UC SOUTHERN REGIONAL LIBRARY FACIUT 
 
 G 000 005776
 
 ^' 
 
 
 THE LIBRARY 
 
 OF 
 
 THE UNIVERSITY 
 
 OF CALIFORNIA 
 
 LOS ANGELES
 
 WW

 
 THE 
 
 NERVOUS CENTRES
 
 TilE 
 
 PATHOLOGICAL ANATOMY 
 
 OF THE 
 
 NERVOUS CENTRES 
 
 EDWARD LONG FOX, M.D. F.R.C.P. 
 
 THYSTCIAJS' TO IHR BlilSTOL I.OYAL INFIRMARY 
 
 I.ATE LElTL'UEll OX THE PRIN'CIPr.KS A\D PRAfTICE HP MEDICINE ANU O.N PATllOLOOICAL 
 
 ANATOMY AT THE BRISTOL MEDICAL SCHOOL 
 
 WITH ILL USTRATIONH 
 
 LONDON 
 SMITH, ELDER, & CO., 15 WATERLOO PLACK 
 
 1874 
 
 [.(// li'jht.- i-.-servd]
 
 1674 
 
 TO 
 
 MY PUPILS 
 
 PAST AND PEESEXT 
 
 Bristol |\od:iI |nfinniinT anir llje Bristol lileikal ^cl)ool 
 
 THESE LECTUKES ARE DEDICATED 
 
 WITH 
 
 MUCH EEGARD
 
 CONTENTS. 
 
 I-KfTl-RE PAQR 
 
 IxTRonrcTiox 1 
 
 I. COXGKXITAL AbXORMALITIES 10 
 
 II. AbxormalitiK'^ of the Vascular System ... 27 
 
 III. IXFLAMMATIOX .'58 
 
 IV. DectEXERATioxs no 
 
 V. TujrorRS 1.32 
 
 VI. Ac0TK Delirifm axd Pelirium Tremens . . . 156 
 
 VII. iNSAXiTr 176 
 
 VIII. Ixsaxity coxrixuEi) — Maxia, MELAxcnoLiA, Dementia, 
 
 General Paraltsis, Idiocy 196 
 
 IX. Aphasia — Glosso-Laryngeal Paralysis — Facial Para- 
 lysis 222
 
 Vlll CONTENTS. 
 
 LECTURE PAGE 
 
 X. Progressive Muscclar Atrophy — Locomotor Ataxy — 
 Infantile Paralysis — Paralysis Agitans — Lead 
 Palsy 2GG 
 
 XL Epilepsy — Chorea 305 
 
 XIL Tetanus — Hydrophobia 344 
 
 XIIL Lesions of the Spinal Cord in Small-pox — Lesions 
 
 OF THE Nervous System in Diabetes . . . 309 
 
 XIV. Ophthalmoscopy in Diseases of the Nervous 
 
 System 382
 
 LIST OF ILLUSTRATIONS. 
 
 Pr.ATF. 
 
 1. Chronic Meningitis 
 
 2. Cysts of Choroid Plexus 
 
 3. Myelitis. Swollen nerve fibres 
 
 4. Atrophy from Myelitis . 
 
 5. Softening of Pons . 
 
 6. Cells from softened Pons 
 
 7. Grey Degeneration of Cord 
 
 8. Grey Degeneration. Amyloid bodies 
 
 0. Disseminated Sclerosis 
 
 10. Fibroid of Cord 
 
 11. Syphilis of Brain . 
 
 12. Glioma of Brain 
 
 13. Glioma of Brain. Diseased vessels more highly 
 
 magnified ........ 
 
 14. Fibroma of fourth cervical nerve pressing on the 
 
 cord 
 
 lo. Miliary Sclerosis in General Paralysis of the Insane 
 
 ](?. Lesion of Medulla Oblongata in Epileptic Mania 
 
 17. Tetanus. New matter on the Dura Mater Spinalis 
 
 18. Tetanus. Colloid Degeneration .... 
 
 10. Tetanus. Colloid and Amyloid Degeneration. 
 Thickened vessels 
 
 Tu face 
 
 PAGE 
 
 GO 
 
 74 
 
 87 
 
 94 
 
 101 
 
 102 
 
 lU 
 
 114 
 
 122 
 
 151 
 
 143 
 
 147 
 
 147 
 
 149 
 
 205 
 308 
 
 35G
 
 PATHOLOGICAL ANATOMY 
 
 NEEVOUS CENTRES 
 
 INTEODUCTION. 
 
 The following lectures have been given, either as a part 
 of the course on Pathological Anatomy at the Bristol 
 Medical School, or as forming portions of clinical lec- 
 tures at the Bristol Koyal Infirmary. 
 
 That anyone giving such lectures should not draw 
 largely from the work of other men would be impos- 
 sible in a country that has been in the foremost rank 
 in the minute investigation of lesions of the nervous 
 system, among workers of no less note than Maudsley, 
 Bucknill, Eeynolds, Eadcliffe, Ogle, Allbutt, Jackson, 
 Broadbent, Sanders, Wilks, Lockhart Clarke, Bastian, 
 and many others, and among microscopists such as 
 Dickenson, Herbert Major, and Batty Tuke, and m.any 
 members of that noble school at the West Riding 
 Asylum under Dr. Crichton Browne. 
 
 To these and many others, whose views are quoted 
 
 )
 
 2 INTRODUCTION. 
 
 in these lectures, I owe most earnest tlianks ; and 
 scarcely less am I indebted to some of the French 
 physicians — Trousseau, Jaccoud, Andral, Gintrac, San- 
 dras, and Bourguignon, as well as to Griesinger, 
 Eokitansky, and other German savans. 
 
 I have also to express my grateful acknowledgment 
 to Dr. Acland for his permission to cull from Van der 
 Kolk's collection in the Oxford Museum ; to Mr. Stirling, 
 of the Edinburgh Anatomical Museum, for much kind 
 help and advice ; and to Mr. Charles Berjeau for the 
 interest he has taken in drawing and lithographing the 
 plates. 
 
 My desire has been to bring together in a conve- 
 nient and readable form, for the use of students and 
 practitioners, much that is now scattered in publications 
 of many kinds, as well as some of the pathological 
 experience that has come in my way in the course of 
 some seventeen years of hospital work in a large city. 
 That it is not presented in a better form, that the 
 imperfections are manifold, that the sins of omission, if 
 not of commission, in the full realisation of morbid 
 lesions, are extremely numerous, is due, partly, to the 
 difficulties of writing at all in the midst of a busy 
 professional life, but far more to the vast extent of the 
 subject. In this department of science, as in so many 
 others, we are indeed but as children picking up pebbles 
 on tlie shore of the ocean of truth. 
 
 Still, some points are struggling out of the ob- 
 scurity of former times, and very much in consequence 
 of the work of the last few years. One is, the ten- 
 dency to give up the word ' functional ' as opposed to
 
 INTRODUCTION. 6 
 
 ' organic' Probably no organ in the body lias been 
 considered to be more frequently the seat of functional 
 disease than the brain. Very many even of the pro- 
 fession at the present day believe that a large number 
 of nervous diseases are associated with no organic 
 change. The difficidty is more of terms than of facts. 
 No doubt many nervous phenomena are met with, and 
 yet nothing is found post mortem that can directly 
 account for them. But this is no proof that lesion 
 has not existed during life. The change in the calibre 
 of the smaller vessels may persist for some time, and 
 yet leave no trace behind, even when nutrition has 
 been for the time materially interfered with. It is 
 only when this interference with nutrition has been 
 extended over a protracted period that so-called 
 organic lesion makes its appearance. But still this 
 variation in the calibre of the vessels is a lesion by 
 itself. Phenomena are not functional because there is 
 no lesion, but because the lesion is transitory and 
 evanescent. It is equally proved by pathological 
 anatomy, and by clinical observation, that no morbid 
 symptom can manifest itself without some alteration 
 in the nutrition of the oro;an affected. 
 
 A second point suggested by this line of work is 
 the close connection between nervous phenomena. 
 Not only are rigor, tremor, spasm, convulsion, mere 
 varieties of the same condition, but they arc closely 
 allied to inco-ordination, and through this to paralysis. 
 The same may be said of the connection of excitement, 
 delirium, and mania, with dementia, fatuity, and 
 coma. It would seem as if loss of regulation of
 
 4 INTRODUCTIOX. 
 
 power was only one stage short of loss of power 
 itself. 
 
 Many fixcts await tlieir explanation in the future. 
 Why the same lesion will at one time concentrate itself 
 solely on the posterior columns of the cord, at other 
 afi'ecting only the posterior or the anterior cornua, it 
 is difficult to say ; still more difficult is it to explain the 
 apparent freaks of nature in causing lesion of the 
 trophic nerve fibrils and centres, leaving the motor 
 and sensory tracts untouched, or vice versa ; or its 
 caprice in marking out as its object of attack the 
 vaso-motor nutrition of one muscle, or even of a part 
 of one muscle. 
 
 One more consideration is the debt we owe to 
 pathological anatomy for our knowledge of the phy- 
 siology of the brain and spinal cord. Without for a 
 moment undervaluing the experimental researches of 
 Brown-Sequard on the spinal cord, or the still more 
 important contributions to the physiology of the cere- 
 bral convolutions by Hitzig and Ferrier, it must be 
 confessed that nearly all we know of the real functions 
 of the various organs of the encephalon and spinal 
 cord has been drawn from observation of the effects of 
 lesions. Disease is nature's most delicate experiment ; 
 and what knowlediTe we have of the seat of language 
 in the brain, of the fimctions of the corpora striata and 
 optic thalami, of the regions specially associated with 
 sensation, with motion, and with thought, is mainly 
 gathered from this, her constant mode of teaching. 
 
 In considering tlie abnormalities of the cerebro- 
 spinal system, the whole class of traumatic lesions has
 
 INTRODUCTIOX. 
 
 been omitted. The effects of injuries of various kinds — 
 hccnioiTliage, iuflanniiation, &c. — will pass under notice 
 in different sections ; but the majority of traumatic 
 lesions are so contained in the regions of pure surgery 
 that they scarcely find a place in lectures devoted to 
 the pathological results of rapid or gradual alterations 
 of nutrition. 
 
 It is proposed to divide the sul^ject into two parts : 
 and, first, to describe the pathological anatomy of the 
 brain and spinal cord, and, secondly, the mode in which 
 these pathological results are grouped in certain condi- 
 tions, which symptomatically have been given special 
 names, as Mania, Melancholia, etc. In pursuing this 
 plan, it will be convenient to divide the first part of the 
 subject into: (I) Congenital Abnormalities of the Cerebro- 
 spinal Centres ; (2) Abnormalities of the Vascular System ; 
 (3) Inflammations; (4) Degenerations; (5) Tumours; 
 while the second part will include the Pathological 
 Anatomy of Mania, Melancholia, Dementia, Idiocy and 
 Cretinism, General Paralysis of the Insane, Delirium 
 tremens, Paralysis agitans, Epilepsy, Chorea, Hydro- 
 phobia, Tetanus, Locomotor ataxy and Progressive 
 Muscular Atrophy, and various local paralyses. 
 
 In making this division of the subject, it will be 
 readily understood that it is simply for the sake of 
 convenience. Its imperfections are manifold ; specially 
 because in several instances it is logically a cross division. 
 As an example, in the first part, the fifth section, on 
 Tumours, stands by itself, without any connection with 
 the second section, on Abnormalities of the Vascular 
 System. Yet the tumours of the brain and spinal cord
 
 6 INTRODUCTION. 
 
 are pathologically divided into those connected with the 
 membranes, those having their origin in the walls of 
 the vessels, and those springing from the neuroglia, the 
 connective tissue of the brain and cord. 
 
 No division, however, can be perfect ; and it will be 
 attempted in each section to bring into due relations 
 each constituent of the cerebro-spinal system. In the 
 same way also it is not logical in a pathological sense 
 to divide Degenerations from Inflammation, on the one 
 hand, and from some Tumours, on the other. It is not 
 only probable, it is certain, that some forms of degenera- 
 tions own an inflammatory origin. 
 
 It would have been possible to make the division 
 according to the anatomical constituents, and to have 
 taken the organs to pieces, as it were, and thus to have 
 considered in detail the abnormalities of the vessels, of 
 the connective tissue, and of the nerve cells and nerve 
 tubes, that go to make up the structure of the nervous 
 system. But a plan of this kind would necessarily 
 have led to much tautology ; a short classification, 
 however, is appended of the lesions to wdiich the various 
 organs within the cranium and spinal column are 
 specially subject. 
 
 Lesions of the Cerebral Dura Mater. 
 
 1. Arrest of development from disease in %itero. 
 
 2. Inflam.mation (Pachymeningitis). 
 
 Thickening. False membranes. Haemorrhage from new 
 vessels (Haematoma). Ulceration. Perforation. 
 
 Apparent Hypertrophy. Abnormal adhesion to the bone, 
 or to the subjacent membranes. Abscess.
 
 INTRODUCTION. 7 
 
 3. Bony growtlis. The ossification consisting of true bone. 
 
 4. Tumours. 
 Myxoma, 
 Lipoma. 
 Sarcoma. 
 
 Fibroma. Fungus of dura mater. 
 Carcinoma simplex. 
 Epithelioma. 
 
 5. Syphilitic disease affecting the dura mater, and often 
 causing ulceration of this membrane, may be classed under 
 inflammation. 
 
 (3. Hfemorrhage of dura mater, without previous inflam- 
 mation — as in purpura, scurvy, injury to the meningeal arteries, 
 perhaps aneurisms. 
 
 7. Disease of sinuses. Rupture from distension. Rupture 
 from ulceration. Phlebitis. Thrombosis. 
 
 8. Malposition of dura mater, owing to arrest of develop- 
 ment of the cranial bones. 
 
 Lesions of the Cerebral Arachnoid, 
 
 1. Malposition, where a portion of the cranial bones may be 
 absent. 
 
 2. Inflammation, acute and chronic. Opacities. Ulcerations. 
 
 3. Arachnoid cysts, the result of ha3morrhage. 
 
 4. Tumour. 
 Pacchionian granulations. 
 Fibroma. 
 Epithelioma. 
 Papilloma. 
 
 Lipoma, fx'om epondyma of the ventricles. 
 Cholesteatoma. 
 
 Tubercle — probably not primarily growing on the arach- 
 noid. 
 Hydatids. 
 
 Lesions op the Cerebral Pia Mater. 
 
 1. Malposition, as in meningo-celc and encephalo-cele. 
 
 2. Inflammation. Meningitis. Idiopathic, traumatic, syphilitic, 
 alcoholic, epidemic ccrebro-spinal, and tuberculous.
 
 8 INTRODUCTIOX. 
 
 3. Fatty degenerations of the walls of the pia mater. 
 
 4. Atheroma. 
 
 5. Calcareous degeneration, either a sequence of atheroma or 
 of fibroid thickening of the vessels. 
 
 6. Cysts on the vessels, especially of the choroid plexus ; these 
 cysts being sometimes filled with a soft material, sometimes with 
 tubercle. 
 
 7. Obstruction of vessels by lymph thrown out around and 
 upon them, causing narrowing of their calibre, and often 
 thrombosis. 
 
 8. Tubercle, especially affecting the sheath of the vessels 
 primarily. 
 
 9. Amyloid degeneration, especially of the choroid plexus. 
 
 10. Aneurism, of various sizes, sometimes as large as a bean, 
 more frequently miliary and multiple. 
 
 11. Embolism. 
 
 12. Rupture from embolism, aneurism, fatty and calcareous 
 degeneration, or sclerosis. 
 
 13. Carcinoma simplex. 
 
 14. Pearl cancer, often found covered upon its surface by 
 the arachnoid. 
 
 15. Epithelioma myxomatodes psammosum. 
 
 16. Papilloma of the pia mater. 
 
 17. Papilloma myxomatodes. 
 
 18. The syphilitic gumma, occasionally attacking the pia 
 mater. 
 
 19. Osseous tumour. 
 
 20. CEdema. 
 
 Lesions of the Brain etc. 
 
 1. Malformation. 
 
 2. Malposition, as in encephalocele. 
 
 3. Anajmia. 
 
 4. Congestion. 
 
 5. All the vascular lesions found in the pia mater. 
 (5. Hfemorrhages in various parts. 
 
 7. Inflammation. 
 
 8. Softening.
 
 INTRODUCTIOX. 9 
 
 9. Sclerosis of various kinds and degrees. Tlie so-called 
 liypertropliy of the brain is duo to increase of connective tissue. 
 lU. Tumours. 
 
 Syphilitic gumma. 
 
 Tubercle. 
 
 Cholesteatoma. 
 
 Fibi-ous and fibro-plastic tumours. 
 
 Carcinoma cerebri sim^ilex. 
 
 Epithelioma. 
 
 Glioma. 
 
 ^lyxoma. 
 
 Psammoma. 
 
 11. Parasites. 
 
 12. Minute changes of cells of grey matter. 
 
 Lesions of the Spinal Membranes and Cord. 
 
 Dura Mater. Inflammation. Cancer. Fibroma. Sarcoma. 
 
 Arachnoid. Inflammation. Spina bifida. Bony plates. Fibrous 
 growths. Possibly tubercle. Cancer spreading from parts 
 contiguous. 
 
 Pirt Mater. Inflammation. HEemori^hage. Occasionally 
 tubercle. 
 
 The Spinal Cord: 
 
 Malposition, as in some cases of Spina bifida. 
 
 ^Malformation. Congenital absence of some portion of cord. 
 
 Enlargement of central canal, congenital or otherwise. 
 
 Inflammation. Abscess rare, except from the breaking down 
 of a scrofulous mass. 
 
 Atrophy. 
 
 Softening. 
 
 Grey degeneration. 
 
 Sclerosis. 
 
 Tubercle. 
 
 Cancer, probably spreading inwards from contiguous parts.
 
 10 
 
 LECTUEE 1. 
 
 CONGENITAL ABNORMALITIES. 
 
 These abnormalities may strike the eye at once or 
 may only be discovered by dissection ; and depend 
 either on arrest of foetal development or on intra-uterine 
 disease of the foetus. 
 
 1. We may find the union of two heads into one 
 or two distinct bodies. The junction is commonly an 
 anterior one, but may be lateral. The two chests and 
 the anterior portions of the abdomen as far as the 
 umbilicus may participate in the union. The posterior 
 portion of the head may be double, while the anterior 
 is single. This abnormality may be divided into several 
 varieties, in proportion to the development of the second 
 face. Thus you liave, as the first variety, two perfect 
 faces opposed ; as the second, an entire fixce on one side, 
 and one ear, or both ears and one eye, on the other ; as 
 the third, an entire face on one side, and one ear or 
 both ears on the other, but without any trace of an 
 eye ; as the fourth, an entire face on one .side, and no 
 vestige, or hardly any vestige, of any organ on the 
 other side. 
 
 2. Two distinct heads may exist on one body, or on 
 two bodies united in the greater part of their extent.
 
 CONGENITAL ABNORMALITIES. 11 
 
 These lieads are generally, but not always, of equal 
 size. They somcthnes both spring from one neck. 
 
 3. There may be a complete absence of the head. 
 When this is the case, there is generally an absence of 
 some other portion of the body. Thus some of the 
 limbs are often wanting, and the vertebral column is 
 very rarely perfect. The two upper vertebrae may be 
 wanting, or the column may be wanting, or the column 
 may begin at the 4th cervical vertebra, or at the 7th, 
 or at the 1st dorsal or the 8th dorsal ; and instances 
 are even not unknown where the vertebral column has 
 been absent down to the level of the 10th dorsal, and 
 even to the 2nd lumbar vertebra. 
 
 A slight deviation from this abnormality is seen 
 where the head is not really wanting, but is deprived 
 of the greater part of cranium and face. 
 
