenty- five. These placed themselves in two ranks, of which the front one kneeling allowed the rear one to see all that was going on. All this was done under the direction M. le Cur6, who took every pains to give us a good view of what was going to happen. “Louise was seated on the edge of her chair; her body,inclined forward, seemed to wish to follow the direction of her eyes, which did not look, but were fixed on vacancy. Her eyes were opened to their fullest extent, of a dull, lustreless appearance, turned above and to the right, and of an absolute immobility. A few workings of the lids were now observed and became more frequent if the eyelids were touched. The pupils, largely dilated, showed very little sensibility to light, and all that remained of vision was shown by slight winking when the hand was suddenly brought close to the eyes. The whole face lacked ex- pression. At certain moments, either spontaneously or as a conse- quence of divers provocations, a light smile, to which the muscles of the face generally did not contribute, wandered over her lips. Then the face resumed its primitive expression, and thus she remained for the half-hour which constituted the 4first station.’ “ The 4 second station ’ was that of genuflection. It had failed at one time, but had again appeared. The young girl fell on her knees, clasped her hands, and remained for about a quarter of an hour in the attitude of contemplation. Then she arose and again resumed her sit- ting posture. “ The 4 third station ’ began at three o’clock. Louise inclined her- self a little forward, raised her body slowly, and then extended herself at full length, face downward, on the floor. There was neither rigidity CEREBRO-SPINAL DISEASES. nor extreme precipitation ; nothing, in fact, calculated to produce in- juries. The knees first supported her body, then it rested on these and the elbows, and finally her face was brought in actual close contact with the tiled floor. At first the head rested on the left arm, but very soon the patient made a quick and sudden movement, and the arms were ex- tended from the body in the form of a cross. At the same time the feet were brought together so that the dorsum of the right was in contact with the sole of the left foot. This position did not vary for an hour and a half. When the end of the crisis approached the arms were brought close to the sides of the body, then suddenly the poor girl rose to her knees, her face turns to the wall, her cheeks become colored, her eyes have regained their expression, her countenance expands, and the ecstasy is at an end.” Further particulars are given, and an apparatus was constructed and applied to Louise’s hand and arm so as to prevent any external ex- citation of the haemorrhage. It was apparently shown that there was no such interference, for the blood began to flow at the usual time on Friday. In addition to the stigmata and the paroxysms of ecstasy, Louise declared that she did not sleep, had eaten or drunk nothing for four years, had had no fecal evacuation for three years and a half, and that the urine was entirely suppressed. M. Warlomont examined the blood and products of respiration chemically, and satisfied himself of their normal character, except that the former contained an excessive amount of white corpuscles. When being closely interrogated, Louise admitted that, though she did not sleep, she had short periods of forgetfulness at night. On M. Warlomont suddenly opening a cupboard in her room, he found it to contain fruit and bread, and her chamber communicated directly with a yard at the back of the house. It was therefore perfectly possible for her to have slept, eaten, defecated, and urinated, without any one know- ing that she did so. The conclusions arrived at by M. Warlomont were, that the stigma- tisations and ecstasies of Louise Lateau were real and to be explained upon well-known physiological and pathological principles, that she c worked, and dispensed heat, that she lost every Friday a certain quan- tity of blood by the stigmata, that the air she expired contained the vapor of water and carbonic acid, that her weight had not materially altered since she had come under observation. She consumes carbon and it is not from her own body that she gets it. Where does she get it from ? Physiology answers, ‘ She eats.’ ” MM. Mauriac and Verdalle 1 give a very interesting account of an ecstatic woman who daily enacted the passion of Jesus, terminating in the usual manner with the representation of the crucifixion. This worn- 1 “ fitudc m6dicale sur l’extatique de Fontet,” Paris, 1875. ECSTASY. 757 an, Beguille, was of nervous temperament, had had many visions of the Virgin and of angels, and was accustomed to prophesy. When visited by MM. Mauriac and Verdalle, Berguille was lying in bed. She is described as a woman of about forty-five years old, brown complexion, muscles and limbs well developed but without much fat, eyes blue, widely open, and staring vaguely. She smiled kindly when questions were put to her, and answered with sufficient intelligence. On being asked why she was in bed, she answered that she was in pain night and day ; and, when requested to state where she felt the most pain, she answered, the backs and palms of the hands, the tips and soles of the feet, and the right side. (It will be remembered that Louise Lateau had her pain and hmmorrhage in the left side, a differ- ence wffiich the miracle-believers ought to find it difficult to reconcile.) Relative to her visions and what she heard during her ecstasies, she said that she saw Jesus Christ in his passion, that she heard voices, but she could not repeat what was told her. Her pulse was from 68 to 72. At about one o’clock the ecstasy began. Her pulse rose to 80. She clasped her hands on her heart, her gaze became fixed, her eyes were widely opened, her lips moved as if she were murmuring prayers, and there were frequent movements of deglutition. Her pupils were slightly dilated, but contracted when a light was brought to them. Her limbs were rigid, but it was noticed that she flexed them very read- ily when she altered her position a little or arranged her dress. In a few minutes she raised herself somewhat awkwardly on her knees, her hands still being clasped and her eyes fixed. Then began the passion or the way to the cross, during which she walked on her knees around the bed, changing her position twelve times, and falling three times in the traditional manner. To make this journey required thirty-six minutes, and, this done, the next act, the crucifixion, was in order. Suddenly she threw herself back on the bed, extended her arms from each side, and remained immovable. The pulse was 112, the res- pirations 100. The muscles of the chest seemed to be paralyzed, only the diaphragm acting. The eyes were closed. The limbs were in a state of forced extension and very rigid; the cutaneous sensibility to pinchings, prickings, and to the electrical stimulus was abolished. The latter, a very strong induced current, caused muscular contractions but no sensation. There was not the least flinching. Things went on in this way for over three hours, and then she sang the Salve Regina, exclaimed “ Oh, what sorrow ! ” and gradually recovered her senses. M. Bourneville1 cites the case of Ler., a hystero-epileptic, to whom reference will be again made, who at one time had a cruciform par- oxysm. Her head was strongly thrown back ; her eyelids, half open, 1 “Louise Lateau,” etc., Paris, 1875, p. 13. 758 CEREBRO-SPINAL DISEASES. Fig. 107. ECSTASY. 759 were in continual motion ; the muscles of the jaws were contracted, and the muscles of the neck were hard and tense. The superior extremities were extended at right angles from the trunk, the hands closed, and the fingers flexed so strongly on the palms as to render it impossible to open them. The inferior extremities were stretched out to their full length, the sole of one foot in contact with the dorsum of the other. In a word, the rigidity was such that the body could have been raised from either end like a bar of iron (Fig. 107). The attack lasted about four hours ; then Ler. opened her eyes and recovered consciousness, exclaiming, “ 0 my God, I was so happy ! ” Two other interesting cases are described by M. Billet,1 but the fore- going are sufficient to give the reader some idea of ecstasy as it ap- pears in Catholic countries. But the phenomena exhibited by Protestant ecstatics have been and are to this day fully as remarkable pathologically as those just de- scribed. Calmeil,3 speaking of the Protestant theomaniacs of Langue- doc and Cevennes, says : “ In general, they gave the name of ecstatic period to the agitation and improvisation which characterized the attack. All the inspired were fully persuaded that the Holy Spirit had entered into their breasts at the moment when they felt themselves constrained by an overwhelm- ing power to prophesy. All expressed themselves as if the Spirit of God spoke to them the words they uttered.” Elizabeth Barton, called the “ Holy Woman of Kent,” announced, during an attack of hysteria, that a child then sick with a brain- fever would die. As she predicted, the event took place soon after- ward, and the fulfillment of this prophecy at once gave the holy woman a great reputation. On this she announced that she was illumined by the Holy Spirit. She had numerous ecstatic paroxysms, during which she, according to her own account, was transported to heaven, and on her emergence she sang hymns, prayed, and made many predictions which astonished her admirers. At last, in obedience to an asserted command of the Virgin, she renounced Protestantism and took the veil. She continued to prophesy, and, growing bold, she predicted the speedy death of the king for his putting aside his wife Catharine of Aragon for Anne Boleyn. Henry VIII. was not of the temper to submit to this sort of holiness, so he had Elizabeth Barton beheaded as a pesti- lent woman, who was better out of the world than in it. An ecstatic, in a paroxysm of rapture, having lost his speech, thus describes his regaining the faculty :3 “At length, after nine months of sobs and convulsions without 1 “ Contributions & l’etude des nevroses extraordinaires,” Paris, 1874. 5 “ De la folie,” etc., tome ii., Paris, 1845, p. 288. 3 Calmeil, op. cii., p. 289. 760 CEREBRO-SPINAL DISEASES. speech, one Sunday morning as I was praying in my father’s house, I fell into an extraordinary ecstasy, and God opened my mouth. During the ensuing three days I was constantly under the operation of the Holy Spirit, neither eating, drinking, nor sleeping, and I spoke often with more or less power, according to the nature of things. All in the family were convinced, as well by the extraordinary state in which they now saw me, as by the wonderful fasting of three days, during which I felt neither hunger nor thirst, that it was surely by the Sovereign Power that such astonishing things were done.” In our own day, instances of ecstatic trance during camp-meetingsj revivals, and the like, are common enough, and the number is greatly increased by spiritualism, mesmerism, and such like absurdities.1 As we have seen, many ecstatics pretend that they do not eat. Cases of the kind are reported very often, and have been noticed from an early period. Thus Schenckius a quotes from Paulus Lentulus the “Wonderful History of the Fasting of Appolonia Schreira, a Virgin, in Bern,” in which it is stated that, being carefully watched by the orders of the magistrates of Bern, it was ascertained that there was no fraud, and she was dismissed as a genuine case of ability to live with- out food. During the first year of her fasting she scarcely slept, and in the second year not at all. Another, and still earlier case, was that of Margaret Weiss, aged ten years, who lived in Rode, a small village near Spires, and whose history is given by Gerardus Bucoldianus.8 Margaret is reported to have ab- stained from all food and drink for three years, in the mean time grow- ing, walking about, laughing and talking, like other children of her age. She, however, during the first year suffered greatly from pains in her head and abdomen, and, all four of her limbs were contracted. She passed neither urine nor fasces. Margaret played her part so well that, after being watched by the priest of the parish, and Dr. Bucoldianus, she was considered free from all juggling, and was sent home to her friends by order of the king, “not without great admiration and princely gifts.” The circumstances seem to have somewhat stag- gered Dr. Bucoldianus, for he asks, “ Whence comes the animal heat, since she neither eats nor drinks, and why does the body grow when nothing goes into it ? ” Of the cases that have been recently reported, that of the so-called Welsh fasting-girl * is one of the most remarkable, and a few years ago an account of its tragical ending excited a good deal of comment in the 1 For a full discussion of this subject, the reader is referred to the author’s work “ On Certain Conditions of Nervous Derangement,” New York, 1881. 5 “ HapaTJ)pr/(J£(i)v, sive observationum medicarum, rararum, novarum, admirabilium et monstrosarum volumen, tomis septem de toto homine institutum,” Lugduni, 1606, p. 306. 3 “ De Puella quae sine cibo et potu vitam transigit,” Parisiis, ann. MDXLII. 4 “A Complete History of the Welsh Fasting Girl, with Comments thereon, and Obser- vations on Death from Starvation,” by Robert Fowler, London, 1871. ECSTASY. 761 medical journals of Great Britain. Like the others, this was a case of hysteroid disease, and when she was so strictly watched that deception was no longer possible, she died in a few days of starvation. The startling heading to an editorial notice in the Lancet1—“ Starved to Death ”—expressed no more than the actual truth. In regard to the rarity of defecation and urination in cases of hys- teroid disease there is no doubt. Such cases are often accompanied with vomiting, and then the matter ejected from the stomach contains urea and sometimes even fecal matter. A lady, not long since under my charge, in whom there were no other very decided hysterical symp- toms, had an operation from her bowels never more frequently than once a month, and generally not so often. Every time she ate any- thing she vomited soon afterward, and the vomited matter always con- tained urea. She urinated about a tablespoonful every eight or ten days. The vomiting of fecal matter in cases of hysteroid disease is not so common. Briquet2 reports a case as occurring in his own experi- ence, in which there was no doubt that substances administered as enemas were vomited a few minutes afterward. Among other experi- ments, and in order to remove all doubt arising from the use of house- hold substances, an injection of tincture of litmus was given immedi- ately after it was brought from the pharmacy. The patient was told that coffee was to be injected. Twelve minutes afterward the tincture of litmus was vomited, its blue color turned to a red through the action of the gastric juice. Less authentic, perhaps, is the following from Henricus ab Heeres: 3 “ A certain gentleman has lived several years without having had any operation from his bowels. About the middle of the day he sits down to his dinner, usually inviting several noble persons to eat with him. In an hour he rises from the table, after having eaten and drunk to his satisfaction, and retiring, vomits the dinner he had eaten the day before, but retaining all the dinner he has just taken. It is ejected putrid and filthy, differing in no respect from other excrement. He vomits with ease, and at once, throwing up the contents of the stomach which have remained from the previous day. Then he washes his mouth with clean water and returns to his friends to finish his repast. He eats no supper or breakfast, and thus he has done for about twenty years.” Stigmata, as occasional symptoms of the hysteroid condition, are well known to dermatologists, many cases of bloody sweat having been noticed. Those observed in the case of Louise Lateau were well studied by M. Worlomont, and they were found to differ in no essential respect from those previously observed, except in regard to the periodicity of 1 Lancet, December 25, 1869. 2 “ Traite clinique et therapeutique de l’bysterie,” Paris, 1859, p. 316. 8 “ Observations medic®,” Lipsi®, 1645, lib. 1, ob. 29. CEREBRO-SPINAL DISEASES. the haemorrhages—a circumstance, however, easily accounted for by the fact that the stages of excitement were regular. Haemidosis, or bloody sweat, is to be regarded as one of the neuroses of the skin. An interesting case is reported by Wilson.1 Mason Good cites authorities to show that it has taken place during coition, violent terror, and great bodily agony. Its occurrence in the hands, feet, and side, is to be ex- plained by the fact that the attention is strongly concentrated on these parts, and it is in all probability kept in these situations by manual irritation. It is by no means certain that this latter was not the case with Louise Lateau, for M. Warlomont’s apparatus was not of such a character as to prevent such action. Causes.—Ecstasy, though not entirely confined to the female sex, is very much more common in women than in men. It appears to be produced in those who are of delicate and sensitive nervous organiza- tions by intense mental concentration on some one particular subject— generally, one connected with religion, or some other abstract train of thought. It was formerly quite common among the inmates of con- vents, and is now not unfrequently met with at camp-meetings and spiritualistic gatherings. There are no points about the Diagnosis requiring special considera- tion, and the Prognosis is always favorable, if the subject can be sub- mitted to proper moral and physical treatment. As the disease is never fatal per se, we know nothing of its Morbid Anatomy. The pathology, as indicated by the symptoms, points to the implication of both the brain and spinal cord, but there is no satisfactory theory of the disorder other than that which refers it to cerebral and spinal pre- occupation—a kind of setting of the current in one direction, whereby all other occupation is for the time prevented. Treatment.—The means of treatment, though not differing essen- tially from those proper for catalepsy, require, nevertheless, special mention of some particulars. The influence of moral force in prevent- ing and curing ecstasy is well marked, and many instances are on record in which epidemics of it have been arrested by arguments addressed to the fears of the subjects. I have several times aborted and prevented ecstatic manifestations by making preparations to cauterize the region of the spine with a red-hot iron. A great deal can be done by giving as little notoriety to ecstatics as possible. They glory in the idea that they are of sufficient impor- tance to excite' attention and discussion, and they are accordingly stimulated to continue their performances so long as they are noticed and an air of mystery is attached to them. Removal from all associations calculated to continue the exciting and morbid train of thought which has developed the disease under notice, should, of course, be a point in the treatment. 