 4. There may be an absence of the brain or of the 
 greater part of the cerebro-spinal system. The shape 
 of the head will depend very much on the extent of 
 deficiency of the cranial bones, or on the amount of 
 distension of the skull by fluid. There are several 
 varieties of this, distinguished by the greater or less 
 extent of deficiency of the cranial contents. Thus the 
 first variety is characterised by the absence of cerebriun, 
 cerebellum, pons, medulla oblongata, and spinal cord. 
 In most of such cases the upper cranial bones and in- 
 teguments are wanting, and the base is exposed to view, 
 whilst in some the integuments exist and are distended 
 by fluid. The nerves may be present. The second 
 variety is characterised by the absence of cerebrum, 
 cerebellum, pons, medulla oblongata, and part of the 
 spinal cord.
 
 12 COXGEXITAL ABNORMALITIES. 
 
 Tlie third, by absence of the cranial contents, whilst 
 the spinal cord is pretty complete. 
 
 The fourth, by absence of the cerebrum or cerebelhmi, 
 whilst the pons, medulla oblongata, and spinal cord 
 are normally developed. 
 
 The fifth, by absence of the cerebrum proper only, 
 whilst the cerebellum, pons, medulla oblongata, and 
 spinal cord are normal. This variety may be ac- 
 companied by absence of the upper cranial bones, or 
 by their distension by hj^drocephalic fluid. 
 
 The sixth, which is exceedingly rare, is characterised 
 by the presence of the cerebrum proper, whilst the 
 cerebellum, pons, medulla oblongata, and spinal cord 
 are all absent. These varieties of arrested development 
 seem to depend on physical injuries to the uterus 
 during pregnancy, and sometimes to mental shock 
 experienced by the mother during tlie same period. 
 
 5. Another form of congenital abnormality is 
 characterised by an extraordinary thickening of the 
 meninges, wdiicii take the place of, and often imitate, 
 the aspect of brain. This condition sometimes coincides 
 with the abnormality last considered. It may be 
 divided into several varieties, according to the amount 
 of cerebro-spinal centres congenitally deficient. 
 
 Thus the first variety shows this thickening of the 
 membranes, with complete absence of cerebrum, cere- 
 bellum, pons, medulla oblongata, and spinal cord. 
 
 The second is associated with the preservation of 
 the whole spinal cord, whilst the cerebral organs are 
 all wanting. 
 
 The third, with preservation of only a portion of the
 
 CONGENITAL ABNORMALITIES. 13 
 
 spinal core], whilst ull the rest of the ccrebro-spiiuil 
 system is absent. 
 
 The fourth, with preservation of the spinal cord, 
 medulla oblongata, and pons, whilst the cerebrum and 
 cerebellum are absent. 
 
 The fifth, with preservation of the spinal cord, 
 medulla oblongata, pons, and cerebellum, whilst the 
 cerebrum alone is wantino;. 
 
 The sixth, with preservation of an imperfect brain, 
 whilst the spinal cord is wanting. 
 
 6. An uncommon form of congenital imperfection 
 is seen in the cyclocephalous condition, in which there 
 is an approximation or fusion of two eyes in a common 
 orbit. The abnormality is of various degrees, according 
 as the nose and mouth are implicated. It evidently is 
 the result of an arrest of development of the central 
 and anterior parts of the head. 
 
 Leaving now, for the present, the abnormalities due 
 to arrest of development, we proceed to those classes 
 of conditions which depend on injuries received or 
 diseases occurring during foetal life. These differ from 
 the preceding in that they are not incompatible with 
 persistence of hfe. 
 
 7. Of these, the most important are those abnor- 
 malities which consist in the incomplete, insufficient, or 
 irregular formation of some of the parts of the ence- 
 phalon. This want of completeness may occur in the 
 membranes, in various portions of the brain proper, 
 the cerebellum, the pons, and the cerebral nerves. 
 
 Whenever there is deficiency of structure in the 
 encephalon, there will always be foiuul an increase of
 
 14 CONGENITAL ABNORMALITIES. 
 
 the cerebro- spinal fluid, just as in atrophy occurring 
 in later life. 
 
 Arixsia of the brain — incompleteness (atelence- 
 phalie) — is of very various degrees. 
 
 (i) Meningeal incompleteness, in which the mem- 
 branes may be altogether wanting, or the dura mater 
 may be absent only at the base of the brain, or the 
 falx cerebri may be absent, or may be perforated with 
 holes, the holes representing the areas of incomplete 
 formation ; or the tentorium cerebelli may be wholly 
 or partially absent. 
 
 (ii) General incompleteness of brain, or such in- 
 completeness affecting several portions of the brain at 
 one and the same time. Such cases have the vault of 
 the cranium thrown back, and the lower jaw very 
 short, whilst the base of the skull is large, the cere- 
 bral convolutions almost effaced, and the cerebellum 
 large. 
 
 In most of such cases the head is small, and 
 seldom shows its normal dimensions ; more frequently 
 it is not only less large than usual, but also flattened 
 on both sides, or on one side, or in front, or at the 
 occiput, and presents various and irregular forms. 
 
 With this microcephalous state are found other 
 conditions : manifestations of atrophy, or of a sub- 
 inflammatory process ; occlusion of the fontanelles ; 
 thickening of the cranial bones ; more or less promi- 
 nent projections of their internal sur&ce ; thickening, 
 and a very white tint of the meninges ; and collec- 
 tions of serum on the surface and in the interior of the 
 brain.
 
 CONGENITAL ABNORMALITIES. 15 
 
 The brain is reduced in volume ; the convohitions 
 small, or, if large, few in number, or interrupted at 
 some points, and replaced by an accumulation of serum, 
 enveloped by the arachnoid and pia mater, or in a 
 cyst. Various parts of the brain are scarcely or 
 imperfectly developed, or of abnormal consistence ; 
 the septum and pineal gland may be wanting. 
 
 The ancient Aztecs afford perhaps the best exam- 
 ples of this microcephalaic condition. Dr. Prichard 
 says : ' The portraits of the ancient Aztecs, as Hum- 
 boldt has observed, and some of their divinities, are 
 remarkable for the depression of their forehead, giving 
 a small facial angle ; and this is a form which seems to 
 have entered into the beau-ideal of the race, and which 
 many other American nations imitate by artificial 
 compression of the head. 
 
 (iii) Incompleteness of the central portions of the 
 brain. The corpus callosum, the septum lucidum, and 
 the fornix, are sometimes absent. 
 
 (iv) Incompleteness of the lateral portions of the 
 brain ; sometimes of one hemisphere, sometimes of 
 the other, partial or entire. The mode of lesion gene- 
 rally consists in a sort of lacuna, a loss of substance, 
 affecting one convolution, or several together. Perhaps 
 loss of substance is hardly the right expression, as a 
 part cannot be lost which has never existed. TJie 
 lacuna is really formed by congenital want of develop- 
 ment of the part. The affected part appears hollowed 
 into a cavity, containing serum, one of the walls of 
 which cavity is formed by the meninges. From this 
 arrangement there residt ampullcc, or cysts ; or, when
 
 16 COXGEXITAL ABNORMALITIES. 
 
 the lesion is more considerable, sacs, or large bags, 
 taking the place of almost all the hemisphere. In 
 some cases the neighbouring ventricle has been opened. 
 The eroded surface is irregular, the grey matter 
 absent, the white matter sometimes indurated. 
 
 There is often serum in the ventricles, with incom- 
 plete development of the corpus striatum, optic 
 thalamus, cornu ammonis, mamillary tubercle, crus 
 cerebri, optic and olflictory nerves on the affected side. 
 
 A similar loss of substance is seen on the same line 
 of the pons, corpora quadrigemina, and pyramid of the 
 same side ; but below the crossing of the nerve fibres in 
 the medulla oblongata the difference in volume is seen 
 on the opposite side. A very remarkable instance of 
 this imperfection of one side of the brain proper is 
 recorded by Van der Kolk. The case was that of an 
 idiot girl, who from her earliest infancy had been para- 
 lysed on the right side, but had lived for twenty-seven 
 years. The left hemisphere was much smaller than the 
 right, and the arachnoid over the entire surfiice was 
 much thickened, and between it and the pia mater a 
 considerable quantity of fluid had collected. The 
 convolutions were much thinner than those of the other 
 hemisphere ; the left ventricle larger than the right, 
 containing a good deal of fluid, and the walls of the 
 left ventricle were much thinner. The right corpus 
 striatum was larger than the left, but was somewhat 
 narrower, and the entire body was as if curved round 
 tlic shortened thalamus. 
 
 Tlie difTercnce between the thalami was particu- 
 larly remarkable. The taenia between the corpus
 
 CONGENITAL ABNORMALITIES. 17 
 
 striatum <aiid thalamus appeared swollen and thickened, 
 in consequence of the thickening of the pia mater lying 
 on it. At the base of the brain the difference between 
 the two hemispheres was especially remarkable, and 
 was in fact so considerable that the length of the right 
 hemisphere exceeded that of the left by twenty-seven 
 millimetres. The left inferior lobe, in particidar, was 
 very much atrophied, and its w\alls were very thin ; the 
 convolutions here were very small or had nearly disap- 
 peared, perhaps in consequence of the constant pressure 
 of the fluid collected in the horn. The left cms cerebri 
 was thinner, and the left corpus mammillare much 
 smaller, than the right. The left half of the pons 
 mammillare and the left corpus pyramidale presented 
 a much smaller circumference than on the right side ; 
 the difference between the corpora olivaria was less. 
 In the cerebellum, on the contrary, the atrophy was on 
 the opposite side, the right hemisphere being in all its 
 measurements much less than the left ; consequently 
 the so-called vermis, posteriorly situated in the middle, 
 between the hemispheres of the cerebellum, was drawn 
 obliquely to the right side. 
 
 It is extremely remarkable that, while the medulla 
 oblongata above the decussation is larger on the right 
 side, the right corpus pyramidale agreeing with it in 
 this respect, beneath the decussation the atrophy of the 
 left hemisphere had transferred itself to the right side 
 of the spinal cord, as well as of the cerebellum. The 
 atrophy of the right side of the cord was very evident 
 at the level of from the fifth to the seventh cervical 
 vertebra. 
 
 c
 
 18 CONGENITAL ABNORMALITIES. 
 
 In some measure corresponding to tliis were found 
 tlie roots (but particularly the ganglia on a level with 
 the brachial plexus) of the fifth, sixth, and seventh 
 cervical nerves on the right side, much diminished in 
 thickness and size ; this difference was particularly 
 strikincf in the fifth and sixth nerves. 
 
 There was also found a very remarkable thickening 
 of the bones of the skull on the atrophied side ; the 
 anterior and lateral portions of the left side of the 
 skull being much thickened ; whilst near the occiput 
 the reverse had taken place, the thickening of the 
 skull in this situation being found on the right side. 
 
 (v) Imperfection of the anterior portion of the 
 Brain only. 
 
 Both the anterior lobes may be affected. Some- 
 times the abnormahty seems only a very partial arrest 
 of development ; at other times the loss is more con- 
 siderable, and the lobes seem, as it were, truncated. 
 
 (vi) Imperfections of the Cerebellum. 
 
 One case only has been recorded of the almost 
 complete absence of the cerebellum, both the lateral 
 lobes and the greater part of the central region being 
 found wanting. 
 
 More often the arrest of development has only been 
 carried to one lobe, causing simple inequality of the 
 two sides. Sometimes there is found a general small- 
 ness of the whole organ. 
 
 There is no rule as to the relation of other portions 
 of the encephalon to an imperfect cerebellum. Some- 
 times the cerebral hemisphere of the same side extends 
 farther back than usual, as tliough to fill up the space
 
 COXGEXITAL ABNOIIMALITIES. 19 
 
 left vacant by the lateral imperfection of the cere- 
 bellum. Sometimes atrophy of one side of the cere- 
 bellum co-exists with a similar condition of the cerebral 
 hemisphere of the same side. 
 
 At other times the absence of one lobe of the 
 cerebellum coincides with relative smallness of the 
 corpus striatum and olivary body of the opposite side, 
 or with a less development of the pons varolii on the 
 same side as the cerebellar atrophy. 
 
 In Van der Kolk's case, the atrophy of the cere- 
 bellum was found on the opposite side to that of the 
 cerebral hemisphere. 
 
 (vii) Imperfection of the Pons and Medulla 
 oblongata. 
 
 Congenital alteration of these parts consists, if life 
 is preserved, only in some modification of form and 
 partial diminution in volume. Entire absence of one 
 side of the pons or of the medulla oblongata is pro- 
 bably unknown, except in anencephalous monsters, 
 stillborn. 
 
 (viii) Imperfections of the Cerebral Nerves. — Some 
 few instances have been observed. Thus, when there 
 is no grave alteration of the brain, the olfactory nerves 
 are sometimes wanting. If the two anterior lobes of 
 the brain are fused together, they may be absent ; and 
 they are sometimes not found in cyclopic individuals. 
 In the same way, the optic nerves are sometimes absent, 
 whilst at other times the tubercula quadrigemina are 
 not developed. 
 
 Although the expression ' arrest of development ' 
 has been used more than once in describing varieties of 
 
 c 2
 
 20 COXGENITAL ABXORMALITIES. 
 
 this incompleteness, it must be generally understood to 
 depend either on injury to the foetus or on some disease 
 occurring during; foetal hfe. The brain, beins; formed 
 late in the order of development, is most likely to suffer 
 from any injiuy to or diseases of the foetus, and the 
 pons and the medulla oblongata will probably suffer 
 next in order. 
 
 8. Congenital Hydrocephalus. — The cases are very 
 rare in which, before birth, fluid accumulates in any 
 portions of the brain or its membranes. Still a few 
 cases are recorded in Avhich this seems to have taken 
 place. Some even of these few are probably due to 
 excessive development of the cerebro-spinal fluid, under 
 conditions of more or less atrophy of some neighbour- 
 ing portion of the brain itself. The recorded cases 
 must be arranged according to the position in which 
 the fluid is found. Thus : 
 
 (i) Fluid has been found between the pericranium 
 and dura mater. This is exceedingly rare. 
 
 (ii) Congenital Hydrocephalus of the Meninges. — 
 Fluid may exist in the cavity of the arachnoid. This 
 also is very rare, although some cases of it are on 
 record. It has been often mistaken for fluid in the 
 cerebral ventricles in those cases where the layer of 
 nervous substance of the cerebral hemispheres has been 
 tliinned to an extreme degree. Under these circum- 
 stances, the fluid has been drawn off by tapping, in the 
 full belief that the case was one of external hydro- 
 cephalus. 
 
 (iii) Congenital Hydrocephalus of the Ventricles. 
 Where this occurs without increase in the cranial
 
 CONGENITAL ABNORMALITIES. 21 
 
 volume, it is due to some condition of incompleteness 
 of some portion of the nervous centre, especially with 
 arrest of development of the corpora striata and optic 
 thalami. But it may be attended with increase in the 
 cranial volume, and may be developed either before or 
 after birth. 
 
 a. Before birth, very rare. — The fluid may begin to 
 collect as early as the second month of gestation, after 
 a blow on the abdomen of the mother. It may be very 
 chronic, and cases are mentioned of patients in this 
 condition living for 2, 9, 29, 33, 38, and even for 41 
 years. It is often associated with spina bifida, or with 
 hydi'orachis without spina bifida. 
 
 b. Developed only after birth. — This may be 
 a true dropsy, depending on disease of the choroid 
 plexus, or it may be a result of inflammation. 
 The brain becomes more or less unfolded, the ventricles 
 distended, the ventricular walls tliin, and even 
 almost membranous, sometimes firm and hard, some- 
 times pulpy. The two lateral ventricles generally 
 communicate freely. The corpus callosum is pushed 
 upward ; the septum lucidum may be entirely effaced, 
 althouoli it is sometimes firm ; the fornix is thinned and 
 flattened out ; the eminences of the ventricles are pressed 
 down. The ependyma lining the enlarged cavities be- 
 comes sensibly thickened, of a certain consistence, and 
 vascular, and capable of being pealed off in thick 
 roughish flakes ; it is sometimes covered with a thick 
 mucous matter. One ventricle may be more distended 
 than the other. 
 
 9. A condition in wliich a considerable portion of
 
 22 CONGENITAL ABNORMALITIES. 
 
 the Brain is situated outside the Cranium. — The cha- 
 racteristics of this abnormality are, that the part of the 
 brain displaced is considerable — that the cranium pre- 
 sents great changes of capacity, form, and constitution, in 
 relation with those that the encephalon has undergone — 
 that life cannot be maintained (or only for a very brief 
 period) with vices of organisation which in their severity 
 are closely allied to those which obtain in anencephalous 
 heads. 
 
 According to the direction the brain takes, this 
 abnormahty may be divided into : (1) Frontal, in which 
 a portion of the frontal bone alone is wanting ; (2) 
 sincipital, in which the parietal bones may be wholly 
 absent, and a part of the frontal, occipital, and temporal 
 also ; and (3) occipital, in which the exit of the brain 
 takes place in one of three ways — either the issue of 
 the brain is through the posterior fontanelle, or by the 
 absence of the upper and middle part of the occipital, 
 or else the issue of the brain, and generally of the cere- 
 bellum, takes place by a large opening at the middle 
 part of the occiput, which often comprises the foramen 
 magnum of this bone, or else the brain, cerebellum, 
 and medulla oblongata are found posterior to the skull, 
 having escaped by a large opening in the posterior part 
 of the head and cervical region of tlie spine. 
 
 Encephalocele is really only a variety of the abnor- 
 mality described above. In this condition there is a 
 displacement of a part, more or less circumscribed, of the 
 encephalon across an abnormal opening in the walls of 
 the cranium. This opening may be frontal, sincipital, 
 temporal, or occipital, and of these the occiput is the
 
 CONGENITAL ABNOEMALITIES. 23 
 
 most frequent seat, and the frontal next. It does not 
 necessarily lead to early death. 
 
 Precisely the same condition may be produced by 
 an opening formed by a wound, or by destruction of 
 some portion of the cranium by syphilis ; but it is also 
 a congenital abnormality. Another variety is encepha- 
 locele in a hydrocephalous subject. Under these cir- 
 cumstances, the fluid distending the ventricles is included 
 in the external tumour. 
 
 According to the situation of the opening, this 
 abnormality may be frontal, fronto-nasal, sincipital, 
 parietal, occipital, and, lastly, sphenoidal. The latter 
 variety is caused by a large perforation of the sphenoid 
 bone, through which tlie pituitary body may descend, 
 and project into the cavity of the mouth. 
 
 This abnormality seems to be caused by one or 
 other of the followino' circumstances : either violence to 
 the abdomen of the mother towards the middle period 
 of pregnane}", or inflammation of the brain or the 
 membranes in the fcBtus, or compression exercised on the 
 neck of the foetus by the umbilical cord, by an adhesion 
 contracted with the placenta or the membranes. A still 
 more rare variety is hydromeningocele, in whicli the 
 dura mater and the serous layer which lines it are 
 lifted up, pressed by the accumulated subarachnoid 
 fluid ; whilst one of the points of the cranial walls, in- 
 completely organised, yields and allows itself to be 
 distended. In this way there may result a tumour 
 very analogous to the former variety, but it differs 
 essentially in the absence of all cerebral expansion 
 unfolded in the hernial sac, or presenting itself at the
 
 24 CONGENITAL ABNORMALITIES. 
 
 abnormal orifice of the cranium. Tlie brain is wholly 
 contained within its normal cranial limits. Sometimes 
 the fluid is from the arachnoid, but this is extremely 
 rare. More often it comes from the ventricle having 
 forced an artificial passage for itself through the thinned 
 layer of cerebral convolutions. The seat of this ab- 
 normality is generally the occiput, and its origin in the 
 foetus seems to date from the beginning or middle 
 period of gestation. 
 
 We proceed now to the abnormahties affecting the 
 cord itself, some of which may exist alone, whilst others 
 are usually associated with some similar condition of 
 the encephalus. 
 
 10. Absence of Spinal Cord. — Complete absence of 
 spinal cord is rare, except in anencephalous subjects. It 
 is not compatible with life. 
 
 11. Congenital imperfection of the Corel: incom- 
 pleteness of Cord corresponding to the same condition 
 affecting the Brain. — The length, breadth, and form of 
 the cord may vary. The central canal may be dilated : 
 it may be capable of holding a crowquill down the 
 whole length of the cord, and this dilatation, though a 
 structural imperfection, does not seem to give rise to 
 any morbid phenomena. In connection with an absence 
 of the Hmbs at birth, the cervical and lumbar swelling 
 may be absent. Inequahties of volume are also found 
 in the lateral parts of the cord. 
 