1 “On Diseases of the Skin,” American edition, Philadelphia 1863, p. 551. HYSTERO-EPILEPSY. Electricity, and the other measures of treatment recommended for catalepsy, will prove serviceable in ecstasy. By galvanization of the sympathetic nerve, I, on one occasion, immediately cut short a parox- ysm of ecstasy, and, by continuing the practice every alternate day for about six weeks, effectually cured the patient, who for several years had been subject to seizures every two or three days. As means for improving the general health are almost invariably required, iron, quinine, and strychnia, in the combination recommended on page 54, may be administered with advantage. I have great confi- dence in the bromides, and the patient should be to a moderate extent brought as soon as possible under the influence of some one of those previously mentioned. III. HYSTERO-EPILEPSY. The combination of hysteria with epilepsy has long been recognized as existing and as giving rise to one of the most frightful affections to be fouod in the whole range of neurological medicine. In the present state of our knowledge it would, perhaps, be going too far were we to pronounce positively in favor of its being a distinct pathological entity with a different anatomical substratum from either hysteria or epilepsy, and yet the phenomena are so distinct that we certainly are warranted in considering it separately from either of these diseases. Symptoms.—An attack of hystero-epilepsy is characterized by the occurrence of convulsions more or less resembling those of epilepsy. There is usually in the first place a well-marked tetaniform spasm, though, sometimes, this is not very decided, and occasionally is not observed at all. Then follow clonic convulsions, during which the patient froths at the mouth and may pass the urine or bite the tongue, though these phenomena, especially the latter, are rare. Loss of con- sciousness exists during this stage. Next ensues a remarkable series of movements, at the beginning of which, or during their continuance, the patient recovers consciousness to such an extent as to answer questions, although there is no after- recollection of the incidents that may have occurred. These move- ments are apparently voluntary, and consist of the most extraordinary contortions of the muscles of the face, neck, trunk, and extremities, so that superstitious people might well imagine the existence of an inter- nal or external diabolical agency. During the continuance of this part of the paroxysm the patient tears with the hands and teeth any thing tearable that comes within reach, and continually utters inarticulate sounds or words apparently in relation with the ideas passing through the mind. Finally, the purely hysterical element ceases to predomi- nate, and the patient alternately weeps and laughs, and gradually ac- quires a knowledge of what is passing around. CEREBRO-SPINAL DISEASES. 764 During the whole of the paroxysm the face is flushed, the pupils are moderately contracted, the pulse is accelerated, the perspiration is in- creased in quantity, and the respiration is hurried and irregular. But there are numerous deviations from this type of a seizure. Sometimes the tetanic spasm is wanting, and again it, or some modifi- cation of it, may constitute the most marked part of the convulsive period. Thus in a lady, who was lately under my charge, the paroxysm began with an opisthotonos, which was immediately relaxed, and again renewed, to be again relaxed, and so on, for over half an hour. In a woman whom I saw in the Pennsylvania Hospital several years ago, in the service of Dr. Pepper, the convulsions consisted of a series of rapid movements produced, as the patient lay on her bed, by the bending back of the body, so as to throw it into an opisthotonotic posi- tion, the head and heels alone touching the bed, and then, the muscles being suddenly relaxed, allowing the buttocks to fall with force on the bed. These actions were continued with great rapidity, and without intermission for an hour or more, and were succeeded by a period dur- ing which there were alternate laughing and weeping. Such cases are what Sauvages designated as hysteria libidinosa. But, in a case now under my care, the patient, a woman, has daily attacks at about the same hour—three o’clock p. M.—which are more dis- tinctly tetaniform in the beginning than any that have come under my observation. They consist of a series of opisthotonotic spasms, during which the body is extremely rigid. The convulsion is, however, unlike the others referred to, very slowly developed. The body extended at full length in the recumbent posture gradually becomes rigid, the legs are slightly abducted, the arms are pressed strongly against the sides, Fig. 108. the jaws are tightly closed, and the gaze fixed (Fig. 108). Respiration is entirely suspended, and the heart beats rapidly, sometimes as fre- quently as one hundred and sixty per minute. Then the body is slowly bowed, so that the head and heels alone touch the bed, and is so rigid and strongly arched that no ordinary force, such as a powerful man can exert, suffices to overcome the tonicity of the muscles. In about a minute from the beginning of the rigidity, the spasm suddenly relaxes, and with a long-drawn inspiration the paroxysm ends—to be again re- IIYSTERO-EPILEPSY. 765 sumed in a few minutes with a like sequence. In the accompanying woodcut (Fig. 109) is an exact representation of this patient when the tetanic spasm is at its height. Fig. 109. In this case there is a distinct aura starting from the left ovary, and strong pressure exerted upon this organ suffices generally, though not always, to cut short the series of paroxysms. Under the name of demonomania many cases of hystero-epilepsy have been described, and the disease, like chorea, has at times prevailed epidemically. At Loudun, in France, it led to the death at the stake of Urbain Grandier, the nuns, who were its subjects, accusing him in their delirium of having bewitched them. At Marseilles, Father Louis Gaufridi, a man of education and of strict morality, was accused by two Ursuline nuns of having debauched them through diabolical agency. At the time of the accusation, these nuns, one of them only nineteen years old, were suffering from attacks characterized by hallucinations and illusions, fearful epileptiform and cataleptiform convulsions, and delirious ravings—all of which were ascribed to the devil moved and in- stigated by Louis Gaufridi. At first, the accused denied the charges made against him, and endeavored by arguments to show the real nature of the seizures. But the effort was in vain, just as is the at- tempt now to convince the credulous and ignorant of the real nature of the seizures of Louise Lateau, Bernadette Soubirous—who evoked Our Lady of Lourdes—and of the hundreds of mediums, ecstatics, and hysterics, who pervade the world. Gaufridi became insane, and con- fessed all that was laid to his charge, with numerous other offenses which had not been imagined. He declared that he had worshiped the devil for fourteen years; that the demon had given him power to render amorous of his person all women on whom he should breathe, and that he had thus overcome several thousand women! Gaufridi, after horrible tortures, was burned at the stake; and the two nuns “continued to be delirious,” as well they might. As showing the nature of the phenomena exhibited in cases of de- CEREBRO-SPINAL DISEASES. moniacal possession and their resemblance to the symptoms of hystero- epilepsy and other forms of hysteria, I subjoin the following questions as proposed by Santerre, priest and promoter of the diocese of Nimes, to the University of Montpellier : Question 1. Whether the bending, moving, and removing of the body, the head touching sometimes the soles of the feet (opisthotonos), and other contortions and strange postures, are a good sign of posses- sion ? 2. Whether the quickness of the motion of the head forward and backward, bringing it to the back and breast, be an infallible mark of possession ? 3. Whether a sudden swelling of the tongue, the throat, and the face, and the sudden alteration of the color, are certain marks of pos- session ? 4. Whether dullness and senselessness or the privation of sense, even to be pinched and pricked without complaining, without stirring, and even without changing color, are certain marks of possession ? 5. Whether the immobility of all the body, which happens to the pretended possessed by the command of their exorcists, during and in the middle of the strongest agitations, is a certain sign of a truly dia- bolical possession ? 6. Whether the yelping or barking like that of a dog, in the breast rather than in the throat, is a mark of possession ? 7. Whether a fixed, steady look upon some object, without moving the eye on either side, be a good mark of possession ? 8. Whether the answers that the pretended possessed make in French to some questions that are put to them in Latin are a good mark of possession. 9. Whether to vomit such things as people have swallowed be a sign of possession ? 10. Whether the prickings of a lancet upon divers parts of the body without blood issuing therefrom are a certain mark of possession ? All these questions, to the credit of medical science—which has always, notwithstanding the weakness of some of its professors even in our own day, been steadily opposed to supernaturalism—were answered in the negative. No one can read them without being struck with the facts that Father Santerre was at least a good symptomatologist, and of the absolute identity of the phenomena cited, in all essential char- acteristics, with those which in our day are said to be of mystical origin, but which in reality are hysterical or hysteroid. We might reproach Father Santerre and his coadjutors more forcibly, if we had not our- selves killed witches and presided at the birth of spiritualism. No one has written with greater effect in regard to the manifesta- tions of hysteria and hystero-epilepsy than Charcot. As a most strik HYSTERO-EPILEPSY. 767 ing case of the latter affection, I cite from him the following instance1 already referred to in another connection under the head of ecstasy. Ler., aged forty-eight years, is a patient well known to all physi- cians who visit the as one of the most remarkable instances extant of hystero-epilepsy. Her menstruation has ceased for four years and yet all the neurotic symptoms persist. She is a demoniac, a Fig. 110. possessed, and presents a striking example of that type of hysteria manifested by the “ Jerkers ” in “ Methodist camp-meetings,” and who exhibit in their paroxysms the most frightful attitudes. The probable origin of these nervous phenomena in Ler. deserves to be noted. She has had, as she says, a series of frights. At eleven years of age she was terrified by a furious dog. At sixteen she was 1 “Lecterns sur lesmaladies du syst&menerveux faites &laSalpGtriere,” Paris, 1872—’73, p. 301, el seq. 768 CEREBRO-SPINAL DISEASES. frightened at the sight of the corpse of an assassinated woman, and again about the same time, when going through a wood, by robbers who attacked her and took her money. With her there are local hysterical manifestations consisting of hemi-anaesthesia, ovarian tenderness, paresis, and at times contraction of the limbs on the right side. Sometimes these symptoms are shown on the left side also. The attacks, wThich are announced by a well-marked ovarian aura, are characterized at first by epileptiform and tetaniform convulsions ; Fig. 111. after which come extensive movements of an intentional character, in which the patient assumes the most hideous postures, recalling the attitudes which history ascribes to demoniacal possession (Figs. 110 and 111). At the moment of the attack she is seized with delirium, which evidently turns on the events which have produced the initial seizures. HYSTERO-EPILEPSY. 769 She hurls invectives at imaginary persons. “ Scoundrels ! robbers! brig- ands. Fire, fire ! Oh, the dogs, they bite me ! ” When the convulsive part of the accession is over, there ensue, gen- erally, hallucinations of sight—she sees frightful animals, skeletons, and spectres ; a paralysis of the bladder ; a paralysis of the pharynx; and a contraction, more or less permanent, of the tongue. It is therefore necessary for several days to feed her through a tube, and to empty the bladder with a catheter. Later, M. Bourneville 1 has- given an account of Ler., somewhat fuller than that of M. Charcot, to which, as showing how Ler. had at one time exhibited phenomena of ecstasy similar to those present in Louise Lateau, reference has already been made. In further illustra- tion of the period of contortions in her case I take from M. Bourneville’s excellent monograph the accompanying woodcut (Fig. 112), made from a sketch taken on the spot by M. Charcot. Fig. 113. In the intervals between the paroxysms the subjects of hystero-epi- lepsy generally exhibit some of the phenomena of hysteria such as hemi- anaesthetic contractions, ovarian tenderness, paralyses, etc. Relative to the Causes, the Prognosis, Diagnosis, Morbid Anatomy and Pathology, and Treatment, there is nothing to add to the remarks already made when hysteria, catalepsy, and ecstasy, were under con- sideration. 1 “Louise Lateau, ou la stigmatisee beige,” Paris, 1875, p. 38, el seq. 770 CEREBRO-SPINAL DISEASES. CHAPTER VII. We have already considered the subject of sclerosis as it affects the brain and spinal cord separately. We have still to treat of it as exist- ing in these nervous centres simultaneously. Although recognized, over thirty-five years ago, by Cruveilhier and Carswell, it is only re- cently, mainly through the observations of Charcot and Yulpian, that attention has been again directed to sclerosis of the cerebro-spinal variety, a form which differs from those already described in this treatise, both in its extent and in the symptoms by which it is charac- terized. Symptoms.—The initial symptoms vary according as the morbid process begins in the brain or spinal cord. In the former case, the first prominent manifestation of disease may be an epileptic fit. In other cases, there are headache, vertigo, ocular troubles, such as ptosis, diplo- pia, or amblyopia, failure of the hearing, and, very often, defective articulation. The mind does not participate to any considerable extent, unless the hemispheres be involved in the lesion. Or, there may be hemiplegia as a consequence of cerebral conges- tion, and even mania, from a like cause. These attacks are sometimes frequent, and usually leave more or less mental weakness after them. Tremor is often first seen in the tongue, more frequently in the eye- ball, of one or both sides, which oscillates when the patient is told to turn it inward or outward, but which is steady when he looks directly to the front. This tremor is called nystagmus, and is, as we have already seen, in«..t with in other diseases of the nervous system. Ac- cording to Femei’s1 observations, it is due to lesion of the cerebel- lum, and when met with in the disease under notice points to this organ as one of the seats of the morbid process. In the case of a woman who attended my clinic at the Bellevue Hospital Medical College, nystag- mus was the only symptom observed for over a year, and then gradu- ally other phenomena of the cerebro-spinal form of sclerosis made their appearance. Tremor is indicative of loss of power, and it gradually becomes more strongly marked and extends to other muscles of the body as other parts of the cerebro-spinal system become involved. It is never, how- ever, a constant phenomenon in any form of sclerosis affecting the spinal cord alone. Its presence is peculiar either to cerebral disease or to lesions occurring in the pons or in the medulla. After a time, which is subject to great variation in different cases, MULTIPLE CEREBR0-SPIN*AL SCLEROSIS. 1 “Experimental Researches in Cerebral Physiology and Pathology,” “ West Riding Lunatic Asylum Medical Reports,” vol. iii., 1873, p. 69. MULTIPLE CEREBRO-SPINAL SCLEROSIS. 771 the loss of power extends to the limbs, and this feature is often accompanied with aberrations of sensibility. If, as is generally the case, the membranes of the cord are congested or inflamed, there are spasmodic jerkings or twitchings of the limbs, but in some cases these are never observed. In the case of a gentleman from South Carolina, who consulted me at the instance of my friend and colleague Prof. J. T. Darby, and who was obviously affected with multiple cerebro-spinal sclerosis, there had never been the slightest involuntary movement, independent of the peculiar form of tremor in the limbs which constitutes so prominent a feature of the disease. The lower extremities are generally very much more paralyzed than the upper, and, when they become involved, festination often makes its appearance. The gait of the patient thus becomes similar to that of a person suffering from paralysis agitans. If the sclerosis begins in the brain before attacking the spinal cord, tremor precedes the paralysis—the affection being then en- tirely cerebral in character ; but when, as is generally the case, the lesion appears primarily in the spinal cord, paralysis is noticed be- fore the tremor. In fact, there is never, as previously insisted on in my remarks on paralysis agitans, any tremor, unless the superior ganglia of the cerebro-spinal system are involved. The fact that it is only shown when a voluntary movement is made also assists us to distinguish it from the tremor of paralysis agitans, as well as from other forms of tremor. In the cerebro-spinal form of the disease, therefore, the patient remains without tremor so long as he is qui- escent. But if he attempts to cross one leg over the other, or to carry a glass of water to his lips, the extremity executing the move- ment is at once seized with tremor, and the act is performed with great difficulty. The ability to place the fingers on any part of the body, unassisted by the eyesight, is impaired, as in paralysis agitans, and in sclerosis affecting the posterior columns of the spinal cord. As the disease advances, symptoms indicative of lesions of the cord appear. These symptoms seldom point to disease of symmet- rical tracts. Thus, in one leg, the symptoms observed may be those of inflammation of the lateral pyramidal tract—that is, slight paresis, stiffness and rigidity of the muscles, exaggerated knee-jerk, and the ankle clonus, while the other leg may evince no abnormal symptoms whatever, or else may show evidence of disease of the posterior col- umns of the same side by the presence of pain, anaesthesia, loss of the knee-jerk, loss of the muscular sense, tactile sense, and temperature sense. The arms may show the same divergence of symptoms. There may also be paralysis of the bladder, constipation, and a tendency to the formation of bed-sores. 