 12. Spina bifida. — Spina bifida is caused by the 
 division or congenital absence of one or several posterior 
 arches of tlie vertebrcc or the sacrum, allowing the
 
 COXGENITAL ABNORMALITIES. 25 
 
 spinal meninges (which are pressed upon from without 
 by serum, and find no spinal wall to hinder their 
 tendency to bulge consequent on this pressure) to make 
 a projection of greater or less extent. This abnor- 
 mality is analogous witli hydromeningocele. In botli 
 we find arrest of ossification, in both accumulation of 
 serum, in both hernia of the menino-es. It is found 
 much more frequently in some countries than in others. 
 Countries more or less circumscribed show the larijest 
 number of cases in a short time — possibly as a result 
 of close intermarriage. In Holland it is specially 
 prevalent. 
 
 Several cases may occur in the same family ; and 
 the state of health of the mother seems to have a de- 
 termining effect, especially as to scrofula, syphilis, &c. 
 The female sex is more liable to it than the male, and 
 it is often coincident with hydrocephalus. Its seat is 
 especially the lumbar regions, and next to this the 
 sacral. It seldom appears in tlie dorsal and cervical 
 regions, but it has been known to exist at the level of 
 the last cervical vertebra, and to extend thence to 
 the last dorsal. It has also been seen at the occiput, 
 tlie atlas, and the axis, and sometimes is found in two 
 regions in the same individuals. It is of variable 
 volume, and its form corresponds to the number of 
 vertebra3 involved. It is generally soft, but not quite 
 always. It projects more when the cliild cries. 
 
 The colour of the tumour varies : it may be 
 reddish violet, pale or livid, opaque, or semi-trans- 
 parent. It is generally covered with the skin more or 
 less altered, and sometimes by a thin membrane. The
 
 26 CONGENITAL ABNORMALITIES, 
 
 skin covering it may show various abnormalities, 
 depending on its often being more or less inflamed. 
 
 The dura mater always forms an essential element 
 in the tumour. The spinal cord is often seen at the 
 bottom of the cavity, sometimes unaltered, sometimes 
 thin and soft. The extent to which it is implicated in 
 the disease seems to vary according to the position of 
 the tumour. The spinal cord is much more apt to be 
 involved if the disease is higher than the lumbar regions. 
 In spina bifida, the spinal cord often extends lower 
 down than usual, and may enter the sacral canal. Even 
 in the lumbar region, however, it may project into the 
 tumour. When implicated, it does not lie free, but is 
 bound down by adhesions. The nerves of the cauda 
 equina are often found in the tumour. The disease is 
 due to arrest in the development of bone. It is most 
 frequently found in the lumbar region, because ossifica- 
 tion here is slower than in other parts of the spinal 
 column. This arrest of development is probably due 
 to local inflammation early in foetal life, which causes 
 points of adhesion between the walls of the spinal canal, 
 meninges, and cord, and provokes hypersecretion of 
 serum. 
 
 The fluid may accumulate in the central canal of 
 the cord, in the sac of the arachnoid, or between the 
 pia mater and araclmoid. 
 
 Consult on this subject — 
 
 Gintrac, ' Maladies de I'Appaieil nerveux.' 
 
 Holmes, ' St. George's Hosp. llep.,' vol. i. 
 
 Pricliavd, ' Natural Hist, of Man.' 
 
 Van der Kolk, ' New Syd. Soc.,' vol. xi. 
 
 'Journal of Mental Science,' Oct. 1873, p. .301. 
 
 ' Brit, and For. Med.-Chir. Rev.,' July 1874. ' Microcephalism.'
 
 27 
 
 LECTUEE II. 
 
 ABNORMALITIES OF THE VASCULAR SYSTEM. 
 
 This subject includes all diseases of the cerebral vessels, 
 cerebral and spinal hemorrhages, and that battle-ground 
 of pathologists, the morbid conditions that are said to 
 result from a variation in the amount, and a modifica- 
 tion in the course, of the blood in the cerebral vessels. 
 It also closely infringes upon the next subject — inflam- 
 mation ; so much so, that by some observers inflamma- 
 tion is found under this classification as a morbid state 
 of the vessels ; and in the case of tuberculous menin- 
 gitis, in which the original lesion is first found in the 
 tissue absolutely forming part of the vessels themselves, 
 the separation of the disease from those of the vessels 
 is in the highest degree unscientific, although for 
 practical purposes it may be convenient. 
 
 I. We take then, first, the diseases of the cerebral 
 vessels ; and these form a natural arrangement, accord- 
 ing to the kind of vessels implicated — arteries, capillaries, 
 or sinuses and veins. 
 
 1. Diseases of the cerebral and spinal arteries. 
 
 a. Aneurisms. — These are most frequently found 
 of the basilar, the middle cerebral, and tlie internal 
 carotid, sometimes within the cavernous sinus, some-
 
 28 ABNORMALITIES OF THE VASCULAR SYSTEM. 
 
 times outside it. But this condition is met with affect- 
 ing most of the arteries of the brain — the middle 
 meningeal, the anterior cerebral, the anterior com- 
 municating, the arteries of the corpus callosum, the 
 posterior communicating, the vertebral, the posterior 
 cerebral, and the cerebellar. It is far more common 
 than is supposed to meet with miliary aneurisms of 
 the brain : miliary aneurisms of the internal vessels of 
 the brain and of the pia mater often co-exist. They 
 constantly co-exist also with aneurisms, small or large, 
 of other vessels of the body ; and as instances of their 
 co-existence with aneurism elsewhere may be mentioned 
 the ftict that with miliary aneurism of the cerebral 
 vessels has been found a similar condition of the 
 vessels of the hands and feet, shoulders, oesophagus, 
 and stomach. They occur also in the retina. 
 
 They seem to be produced quite independently 
 of atheroma, but rather to depend on a peculiar altera- 
 tion of the tissue of the vessels, and primarily of the 
 inner coat, to which the name ' Arterio-sclerosis ' has 
 been given. This condition is sometimes found co- 
 incident with sclerosis of the spinal cord. MM. Charcot 
 and Ch. Bouchard deny tliis condition of sclerosis, and 
 say that the inner coats of the arterioles first become 
 ruptured, and thus give rise to the formations of a 
 dissecting aneurism. This state of things may continue 
 for some time ; or, in consequence of a process of re- 
 gression, nothing remains but a little pigmentary 
 tubercle. Lastly, in other cases the adventitious tunic at 
 length becomes ruptured, and gives rise to a cerebral 
 ha3morrhage.
 
 ABNORMALITIES OF THE VASCULAR SYSTEM. 29 
 
 Zenker, liowever, upliolds the view of sclerosis of 
 the inner coat, either at the seat or in tlie immediate 
 neisjlibourliood of the aneurism. 
 
 Instances are met witli of the vessels of the brain, 
 cerebellum, pons, and spinal cord being thus affected at 
 the same time. No age is exempt from this ' premature 
 old age of the arteries ': it occurs even in children. 
 
 In many people there seems to be a true aneurismal 
 diathesis ; and certainly a predisposition to aneurism is 
 influenced by the speciality of tlie race. It is more 
 common in England than elsewhere, and in men than 
 in women. 
 
 Miliary cerebral aneurisms exist in various cachexias, 
 and in some general maladies ; and although they may 
 persist for some time without giving rise to any symptom, 
 yet often enough they are accompanied by headache 
 and vertigo ; and successive attacks of paralysis, quickly 
 recovered from, afford almost certain proof of their 
 existence in the brain. 
 
 They may co- exist with and be more or less caused 
 by cancer, the tuberculous cachexia, in which the retina 
 is sometimes thus affected, Bright's disease, and chronic 
 alcoholism, in which, again, the retina suffers in the same 
 way, even in those cases in which the kidneys have not 
 become diseased. Alcohol, indeed, is a frequent cause 
 of aneurism, as being probably a frequent cause of the 
 arterio- sclerosis just mentioned. 
 
 This abnormahty of the small vessels of the brain 
 is found also in cases of general paralysis, lead-poison- 
 ing, rheumatism, gout, leucocythemia — the capillaries, 
 distended with white corpuscles of the blood, not un- 
 freqiiently giving way — pregnancy, and purpura.
 
 30 ABNOEMALITIES OF THE VASCULAE SYSTEM. 
 
 The larger aneurisms depend on a condition of 
 arteries somewhat different from the arterio-sclerosis. 
 The waUs are sometimes thin and transparent ; some- 
 times thick, hard, cartilaginous, encrusted with lime- 
 salts, or spotted with bony plates. 
 
 Their effects vary immensely according to their seat. 
 They may compress a nerve, or give rise to a sensation 
 of palpitation in the head that is almost insupportable ; 
 or, if aneurism exist within the cavernous sinus, the 
 circulation of the blood may be arrested, the veins of 
 the retina will be dilated, and even exophthalmia be 
 produced. 
 
 If rupture occurs in the sac, a sort of arterio-veuous 
 aneurism is caused. Serous effusions, both in the 
 arachnoid and in the ventricles, may be the effect of 
 aneurism of the cerebral vessels. 
 
 In a man, aged 45, who died of cancer of the 
 stomach, all the arteries of the circle of Willis were 
 very atheromatous. On the left posterior cerebral 
 artery, just as it crosses the crus cerebri, was a small 
 aneurism, the size of a large pea. The crus beneath 
 this was rather softened, and the locus niger exposed. 
 
 h. Atheroma. — The interference with the calibre 
 of an artery by atheroma is a common cause of 
 thrombosis. It is practically an arrangement of greyish 
 or yellowish-white patches interposed between the 
 internal and middle coats of the artery. These patches 
 may be dissolved in alkalies and in ether. They con- 
 stitute a fatty degeneration of the internal and middle 
 coats, perhaps specially of the latter. 
 
 c. Cartilaginous, osseous, or calcareous state of the
 
 ABNORMALITIES OF THE VASCULAR SYSTEM. 31 
 
 Arteries This condition is most common in the arteries 
 
 of the base, and specially in the principal trunks. It 
 occupies the same position in the arterial wall as 
 atheroma, and indeed is very frequently a further 
 stao'c of deo'eneration. It is most common in advanced 
 age, but is found at all ages. In some cases it seems 
 to be a degeneration occurring upon chronic arteritis. 
 The arterial walls are rendered very brittle, and 
 ha3morrhage is a frequent result. Yet the rupture 
 of the artery does not always take place at the most 
 diseased part. The disease interferes not only Avith 
 the resilience, but actually with the calibre of the 
 vessel, and there results either congestion without 
 hcemorrhage, or such a modification in the course of 
 the blood that great pressiure is brought to bear upon 
 some other part of the vessel, and so hasmorrhage. 
 As a further result of the lesser evil — congestion — we 
 find serous effusion into the arachnoid cavity, the pia 
 mater, and the ventricles. 
 
 For a statement on hyahne-fibrosis, and hyper- 
 trophy of the muscular coat, see Lecture VII. 
 
 d. Perforation. — Sometimes perforation occurs 
 without our being able to detect any lesion of the 
 vessel that could have led to it. More often, however, 
 it results from a local alteration of the arterial walls 
 (differing somewhat from arteritis), by which they 
 become thickened and softened, and in some places 
 eroded, ulcerated, and destroyed. Of course we are 
 leaving out of the question perforation from traumatic 
 lesion of any kind, but it may be connected with 
 gradual erosion of the bony walls from sy[)hilitic or 
 other causes.
 
 B2 ABNORMALITIES OF THE VASCULAR SYSTEM. 
 
 e. Thrombosis. — Eare in arteries. It is practically 
 a concretion or coagulation of blood contained in the 
 vessels ; formed in situ, not brought from a distance. 
 It may occur without any appreciable lesion of the 
 arterial walls ; and in this case it is from what we are 
 accustomed to call hyperinosis of the blood, an excess 
 of fibrine, as in several acute diseases, and markedly 
 in acute rheumatism. But more generally it seems to 
 depend upon some condition that interferes with the 
 normal calibre of the vessel itself, or which renders 
 the internal coat rough or unequal. This may be 
 from inflammation, but net very frequently. Atheroma 
 is a more common cause. 
 
 The thrombi are more dense at their circumference 
 than at the centre. Sometimes they contain small 
 calcareous deposits. Men are more subject to this 
 lesion than women ; but old age seems not to be more 
 liable than the other periods of life. The internal 
 carotid, the middle cerebral, the basilar, and the 
 vertebral arteries are most commonly affected. 
 
 /. Embolism. — Due to a coagulum brought from a 
 distance, and not formed in situ. It may be brought 
 from the heart itself, or its valves, from the walls of 
 the aorta, or from the cavity of an aneurism. 
 
 Several arteries may be obstructed at one and 
 the same time ; sometimes all on one side, at other 
 times some arteries of one side of the brain and some 
 of the other. 
 
 We may meet with embolism obstructing the main 
 trunk of an important artery, causing perhaps sudden 
 aphasia, or hemiplegia ; or the main trunks may escape,
 
 ABXOEMALITIES OF THE VASCULAR SYSTEM. do 
 
 aud the smallest branches be thus blocked, as they 
 have been found to be in the corpus striatum in 
 chorea. 
 
 The left middle cerebral artery is the most frequent 
 seat of embolism, and next tlie right Sylvian artery. 
 It is a constant cause of hajmorrhage. The female sex 
 is much more liable to embolism than the male ; and 
 youth and adult age more than other periods of life. 
 
 2. Diseases of the Capillaries. — The cerebral capil- 
 laries do not seem to be affected with aneurism. Even 
 the smallest miliary anemisms are connected with the 
 arteries, and do not attack the capillaries. But these 
 latter vessels may be dilated from various causes, some- 
 times from backward pressure of blood, owing to 
 venous obstruction, and sometimes from the augmented 
 vis a tergo due to hypertrophy of the heart. 
 
 They are also liable to atheroma, though less so 
 than the arteries, and, probably as a consequence of 
 atheroma, to calcareous infiltration. 
 
 When the calibre of the capillary vessel is partially 
 interfered with and obstructed by atheroma or cal- 
 careous degeneration, a thrombus may form in it ; but 
 embolism of the capillaries is rare. Blandford and 
 Charlton Bastian, however, mention it. The so-called 
 capillary heemorrhages are generally due to rupture of 
 the smallest arteries. Sometimes, however, rupture of 
 the capillaries takes place, especially in those minute 
 vessels that often encircle an old hgemorrhoge in the 
 brain, or a spot of softening. 
 
 3. Diseases of the Cerehiv-sjnnal Venous System. — 
 a. Inflammation of the Cerebral Veins and Sinuses of 
 
 D
 
 34 ABNORMALITIES OF THE VASCULAR SYSTEM. 
 
 the Dura Mater. — Inflammation of the veins and sinuses 
 generally co-exist. The vascular walls lose their 
 transparency, and become thick, rugose, soft, and 
 reddened. The vein or sinus attacked contains clots 
 of various colours and consistence, according to their 
 age. These clots form true thrombi, and inflammation 
 of the veins and sinuses is a not unfrequent cause 
 of cerebral thrombosis ; they also contain pus, false 
 membranes, &c. 
 
 This inflammation may depend on various causes. 
 Damp, scrofula, alcohol, misery, all predispose to it ; 
 whilst accidents, ulcers, or abscesses of the scalp, 
 anthrax of the neck, pus in the pleural cavities, and 
 scarlatina, are all exciting causes. But perhaps the 
 most common cause of inflammation of the sinuses, 
 and more frequently than is supposed of the cerebral 
 veins themselves, is inflammation of the internal ear 
 and the pars petrosa. Under these circumstances the 
 lateral sinus is the one most usually affected : the dura 
 mater is often raised by pus, becomes thick, spongy, 
 grey or black, and ulcerates. The corresponding lobes 
 of the brain are covered with pus, or with brown, grey, 
 or slate-coloured matter. There is effusion of pus or 
 serum under the arachnoid, or in its cavity, or in the 
 ventricles. The cerebral substance is injected, or 
 studded with small clots or with larger haemorrhages, and 
 in many cases softened. When the cerebral veins are 
 likewise implicated, there is found also cerebral abscess. 
 Secondary abscesses of the lungs, liver, spleen, and 
 kidneys may be met with. 
 
 h. Thrombosis. — Sometimes the result of phlebitis, as
 
 ABNORMALITIES OF THE VASCULAR SYSTEJNf. 35 
 
 above stated. It may arise from other causes, especially 
 from anything that forms an obstacle to the circulation of 
 tlie blood in the brain, such as tumours, preventing the 
 retmii of blood from the head ; probably, also, any condi- 
 tion that leads to partial asphyxia, such as asthma. It is 
 most common in early life. The vein is seldom attacked 
 alone : it is associated with thrombus of a neighbouring 
 sinus, on the one hand, or more commonly with thrombi in 
 the capillaries and small artery with which it is connected. 
 The thrombus is occasionally found partially organised. 
 
 As a result of venous thrombosis, we may meet 
 with serum in the cavity of the arachnoid in some 
 cases, or a hyperaimic condition of the pia mater, or 
 sometimes with small hajmorrhages on the surface of 
 the cerebral hemispheres or within them. The brain 
 is sometimes healthy, sometimes more or less softened 
 in the neighbourhood of the affected vein. 
 
 Th. von Dusch collected fifty-seven cases in wliich 
 the formation of the thrombi in the sinuses of the 
 brain is mentioned. A comparison of these cases in 
 reference to their causation shows that in thirty-two 
 the tlirombosis was the result of gangrenous, erysipela- 
 tous, and suppurative inflammations of those parts of 
 the body (neck, face, orbits, bones of the skull, brain 
 and its membranes) whose vessels are in close connec- 
 tion with the sinuses. In four it appeared to result 
 from a diminution of the calibre of the sinus, by the 
 intrusion of foreign bodies and tumours, or from pres- 
 sure from without upon the sinus, or upon the internal 
 jugular vein. In fifteen it appears to have been occa- 
 sioned by circumstances which lessened the force of 
 
 D 9.
 
 26 ABNORMALITIES OP THE VASCULAR SYSTEM. 
 
 the circulation, namely, by previous debilitating diseases 
 in individuals for the most part feeble already, as aged 
 persons and children. Lastly, in six cases nothing 
 positive as to the cause could be ascertained from the 
 history. 
 
 c. Cartilaginous and osseous conditions of the Cere- 
 bral Veins. — This abnormality, which is found in the 
 inferior cava and other veins, is very rare in the cerebral 
 veins, and probably unknown in the sinuses. 
 
 d. Eupture of the Cerebral Veins and Sinuses. — 
 Eupture of veins is very rare. At the point of con- 
 fluence of the sinuses the walls of the sinuses are 
 often much thinned by the constant pressure of the 
 blood arrested in its course from the brain. Under 
 these circumstances, the walls may yield at this point, 
 and venous blood be effused along the base of the 
 brain, and down the spinal canal. 
 
 II. HAEMORRHAGES. 
 
 1. Hcemorrhage outside the Brain and Spinal Cord, 
 a. Between the Cerebral Dura Mater and the Bone. — 
 This depends on fracture of the skull ; on blows on the 
 head, without fracture of the skull ; on erosion from 
 syphilis ; on congestion of the meningeal vessels ; on 
 morbid conditions of the blood itself, as scurvy or 
 piu-pura ; and, lastly, Gintrac mentions as a cause of 
 hasmorrhage in this position, vascularity of the Pac- 
 chionian glands that have pushed through the dura 
 mater. It is an uncommon condition, except from a 
 traumatic cause.
 