772 CEREBRO-SPINAL DISEASES. Thus, it is evident that, in the affection under consideration, we are not confronted, as a rule, with lesions confined to one or more of the “system tracts.” On the contrary, it is quite apparent that the diseased areas are scattered about in patches or islets, at one level affecting one tract, at another level another tract, while at many other levels the entire segment of the cord may be normal. The head symp- toms likewise increase in intensity, but the mind remains clear to the last in the great majority of cases. Indeed, my observation of many cases has convinced me that in the cerebro-spinal form of sclerosis the hemispheres are not often involved, even when the disease has lasted several years. The difficulties of articulation notably increase, and the muscles of deglutition likewise become involved. In consequence, the saliva is not swallowed as often as it should be, and it therefore dribbles from the mouth. Mastication is difficult, and the facial muscles gradually become involved. The countenance of the patient at this period is not unlike that of a person suffering from glosso-labio-laryngeal paral- y sis, as in fact might be expected, the same nerves and muscles being involved. Finally, the patient dies from exhaustion, or from some in- tercurrent disease. Few diseases are so irregular and ununiform in their phenomena as the cerebro-spinal form of sclerosis. This is due to the fact that the organs liable to be the seat of the disease are numerous and of varied functions. The essential feature of the affection is tremor occurring generally after paralysis, and only manifested during the performance of voluntary movements. It is not always necessary, however, that the movements should be of the partially-paralyzed limbs, for I have seen cases in which tremor was excited in a paretic leg by the act of executing voluntary movements with a sound hand. The following histories will contribute to a fuller understanding of the subject: Cruveilhier1 reports the case of a cook, aged thirty-seven, who six years before coming under observation noticed that he was losing power in the left leg, so that he nearly fell in the street. Three months sub- sequently the right leg became similarly affected, and then the superior extremities followed. They were tremulous and weak, but the patient was still able to use them to some extent. The sensibility remained intact, and the reflex faculty of the cord was unimpaired. In other respects the patient was condemned to immobility. There were no spasmodic retractions of the limbs, and no painful contractions. The articulation was imperfect, but the intelligence was unaffected. There appear to have been no marked head-symptoms in this case. “ Point de cephalalgie, jamais de cephalalgie, le malade entendait & merveille.” 1 “ Anatomie pathologiquo du corps humain,” Paris, 1835, 1842, tome ii., liv. xxxii., Fig. 4, PI. 2. MULTIPLE CEREBRO-SPINAL SCLEROSIS. 773 After death there was found gray degeneration of the spinal cord, of the medulla oblongata, of the pons Varolii, of the right cerebral pedun- cle, of the right optic thalamus, of the corpora callosa, and of the for- nix. The hemispheres were not involved. Two other cases, similar in general character to the foregoing, are given, in neither of which were the hemispheres involved. Another case, that of Josephine Pajet, is cited by Cruveilhier.1 In this there was almost complete insensibility of the inferior extremi- ties, though the patient was able to move the toes, the feet, and the legs. There were no cramps and no contractions. There was also diminished sensibility of the superior extremities. All the limbs were weak, and the arms were affected with tremor. The patient could walk and sew when first seen. The right hand was stronger than the left. There was a sensation of a tight band around the abdomen. After death there was gray degeneration of the cord, and of the pons Yarolii. In none of these cases were there spasmodic jerkings or tonic con- tractions of the limbs. Two cases have been reported by Friedreich.2 In one of these a man, aged twenty-one, was the subject. Among the first symptoms were mental excitement, vertigo, pain in the head, and weakness of the lower extremities. The gait was unsteady, and there was tremor upon any emotional excitement, or on the attempt to exe- cute movements. This affected the upper and lower extremities, the head, and the eyeballs. After death, patches of sclerosed tissue were found on the tubercula mammillaria, the cerebral peduncles, the pons Yarolii, and the medulla oblongata. The other case was that of a woman, aged twenty, who was attacked, when seventeen years of age, with weakness of the right leg. Soon afterward the left became affected, and subsequently the arms. These latter were rendered tremulous at every attempt to move them. The speech was implicated, and there was nystagmus. The mind was weak- ened, and the sensibility was impaired. In the first of these cases the disease appears to have begun in the brain ; in the second in the spinal cord. Yulpian,3 under a title which goes to show how even the best au- thorities have confused the whole subject of sclerosis, describes an in- teresting case communicated by Charcot. In this instance a woman, aged forty-three, of nervous temperament, had been subject to frequent attacks of facial neuralgia, and had often suffered from vague pains 1 Op. cit., liv. xxxviii., Fig. 1, PI. 5. 2 “ Deutsche Klinik,” No. 14, 1856. 3 “ Note sur la sclerose en plaques de la moelle epiniere,” Id Union Medicale, No. 70, Join 14, 1866, p. 507. Like other writers, Yulpian, in this paper, brings together cases which have no affinity except as regards the general character of the lesion. 774 CEREBRO-SPINAL DISEASES. without determinate seat. In 1856, she suffered from attacks of ver- tigo, which, from being rare at first, subsequently came on five or six times a day. Sometimes she fell, but never lost consciousness, or had any convulsive movement. Shortly afterward, during the night, she was seized with vomiting, cramps in her limbs, and a numbness of the right side. In the morn- ing she was hemiplegic. Fifteen days afterward motion reappeared in the arm, but the leg remained paralyzed. In 1859, she had anoth- er attack of hemiplegia, and this time was deprived of speech for fifteen days. After this seizure, there were contractions of the flexors of the fingers, and of the forearm of the right side. In 1861, she had a third attack. In 1862 (January 1st) she came under M. Charcot’s care. The intellectual faculties were not involved. The right superior extremity was almost entirely paralyzed, and w’as in a state of rigidity and contraction. The lower extremities were permanently extended, and could not be flexed but by great effort. Sensibility was perfect throughout, and reflex movements could still be excited. She died February 9th. On post-mortem examination, patches of sclerosed tissue were found in the right middle cerebral peduncle, the pons Yarolii, the medulla ob- longata, and the cervical region of the spinal cord. The hemispheres were perfectly healthy. In this case, it is probable that the contractions were mainly due to secondary degeneration of the cord, a condition which, as we have seen, is analogous to sclerosis. It will be observed that there were no tre- mors, either with or without voluntary motions. Another important case has been reported by M. Magnan :1 A woman, aged thirty-four, came under observation. In 1848, when thirteen years of age, she had an attack of typhoid fever, from which she lost her sight. The first symptom of her disease occurred in 1867, and consisted of trembling of the hands and arms she endeavored to execute any difficult movement. Before long, the tremor involved the lower extremities; but there was no paralysis till about eight months previous to her admission to the hospital. At this time, every effort at motion caused tremor. The hands, arms, legs, eyeballs, and even the muscles of the trunk, were involved. The articulation was defective, and there were various painful sensations in different parts of the body. Ophthalmoscopic examination showed atrophy of the optic disks and nerves. The diagnosis in this case was multiple cerebro-spinal sclerosis— an opinion which I do not think is warranted by the facts. The lesion was probably entirely confined to the brain. The main reason which 1 “ Memoircs de la society de biologie,” Paris, 1869. MULTIPLE CEREBRO-SPINAL SCLEROSIS. 775 leads me to entertain this view is, that the tremor appeared before the paralysis. I cite the case for the purpose of showing how little accord there is among authors relative to the association of symptoms with lesions in the several forms of sclerosis. Thirty-one cases of what the symptoms indicated to be the cerebro- spinal form of sclerosis have been under my care ; and, though I have not had the opportunity of verifying my diagnosis in a single instance, I think the symptoms have been of such a character as to indicate the existence of the lesion so graphically described by Char- cot, Friedreich, and Bourneville and Guerard.1 The fact, that sev- eral of the histories were written out before Charcot’s investigations gave me a clew to their real import, will tend, I think, to increase their value. Mr. M., a gentleman fifty-three years of age, consulted me, at the instance of my friend Prof. Fordyce Barker, M. D., for partial paralysis with tremor, mainly affecting the right arm and leg. Two years previously he had suffered from vertigo and headache, which were followed by a slight attack of hemiplegia of the right side, unattended by loss of consciousness. He gradually recovered from this, but, about six months befoi’e he came under my observa- tion, he noticed that his right leg began to drag, and, soon after- ward, that the arm of the same side became weak. About the same time he had headache, vertigo, and weakness of sight. A short time subsequently—about a month, as well as he could recollect— the arm was seized with tremor while attempting to carry a glass of wine to his lips. The agitation continued to grow more violent on any voluntary movement of the arm, and gradually his. speech be- came involved. When I saw him he was still suffering from occasional attacks of vertigo and headache ; the lips were agitated whenever he attempted to move them, the tongue was tremulous, and his speech was conse- quently halting and jerking. There was also nystagmus, a symptom which he had not noticed. The right arm was unaffected with tremor so long as he allowed it to rest on his knee or to hang by his side ; but, in the act of moving it, the whole extremity was agitated by a series of short, vibratory mo- tions, consisting of flexions and extensions, which continued so long as he persevered in the movement, or kept the arm in any position requir- ing muscular exertion. The right leg was weak, and dragged so that he struck his foot against any slight obstruction. There was a little tremor in it when he attempted to cross it over the other as he sat in a chair. 