 ABNORMALITIES OF THE VASCULAR SYSTEM. 37 
 
 b. Cerebral Ifemorrhage beneath the Dura Mater, 
 in the cavity of tlie Arachnoid. — The blood is found in 
 this situation under circumstances varying according to 
 the time at which it has been effused, and also accord- 
 ing to the presence or absence of surrounding inflam- 
 mation. Tlius we meet with blood in a liquid state, 
 or partly coagulated, or wholly coagulated, lying in 
 the cavity of the arachnoid, surrounded by the parts 
 in a normal state, without any sign of inflammation ; 
 or, on the other hand, we may meet with blood sur- 
 rounded by a false membrane of various degrees of 
 thickness, sometimes unorganised, sometimes partially 
 organised ; and, lastly, it may be surrounded by an 
 old thick cyst wall thoroughly provided with vessels. 
 Hasmorrhage from the under-surface of the dura mater 
 usually occurs as a sequence of inflammation of that 
 organ, the blood coming from the tender vessels of the 
 partially organised effused products. 
 
 For further reference to the arachnoid cysts, so 
 formed, see Lecture VII. 
 
 c. Ha3morrliage : sub-arachnoid, cerebral. — This 
 may occur either on the convex surface of the brain 
 only, or at the base only, or both at the base and on 
 the convexity together. It is said that subarachnoid 
 haemorrhage at the base of the brain is never met witli 
 in the insane. The symptoms are grave, and the 
 prognosis serious in proportion to the extent of the 
 hcemorrhage. Hasmorrhage of the convexity depends 
 most frequently on mihary aneurisms of the pia mater. 
 It is usually very small in amount, forming one or 
 more ecchymoses, and probably then giving rise to
 
 38 ABNORMALITIES OF THE VASCULAR SYSTEM. 
 
 no symptom. At other times, many of the miUary 
 anenrisms are found, and the results of their rupture 
 are seen on the convexity, varying in colour and con- 
 sistence according to the date of the haemorrhages. 
 At other times, again, these miliary aneurisms co-exist 
 with one of a larger size, from the rupture of which 
 the whole of the convex surface of the brain is covered 
 with blood. A large haemorrhage of this kind may, 
 moreover, depend on external injury to the skull, or 
 on scurvy or purpura. 
 
 When subarachnoid hemorrhage of the base is met 
 with, it is generally due to fracture of the skull, with 
 rupture of the membranes or laceration of the brain, 
 or both ; or to the giving way of an artery at the base, 
 especially the basilar ; or to the fact that a large 
 cerebral hasmorrhage has partially found its way 
 externally. 
 
 Subarachnoid hsemorrhage of the convexity and 
 base together will generally be found, excluding very 
 severe local accidents, to depend on the co-existence of 
 large and miliary aneurisms, a condition, so to speak, 
 of aneurismal diathesis ; but, once again, it may be well 
 to remind you that an aneurism which by its rupture 
 leads to great hiemorrhage of the base need uot be of 
 any vessel external to the brain itself. 
 
 d. Hgemorrhages of the Spinal Meninges. — This may 
 be outside the spinal dura mater, or in the cavity of 
 the arachnoid or sub-arachnoid. All three forms may 
 be due to external injury to the spine, but they may 
 depend on other causes. The two latter varieties 
 especially may be caused by great muscular efforts,
 
 ABXORMALITIES OF THE VASCULAR SYSTE.M. 39 
 
 by venereal excess, perhaps by the abuse of alcohol. 
 Certainly rupture may occur after great congestion, 
 such congestion being induced by suppression of the 
 catamenia, or by interference with respiration. Unless 
 the hsemorrhage be of great amount, much of the clot 
 is rapidly absorbed, but it generally sets up some 
 inflammatory action of the meninges in its neighbom'- 
 hood, the membrane becoming thickened and opaque ; 
 and very often the nervous tissue beneath the seat of 
 effusion is softened. This obtains also in haemorrhage 
 of the cerebral membranes. 
 
 2. Hcemorrhage of the Brain. — Hasmorrhage may 
 occiu- in any portion of the nervous centres,and in several 
 spots at one and the same time. Thus clots of various 
 sizes may be found in the cortical substance of the 
 brain, in one or both of the anterior, middle, and 
 posterior lobes, in one or both of the corpora striata, or 
 optic thalami, in the ventricles, in the cerebellum, the 
 pons, the medulla oblongata, and spinal cord. 
 
 (i) Haemorrhage of the Cortical Substance.— Seldom 
 of one spot only, or of very small extent. When it is 
 so, it depends generally on local disease, such as adhe- 
 sion of the membranes to the part, disease of the pars 
 petrosa, otitis, &c. More frequently it is found in 
 larger amount or in numerous spots, and the blood 
 may be seen mingled with the nerve matter, from local 
 encephalitis or local softening having been set up in 
 the immediate neighbourhood of the clot. These spots 
 may be surrounded by cysts. 
 
 At the periphery of the brain, and especially 
 on the convex surface, hasmorrhage of the cortical
 
 40 ABXOEMALITIES OP THE VASCULAR SYSTEM. 
 
 substance occurs in a miliary form, ' Capillary 
 apoplexy,' as it has been termed. If no inflammation 
 lias been set up around these spots, we fnid a few 
 globules of blood, or merely some blood-crystals. This 
 form occurs under several conditions, such especially 
 as miliary aneurism, purpiu^ic alteration of the blood, 
 thrombosis of the sinuses or of the veins of the pia 
 mater. Old age is most subject to it. 
 
 It is not very unusual to meet with the co-existence 
 of ha3morrha2:e of the cortical substance and of the 
 meninges. The arteries are sometimes atheromatous, 
 cartilaginous, calcareous, sclerosed, or aneurismal ; and 
 Gintrac says that the corpora striata, in cases of 
 hsemorrhage of the cortical substance, are sometimes 
 found injected, softened, of various colours, and pitted 
 with small irregular cavities. 
 
 The brain substance is more often injured by 
 haBmorrhage in tlie middle lobes than in either the 
 anterior or posterior lobes ; and the lesion in the middle 
 lobes is of greater gravity, partly because of the near 
 neighbourhood of the corpora striata, partly because of 
 the tendency of the effused blood to find its Avay into 
 tlie ventricles. 
 
 In the anterior lobes the haemorrhage is generally 
 circumscribed, but it may open into the lateral ventricles 
 or externally, or in both situations at once. Coincident 
 hasmorrhage may occur in tlie anterior and some one 
 of the other cerebral lobes, or in the interior of the 
 lobes and the cortical substance, or in the lobes and 
 tlie meninges, at one and the same time ; but hasmor- 
 rhage of the corpus callosum alone is extremely rare.
 
 ABNORMALITIES OF THE VASCULAR SYSTEil. 41 
 
 Htemorrliage of tlie middle lobes may be met with 
 ill one lobe only, and then the gravity of the case will 
 be in direct proportion to the extent of the lesion. 
 Death may occur in a tew hours, or not for several 
 years. The lesion may attack both lobes simultaneously 
 or successively ; or rupture may take place at the 
 surface of the brain, and the blood originally effused in 
 the middle lobe may find its way into the meshes of the 
 pia mater ; or this rupture may take place into a lateral 
 ventricle, causing symptoms that usually are quickly 
 fatal, though cases are on record where life has been 
 prolonged, but probably only where the amount of 
 blood poured out into the ventricle has been small ; 
 or, again, this complication may arise not from an 
 extension to the ventricle of the original lesion, but 
 from rupture of a cyst that had formed round a previous 
 clot ; or, again, the effused blood may find its way 
 simultaneously into a ventricle and at the surface of 
 the brain. 
 
 The posterior lobes are less often affected than the 
 nfiddle, and haemorrhage there seems to be of far less 
 serious import. 
 
 It may be circumscribed in one or both posterior 
 lobes, or it may occur in one of the posterior lobes, 
 and open at the surface of the hemisphere or into one 
 of the ventricles, or simultaneously into one of the 
 ventricles and at the surface of the hemisphere. This 
 haemorrhage has been known to occiu" in early childhood, 
 at four years of age. The duration of life may be 
 much greater after haemorrhage in the posterior than 
 after haimorrhase in the middle lobes.
 
 42 ABNORMALITIES OF THE VASCULAR SYSTEM. 
 
 Extravasation of blood occurs in tlie brain in bulk 
 or in a punctated form. This punctated form may 
 depend on one or other of the following causes : 
 Hyper£emia, inflammation, embolism of the small 
 arteries of the brain, internal inflammation of vessels, 
 minute aneurism, and purpura hsemorrhagica. It is 
 seen in the form of many blood-points, arranged very 
 close together, in a very limited area. Each point 
 is surrounded by a delicate capsule, furnished, as 
 Eindfleisch says, by the fibrogenous substance of the 
 circumfluent nutritive fluid. The changes that take 
 place in this minute extravasation are either to yellow 
 softening, or to suppuration, or to direct organisation 
 of the clot. Of this latter process, Eindfleisch's account 
 is, that organisation of the capsule occurs first, and then 
 of its contents. Colourless blood-cells gradually take 
 the place of the red ones, without the capsule being 
 opened at any place, and so this germinal tissue is 
 directly transformed into fibrinous connective tissue. 
 In the capside itself cleft spaces occur, which divide the 
 capsule into multiple layers. In these spaces connective 
 tissue corpuscles become visible ; and, finally, the inner 
 connective tissue fuses completely with the outer, and 
 a small compact nodule is formed. 
 
 Bulky haemorrhage can only find space by displace- 
 ment of the cerebro-spinal fluid and by emptying the 
 cerebral vessels. If the first injury is withstood, 
 the contraction of the fibrine enables the vessels to fill 
 again, and thus the brain is nourished. The clot becomes 
 encapsulated, and goes through changes as in the 
 punctated form. Part of the blood is changed into
 
 ABNORMALITIES OF THE VASCULAR SYSTEM. 43 
 
 pigment, part becomes connective tissue, and forms the 
 cicatrix ; or, if the process does not go so far, a cyst is 
 formed, filled with clear fluid. This connective tissue 
 growth may not be complete for a long time : round an 
 extravasation of any size it is probably not thoroughly 
 developed before the end of the second year. 
 
 (ii) Hsemorrhage of the Corpora Striata. — These organs 
 are the most frequent seat of cerebral hajmorrhage, from 
 their special texture, from the abundance of grey matter 
 in them, and from their richness in vessels. The lesion 
 may occur in and be confined to one corpus striatum 
 only, and may either destroy life rapidly, without any 
 attempt at local repair, or not for twelve months, in 
 which case a more or less complete cyst may have 
 formed, the corpus striatum being to a great extent a 
 mingled debris of blood and brain tissue ; or life may be 
 prolonged with paralysis for a much longer period, and 
 when death occurs, either from a second haemorrhage 
 or some other cause, a cyst is found of some thickness, 
 traversed by bands, and causing either a depression or 
 a projection in the corpus striatum, according to the 
 original position of the lesion and the amount of con- 
 traction the connective tissue has undergone. Or the 
 haemorrhage into one corpus striatum may be compli- 
 cated by rLi])ture of the organ towards the lateral ven- 
 tricle and extravasation of blood into this cavity — a lesion 
 generally very rapidly fatal, though not necessarily so. 
 The left corpus striatum is more frequently affected in 
 this way than the right ; or, again, hasmorrhage may 
 be met with in both corpora striata, these organs be- 
 ing sometimes attacked successively, sometimes simul-
 
 44 ABXORMALITIES OF THE VASCULAR SYSTEM. 
 
 taneously. HEemorrhage of the neighbouring organs, 
 the optic thalami, is not so common, and the effects are 
 often less marked, the paralysis being less intense, even 
 if there is any diminution of motor power from lesion 
 of these organs alone. The lesion may be circumscribed 
 in the optic thalamus, or may extend into the cor- 
 responding cerebral peduncle, or may open at the 
 circumference of the brain, or more frequently may 
 extend and allow extravasation into the neighbourinci; 
 lateral ventricle ; and, lastly, haemorrhage of one corpus 
 striatum and one optic thalamus may occur simul- 
 taneously, sometimes with one spot of lesion common 
 to both, at other times with lesions distinct in each 
 organ. When heemorrhage occurs into the ventricle to 
 an extent that is not rapidly fatal, the ependyma is 
 generally after a time found a good deal thickened. 
 This lesion is met coincidently with haemorrhage of 
 other parts of the brain. We find haemorrhage of an 
 optic thalamus and a corpus striatum with haemorrhage 
 of the cerebral lobes and of the meninges, or of a cerebral 
 lobe with the meninges intact. 
 
 Haemorrhage of the cerebral ventricles may occur 
 from various morbid conditions of the plexus ch oroides. 
 The plexus may be more vesicular than usual, with 
 vessels greatly distended with blood, and showing rup- 
 tures in several places ; or, indeed, engorged from any 
 cause that interferes with the normal flow of blood 
 through these vessels. This lesion is sometimes co- 
 incident with a breaking down of the septum lucidum ; 
 at other times the ventricular walls are injured, 
 softened, or eroded, either from pressure of the effused
 
 ABNORMALITIES OF THE VASCULAR SYSTEil. 45 
 
 blood upon them, or in consequence of mal-nutrition 
 from impeded blood supply, or from extension of 
 lesion from a corpus striatum or optic thalamus. In 
 very rare cases, blood is found in the ventricles without 
 any lesion that can readily accoinit for it, with healtliy 
 plexus choroides and venai Galeni, with lloor, and 
 walls, and roof of the ventricles ])erfectly healthy. 
 In these cases the ha3morrhage has been supposed to 
 have been due to a kind of exhalation, but of this 
 there is no sufficient proof. It probably, however, 
 depends upon some abnormality of the blood itself, 
 rather than of any vessel. Ilajmorrhage of the ven- 
 tricles may co-exist with haemorrhage of the corpora 
 striata, optic thalami, cerebral lobes and meninges, or 
 of any of them. 
 
 Haamorrhage of the cerebellum is very rare, and 
 when it occurs it is usually in advanced age. The 
 course of the malady is generally continuous, but some 
 cases are recorded in which there has been marked 
 amelioration. The most rapidly fatal cases are those 
 in which the blood has found its way into the fourth 
 ventricle. Haemorrhage may occur in the cortical 
 substance, in the right or the left lobe, or in both, or 
 in the central region of the cerebellum ; and such 
 lesions may co-exist with similar hasmorrhage in any 
 one or more of the following regions — the meninges, 
 the cerebral lobes, the corpus striatum, the optic 
 thalamus, the cortical substance of the brain, the lateral 
 ventricles, and the pons. 
 
 Heemorrhage of the pons is a very serious con- 
 dition, and the gravity of the case is again in direct
 
 46 ABNORMALITIES OF THE VASCULAR SYSTEM. 
 
 proportion to the size of the hasmorrhage. It is not 
 very unusual to find two, three, or even four mihary 
 ha3morrhages in the pons, and yet hfe has been pro- 
 longed. In some cases the blood is contained in the 
 pons itself, and the symptoms, of course, vary accord- 
 ing to the exact position of the hasmorrhage. The 
 blood, however, may find an exit into the fourth ven- 
 tricle, or at the inferior surface of the pons itself, or 
 in both directions in the same case ; or, again, it may 
 break into the crus cerebri on one side, or both, or 
 into the crura cerebelli. 
 
 Haemorrhage may also occur in one or both of 
 the crura cerebri, and perhaps specially in the locus 
 niger. 
 
 The two following cases are instances of haemorrhage 
 into the pons : — 
 
 Woman, aged 73, with purpiu\a. A little dark 
 fluid was smeared on the outside of the right hemi- 
 sphere. In the right lateral ventricle was a ragged 
 opening in the optic thalamus, from the rupture of a 
 vessel. Almost all the central part of the right hemi- 
 sphere was broken down by the blood, and the left 
 ventricle was filled with fluid blood, from rupture of 
 the septum. The pons, on transverse section, showed 
 five or six small extravasations in its substance. 
 
 Man, aged 45, with purpura. A large clot extended 
 over almost all the convex surface of the right cerebral 
 hemisphere. On making sections of the brain, a small 
 clot was found in the posterior angle of the left lateral 
 ventricle, and one about the size of a nut in the anterior 
 portion of the corpus caUosum. A very small clot in
 
 ABNORMALITIES OF THE VASCULAR SYSTEM. 47 
 
 the right optic thalamus. Both corpora striata hcaUhy. 
 A small clot in the posterior portion of the third 
 ventricle, the blood passing through the iter a tertio 
 ad quartum ventriculuni, and distending the fourth 
 ventricle, making its way romid to the lower portion 
 of the cerebellum. The medulla oblongata was healthy ; 
 but on section of the pons, the fibres of this organ 
 seemed to be laid alternately with horizontal clots, as 
 if all the vessels here had given way. 
 
 Hsemorrhage of the medulla oblongata is also rare. 
 Death occurs very rapidly under such circumstances, 
 but even then never quite suddenly. Sudden death, 
 unless induced by certain poisons, as prussic acid, is 
 always due to disease of the heart. No brain lesion, 
 however intense and however rapidly fatal, ever in- 
 duces an absolutely sudden fatal event. 
 
 Hsemorrhage into the fourth ventricle seldom, if 
 ever, results from the breaking through of the blood 
 from the medulla oblongata. Death, in haemorrhage 
 into this latter organ, is too rapid for that. It com- 
 monly arises from blood that has found its way in the 
 ordinary channel from the lateral ventricles, or the 
 third ventricle, or else from the giving way of the 
 substance of the cerebellum or of the pons. 
 
 The conditions that precede cerebral haemorrhage, 
 some of which cause it, whilst others are coincident 
 with it, are : 
 
 (1) Blows or wounds, mental alienation, and 
 epilepsy. The two latter probably depend on the 
 same conditions that predispose to or excite the cerebral 
 haemorrhage.
 
 48 ABNORMALITIES OF THE VASCULAR SYSTEM. 
 
 (2) Morbus cordis, hypertrophy, fatty heart, 
 fibrinous concretions in the heart, valvular disease, 
 disease of the origin of the aorta and of vessels. 
 
 (3) Diseases of the respiratory organs, acting only 
 indirectly, and leading mainly to hasmorrhage from 
 veins or sinuses. 
 
 (4) Diseases of the digestive organs ; hypersemia 
 of stomach, intestines, and liver (?) ; suppression of 
 hremorrhoidal flux. 
 
 (5) Diseases of the kidney, especially the small 
 granular kidney, and this particularly when found in 
 connection with rigid cerebral arteries and hypertrophy 
 of the left ventricle of the heart. 
 
 (6) Diseases of the sexual organs ; arrest of men- 
 struation ; venereal excess, especially in elderly people. 
 
 More rarely rheumatism, gout, and lead-poison. 
 
 In the following cases of Calmeil the effects on the 
 brain of recent hemorrhage, and of hsemorrhage of 
 older standing, are well seen. 
 
 He gives a resume of fifteen cases : 
 
 In 3 there were old cicatrices on the right side of 
 the brain ; in 3 on the left side ; in 2 in the pons. 
 
 In 3 the spots of encephalitis with clot were 
 situated on each side of the median line. In one of 
 these cases the blood had filled the cavities of the 
 lateral ventricles. 
 
 In 3 the spots were of the right lobe only ; in 2 of 
 the right lobe and the right lateral ventricle ; in 2 of 
 the right lobe and both lateral ventricles. 
 
 In 1 the lesion was in the left cerebral lobe only ; 
 in 1 in the left lobe and both lateral ventricles.
 
 ABNORMALITIES OF Tllh] VASCULAR SYSTEM. 49 
 
 III 4 ha3moiTliage existed in the pons, as well as 
 ill the brain. 
 
 In 3 in the cerebellum alone. In two of these cases 
 the blood was found in the fourth ventricle. 
 
 In 2 other cases it existed at one and the same 
 time in the cerebellum and cerebral hemispheres. In 
 both blood existed in the cavity of the ventricle of the 
 cerebellum. 
 
 In 5 the nervous substance of the spots was 
 moderately softened ; in 5 much softened ; in 5 softened 
 or disintegrated. 
 
 The spots of encephalitis with clot were examined 
 microscopically in nine cases. They have never shown 
 anything but fibrinous elements, liquid or scarcely 
 coagulated globules of blood, hiematosin, and cerebral 
 fibres detached from each other, when the patient 
 had only survived the attack from two to eight hours. 
 In all these cases the clot only contained the ele- 
 ments of blood, and the cerebral fibres and lumps 
 of nerve substance had been sometimes dragged 
 alonu: in the midst of these elements. The cerebral 
 vessels were sometimes filled with blood in the neigh- 
 bourhood of, or at a certain distance from, the morbid 
 spots. 
 
 The recent softened spots were not constituted 
 otherwise than those which were less soft ; they con- 
 tained only more liquid librine and more serum. 
 
 In all the cases in which the patients had survived 
 tlie extravasation of blood beyond twelve to fifteen 
 hours, the spots contained molecular granules, and 
 numerous granular cells, mixed with the products 
 
 E
 
 50 ABNORMALITIES OF THE VASCULAR SYSTEM. 
 
 above mentioned, namely, tlie elements that constitute 
 the blood. 
 
 The clot, as well as the surrounding walls, con- 
 tained granular cells and granules. 
 
 In cases of this kind the nerve substance was often 
 broken into particles, and more or less disintegrated. 
 
 The calibre of the vessels of the spots was some- 
 times considerable. 
 
 In observation 177, where the case was one of 
 traumatic ha3morrhage, the inflammatory spots con- 
 tained a good many pus globules, independently of the 
 products which we have generally found in patients 
 who have lived for some days. 
 
 In eleven cases of non-recent haemorrhage, there 
 were found in 4, local spots in the two cerebral 
 hemispheres only ; in 2, in the cerebral hemispheres, 
 the cerebellum, and the pons ; in 2, in the cerebellum 
 and the cerebral hemispheres ; in 2, in the cerebral 
 hemispheres and the pons; in 1, in the right cerebral 
 lobe only. 
 
 In the cases in which the cerebral hemispheres were 
 also injured, there were found on the right side 5 spots in 
 one cell, 5 in another, 1 in three cases ; on the left side, 3 
 spots in one case, 2 in two, more than 20 small spots in 
 another. When the brain and cerebellum were injured 
 simultaneously, the number of the spots was 5 in one 
 case, 3 in the other. When the brain, cerebellum, 
 and pons were injured simultaneously, the number of 
 spots was more than 5 in one case, and of an undeter- 
 mined number in the other. When the brain and 
 pons were alone affected, the number of the spots was 
 12 in one case, 7 in the other.
 
 ABNORMALITIES OP THE VASCULAR SYSTEM. 
 
 51 
 
 The walls of some spots were still softened in three 
 or four cases. Some spots, in three cases, contained 
 natural blood. In almost all the cases the principal 
 spots were in the state of cellular cicatrix. 
 
 Haemorrhage of the spinal cord is rare. It is more 
 common in the upper part of the cord than in the 
 lower. The cord is generally swollen in the region 
 occupied by the haemorrhage. The lesion is commonly 
 found in the grey matter in the centre of the cord. 
 Around the seat of hiemorrhai:ye the cord softens, some- 
 times without any preceding myehtis, but often as the 
 result of inflammatory action. Occasionally, and much 
 more rarely than in the brain, there is found a cyst- 
 like false membrane round the hrcmorrhage. In 
 cerebral haemorrhage the dura mater is more liable to 
 haemorrhage than the pia mater, though less vascular ; 
 the cortical substance less liable to haemorrhast'e than 
 the medullary, yet more vascular ; the corpus striatum 
 more liable than the optic thalamus, which is equally 
 vascular. 
 
 Gintrac, in 751 recorded observations of haemor- 
 rhage of the nervous system, found — 
 
 Haemorrhajrc of the menino'es 
 
 „ „ middle lobe of l)raiu 
 
 „ „ . pons and peduncles 
 
 5, „ corpora striata . 
 
 „ „ cerebellum 
 
 Corpora striata and optic thalami 
 Ventricles (septum and plexus) 
 Cortical substance of tlie brain 
 
 Optic thalami 
 Posterior lobes of brain 
 
 . 172 
 
 times. 
 
 . 127 
 
 5? 
 
 . 76 
 
 ?? 
 
 . 72 
 
 ?? 
 
 . 55 
 
 55 
 
 48 
 
 55 
 
 . 46 
 
 55 
 
 . 45 
 
 55 
 
 38 
 
 55 
 
 . 33 
 
 55 
 
 E 2
 
 OZ ABNORMALITIES OF THE VASCULAR SYSTEM. 
 
 Spinal cord . . . . .19 times. 
 
 Anterior lobes of brain . . . . 17 „ 
 Medulla oblongata ..... 2 „ 
 Corpus callosum ..... 1 „ 
 
 III. V^UIIETIES IN THE AMOUNT OF BlOOD SUPPLY TO THE 
 
 Brain and Spinal Cord. 
 
 It is scarcely necessary to do more than mention 
 the fact of this variation. The proof of its possibihty 
 is due to the observations and experiments of men of 
 our own day — Dr. Burrows, Dr. Symonds, and others. 
 We meet with ana3mia from various causes, and hyper- 
 a3mia active and passive, general and local. Ana3mia 
 of the nervous centres is often only dependent on 
 general anaemia. It may, however, occur when the blood 
 itself is normal, and then it is due either to plugging 
 of vessels, to any condition that interferes with their 
 calibre, or to the pressure of tumour or of abscess ; in 
 all which cases the anaemia will be local, and the 
 venous tissue will eventually pass, more or less, into a 
 state of white softening ; or it will be general over the 
 wdiole surface of the brain, from deficient heart action, 
 or over one hemisphere, from pressure on the common 
 or the internal carotid by tumour &c. Besides the 
 general pallor of the brain, however, and the extreme 
 whiteness of the white matter, there is little to be seen 
 in such cases, except where the anaemia has been not 
 only general but of long duration. Under such cir- 
 cumstances, there is often some atrophy of the whole 
 organ, willi compensathig increase of cerebro-spinal 
 fhiid. In one case I have met with this condition in a 
 very extreme form, the atropliy of the wliole brain
 
 ABXORMALITIES OF THE VASCULAR SYSTEM. 53 
 
 having proceeded to such an extent that tlie organ re- 
 sembled the brain of clironic senile dementia, althougli 
 the mental faculties had been preserved until within a 
 few days of death. This atrophy is frequently seen over 
 spots of tlie brain, where the interference with the 
 blood supply has not been complete. When it occurs 
 at the surface of the brain, there is no apparent altera- 
 tion in the shape of the cerebral surface until the pia 
 mater and the arachnoid has been stripped off, the 
 depression caused by the atrophy being filled in by the 
 cerebro-spinal fluid. 
 
 But cerebral anaemia owns other causes. It may 
 be connected with general ana3mia, and be caused by 
 inanition, by dyspepsia, an indirect mode of inducing 
 inanition, or by a drain on the sj^stem, such as 
 menorrhagia and other exhausting discharges. The 
 circulation through tlie brain is interfered wdtli by 
 the pressure of clot, of serous effusion, or of intra-cranial 
 tumour. Venous stasis, such as may be met with in 
 aggravated cases of heart disease, must impede arterial 
 circulation. The same phenomenon may be induced 
 by mental emotion, and notably by shock ; and, lastly, 
 the presence of an excess of the products of waste of 
 tissue in the blood will lead to a similar condition. 
 
 Hypersemia, that is active and general, will depend 
 on hypertrophy of heart ; and this condition is so often 
 met with in connection with small granular kidney, that 
 the state of the brain may be complicated with those 
 changes in the structure of the smaller arteries that 
 often accompany, if they do not depend on, this renal 
 abnormaUty. The morbid appearances are similar,
 
 54 ABNOEMALITIES OF THE VASCULAR SYSTE^tl. 
 
 whether the chanQ;e be i^eneral or local, viz. a larsre 
 number of vascular puucta on transverse section of 
 the white matter of the brain, and in spots, especially 
 where the hyperosmia has been more localised, a sieve- 
 like appearance of the nervous matter, the tissue being 
 the seat of numerous little depressions, due to the 
 pressure exercised upon it by the dilated vessel. 
 Added to this, the calibre of the vessels may be 
 permanently altered, constant dilatation having given 
 rise to a persistent enlargement of the vessel. This 
 condition was found by Van der Kolk in the vessels of 
 the medulla oblongata in patients who had died of 
 epilepsy, the dilatation having probably been the 
 consequence of the previous contraction of the arteiies, 
 the first factor in the series of epileptic phenomena. 
 This, however, is not found in all epileptics, and, where 
 it is, is doubtless the result of the attack rather than 
 the cause. 
 
 Passive hyperasmia is more common, and is caused, 
 in a word, by any obstruction to the flow of blood 
 through the cerebral veius and sinuses. Mitral re- 
 gurgitation, mitral stenosis, tumour in the neighbourhood 
 of and pressing on the vena cava superior, the jugular, 
 &c., disease of one of the important sinuses, any form 
 and every degree of suffocation, even in some persons 
 stooping or hanging the head down, may all cause 
 general or local congestions of the brain, that can bo 
 recognised post mortem, if only the skull be opened 
 before any other part of the body. 
 
 These appearances will vary according to the position 
 and the de<]^rcc of the cono;estion. The cortical
 
 ABNORMALITIES OF THE VASCULAR SYSTE:\I. 55 
 
 substance may be generally injected, and more or less 
 discoloured ; the corpora striata may be of a violet 
 colour ; the white substance of the brain may look as if 
 it were sanded with little drops of blood ; the injection 
 may penetrate the pons ; the vessels of the pia mater 
 may be engorged, the internal surface of the dura 
 mater furrowed by capillary arborisations ; the sinuses 
 may stand out with peculiar prominence, filled with 
 venous blood ; and at a stage further we may meet with 
 extravasations either into the tissue of the brain itself 
 or into the ventricles, or on the surface of the hemi- 
 spheres ; or, again, the congestion may have been the 
 starting-point of a diffuse inflammation of the external 
 layers of the grey matter of the convolutions, or even 
 of a more complete encephalitis ; whilst in cases some- 
 what rare the cerebral sinuses may give way at the 
 spot where the blood-pressure is most intense. 
 
 The incrustation of the capillary vessels with 
 granules and granular cells in congestion followed by 
 inflammation of the cortical tissue will be noticed under 
 tlie head of ' Inflammation.' 
 
 The spinal vessels may be distended even to an 
 extreme extent without exercising a proportionate 
 pressure upon the cord. The causes that have been 
 mentioned as influencing spinal congestion are gi;eat 
 muscular efforts, exposure to a hot temperature, 
 especially to the sun's rays, some epidemic influence in 
 the newly born, suppression of the evacuations, par- 
 ticularly of the catamenia, irritation of neighbouring 
 organs, venereal excess, and the rigors of ague. It is 
 certain, however, that temporary [)aralysis may follow 
 spinal congestion.
 
 56 ABNOEMALITIES OF THE VASCULAR SYSTEM. 
 
 Desnos describes a very peculiar case of paralysis, 
 with rotation of the head and lateral deviation of the 
 eyes, following a condition of intense congestion (with- 
 out other lesion) of the hemispheres, optic thalami, 
 corpora striata, cerebellum, peduncles, pons, and 
 medulla oblongata. 
 
 Calmeil's account of the pathological anatomy of 
 cases of intense cerebral congestion of temporary 
 duration is of great interest. 
 
 In three cases the cranial bones were notably in- 
 jected ; in three the vessels of the dura mater were 
 congested ; in one case there was fibrinous coagulation 
 in the longitudinal sinus ; in one the internal surface 
 of the dura mater was furrowed by capillary arborisa- 
 tions ; in two the cavity of the arachnoid contained liquid 
 blood and bloody humidity ; in four the cerebral pia 
 mater was generally congested ; in three cases it was 
 reddened by extravasated blood ; in one the pia mater 
 adhered in spots to the subjacent convolutions ; in one 
 these convolutions on the right side were swollen ; in 
 four the cortical substance of the brain was generally 
 injected and more or less coloured by heematosin ; in 
 two cases it was injected, and much coloured on the 
 right side ; in one it was of a yellow colour ; in seven 
 the* white substance of the brain was injected, and, as 
 it were, sanded with little drops of blood ; in two the 
 corpora striata were of a violet colour ; in four the 
 pia mater of the cerebellum was tinted with violet 
 l3y ha^matosin, or by suffusion of blood ; in three, in- 
 jected in its vessels ; in two the injection had penetrated 
 into the pons ; in one the sinuses of the spinal cavity
 
 ABXOEMALITIES OF THE VASCULAR SYSTE.M. 57 
 
 were engorged with blood ; in two cases tliere lind 
 occurred efTusions of blood inider the spinal arachnoid. 
 
 Consult on these subjects — 
 
 Hammond on ' The Nervous System.' i 
 
 Gintrac, 'Maladies de I'Appareil nerveux.' 
 
 Rindfieisch, ' Path. Anatomy.' 
 
 "Wilks, ' Path. Anatomy.' 
 
 Jaecoud, * Pathologie interne.' 
 
 Rokitansky, ' Path. Anatomy.' 
 
 Bright's * Med. Reports.' 
 
 Carswell's Plates. 
 
 Reynolds' 'System of Med.' Art: 'Apoplexy and Congestion 
 
 of the Brain.' 
 Calmeil, ' Maladies inflammatoires du Cerveau.' 
 Beale on * Kidney.' 
 Liddell on ' Apoplexy.' 
 Lionville on ' Aneurism.' ' 
 Th. von Dusch, * New Syd. Soc' * Thrombosis of Cerebral 
 
 Sinuses.' 
 ' Lond. IIosp, Rep.,' vol. i. p. 350. 
 ' St. Barth. IIosp. Rep.,' 1872. 
 
 'Brit. Med. Jour.,' .Tune 13, 1874. 'Aneurism of Brain.' 
 'Med. Record,' vol. i. 2G.3. 'Sclerosis of Arteries.' 
 * Med. Record,' vol. i. 472. * Congestion of Brain.'
 
 58 
 
 LECTUEE III. 
 
 INFLAMMATION. 
 
 Dura Mater. — Inflammation of the dura mater (pachy- 
 meningitis) is scarcely ever general, although the whole 
 of the convexity may be involved at one time. 
 
 It may be purulent or non-purulent. 
 
 It arises from a great variety of causes. Blows or 
 falls on the head may lead to the purulent, but much 
 more frequently to the non-purulent variety. Syphilitic 
 caries of the bone may lead to either form. The in- 
 flammation of the dura mater, consecutive to disease 
 of the petrous portion of the temporal bone, is local 
 and generally purulent, whilst not unfrequently the 
 portion of membrane attacked becomes gangrenous. 
 The vasa propria of the dura mater are specially 
 liable to thrombosis. In the non-purulent form the 
 new formation, the result of the inflammation, becomes 
 very quickly the seat of vessels, and is composed of 
 several layers ; those nearest the dura mater being 
 composed of compact lustrous connective tissue fibres, 
 almost as dense as the dura mater itself; whilst the 
 layer further removed from the dura mater is rich in 
 cells, with small and narrow vessels, and the layer 
 nearest the arachnoid often firmly uniting the arachnoid
 
 IXFLAMMATIOX. 59 
 
 to the dura mater, is remarkable for very large capil- 
 laries. It is from rupture of these vessels that the 
 haemorrhage spoken of in the last Lecture occurs ; the 
 blood being not unfrequently locked up in the lacunaj 
 of false membrane poured out beneath the dura mater. 
 From further alteration of these inflammatory products 
 result the lamince of bone that are sometimes met with 
 on the visceral surface of the cranial dura mater, espe- 
 cially in the falx cerebri and cerebelli, and still more 
 frequently on the dura mater spinalis. So far as I 
 know, this ossification is never preceded by the forma- 
 tion of cartilage. The bone, true bone as it is, is 
 formed from fibrous tissue, this fibrous tissue being a 
 further development of the inflammatory exudate from 
 the vessels of the dura mater. In old cases of chronic 
 spinal meningitis, such lamina) of bone are met Avith, 
 not continuous, but sporadically arranged over portions 
 of the cord. 
 
 An inflammation of tlie dura mater, ori^-inallv 
 non-purulent, may become purulent by the occurrence 
 of haemorrhage, as diffuse suppuration of the whole 
 neo-membrane may occur as the result of the pressure 
 exercised upon the eff'used product by the haemorrhage. 
 
 Except as a complication of tumour, or traumatic 
 lesion, inflammation of the dura mater at the base of 
 the skull is rare. 
 
 The dura mater may be perforated by sloughing 
 ulceration, and in this case the condition almost 
 invariably depends on tlic extension to tliis membrane 
 of disease commencing in the bone in its immediate 
 neighbourhood, or upon the irritation either of a wound
 
 60 INFLAMMATION. 
 
 or of a foreign body pressing upon the dura mater. 
 This foreign body is not unfrequently a portion of the 
 cranial bones depressed on the subjacent membrane by 
 some accident. 
 
 The spinal dura mater, liowever, may be secondarily 
 attacked by the extension to it of suppurative disease 
 of the bodies of tlie vertebra3. 
 
 For inflammation of tlie sinuses of the dura mater, 
 see last Lecture. 
 
 Inflammation of tlie Arachnoid. — It is not always 
 possible to isolate diseases of the arachnoid from 
 abnormalities of the under-surface of the dura mater ; 
 and still less possible is it to separate morbid conditions 
 of the arachnoid from those of the subjacent pia mater 
 so closely blended with it. 
 
 But we do find various degrees of thickening of the 
 arachnoid, with sometimes deposit of lymph on the 
 upper or under surface of its visceral layer, if not of 
 both. 
 
 The arachnoid may appear milky from two causes : 
 either from the presence beneath it of slightly turbid 
 fluid, such as the cerebro-spinal fluid in not quite a 
 normal condition, or from the faintest commencement 
 of the thickening of the membrane itself. 
 
 Thickening and opacity of tlie arachnoid occurs 
 under somewhat varied conditions ; thus it is not 
 uncommonly found — 
 
 (i) In cases of small granular kidney. 
 
 (ii) In cases of delirium tremens, with epileptiform 
 attacks. In one such case I have found chronic 
 thickening of the arachnoid of the convex surface of
 
 INFLAMMATlOxV. Gl 
 
 the cerebral hemispheres, with opaque spots and plates 
 quite distinct from the Pacchionian bodies. 
 
 (iii) There may be very chronic thickening of tliis 
 membrane in cases of senile dementia. In such cases, 
 as in many other instances of chronic thickening, there 
 is often an atheromatous condition of the cerebral 
 vessels. 
 
 (iv) In heart disease ; where we sometimes fmd 
 patches of thickening of the arachnoid at the convexity. 
 
 (v) In cancer, especially of the stomach and liver ; 
 generally associated with atheroma of the cerebral 
 vessels. 
 
 (vi) In cerebro-spinal meningitis ; in which the 
 arachnoid of the convexity is not free from disease, 
 although the membrane of the base is chiefly attacked. 
 
 (vii) In tuberculous cases, in which thickening of 
 this membrane is generally associated with effusion of 
 lymph and with tubercle of the pia mater. This 
 abnormality is, in most cases, confined to the base, but 
 occasionally the convexity participates ; and sometimes 
 the convexity is alone attacked. 
 
 (viii) In cases of diseased spinal cord, as, for instance, 
 where there has been tubercle of the cord ; but the 
 plates on the spinal arachnoid, which may be soft or 
 cartilaginous or osseous, may be the result of very 
 chronic inflammation, not associated with tubercle. 
 
 (ix) In cases of arachnitis, consequent on disease ot 
 the bone or dura mater — as idceration, haemorrhage, 
 cancer, tubercle, &c. — causing pressure on the arachnoid 
 from above downwards ; or from pressure from below 
 upwards, as from a clot in the })ia mater.
 
 62 INFLAMMATION. 
 
 (x) In cases of arachnitis occurring after severe falls, 
 with or without fracture of the skull. 
 
 (xi) Thickening of the arachnoid is met with also 
 where no cause can be discovered, as in the following 
 case : — 
 
 A woman died without any cerebral symptoms. 
 There was great thickening and toughness of tlie 
 arachnoid and pia mater over the cerebellum, pons, and 
 medulla oblongata. The condition was evidently of 
 Ions; standing;. The floor of the fourth ventricle was 
 in a similar condition, except that here the thickening 
 was slightly nodular. A very large amount of fluid 
 in tlie ventricles, with some softening of the third 
 ventricle ; brain otherwise firm. Vessels healthy. 
 