1 “ De la sclerose en plaques disseminecs,” “ Nouvelle etude sur quelques points de la sclerose en plaques disseminees,” Bourneville, Paris, 1869. CEREBRO-SriNAL DISEASES. I treated him solely with the primary galvanic current, which I passed through the brain and spinal cord—the first time such an oper- ation was performed in this country for the treatment of disease. My diagnosis was incipient softening of the ganglia at the base of the brain and of the upper portion of the spinal cord. My opinion was, that the hemispheres were not involved, as there were no symptoms indicat- ing mental weakness or disturbance. I made an application of about fifteen minutes’ duration every day. He gradually but rapidly improved, and to such an extent that on the 19th of April he wrote to me as follows : “Yesterday must be marked with a white stone as the best day yet. Foot active, hand and arm steady, and spirits good. If we can manage to fix these good effects, cure is certain. “ I hope the magic pile will be ready to repeat its good work on Saturday next.” He continued to improve for several weeks, then gradually went back to his former condition, and from that rapidly grew worse. The paralysis invaded the other side, then tremor followed, the speech became much more difficult, and he died in the country two years sub- sequently. Miss H., of Connecticut, aged thirty-five, consulted me for paralysis and tremor. About two years previously, she had noticed a weakness of the right arm, which had been preceded by occasional attacks of not very severe headache and vertigo. The arm gradually became weaker, and in the course of a few months began to shake whenever she attempted to use it. Before the year had expired, the right leg began to drag a little, and lost a good deal of its natural strength. Her speech also became difficult, not from any failure to remember W’ords, but from tremor of the tongue and weakness, with a little rigid- ity of the lips. When I saw her, the articulation was halting and syllabic ; there was nystagmus in both eyes ; the right arm was very weak ; she could only move the index of my dynamometer four degrees, equivalent to a pressure of two pounds and a half, wThile with the left hand she could move it twenty-eight degrees. Every attempt to move the arm caused trembling of the whole extremity. So long as she refrained from any exertion of voluntary power, it remained free from agitation. She could not write, owing to the tremor which the effort to do so excited. There was slight tremor in the leg, when she slowly raised the foot from the ground. The mind was perfectly intact, and she was entirely free from any emotional weakness. In this lady’s case I diagnosticated multiple cerebro-spinal sclerosis —the “ sclerose en plaques disseminees ” of Charcot. I treated her with the iodide of potassium and the primary gal- MULTIPLE CEREBRO-SPINAL SCLEROSIS. 777 vanic current. By the following autumn she had improved so much that she could walk several miles without fatigue, lifted her foot clear of the ground, could move the index of the dynamometer to thirty degrees, was free from tremor, except when she attempted to write, and then it was only manifested to a slight extent. I now ceased using the galvanism, but continued the iodide of potassium. One year later she paid me a visit. She was then walking well, but there was still a very slight tremor when she attempted to execute delicate or difficult movements with the right arm. I directed the continu- ance of the iodide. Mr. II., of South Carolina, a highly-educated and intelligent gen- tleman, consulted me for paralysis and tremor. As he entered my consulting-room, the tendency to festination was exceedingly v/ell marked. On examination, I found his mind perfectly clear. There were nystagmus and syllabic articulation. On moving the left arm or left or right leg, the limb became tremulous. There had never been any head-symptoms. One week later, at my request, he wrote a short account of his dis- ease, which I here transcribe : “ I was never robust in health, but, on the other hand, I have never had, since childhood, a serious spell of sickness. My manner of life has been sedentary—that of a student. I was always careful not to overtask myself until I became engaged, in the year 1864, in a mathe- matical research. I was for a considerable length of time very much absorbed in this work, and allowed it to encroach seriously upon my hours of recreation and sleep. “ In the fall of 1865, after having accomplished the above work, I observed a slight lameness in my left foot—a tendency to strike the toe against the inequalities of the ground—an inability to raise quickly enough the front part of the foot. “After my return home, in the summer of 1866, from Europe, where I had spent five or six years, the lameness in my foot in- creased rapidly, and in the winter of 1866-’6T a lameness in my left hand was very perceptible—an inability to move the fingers quickly, and a tremor, particularly of the thumb, when I attempted to do so. “ The above symptoms have gradually grown worse, and within the last year the right leg has become involved, to the extent that it begins to shake when I stand upon it, and it shakes even while sitting, when I am under excitement, or wffien I execute difficult voluntary motions with my hands. “ The disease seems to make greater progress in hot weather. I have at no time suffered pain, my appetite and digestion are good, and I generally sleep well.” This gentleman improved greatly through the use of the primary 778 CEREBRO-SPINAL DISEASES. galvanic current, iodide of potassium, and tincture of hyoscyamus, during the two weeks that he remained in New York under my care. On his return to South Carolina he took a primary-cell battery with him. Four months later he wrote to me as follows : “ Sometimes I thought I was improving slowly, or at any rate not losing ground, and then again, for several days together, I would feel confident that I was falling back. But now I think I can certainly say I am growing worse. All my symptoms have been worse—lamer, more nervous, and the disease more general in its effects. My right hand, which has heretofore been comparatively unaffected, is now seriously implicated, and yet I still manage to write after a fashion. I find it very difficult to dress myself, and I must make several attempts before I can get up from a sitting or a lying posture. “ What could have caused the improvement that took place while I was under your immediate treatment?” In this case I diagnosticated multiple cerebro-spinal sclerosis, and I think those acquainted with the disease will agree with me in my view of the case ; and yet there was as strongly-marked festination as I have ever seen. The gentleman could trot well, could mount a staircase without much difficulty, but walking slowly, or descending stairs, troubled him greatly. According to some authors, this symptom would, of itself, have been sufficient to contraindicate the existence of sclerosis, and to have placed the disease among the neuroses. My views on this point have already been expressed under the head of multiple cerebral sclerosis. J. F., a gentleman of this city, forty-two years of age, consulted me November 29, 1870. On the 4th of July previously he had indulged rather freely in champagne, and the following morning awoke with severe headache, vertigo, and nausea. Although he recovered from this attack, he never felt quite as well as before, and was frequently subject to headache and vertigo—symptomatic, as he thought, of gastric disorder. About a month after his first symptoms he was sud- denly conscious of a singular sensation about his left eye, and on look- ing in the glass discovered that the upper lid had dropped, and that he could not raise it. This was about five o’clock in the afternoon, and by ten that night the lid entirely covered the pupil. The following morn- ing it was not so low, but he found that he saw double. He continued to attribute all his troubles to the stomach, and began taking some quack remedy recommended to him for dyspepsia. In the course of a few days, feeling no better, he went to the sea- shore, and while there noticed that his right arm became weak, and that he frequently let things drop from his hand. He had difficulty in shav- ing and in dressing himself, from inabilit}' to coordinate the muscles, and there was numbness of the ends of the fingers. During all this MULTIPLE CEREBRO-SPINAL SCLEROSIS. 