 Arachnitis^ ivith efjusion of Lymi^li or of Pas. — This 
 is generally a further stage of mere thickening and 
 opacity ; certainly the effusion of inflammatory products 
 never occurs without some decided opacity at least 
 of the arachnoid. 
 
 The effused product is most frequently found on 
 the under-surface of the arachnoid, and it is probable 
 that under these circumstances the arachnoid is only 
 secondarily affected, the pia mater being the tissue 
 primarily inflamed. 
 
 This is especially seen to be the case in tuberculous 
 and in cerebro-spinal meningitis. In the former case, 
 indeed, the arachnoid, when inflamed, seems only so in 
 direct ratio and extent with the pia mater, and the pia 
 mater may be affected whilst the arachnoid is almost 
 wholly or wholly free. 
 
 We sometimes, however. And the upper surface of
 
 INFLMIMATIOX. 63 
 
 tlie visceral araclmoid coated witli lymph, from irritation 
 reflected ou it from above, as from various abnor- 
 malities of the dura mater. In such circumstances the 
 pia mater may be liealthy. The upper surface of tlie 
 visceral araclmoid of the convexity may be covered 
 with lymph, whilst the subjacent pia mater is in a 
 similar condition, as is seen sometimes after falls on the 
 head without fracture of the skull. Occasionally also 
 lymph is found on the upper surfoce of this membrane 
 under circumstances wliicli can only be considered due 
 to inflammation. This was seen in the case of a woman 
 w^lio died with light hemiplegia and softening of the 
 brain ; the two cerebral hemispheres were united 
 together over the corpus callosum by soft adhesions on 
 the arachnoid. 
 
 I published a case in ' St. George's Hospital Eeports,' 
 Vol. 4, of a young man who had died of an attack of 
 haemorrhage from rupture of the right middle meningeal 
 artery ; the dura mater all over the convex surface of 
 the hemispheres was somewhat adherent to the sub- 
 jacent arachnoid, whilst the arachnoid was thickened 
 and yellow all over. This patient liad been under a 
 surgeon's care a year before with great pain over the 
 whole of the upper part of the head, and had been 
 treated with entire success with iodide of potassium. 
 
 Although it is difficult to separate the abnormahties 
 of the pia mater from those of the arachnoid, yet it is 
 generally easy to speak with certainty of these abnor- 
 mahties as having their origin in the pia mater. 
 
 1. Meningitis of the convexity is much less often 
 accompanied with softening of the central portion of
 
 64 INFLAMMATION. 
 
 the brain than meningitis of the base. Hypera3mia of 
 the vessels is seen first, and there generally results an 
 effusion of pus or lymph in the sub-araclmoid spaces. 
 This may be partial — over a spot, for instance, no larger 
 than half-a-crown — or general over the whole convexity. 
 Sometimes, though rarely, both convexity and base are 
 attacked in the same manner. The pia mater may be 
 affected very intensely, and the arachnoid hardly at all. 
 The congested vessels and the effused products are 
 seen occupying the sulci between the convolutions. 
 As a general rule, meningitis of the convexity is not 
 associated with tubercle, whilst meningitis of the base 
 is tuberculous ; but to this there are many exceptions. 
 Thus in one case ' a good deal of lymph, mixed with 
 granules of tubercle, was found on the convex surface 
 of the left hemisphere. A similar condition over base. 
 The lymph seemed to dip in between the convolutions, 
 following the course of the pia mater.' 
 
 Again, in another case, ' the arachnoid and pia 
 mater, at the upper parts of the hemispheres, contained 
 much clear fluid, but were natural ; between the 
 hemispheres of the brain, in the longitudinal fissure, 
 were many miliary tubercles ; and at the lower part of 
 this fissure, the opposed hemispheres were adherent to 
 each other by means of a mass of scrofulous matter, 
 equal in size to a hazel nut. A small portion of a 
 similar growth was found at the upper part of the 
 cerebellum, connected with the arachnoid.' 
 
 As an instance of non-tuberculous meningitis of 
 the base : 
 
 ' Woman. a2;ed 18. On tlie under-surface of 
 the arachnoid, along the course of the blood-vessels,
 
 INFLAMMATION. 65 
 
 inucli soft material existed at the upper and lateral 
 parts of the cerebral liemispheres ; and at the base of 
 the brain, at a point chiefly corresponding to the base 
 of the third ventricle, and the pons, the membranes 
 Avere adherent to the cerebral tissues by means of a 
 thick deposit of the same soft material.' 
 
 If the disease is of slight intensity, and over a 
 region of very limited extent, the effused products may 
 be reabsorbed. Tlie only abnormality attending this 
 condition may be a slight atrophy of the cerebral con- 
 volutions immediately subjacent to the spot of thickened 
 membranes, and a corresponding increase of cerebro- 
 spinal fluid at the same spot. 
 
 It will be seen in a future lecture how a thickened 
 state of the pia mater is constantly found in cases of 
 general paralysis of the insane. 
 
 Whether meningitis ever occurs independently of 
 syphilis, rheumatism, alcoholic poisoning, tubercle, 
 anaemia, or mechanical irritations is at least an open 
 question. Dr. Bright, however, gives a beautiful plate 
 of puriform fluid beneath the arachnoid. If cerebro- 
 spinal meningitis is excluded, the only case I have known 
 was that of a young lady, whose mother was rheumatic, 
 although she herself had never suffered from rheuma- 
 tism affecting the joints or the heart. But it certainly 
 occm's from irritation from above downwards, and 
 that over a space corresponding to the extent of the 
 irritating lesion. Thus it is not unusual to find thick- 
 ening of this membrane over surfaces subjacent to 
 diseased cranial bones, ulcerated dura mater, &c. ; or 
 pressed upon by exostoses or other tumours from 
 
 F
 
 66 INFLAMMATION. 
 
 above: and the St. Bartholomew's Museum contains a 
 specimen of the pia mater opaque and indurated over 
 the convexity of the brain and between the convohi- 
 tions, in a case of hasmorrhage outside the dura mater. 
 This non- tuberculous meningitis may be chronic. Plate 
 1 is taken from a specimen of this kind, from the 
 collection of Van der Kolk in the Oxford Museum. 
 
 2. Cerebro-sjnnal Meningitis. — Sometimes sporadic, 
 generally epidemic. The post-mortem appearances 
 are not always the same, even where death occurs at 
 precisely the same stage of tlie disease. 
 As an instance of the sporadic form — 
 ' Man, aged 28. Dura mater healthy. On re- 
 moving the dura mater a yellow spot, the size of 
 half-a-crown, was seen beneath the arachnoid on the 
 anterior convolutions on the left side, close to the 
 central division. This was composed of lymph effused 
 between the arachnoid and the pia mater. Tlie whole 
 of the convex arachnoid was milky in appearance. At 
 the base of the brain the whole of the region compre- 
 hended in the circle of Willis was covered with a 
 compact thick yellow Mse membrane, in which the 
 nerves were imbedded. In a very slight degree it 
 existed in the fissures of Sylvius, but it became intense 
 at the iufundibulum, covered the pons, the medulla 
 oblongata, and part of the cerebellum, and ran up 
 between the lobes of the cerebellum. Many puncta 
 on section of the brain. Much turbid Iluid in the 
 ventricles, and the lateral, tlie third, and the fourth 
 were lined in their lower part by a similar yellow 
 coating of lymph. The septum, and much of the 
 central white matter around the ventricles were creamy.
 
 Plate 1 
 
 '^ 
 
 t 
 
 '^ 
 
 'J M . U M £ N I N G
 
 IXFLAMMATIOX. 67 
 
 Choroid plexus very tortuous, and covered witli yellow 
 lymph. The spiual cord was covered on its cervical 
 portions with yellow lymph.' 
 
 The most usual appearances are great vascularity 
 of the dura mater, both of the brain and cord, and 
 sometimes extravasation of blood outside the spinal dura 
 mater. The diploc of the bones is often highly in- 
 jected. Great congestion of the cerebral sinuses. The 
 pia mater and the arachnoid are injected, sometimes 
 more or less thickened ; the layers of the arachnoid 
 may be adherent by means of false membrane. Some- 
 times there is fluid in the cavity of the arachnoid, 
 especially in the spinal canal. Exudation is very fre- 
 quently found beneath the arachnoid : very often this 
 is purulent, and occupies very various seats. It may 
 be situated over the whole convex surface of the brain, 
 and at the base of the brain, and over a considerable 
 portion of the spinal cord : or it may occupy a very 
 small portion of the convexity of the brain, or more 
 frequently it is found over a great part of one surface 
 of the cord, especially the posterior. In the lower 
 portion of the cord the whole organ may be surrounded 
 by pus. There is often a turbid, serous, or purulent 
 exudation in the lateral ventricles of the brain, and 
 the vessels of the choroid plexus are much engorged. 
 
 The condition of the brain and spinal cord has 
 seemed to vary in different epidemics. Sometimes the 
 organs are healthy, or nearly so ; in other cases the 
 external cortical layer is found adherent to the pia 
 mater, and is detached with it. In others, again, there 
 is simply hypersemia, or more or less induration ; but 
 
 ¥ 2
 
 68 INFLAMMATION. 
 
 softeniug is more comniou, varying mucli in degree, but 
 not unusually very general. 
 
 In Dr. Collins' cases, microscopical examination of 
 the exudation showed that it consisted of granular 
 debris, imbedded in which were numerous small 
 granular cells, chiefly circular in form, measuring about 
 4'oVo" ^f ^^^ ^^^^^^ ^^^ diameter, very similar in character 
 to pus corpuscles, save that they were much smaller 
 in size. He says, too, that 'Mayne long ago drew 
 attention to the fact, that the nervous matter seldom 
 suffered, and, when involved, was only so accidentally, 
 owing to the propagation of its disease from the 
 membranous investments. We can fully bear out this 
 testimony in the cases we have observed, both as 
 regards the brain and spinal marrow. The cords we 
 have examined with care, but in only one of them 
 could we find any evidence of disintegration under 
 the microscope. Specimens, how^ever, have been 
 submitted to the Pathological Society of Dublin by 
 Drs. B. M'Dowel and Hayden, in which the marks 
 of localised softenings of the spinal cord were present. 
 Softening of the substance of the encephalon, though 
 also uncommon, appears to be more frequent than the 
 corresponding condition of the cord. Allusion is here 
 made only to cases of wdiite softening, but Klebs, on 
 two or three occasions, in rnpid cases of cerebro-spinal 
 meningitis, has ibund foci of softeniug, varying in shade 
 from straw-colour to red in the centrum ovale, and in 
 each of these cases he has found indications of recent 
 endocarditis.' 
 
 3. Acute Basilar Meningitis. — This is said by Gintrac 
 to be sometimes non-tuberculous. It is certain that
 
 INFLAMMATIOX. G9 
 
 meningitis of tlie base, and of tlie base only, exists 
 when it is impossible to detect tlie granulations of 
 tubercle with tlie naked eye. This, however, is no 
 proof of its non-tuberculous origin. 
 
 For practical purposes it may be considered either 
 a syphilitic or a tuberculous meningitis ; and when 
 tuberculous, it is generally associated with the presence 
 of tubercle elsewhere, so generally that the rule is 
 almost without exception at all ages beyond early 
 childhood, though in the first five years of life the 
 exceptions are slightly more numerous. 
 
 With reference to the situation of tubercle, Dr. 
 Green's account is very clear: 'The sheaths of the 
 arteries, especially in the fissures of Sylvius, are the 
 preferred seats of development. The tubercles are 
 placed as lateral projections, singly or united into small 
 groups upon the larger branches, while upon the more 
 minute branclies and the almost capillary vessels they 
 present themselves as spindle-shaped varicosities, which 
 occupy the whole circumference of the vessels. Tliey 
 injure the lumen of the vessel, at first by pushing into the 
 tunica media and intima, and then by perforating them. 
 Tliis interference with the calibre of the vessels may 
 2;ive rise to comxestion and haimorrhai2;e : and if 
 active hypersemia supervenes, basilar meningitis is the 
 result.' 
 
 When this condition of meningitis is set up, the 
 whole of the base of the brain is often covered with 
 effused products, especially with a softish lymph or 
 pus, matting together all tlie nerves as they emerge. 
 
 Occasionally some portion of the convexity is 
 imphcated as w^ell, and it is not unusual for tlie convex
 
 70 INFLAMMATION. 
 
 surface of the cerebellum to be affected. There is 
 dryness of the arachnoid of the convexity. A venous 
 congestion of the pia mater there ; sometimes a little 
 lymph in the sulci, and occasionally, on removing the 
 pia mater, a small portion of the external layer of the 
 convolutions is removed adherent to it. Tubercle is 
 generally found not only along the fissures of Sylvius, 
 but coating a considerable space over the infundibulum 
 and the neiofhbourino- orsjans. 
 
 This abnormality of the pia mater is almost 
 universally associated with more or less distension of 
 the lateral ventricles with shghtly turbid fluid, and with 
 softening of the septum, and, indeed, of all the white 
 matter forming the roof and walls of the ventricles. 
 
 The third, fourth, and fifth ventricles may be 
 similarly distended and their walls softened. The 
 ependyma of the ventricles is thickened and raised into 
 small granular elevations by collection of cells. Some- 
 times small tubercles are seen on the velum interpositum. 
 
 Capillary haemorrhages of the cortical substance 
 are not unfrequently coincident with basilar meningitis. 
 
 Tubercles are very seldom found in the plexus 
 choroides, but they are met with in situations in which 
 there is no pia mater, as on the walls of the ventricles, 
 on the internal surface of the dura mater, the parietal 
 layer of the arachnoid, or the free surface of the 
 visceral arachnoid. 
 
 4. BydroceplLalus. — This may be acute or chronic. 
 I cannot agree with authors who draw a marked dis- 
 tinction between acute liydrocephalus and the condition 
 of the ventricles in tuberculous meningitis. It is said 
 by some thot acute hydrocephalus is a flux, and should
 
 INFLAMMATION". 71 
 
 show little or no trace of inflammation ; that it is best 
 described by the old term, ' Water-stroke ;' that it is a 
 flux caused by extreme fulness of vessels, especially if 
 the blood is spana^mic, as it may be in scrofula, 
 tubercle, cachexia, albuminuria, &c. ; and that this is 
 the connection between these conditions and acute hy- 
 drocephalus. This latter abnormality, in most cases at 
 least, seems not to be due to any impediment in the 
 course of the vense galeni, the passage of the blood being 
 generally found free from all obstacle. It is really 
 due to the inflammation of the ependyma, a condition 
 that may take place (piite by itself, without any im- 
 ■plication of other parts of the brain or membranes, 
 except indeed the portions of the brain immediately 
 subjacent to the ependyma itself. It is not absolutely 
 necessary that it should be associated with tuberculous 
 meningitis, but it very often is so, and in almost all 
 cases seems to depend upon the same causes. In a 
 word, acute hydrocephalus is generally tuberculous 
 meningitis, with the lining membrane of the ventricles 
 more implicated than is usually the case in ordinary 
 meningitis of the base. This inflammation of the 
 ependyma, with efiiision more moderate than in acute 
 hydrocephalus, is not an unusual appearance in several 
 conditions of brain disease. It may be found in chronic 
 hydrocephalus, in general paralysis of the insane, in 
 chronic mania, and sometimes also in melancholia. 
 
 An instance of this was seen in a man wlio died 
 with pulmonary abcessses. 
 
 Skull cap very thick. Dura mater very adherent 
 all along the superior longitudinal sinus. This sinus
 
 72 INFLAMMATION. 
 
 was empty. More than four ounces and a half of fluid 
 was collected from beneath the arachnoid. This mem- 
 brane was milky and slightly thickened everywhere. 
 Cerebral hemispheres tolerably firm, a little flattened 
 at the anterior portion. More tlian three ounces of 
 fluid in the lateral ventricles. Their cavities enlarged, 
 and walls almost diffluent. The third ventricle was 
 opened out by the pressure of fluid, and the soft 
 commissure destroyed. The hning membrane of the 
 lateral, third, and fourth ventricles was much thickened 
 and very granular, being quite rough to the touch. It 
 was impossible to detach it from the subjacent brains. 
 This granular condition was composed of granules,' 
 small cells, and a few exudation corpuscles. The 
 membrane surrounding the pituitary gland was thick 
 and white. Cerebellum healthy. Pons and medulla 
 oblongata rather soft. 
 
 5. This seems perhaps the most convenient place 
 to say something about chronic hydrocephalus, although 
 inflammation plays a less important part in its causation 
 than in the case of the acute condition. Still, a low 
 form of inflammation attacking the arachnoid lining of 
 the ventricles, during foetal life and in earliest infancy, 
 sometimes even later in life, is more often the cause of 
 this peculiar abnormality than lias been recognised by 
 some authors. Dr. Bright's plates of ' Cardinal ' are 
 well worth study on tliis subject. 
 
 I find few accounts of post-mortem appearances 
 that seem to justify the idea of external hydrocephalus. 
 Kindfleisch's account of the causation of the disease 
 appears to be wholly tlieoretical. lie says : ' The seat
 
 INFLA]\[MATION, 73 
 
 of tliis disease is the region of tlie cerebral veins of the 
 vertex along the longitudinal sinus ; the first result 
 heino: elono-ation of tlie veins and dilatation ; second, 
 oedema of the pia mater and efiusion of serous fhiid. 
 The gyri are pressed asunder, the sulci dilated. 
 Decrease of thickness in tlie hemispheres. Milky 
 clouding of tlie pia mater due to infiltration of colour- 
 less cells, and even afterwards a gradual fibrous trans- 
 formation.' 
 
 All this is little more than a description of what 
 occurs in atrophy of the brain or defective develop- 
 ment, ill which tlie cerebro-spinal fluid takes the place 
 of the atrophied convolutions ; and the membranes 
 over the convexity appear at first sight like a bladder 
 partly filled with water. Those cases of reputed ex- 
 ternal hydrocephalus, and of recovery after tapping the 
 head, were either instances of this atrophy of the brain 
 or of internal hydrocephalus, in which the pressure of 
 fluid from within had caused absorption of a large 
 amoimt of the brain substance, and the trocar had 
 passed not only through the bone and membranes, but 
 also through the thin layers of cerebral substance 
 surrounding the mass of fluid \vithin, or some sudden 
 accident had caused the rupture of this thin layer 
 of brain substance, and the fluid which originated in- 
 ternally had escaped through the rent to an external 
 situation. 
 
 It seems on the Avhole most in accordance with 
 
 experience to say that external hydrocephalus has no 
 
 existence, except in those rare cases in which fluid in 
 
 the cavity of the arachnoid is the result of ]ia3morrhage 
 
 nto the araclinoid sac.
 
 74 INFLAMMATION. 
 
 Chronic hydrocephalus of the ventricles is sometimes 
 a result of tlie acute disease, or, at any rate, is a con-' 
 sequence of inflammatory action. Dr. West, in his 
 sixth edition of his work on diseases of infancy and 
 childhood, says : ' I may further add that each year leads 
 me to estimate more highly the share of inflammation 
 of the Hning membrane of the ventricles in the produc- 
 tion of chronic hydrocephalus.' 
 
 In many cases, however, it is a simple flux depending 
 on some impediment to the flow of blood through the 
 vense galeni. It has been seen as the result of closure 
 of the fourth ventricle by a thickened arachnoid ; also 
 as a consequence of disease of the clioroid plexus, which 
 is sometimes tuberculous. 
 
 When not tuberculous, the surface of the choroid 
 plexus is found beset with numerous papillas, consisting 
 of a thick mantle of epithelial cells, and a central part 
 made up of the lumina of vessels. 
 
 A cystic condition of the choroid plexus may be 
 found without hydrocephalus resulting from it ; but a 
 very intense form of this disease would lead to a very 
 considerable effusion. 
 
 Plate 2 represents a very unusual condition of cysts 
 of the choroid plexus from the Oxford Museum. 
 
 It is easy to luiderstand how the reflux of the 
 venous circulation from the brain would be interfered 
 witli by a tumour attached to the choroid plexus, such 
 as is seen in specimen 811, one of Van der Kolk's, in 
 the same museum : ' in the left ventricle is a large white 
 tumour of moderate consistence, resembling brain 
 substance in appearance, but not springing from the
 
 r'cix M D 
 
 Pla'.e 2 
 
 F 
 
 
 
 r-;i 
 
 mnv-i,KX 
 
 
 
 Be-sf-ii Li-i 
 
 CYSTS OF CHOROID PLEXUS.
 
 INFLAMMATION. 75 
 
 brain, only loosely adherent to the choroid plexus. 
 There was no mania nor paralysis.' 
 
 The anatomical appearances of chronic hydrocephalus 
 vary according to the amoinit of fluid, and to some 
 extent, also, according to the period of life at which the 
 disease originated. 
 
 These appearances are, distension of the ventricles, 
 compression of their walls, and especially of the floor 
 of the ventricles, a very patent condition of the channels 
 which lead from one ventricle to another, thinning 
 or even unfolding of the superjacent convolutions, a 
 thickened ependyma, if the disease has had an inflamma- 
 tory origin. The state of the bones varies considerably; 
 either the sutures have never united, and a large portion 
 of the calvarium is not ossified ; or the union is less 
 firm than normal, with the interposition of many ossa 
 triquetra ; or the bones are much thinned ; or, lastly, 
 the bones are found either thicker than usual, or of the 
 normal density. 
 
 The pressure of a tumour may frequently, by 
 irritation, set up a certain amount of meningitis in its 
 neighbourhood. This, being generally very locahsed, 
 is only of importance if it implicates any nerves. As 
 a matter of fact, meningitis so caused does sometimes 
 thus implicate the optic nerves, and the low form of 
 inflammation spreading to them may lead to true optic 
 neuritis, or, by causing increase of connective tissue 
 growth in the nerve, induce atrophy. 
 
 6. Spinal Meningitis. — Very often spinal meningitis 
 occurs coincidently with cerebral, as in sporadic and 
 epidemic cerebro-spinal meningitis, and occasionally 
 also in the tuberculous form.
 
 76 INFLAMMATION. 
 
 The post-mortem appearances vary somewhat ac- 
 cording to the cause of the disease. It may be that 
 the disease lias been set up by lesion of the bones or 
 of the ligaments ; and we fmd corresponding altera- 
 tions in these organs, or the dura mater is thickened 
 and adherent to the bone, or gangrenous. The arach- 
 noid is less often primarily attacked than the pia mater, 
 but is sometimes the seat of opacities, and in chronic 
 cases even of cartilaginous or bony plates. The pia 
 mater is the most usual seat of inflammation. The 
 vessels are turgid, and there is effusion of clear, or 
 flocculent, or sanious, or purulent fluid. The spinal 
 cord may be somewhat compressed by the fluid and 
 its vessels empty ; or it may be injected, or softened, 
 or indurated ; and, lastly, it may in no way participate 
 in the disease of the membranes. 
 
 It is not very uncommon to find thickening of the 
 spinal meninges in cases of fatal tetanus. 
 
 Encephalitis. — This term will include inflammation 
 of any or all the contents of the cranium, except the 
 meninges and the nerves. Meningitis, however, is a 
 frequent complication. 
 
 It may be general, or at any rate difliised in many 
 spots over the various oigans contained in the cranium, 
 or it may be confined to one region, or to one organ. 
 The cortical substance alone, or the grey and white 
 matter in any one lobe, may be affected. If, however, 
 one lobe is attacked, the opposite corresponding one 
 will most probably suffer in unison, unless the inflam- 
 mation is from a local traumatic cause. The great 
 centres at the base of the brain, the corpora striata
 
 IXFLAMMATIOX. 77 
 
 and optic tlialaiiii, eillicr .singly or together, or Uio 
 crura cerebri, tlic cerebellum, the floor of the Iburth 
 ventricle, and the pons, may be the seat of this abnor- 
 mality. The whole of the medulla oblongata has been 
 said to have been so affected ; but this condition is 
 extremely rare. 
 
 The post-mortem appearances vary exceedingly, 
 according to the conditions under which the disease is 
 set up. They are partly recognisable by the naked 
 eye, and partly to be realised by high magnifying 
 powers. Of the first, the appearances vary according 
 to the stage of the disease at which the examination 
 is made, and also according to the chronicity of the 
 disease itself. Thus the lesions are : — 
 
 (i) Injection of the cortical substance, with or 
 without a certain friability of this substnnce, and most 
 commonly of the external layer. 
 
 (ii) Or injection of both white and grey matter ; this 
 condition of the white matter being evidenced by the 
 numerous bloody puncta on transverse section. 
 
 (iii) Spots or regions of induration, especially of the 
 grey matter. 
 
 (iv) Spots or regions of red softening. 
 
 (v) The formation of pus, either as one large abscess, 
 or in multiple abscesses. These abscesses may be 
 bounded by a cyst-wall, or may merge gradually into 
 regions of softening ; or they may cause bands of 
 secondary degeneration. 
 
 (vi) A gangrenous appearance, generally very 
 localised. 
 
 In connection with the iburth variety of this series
 
 78 INFLAMMATION. 
 
 is a form described by Dr. Moxon and others, and 
 named by him ' Congenital Encephahtis.' Its characters 
 are softened patches containing granule cells (which 
 represent fattily degenerated neuroglia cells), spindle- 
 shaped clear bodies, not provided with nucleus or 
 nucleolus, and caused, according to Virchow, by swell- 
 ing and severance of the axis cylinders of the nerve 
 tubercles. The proper tissue of the brain in these cases 
 is almost utterly destroyed by hyperplasia of the 
 neuroglia. 
 
 Taking these coarser varieties first, we find under 
 the head of injection some differences, according as the 
 disease is acute or chronic. In the acute form the 
 calibre of the capillaries is increased : there is some- 
 times an increase of the sub-arachnoid fluid both over 
 the convex surface of the hemispheres and in the 
 ventricles. 
 
 The vessels of the choroid plexus are often large ; 
 the white matter of the brain seems increased in 
 density, probably from pressure. This pressure is ex- 
 plained by the appearance of the vessels in the more 
 chronic form. There is often a tortuous condition of 
 the minute vessels ; sometimes they are aneurismal, 
 occasionally also they have given way,' and small 
 granules of ha^matine are found in the immediate 
 neighbourhood of vessels ; whilst the hemispheres show 
 on transverse section a cribriform appearance, from the 
 presence of numerous little holes, probably caused by 
 the pressure of the small vessels, enlarged during life 
 and contracted after death. 
 
 Of the spots of induration, an occasional form of
 
 INFLAMMATION. 79 
 
 degeneratiou that sometimes owns an inllammatory 
 origin, something will be said by-and-by, under the 
 head of Sclerosis. 
 
 Eed softening gathers its colour from minute 
 hsemorrhages ; but non -inflammatory softening, de- 
 pending only upon obstructed circulation, may be red 
 from hsemorrhages or from capillary congestion. The 
 softened mass is composed of pus, disconnected frag- 
 ments of nerve fibres, granular cells, and pigmentary 
 ganghon cells, but all the appearances hitherto sup- 
 posed to be characteristic of inflammatory softening 
 have been found in softening manifestly non-inflam- 
 matory ; so that I confess myself unable to determine, 
 by post-mortem appearances alone, whether a patch of 
 softening has depended on an inflammatory origin 
 or no. 
 
 Wlien abscess is formed, the pus comes partly 
 probably from proliferation of the neuroglia cells, but 
 mainly from the emigration of white cells from the 
 vessels. 
 
 Beyond the dej^ot of pus proper we meet with a 
 zone of cedematous saturation, by which both nucleus 
 and cell swell up. Calcification and excessive pig- 
 mentary infiltration may occur. Cerebral abscess is 
 generally encapsulated by a thin compact connective 
 tissue capsule. This capsule is formed from the neu- 
 roglia, and is composed from within the abscess out- 
 wards. It is composed of: (1) A layer of fatty 
 degenerated cells ; (2) A layer of germinal tissue, 
 which by its irregular thickness causes wave-like irre- 
 gularities of the surface. This merges into (3) very
 
 80 INFLAMMATION. 
 
 loose spindle-shaped tissue, which is stratified distinctly 
 parallel to the surface ; (4) fatty granular cells, making 
 a zone of yellow softening at the boundary of the 
 abscess membrane towards the brain. (Rindfleisch.) 
 
 The following case is an example of cerebral 
 abscess ; — 
 
 ' Man, 38. Dura mater healthy, except at a spot at 
 the upper and posterior portion of the middle right cere- 
 bral lobe, where it was very adlierent to the subjacent 
 tissues. The longitudinal sinus close to this spot was 
 full of a light-coloured clot. At this spot, and extending 
 forwards, and laterally over a space about two inches 
 square, the convolutions were flattened smooth and 
 shining, and darkish with the colour of an old bruise. 
 On removing the arachnoid and pia mater, about the 
 centre of this patch the brain substance gave way, and 
 a little healthy pus escaped. On enlarging the open- 
 ing a cavity was shown, large enough to contain a 
 small orange, and full of pus. The roof of this cavity 
 was found mainly of grey matter about a quarter of 
 an inch thick, except in the one spot Avhere the brain 
 substance had softened, and allowed the pus to reach 
 the convex surface of the hemisphere. This cavity 
 was lined with a firm tense rougliened false mem- 
 brane, about two or three lines thick, forming a kind 
 of cyst. The abscess lay wholly in the white substance 
 of the hemisphere, and did not reach the ventricle at 
 all. Cerebral vessels healthy.' 
 
 It is quite possible to find in different spots in the 
 same individual depots of pus encysted in the manner 
 just described ; pus encircled witli cerebral tissue, soft
 
 IXFLAMMATIOX. 81 
 
 or indurated, or iniu-li injected, but not forming a 
 regular cyst-wall, and mere regions of softening, of 
 Avliich tlie centre is softer tliau tlie circumference, the 
 latter gradually losing itself in the healthy parts. 
 
 Of multiple abscesses, the number is generally 
 in inverse ratio to their bulk. 
 
 The white and grey matter are almost equally 
 liable to inflammation. The middle lobe is a frequent 
 seat ; the anterior and posterior less so. The corpora 
 striata, optic thalami, and ventricles are often the seat 
 of inflammation ; the cerebellum and pons are less 
 subject to it ; but many parts may be affected simul- 
 taneously. 
 
 The stages, then, of encephalitis are, according 
 to Eindfleisch : (1) Hypereemia. (2) Infarction. (3) 
 CEdema, and in some cases haemorrhage. (4) Prolife- 
 ration of the elements of the brain tissue, cellules, 
 and nuclei. (5) Hypertrophy. (G) In some cases, 
 especially in chronic cases, Induration, generally not 
 occupying the whole seat of inflammation, but accom- 
 panying softening either at the centre or at the circum- 
 ference. (7) Softening; when inflammatory, accom- 
 panied by a small infiltration of blood. The softened 
 region contains inflammatory granules, which also, 
 however, exist sometimes in non-inflammatory soften- 
 ing (as also do the small haemorrhages). (8) Suppu- 
 ration. The cyst round the abscess may begin to form 
 from the 13th to the 24th day. (9) Earely false 
 membrane. (iO) A condition of foetid suppuration 
 or softening, resembling gangrene. (11) More or less 
 atrophy, the result of inflammation. Many instances 
 
 G
 
 82 INFLAMMATION'. 
 
 of so-called acute abscess have really been examples 
 of local softening, due merely to intercepted blood 
 supply. 
 
 It is very remarkable how seldom we meet with 
 abscess of the brain that may be called idiopathic. 
 Thus of 76 cases collected in Reynolds' ' System of 
 Medicine,' 18 were secondary to suppuration elsewhere, 
 17 were due to direct injury of the head, 27 to disease 
 of the internal ear or of the petrous portion of the 
 temporal bone, 3 to various diseases of the nose, 1 to 
 syphilitic disease of the bones of the head, 1 to carci- 
 noma of the roof of the orbit; in 8 the cause was 
 unknown, and in only 1 case could the abscess with 
 any probability be termed idiopathic. 
 
 I add the following cases, as in each the cerebellum 
 was affected — a rare condition : — 
 
 Man, 23. Numerous abscesses, of a size varying 
 from a pin's head, at various parts of the brain. In 
 the right hemisphere, almost half an inch from the 
 surface, were two small abscesses, each about the size of 
 a filbert. In the left hemisphere, about its centre, was 
 a small abscess, surrounded by a number of small col- 
 lections of pus ; there were two others, one in the back 
 part and another in the front part. Much purulent 
 lymph in the left lateral ventricle, at the back part, 
 and filling its descending course. Septum lucidum 
 soft. Separate collections of jous in the left hippo- 
 campus major and left optic thalamus. A small abscess 
 in the centre of the cerebellum. Each of these collec- 
 tions of pus was surrounded by a zone of congested 
 vessels, and appeared of recent formation. There were 
 also many abscesses in both lungs.
 
 INFLAMMATION. 83 
 
 Man, 23. Occasional nystagmus. Left [)ni)il larger 
 than the right. Left arm weaker than the other, and 
 was tremulous at times. No other paralysis. Intense 
 intermittent pain over the whole head. No vomiting. 
 No loss of co-ordination. Sight very defective. Optic 
 neuritis of left eye. 
 
 P. M. Ex. Brain quite healthy, except tliat the 
 lateral and third ventricles were very much distended 
 with clear fluid. A very little softening of the septum. 
 In the centre of the left hemisphere of the cerebellum 
 was an abscess, lined with thick false membrane, and 
 containing nearly one ounce of pus. Sinuses healthy. 
 Left internal ear healthy. Other organs healthy. This 
 seemed to be a case of idiopathic abscess. 
 
 There are other conditions, not recognisable without 
 magnifying powers : 
 
 1. Changes in the neuroglia. 
 
 General sclerosis — rare. 
 Disseminated sclerosis. 
 Miliary sclerosis. 
 
 2. Changes in the vessels. 
 
 Microscopic aneurism, or rupture. 
 Dilatation of vessels. 
 
 Eesults of exudation in the tunica adventitia. 
 Masses of ha^matoidine, or of pigment, de- 
 posited outside the vessels. 
 
 3. Pigmentation of cells. 
 
 Sometimes large cells are found in the middle 
 layer of the cortex, with many large 
 branches. 
 
 Small granular cells nre often rapidly formed. 
 
 G L>
 
 84 INFLAMMATION. 
 
 Of the fifteen cases given by Calmeil uniler the 
 head of acute cerebral softening, or local acute 
 encephalitis without clots of blood, he found in one 
 fibrine in the sinuses of the dura mater ; in one this 
 membrane was bathed in purulent liquid, and it was 
 also perforated at one point. 
 
 In five there were recent spots of encephalitis on 
 the right and left sides, in six on the left only, in three 
 on the right only. 
 
 In three there were cellular cicatrices in the right 
 lobe of the brain, in one in the left lobe. 
 
 In two the right hemisphere of the cerebellum was 
 the seat of an acute inflammatory spot. 
 
 In four the principal recent inflammatory spots 
 were still in a state of red hepatization. In seven they 
 were in a state of softenincf, with disinteo-ration of the 
 nervous substance. In four they were in a state of 
 disintegration of the nervous substance, with a mixture 
 of a hquid that resembled pus. 
 
 In four the spots of acute local encephalitis without 
 clot were studied microscopically. Of these, in one 
 they were still in the state of red hepatization ; the 
 diseased regions were reddened by the widening of the 
 capillaries, and by the presence of extravasated globules 
 of blood ; the cerebral fibres were not yet disintegrated ; 
 already small granular cells had begun to be formed 
 in Ihe inflamed parts. 
 
 In three the nervous substance of the diseased 
 seats was disintegrated, and more or less reduced to 
 fragments ; it was soaked in plasma, mixed with a 
 considerable number of great cells collected together, 
 
 JL
 
 INFLAMMATION. 85 
 
 and molecular granules ; sometimes in the preparation 
 there were seen rare globules of pus scattered. The 
 vessels and their principal branches were constantly 
 very apparent. 
 
 Myelitis. — Opinions are divided as to the nature of 
 the change in so-called myelitis. Some observers 
 affirm that what is called myehtis is only a form of 
 meningitis, an inflammation of the connective tissue 
 supporting the cord ; that inflammation of the spinal 
 cord is of an interstitial character, leading to the 
 degeneration and disintegration of the nerve structure 
 instead of the production of epithelial elements and 
 pus. 
 
 Without doubt, also, the breaking up of the 
 softening surrounding a clot in the cord, or a scrofulous 
 mass, has not unfrequently been mistaken for abscess of 
 the spinal marrow. 
 
 Still, inflammation, with true inflammatory products, 
 may be found in the cord, involving not the neuroglia 
 only, but the other component parts of the white and 
 grey matter ; but under all circumstances the neuroglia 
 is probably the first and always the main structure 
 affected. 
 
 Inflammation, according to Hammond, Jaccoud, 
 and other observers, may attack the grey and white 
 matter (in which case it becomes impossible to distin- 
 guish the two substances from each other) or one o\\\y. 
 When it affects the white matter, the membranes of 
 the affected portions are congested, thickened, oiJiique 
 in patches, and adherent to the cord. The cord is 
 softened to a variable de})th, and detaclied in pieces
 
 86 INFLAMMATION, 
 
 with the membranes on their removal. Tlie softened 
 portion is in the early stage rose-coloured and studded 
 with red points, marking the situation of the enlarged 
 blood-vessels. As the disease advances, the colour 
 deepens to a reddish-brown, then becoming lighter, 
 passing through several shades of yellow, until at last 
 all colour is lost. Similar changes are seen in the grey 
 matter. 
 
 Microscopically we find congestion and increase of 
 the connective tissue of the cord. The evidences of 
 this hypertrophy are seen in the increase of fusiform 
 cells, and in the production of multi-nuclear cells 
 and free nuclei. These formations take place at the 
 expense of the proper nervous tissue of the cord, the 
 anatomical elements of wdiich undergo atrophy and 
 fatty degeneration. The nervous tubules are thus 
 often disintegrated, and their contents disseminated 
 through the extraneous tissue. The axis cylinders are 
 entirely surrounded by oil globules, or altogether 
 broken up. Should suppuration occur, the elements 
 of pus are observed among those already described, 
 and take their place to a considerable extent. As 
 acute myelitis becomes chronic, the centre of inflam- 
 mation undergoes other changes, still characteristic of 
 hypertrophy of the neuroglia, at the expense of the 
 proper nervous tissue. Sclerosis is the result. 
 
 Occasionally, however, the softening persists, and 
 becomes tlie permanent structural condition of the 
 diseased portion of the cord. These conditions of 
 softening and induration of the cord, like similar 
 changes in the brain, seem to mark the acuteness or 
 chronicity of the inflammatory action.
 
 C. Ber)9au,Lilli, 
 
 Banks & Co.. Edm' 
 
 MYELITIS. SWOLLEN NERVE FIBRES
 
 INFLAMMATION, 87 
 
 Micliaud's plates give an excellent idea of the 
 extent of degeneration and distortion the cord niiiy 
 undero'o from inflammation attackin<:j either its sub- 
 stance or its meninges. They also show very beauti- 
 fully the gradual passage of inflammation into sclerosis, 
 or rather the mode of orig-in of sclerosis from iuHam- 
 mation. 
 
 The condition of softening will very generally affect 
 the grey matter first, probably from its greater richness 
 in blood-vessels ; it may be found only in one spot, 
 or in a few isolated spots ; but it has been met with 
 along the whole leno;th of the cord. 
 
 Hasmorrhage often occurs in the softened portions, 
 and may even be of considerable extent. Such cases 
 must be distinguished from inflammatory softening 
 round haemorrhages, the hcemorrhage being the primary 
 lesion. 
 
 Myelitis may co-exist with chronic cerebral soften- 
 ing from encephalitis. Calmeil mentions three such 
 cases, in one of which the cord was thin and indurated, 
 in one softened and disintegrated, in one of a violet 
 colour. 
 