779 time he had suffered more or less from headache, vertigo, and double vision, and the ptosis still continued. Gradually the left arm became involved, and, by the time the paresis in this extremity was well estab- lished, the right arm was affected with tremor, but only when he at- tempted to execute movements with it. Thus, as he said, he could place the hand on a table and it would continue perfectly quiet ; but, as soon as he took a pen to write, or even endeavored to raise the hand from the table, it was seized with tremor. The left arm soon became similarly affected, and eventually the left leg lost strength and was rendered tremulous by any attempt at muscular exertion. He noticed also, what, as I afterward learned, his friends had perceived several weeks before, that his articulation was imperfect, and that is was ne- cessary for him to make a mental effort to talk distinctly. He returned to the city about the middle of October, and employed a “ rubber ” to restore, as he said, the circulation to his limbs. Con- tinuing to get worse, he consulted me. At this time there was festination. The speech was syllabic and accentuated, the tongue and lips were paretic and tremulous, there was nystagmus in both eyes, ptosis and diplopia from paralysis of the left sixth nerve, and dilated pupil of the right eye. There were also occa- sional headache and vertigo, but not to the same extent as at first. Both arms and the left leg were partially paralyzed. He could not raise either upper extremity out from the side, owing to the complete paralysis of the deltoids, but he could flex both forearms, and move his nands and fingers tolerably well. There was no tremor while he re- frained from using them, but the least attempt at voluntary motion excited them to agitation. The same was true of the left leg. Exami- nation with the ophthalmoscope showed both optic disks to be white, and the retinal vessels small and straight. With the dynamometer he could only exert a pressure of nine de- grees with the right hand and eleven with the left. The line made with the dynamograph was descending, showing his inability to main- tain, even for a short time, a uniform muscular contraction. There was no loss of sensibility, except in the upper extremities. He had occasionally suffered from pains in the back, about the region of the shoulders. The power over the sphincters was intact. This gentleman could stand and walk as well with his eyes shut as with them open. On rising from his chair, which he did with difficulty, he always felt impelled to take a few steps forward, which were a stag- ger rather than a voluntary movement. In walking, the body was in- clined forward, and he went in a kind of jog-trot. He attributed his disease to dissipation of all kinds, in which opinion I expressed my concurrence. Under treatment with galvanism, hyoscyamus, and iodide of potas- 780 CEREBRO-SPINAL DISEASES. sium, this patient has improved, but not as yet sufficiently to warrant any hope of a permanent cure. A gentleman from the northern part of the State of New York con- sulted me in January, 1871, and again in March. His symptoms, though decided, were not very severe in character. Gradually, however, there; had been for two years a loss of power supervening in the muscles of the right side of the body, and lately ocular troubles had made their ap- pearance. Tremor, on making any voluntary movement, was just be- ginning to appear when I last saw him. Its influence over his hand- writing is seen in the following facsimile: Fig. 113. One patient, with multiple cerebrospinal sclerosis, attends the out- door department of the New York State Hospital for Diseases of the Nervous System. He has marked head-symptoms. And another, from Philadelphia, who was supposed to be suffering from cerebral disease, consulted me a few days ago. In this case the affection probably re- sulted from a fall. The remaining cases do not present any such peculiar phenomena as to warrant their histories being given in detail. Causes.—Nothing very definite is known of the etiology of the affec- tion in question. It probably is induced by such causes as give rise to the purely cerebral form of the disease. Age does not, however, ap- pear to exercise so important an influence. Eleven of my cases were over fifty years, and one of them, the gentleman from Philadelphia, was over sixty ; seventeen were over forty and under fifty, and three were between thirty and forty. All were males but four. In seven cases it was apparently caused by excessive mental appli- cation, in two by anxiety, in one by a fall, in six by dissipation. ’ In the remaining cases I could discover no obvious cause. In none of them was there a rheumatic, syphilitic, or other morbid diathesis. Diagnosis.—The facts of the tremor making its appearance after the paralysis, and of its only—or, at least, with rare exceptions, and then only in the latter stages of the disease—being manifested when volun- tary movements are being made, will suffice to distinguish the cerebro- spinal form of sclerosis from any other affection. The points to recol- lect are these: that, in paralysis agitans, the tremor appears before the paralysis, and does not depend on the voluntary contraction of muscles for its excitation. The tremor is rhythmical, and the muscu- lar movements are performed slowly on account of the stiffness and contraction of the muscles : In simple spinal sclerosis there is no tremor MULTIPLE CEREBRO-SPINAL SCLEROSIS. 781 at all. I have already insisted on these distinctions in my remarks on the other forms of sclerosis of the nervous centres. Prognosis.—This is very generally unfavorable. In only one case have I had reason to expect a cure. It often happens that amendment very decided in its character takes place soon after the beginning of the treatment with galvanism and hyoscyamus. This has been the case in every instance of the disease that has been under my charge ; but in only one has it been permanent. In those now under treatment, there has as yet been no relapse; but the time is too short to speak with any confidence in regard to the ultimate result. Morbid Anatomy and Pathology.—The remarks made under this head, when the cerebral and spinal forms of sclerosis were being con- sidered, apply to the cerebro-spinal variety. Charcot1 has considered the subject of sclerosis mainly in its histological relations. The main points are—and these have already been stated several times—that the morbid process essentially consists in hypertrophy of the neuroglia at the expense of the proper nerve-substance, and that this is a conse- quence of inflammatory action. In the present form of the disease, the sclerosed tissue appears in the form of plates or nodules in different parts of the brain and spinal cord. Treatment.—The treatment of multiple cerebro-spinal sclerosis is more palliative than curative. Galvanism to the brain and vertebral column, iodide of potassium, nitrate of silver, and preparations of hyos- cyamus, have very generally caused improvement for a time, but my experience goes to show that this is not permanent. The galvanic current should be used of less tension when applied to the head, but as strong as the patient can endure, to the spine. The iodide of potassium, which, I believe, prevents to a certain ex- tent the formation of new connective tissue, should be given in mod- erate doses at first, but should be gradually increased up to the point of toleration. I have sometimes given the nitrate of silver in fourth-of-a-gram doses, three times a day, and very generally recommend cod-liver oil with each meal. Occasionally I have also administered the bichloride of mercury, with the view of counteracting a possible syphilitic dia- thesis. Hyoscyamine may be advantageously employed, according to the formula given on page 293, for the treatment of paralysis agitans. Whatever measures are adopted should be continued for several months at least, and, if the improvement persists, for a much longer period. 1 Gazette des Hopitaux, Nos. 102, 103, 140, 141, 143. 1868. 782 CEIIEBRO-SPINAL DISEASES. CHAPTER VIII. PARETIC TREMOR. The affection which Parkinson1 described, and to -which he applied the name “ shaking palsy,” has since been very carefully studied by many writers, and the fact has been clearly made out that it is not a single disease, but includes several affections which are very different in character. I have already considered two of them—paralysis agi- tans and multiple cerebro-spinal sclerosis; a third I propose to treat under the name of paretic tremor. Symptoms.—The primary manifestation is tremor, and this, like the same symptom in the severer forms of disease already considered, in which it forms an essential feature, may begin in a very restricted or more extensive region of the body. It is present whether voluntary movements are performed or not with the affected limbs, but is in- creased by mental excitement of any kind, by physical exertion, or by any cause capable of depi'essing the powers of the system. It is not generally the case that the tremor shows any tendency to advance much beyond its original limits, however small or extensive these may be. When it does exhibit such a disposition, contiguous muscles are first attacked, and then the corresponding ones on the oppo- site side of the body. From the very first there is slight muscular weakness, not to any very great extent, and often not severe enough to attract the patient’s attention, but still sufficiently evident to careful examination with the dynamometer? As the tremor increases in violence or extent, the paralysis becomes more obvious. Sensibility is i*arely affected, there is no bending of the body for- ward, no festination, and no head-symptoms. The tremor always ceases during sleep, except in very extreme and long-continued cases, and there may be intermissions of longer or shorter duration while the patient is awake. Causes.—Paretic tremor may result from emotional disturbance, from continuous or severe muscular exertion, from some exhausting disease, such as dysentery, typhoid or typhus fever, or rheumatism, or from blows, falls, or other injuries. In many cases the. cause cannot be ascertained. Of twenty-five cases of wdiich I have records, ten were apparently due to mental causes, four to excessive physical exertion, four to dis- eases of various kinds, two to injuries, and in five no cause could be discovered. Two cases of mercurial trembling, the symptoms of which affection 1 “Essay on the Shaking Palsy,” London, 1817. PARETIC TREMOR. 783 are very similar to those of non-toxic paralysis agitans, are not included among the foregoing. Diagnosis. — From paralysis agitans, paretic tremor is distin- guished by the facts that there are no head-symptomis, no destina- tion, and no derangements of sensibility. It is more apt to occur in persons under the age of fifty, and may be met with in quite young persons. The reverse of both these circumstances is true of paralysis agitans. From multiple cerebro-spinal sclerosis, it is diagnosticated mainly by the absence of any head-symptoms, by the fact that the tremor usu- ally comes on before the paralysis, and is independent of voluntary movements. From convulsive tremor it is readily distinguished by the facts that the tremor is not paroxysmal, and that it is accompanied by paresis of the affected muscles. The character of the muscular action, and the history of the case, will prevent its being confounded with chorea. Prognosis.—Paretic tremor rarely terminates fatally, and when it does it is because the tremor has become so general that death results from exhaustion. It, however, often happens that all measures fail to relieve the agitation. Of the twenty-five cases occurring in my own experience, eight were cured, five partially so, and in the rest no per- manent effect was produced by any means I employed. Morbid Anatomy and Pathology.—Nothing is known of the morbid anatomy. In a few cases, patients have died either from the disease or from some intercurrent affection, and post-mortem examinations have been made with negative results. Petrasus, quoted by Dr. Handheld Jones, relates two severe cases, one of which proved fatal. At the autopsy nothing was found but fatty degeneration of the heart and pneumonic consolidation of the right lung. He remarks on the tremor not being constant in many cases, ceasing for some days and then re- turning with fresh force, or changing its seat from one part to another. In my opinion, the disease under consideration is due to an irregular and diminished evolution of nerve-force from the motor nerve-cells in relation with the nerves supplying the muscles in which the agitation exists. The pathology of tremor, not the result of structural lesions, is a subject which is beginning to be studied, but which is not yet clearly understood. We know that, when we have strongly exerted an arm, for instance, the muscles are tremulous for some time afterward, and that the agitation is rendered very evident when we attempt to write or do any other act requiring delicate muscular adaptation. A period of rest must take place before steadiness is regained. Now, in such a case the agitation is not probably due to any cause inherent in the muscle, but is the result of exhaustion in the nerve-cells and the disengagement of insufficient force in an intermittent manner. I sup- CEREBRO-SPINAL DISEASES. pose paretic tremor to be due to some such action in tbe motor nerve- cells in the gray matter of the spinal cord. In those cases in which the tremor becomes permanent, structural lesions of profound character—as in permanent hysterical contractions and epilepsy—doubtless occur. Treatment.—I have used electricity, both of the galvanic and fara- daic kinds, in all the cases of paretic tremor that have been under my charge, and in conjunction have employed many internal medicines, such as arsenic, iron, manganese, zinc, copper, phosphorus, strychnia, and sedatives of various kinds, including opium, bromide of potassium, conium, stramonium, Indian hemp, and many others. I am very de- cidedly of the opinion that the best treatment consists in the use of the constant primary current to the spinal cord, sympathetic nerve, and the affected muscles, while at the same time strychnia and phosphorus, ac- cording to the formula given on page 67, are administered internally. By these means four of my eight successful cases were entirely cured within two months. One of these was sent to me by my friend Dr. F. N. Otis. The affection was confined to the right arm, and was probably due to inordinate gymnastic exercise; the other was a gentleman from St. Louis, in whom the disease was also confined to the right arm, and had apparently resulted from writing excessively. Both had lasted several months. Another was a railway engineer, in whom the disease was the result of over-mental excitement; and the fourth was a distinguished clergy- man of the Catholic Church in whom a like origin existed. The six other cases were, two of them, consequent on other diseases, and four were without known cause. Three were women ; the tremor in two was in both arms, and in two in one leg in each. The duration of the treatment was from three to seven months. A full and nutri- tious diet, and the avoidance of all mental excitement or strong physi- cal exertion, are important features in the treatment. CHAPTER IX. ANAPE1RA TIG PARALYSIS. Tiiere is a class of paralyses produced by the habitual use of a par- ticular class of muscles in the same way for a long time. Thus we have writer’s paralysis, telegrapher’s paralysis, hammer paralysis, and so on. To describe these as separate and distinct affections is scarcely, in the present state of our knowledge, permissible. I shall, therefore, em- brace these under the designation of anapeiratic (Avaneipau, to do or ANAPEIRATIC PARALYSIS. 785 attempt again) paralysis, as being caused by the frequent repetition of some particular muscular action. Symptoms.—The first symptom usually observed is a feeling of fa- tigue experienced in the muscles which have been grouped together for frequent use in some especial way. Thus in writers, engravers, violinists, type-setters, and telegraphers, the tired sensation is felt in the muscles of the hand, forearm, arm, and shoulder. The thumb is especially affected, and is also the seat of a dull, aching pain. Pains, not very severe or fixed, are also common in the muscles higher up ; this fatigue the patient endeavors to correct by grasping the pen or burin, for instance, more firmly, or by making an intense mental effort to regulate the muscular contractions by which the instruments are held, the type seized, or by which the fingers are moved over the strings of the violin, or the lever of the telegraph-instrument. But he only thereby adds to the difficulty, for the weariness and pain are increased, the muscles become weakened, and moreover irregular and incoordi- nate actions ensue which render the results of either writing, engraving, etc., more or less imperfect. If he perseveres day after day in his occupation he soon reaches that stage of the disease in wffiich the ability to direct the pen, for in- stance, in accordance with his will, is lost, and the automatic actions, which are of great importance in writing, are likewise very much di- minished. For a time, then, he writes better when his mind is not occupied in directing the formation of every letter, but in which he allows the muscles as it were to take care of themselves. Constantly, however, he feels the necessity of mental action, and this action invari- ably increases the trouble, until, at last, the moment the attempt is made to write, the pen, actuated by the muscles of the fingers, executes such disorderly movements as to bear, in extreme cases, little or no analogy to the wrords attempted to be written. A distinct paroxysm is thus induced, which lasts as long as the patient persists in the attempt to write. When he discontinues, the spasm ceases, and he can perform any other act with the fingers without there being the slightest convul- sive movements. In some cases there is pain in the fingers, the muscles between the metacarpal bones, and in those of the forearm. The spasm is much worse if the patient be excited or particularly anxious to do his best. In the accompanying wToodcut (Fig. 114) are represented three attempts of a patient to write the name “James Ely.” At first some resemblance to the letter J is made, but in the second trial it is less distinct, and in the third is lost altogether. All of my patients had resorted to various expedients to obviate the spasms, under the idea that they were produced by metallic pens carry- ing off the electricity from the arm ; several had, for a time, made use of quills, or hard rubber pens, and for a time relief had been ob- 786 CEREBRO-SPINAL DISEASES. tained, but the paroxysms soon became as bad as ever. Others had used very thick pen-holders, and this expedient was also, for a time, successful. In the end, however, all such efforts to prevent the spasms proved futile. In one case under my charge, the patient, an engraver, was utterly incapable of using his burin, although he could write for hours perfect- Fig. 114. ly well, and those who had contracted the disease by excessive writing could execute any other delicate movements, such as drawing, playing the piano or violin, threading needles, etc., without inconvenience. In several cases the individuals had acquired the power to write with the left hand, but before long this was also affected. Dr. G. V. Poore 1 has recently published an interesting memoir on the affection as produced by excessive writing, and argues that, although it is true that patients can execute other actions than writing with the affected hand, the muscles employed in these movements are not the same as those used in Avriting. This is doubtless true of advanced stages of the disease, but it certainly is not so of early periods. 1 have a patient at this time under my charge wdio cannot Avrite without great inconvenience, but avIio uses a pencil in drawing with the greatest fa- cility and precision. Dr. Frank Smith 2 describes the disease I have designated anapei- 1 “Writers’ Cramp, its Pathology and Treatment,” The Practitioner, June, July, and August, 1873. 2 Lancet, March 27, 1869, also “On Ilephaestic Hemiplegia or Hammer Palsy,” British Medical Journal, October 31, 1874. ANAPEIRATIC DISEASES. 787 ratic paralysis, as it occurs in workmen who use the hammer almost continually in certain processes, and gives it the name of hephaestic (K