 Plate 3 is an example of myelitis following fracture 
 of the bodies of some of the vertebrae and consequent 
 haemorrhage. Plate 4 shows how completely the 
 nervous substance of the spinal cord can be destroyed 
 by myelitis. The case was as follows : — 
 
 Fanny , aged 37, married. Has been ill 
 
 for the last fourteen days. Was first taken with 
 numbness in the left leg and motor paralysis ; the 
 right leg l^ecame gradually affected in the same way
 
 88 INFLAMMATION. 
 
 a few days later. She lost her sight suddenly fourteen 
 days ago. Was then constipated, and had difficulty 
 in passing water. On admission is almost Avholly 
 blind ; she can just distinguish the form of a person 
 near her, but not tlie features. Is quite paraplegic, 
 being unable to move the leg in the least degree. 
 Has lost sensation to a great extent over the whole 
 region of the motor paralysis. No power over the 
 sphincters. Urine dribbles away, and yet much is 
 retained, and has to be drawn off by the catheter. 
 No paralysis of the upper limbs, or of face, or of the 
 muscles of the eyeball. Eetinal vessels very small, 
 and discs cloudy. Is very hungry and very thirsty. 
 Has a large deep bed-sore on each buttock, and her 
 feet are blistered in many places from having been 
 burnt by hot bottles. Complains of pains in the arms. 
 Abdomen tympanitic. She feels cold in the legs, 
 though anaesthetic to touch. Has been subject to 
 pain in the head ever since her marriage. Four days 
 after admission she was able to see much better. At 
 the end of three weeks she was beginning to move the 
 right leg, but she died in about a month from ex- 
 haustion from the bed-sores. 
 
 P. M. Ex. Brain healthy. Spinal cord, at a point 
 corresponding to the last dorsal and first lumbar 
 vertebra;, was much disorganised, being a dark brown 
 over much of its thickness. A similar condition, 
 though of less degree, existed about the middle of the 
 dorsal region. Plate 4 shows very little remaining 
 besides the vessels, with some thickening of connective 
 tissue, and a somewhat gelatinous appearance of what 
 remained of the columns of tlie cord.
 
 INFLAMMATIOX. 89 
 
 Dr. Von Eabcnau describes three cases of chronic 
 mental derangement, in all of which there were peculiar 
 alterations in the posterior columns of the cord, due to 
 chronic myelitis. 
 
 Consult — 
 
 Hammond, ' Diseases of the Nervous System.' 
 
 Calmeil, ' Maladies inflammatoires du Cerveau.' 
 
 Ileynolds' ' System of Medicin«>.' 
 
 Rindfleisch, ' Path. Histology.' 
 
 Bright's ' Med. Reports.' 
 
 Green, 'Path. Anatomy.' 
 
 Gintrac, ' Maladies de I'appareil Nerveux.' 
 
 AVilks, 'Path. Anatomy." 
 
 Rokitansky, * Path. Anatomj'.' 
 
 'Med. Times.' 1870. Dr. Moxon. 
 
 ' Jour, of Mental Science.' July 1873. Dr. Jastrowitz. 
 
 * West Riding Asylum Rep.,' i. 218. ' Arachnoid Cysts.' 
 < St. Earth. Hosp. Rep.' 1872. Mr. Kesteven. 
 
 Dr. Collins' ' Report on Epidemic Cerebro-Spinal Meningitis. 
 
 ' Privy Council Rep. on Cerebro-Spinal Meningitis.' Drs. Whitley 
 and Sanderson. 
 
 West, ' Dis. of Infancy and Childhood.' 6th edit. ' Ch. Hydro- 
 cephalus.' 
 
 * St. George's Hosp. Rep.,' vol. iv. ' Tuberculous Meningitis.' 
 
 Dr. E. L. Fox. 
 'Med. Record', i. 296. 'Myelitis in the Insane.' 
 'Michaud, *Sur la Meningite et la Myelite,' &c.
 
 90 
 
 LECTUEE IV. 
 
 DEGENERATIONS. 
 
 Degenerations include atrophy, softening, and tlie 
 various forms of sclerosis. 
 
 The distinctions between these varieties are arbi- 
 trary, and can only be defended on the ground of 
 convenience. Thus atrophy may depend upon, or be 
 intermingled with, softening, or, again, with sclerosis. 
 It may be due to inflammation, as also may at least 
 one variety of softening, and it is an open question 
 whether all forms of sclerosis do not own a similar 
 inflammatory origin. 
 
 Atrophy may be met with under several forms. 
 Thus we find distinct losses of substance, forming 
 cavities, either at the circumference of the organ or 
 in its interior ; or there may be a general wasting of 
 the whole contents of the encephalon or the spinal 
 canal, the space formerly occupied by the nervous sub- 
 stance being filled with cerebro-spinal fluid ; or more 
 commonly there is diminution in the bulk of one organ 
 or a small part of an organ, of a hemisphere of the 
 brain or cerebellum, or of one lobe of either, or one 
 half of the pons, of one corpus olivare, &c. 
 
 It may be a congenital condition, or one acquired
 
 DEGENERATIONS. 
 
 91 
 
 as a sequence to an accident, or to some disease, 
 especially anything that slowly interferes with the 
 nutrition of the organ. Of the first variety, in which 
 there is a distinct loss of substance, it is most usual to 
 find one spot in the brain, but in some few cases there 
 are several. The cavity is generally lined with a 
 thin membrane of great vascularity ; the sides of the 
 cavity are somewhat indurated ; the contents may be 
 pultaceous, or only a turbid lluid. It is probable that 
 this form is strictly a sequence of inflammation. 
 
 Far more frequently we meet with a gradual loss of 
 bulk in some organ or part of an organ, the general 
 relations and shape of the organ being retained. 
 
 In the brain the volume and weisiht of the ortran 
 are diminished. The whole brain, or at least all the 
 convolutions of the convex smface of the hemispheres, 
 may be found sunk, and their place taken by a con- 
 siderable amount of fluid. This is common enough in 
 old age, with feebleness of mental effort, in clu'onic 
 mania, and dementia. I have met with it, however, 
 once m the brain of a very intellectual person, who 
 retained not only consciousness, but brightness of 
 mental power to the last ; in this case it was associated 
 "with sclerotic lesions of the cord. Unless it depends 
 on senile conditions, it is frequently associated with 
 various deformities of the cranial bones, thickening of 
 the meninges, and patches of meningeal ossification, 
 with fluid in the ventricles, or, if the atrophy is 
 unilateral, with fluid in the ventricle of the affected 
 hemisphere, with thickened ependyma, and indunitions 
 of the ventricular wall. All these concomitant lesions
 
 92 DEGENERATIONS. 
 
 point to an inflammatory origin for the atrophy ; the 
 process in order of sequence being inflammation, then 
 softening with fatty degeneration, then partial absorp- 
 tion, and so atropliy. Sometimes the brain is diminished 
 in thickness, sometimes in length. The cerebellum may 
 be atrophied in the half opposed to that of the brain ; 
 thus atrophy of the right cerebellum may coincide with 
 atrophy of tlie left cerebrum. 
 
 If tlie lesion have an inflammatory origin, we find 
 traces of fatty degeneration of all the tissues of the 
 vessels, the nerve-tubes, and even the cells, with debris of 
 broken-up nerve-cells. Sometimes the nem^oglia itself 
 has softened down in the same manner ; at other times, 
 when the inflammatory action has been of less intensity 
 and more chronic, this tissue will have been the seat of 
 proliferation, and some sclerosis is the result. Amyloid 
 bodies will also be found most generally. 
 
 If the lesion have no inflammatory origin, we meet 
 only with a shrunken condition of the nerve-tissue, 
 especially of the calibre of the nerve-tubes. The cells 
 seem smaller than usual, or, if the disease be unilateral, 
 the cells are proportionately smaller than those of the 
 corresponding portion of the brain on the unaffected 
 side. The size of the arteries is often somewhat de- 
 creased, or the lumen botli of arteries and capillaries may 
 be found encroached upon by atheroma. In this case 
 the border line between atrophy and softening is a very 
 fine one, and the two lesions are conditioned very much 
 by tlie gradual manner in which the disease of the 
 vessels occurs ; any rapid interference with their calibre 
 leading probably to softening, more gradual interrup- 
 tion to a free circulation causing atrophy.
 
 DECiEXEllATlUXS. 93 
 
 A marked case of atrophy of tlie brain, with absence 
 of the corpus callosum, is reported by Dr. Pahnerini, 
 and quoted in the Medical Record^ December 31, 1873. 
 The patient, a girl, was born of healthy ])arents ; but 
 wlien a year old showed signs of mental weakness, and 
 grew up in this state till her sixteenth year, when she 
 was received into the asylum at Siena. Her skull was 
 small and symmetrical, her forehead small, the teeth 
 long and large ; her aspect was imbecile, and her 
 growth stunted. All the mental faculties were very 
 weak ; she did nothing except by imitation, or in 
 obedience to orders. Sensation, motion, and taste were 
 perfect ; hearing and smell were rather weak. She 
 improved while in the asylum so far as to be able to 
 do some work, and to abandon some foolisli and 
 destructive habits, to which she had become accus- 
 tomed. In the second year of her residence she died 
 of phthisis. The necropsy gave the following result : 
 
 The cerebrum weighed oo^ ounces avoirdupois ; tlie 
 convolutions were small, with few tortuosities, and the 
 sulci were shallow ; the frontal lobes were imperfectly 
 developed in proportion to the other parts of the brain. 
 The corpus callosum was completely wanting, as were 
 also the septum lucidum and the anterior and soft com- 
 missures. The olfactory nerve was absent on the right 
 side, and was merely rudimentary on the left. The audi- 
 tory filaments were slender ; the cortical and medullary 
 substance of the cerebrum and cerebellum were anaemic. 
 
 Atrophy of Cord. — There is comparative absence 
 of nerve-tubes, and presence of amyloid bodies. 
 It is in the cord even more than in the brain 
 that we see in a strikinf:^ manner the difficulties of
 
 94 DEGENERATIONS. 
 
 pathological distinctions. It is perfectly true that 
 atrophy of the cord may exist per se, depending 
 on atheroma of the capillaries, and manifested by 
 a tolerably universal shrinking of the whole organ. 
 This is seen most decidedly in the upper portion 
 of the cord, as the condition is due sometimes to lesions 
 of the brain that have practically cut off much of the 
 use of the cord below them, or to lesion of the . cord 
 that has a similar effect on the part of the cord lying 
 further down. The white matter of the cord is solely 
 or mainly affected. 
 
 But the more common varieties of atrophy of the 
 cord are due to other conditions, to which the atrophy 
 is merely the sequence. We may meet with atrophied 
 appearance of the cord in cases of general or locahsed 
 sclerosis, when disseminated sclerosis attacks the whole 
 thickness of a cord in various portions of its length ; 
 when it confines itself to one column or set of columns ; 
 when sclerosis in the non-disseminated form attacks a 
 small portion of the cord ; when grey degeneration affects 
 a spinal region, the posterior columns for instance, or the 
 groups of cells in the posterior cornua ; and lastly, we see 
 it in great perfection in some cases of chronic myelitis, 
 as in Plate 4. In one case observed the calibre of the 
 cord on transverse section did not exceed half what is 
 normal, and this, too, in its whole length. Much more 
 frequently, even where atropliy depends on chronic 
 myelitis, it is partial. In the case above alluded to 
 almost all tlie nerve-structure had disappeared. 
 
 In the other forms the loss of nerve-tube has 
 depended on ihe ])rcssure consequent u})on tlie sclerosis, 
 the contraction of tlie hyperplasic connective tissue.
 
 C. Ber|ea'u.Li;^. 
 
 BsLBKS Sc Co Edm' 
 
 ATP.OPKY FROM MYELITIS.
 
 DEGEXERATIOiVS. 95 
 
 Atrophy of the cord, tlierefore, slioiild lead to further 
 investigation. It will then be found to depend either 
 on atheroma of the smallest vessels, or myelitis most 
 usually chronic, or grey degeneration, or general or 
 partial sclerosis, disseminated or non-disseminated. 
 
 The so-called hypertrophy of the brain is merely an 
 extreme hyperplasia of the connective issue. There is 
 no real hypertrophy of nerve-cells or nerve-tubes. It 
 is pretty much the same condition as sclerosis, only in 
 the latter there is retraction of the connective tissue and 
 consequent destruction of the nerve elements. In hyper- 
 trophy of the brain the retraction has not taken place, 
 and the nervous elements exist in their normal amount. 
 Localised hypertrophy of one hemisphere of the brain 
 may coincide with atrophy of the opposite side of the 
 body. 
 
 Eokitansky states, as the result of many microscopical 
 examinations, that its augmented bulk is not produced 
 by the development of new nervous fibrils, or by the 
 enlargement of those already existing, but by an increase 
 in the intermediate granular matter, most probably due 
 to an albuminoid infiltration of that structure. This is 
 doubtless but the first stage of the process of connective 
 tissue crrowth. Neither the base of the brain nor the 
 cerebellum is liable to this affection. 
 
 Softening. — For the production of softening the most 
 important element is suppression of the circulation ; and 
 the varieties of softening depend more or less on the 
 nature and mode of this suppression. Obliteration of 
 the arteries, of the capillaries, of the sinuses, will form 
 the main causes of cerebral softcniim-.
 
 96 DEGENERATIONS. 
 
 It may be clue to inflammation, to hasmorrhage, to 
 infiltration of serum, to the neiglibom^hood of tumours, 
 to interruption to the conrse of the blood by embolism, 
 by thrombosis, by disease of vessel such as atheroma, 
 not necessarily leading to thrombosis, by artificial 
 means, such as ligature of vessels, &c. But all these 
 conditions own a common point — the suppression, total 
 or partial, of the circulation. The stasis or the throm- 
 bosis existing in inflammation, the rupture of vessel in 
 ha3morrhage, and the consequent cutting off of the cir- 
 culation beyond the seat of rupture, the pressm^e of a 
 tumour on the surrounding vessels, may all either lead 
 to, or imitate in their effects, the embolic or thrombotic 
 obliteration of vessels to which softeninc? is due. 
 
 In inflammatory softening new formations exist. 
 Connective tissue is generated ; an exudation of albu- 
 minous fluid containing fine granules takes place, and, 
 mixed with red globules, forms a reddish pultaceous 
 mass. The pulpy mass undergoes partial absorption, 
 and is replaced by a white turbid fluid. There are often 
 also small htemorrhages met with. 
 
 Jaccoud's remarks on softening are so pertinent 
 that I am tempted to give you a free translation of them. 
 
 Partial anaimia and softening by necrosis of the cere- 
 bral regions nourished by the obstructed artery are, in 
 chronological order, the two phenomena whicli follow 
 the interruption to the course of the blood. When 
 death occurs before softening takes ])lace, there is no 
 need to look for an abnormal white colouring to recog- 
 nise local anaemia ; several circumstances may mask or 
 efface all difference of colour between the anaemic part
 
 DEGENERATIONS. 97 
 
 and the neighbouring regions ; when an arterial branch 
 is obstructed, a collateral or compensating circulation is 
 developed in the vessels that have remained patent ; this 
 aQlux of blood produces hypera^mia of the tissue which 
 surrounds the anaemic sphere, and this congestion, extend- 
 ing itself nearer and nearer by the capillaries, causes the 
 ischa^mic colour to disappear. On the other hand, the 
 obliteration of the artery is frequently followed by that of 
 the corresponding venous branches ; thence a, congestion 
 by stasis, the dee[) red hue of which masks the anaemic 
 pallor. Consequently it is well not to trouble oneself 
 with the illusory appreciation of colour, and only to 
 judge of the partial anaemia by the state of the arteries ; 
 we shall find the occlusion ; and the examination of the 
 walls, the coagulum, and the heart will allow us to 
 'decide whether one has to do with a spontaneous 
 obstruction or an embolism. 
 
 Softening is circumscribed in one or more strictly 
 limited spots ; it results from the suspension of the nutri- 
 tive process in the parts which were nourished by the 
 obliterated vessel ; in its mechanism and its cause this 
 softening does not differ from the mortification produced 
 in all organs by the uncompensated obstruction of a 
 nutritive artery ; thence the very good name of 'Cerebral 
 Necrosis,' which is generally given to it to distinguish 
 it from all other kinds of cerebral softening. With the 
 exception of the very rare cases in which death is so 
 rapid that the centre of the necrosed spot is found 
 white and bloodless, softening presents three stages 
 characterised by a special colour ; the first is the stage 
 of red softening, the second of yellow, the third of white. 
 
 n
 
 98 DEGENEEATIONS. 
 
 Eecl softening is only developed 3G or 48 hours 
 after tlie occlusion of a vessel : during this interval the 
 collateral circulation is established ; and if it is sufficient 
 to prevent the death of the tissue, all the ulterior ac- 
 cidents may be avoided. This stage is characterised 
 by a diminution in the consistence of the tissue, and a 
 colour which varies from a rose to a deep red ; the 
 tint is more intense at the circumference of the spot, 
 where the vessels are strongly dilated and hyperasmic. 
 
 It is not only a simple congestion which is pro- 
 duced ; often the small vessels are ruptured under the 
 influence of the increase of pressure, and we observe 
 here and there in isolated or confluent spots small 
 punctiform haemorrhages which give to the tissue the 
 aspect of a reddish pulp ; in other cases, the external 
 appearance being almost the same, there has been no 
 true ha3morrhage ; the vessels are not ruptured, but 
 the increase of pressure has caused the transudation of 
 a serum, coloured red by the dissolved hasmatine : 
 hence a pseudo-hsemorrhagic imbibition, which con- 
 tributes in a great degree to the separation of the 
 histological elements and to softening of the spot. 
 Under the microscope the cells and the nerve-fibres 
 are separated : the most part present still their normal 
 characters ; some may be already ruptured and 
 granular. Except in the case of liEemorrhage, the 
 capillaries are intact or filled with coagulated blood. 
 The duration of this stage varies from 8 to 14 days. 
 
 In the stage of yellow softening, the contents of 
 the spot have already the aspect of a ' bouilli ' more 
 or less thickened ; the fibres and the nerve-cells are
 
 DEGENERATIONS. 99 
 
 ruptured, separated, granidar, and in course of retro- 
 gressive or flitty metamorphosis ; they are often even 
 scarcely recognisable ; the walls of the vessels are 
 covered with fatty granulations ; they contain the 
 elements of tlie blood, and particularly elements of 
 free ha^matine and white globules ; these degenerated 
 leucocytes and fatty granulations constitute the cor- 
 puscles described by Gluge under the improper name 
 of inflammatory corpuscles, or granular bodies of in- 
 flammation. It is these elements that give to the spot 
 its characteristic yellow colour. 
 
 White softening is only effected after several 
 months ; the contents of the spot, perfectly white, 
 appear as a milky pulp more liquid than solid, in 
 which are suspended whitish flocculi. The nerve 
 elements, the blood-globules, the capillaries have dis- 
 appeared : the microscope shows nothing but numerous 
 granulations, drops of fat, and granular cells, so that 
 the liquid presents an accurate resemblance to 
 colostrum. 
 
 When the spots are not too considerable, absorption 
 is possible ; it often leaves after it a depressed cicatrix 
 or a small lacuna, a persistent vestige of a former 
 pathological condition. This is tlie most complete mode 
 of repair ; in other circumstances absorption is not 
 complete, but a cyst is formed, which isolates the spot 
 from the healthy tissue. These various curative pro- 
 cesses represent the fomth stage of necrosed softening. 
 
 In certain cases the examination of the brain 
 demonstrates plainly a spot of necrosis, but the 
 obstructing clot cannot be found. As tliis difTiculty 
 
 H 2
 
 lOO DEGENERATIONS. 
 
 only presents itself in old-standing cases, we must 
 admit, with Bamberger and Hasse, a complete ab- 
 sorption of the clot or a total atrophy of tlie artery. 
 (Meissner.) 
 
 The spots of cerebral necrosis often coincide with 
 similar lesions of other viscera, especially the spleen 
 and the kidneys. 
 
 For the occlnsion of an artery to result in necrosis, it 
 is necessary that a sufficient collateral circulation should 
 not be immediately established ; it is necessary, there- 
 fore, that in the case of the anterior cerebral regions 
 the obstruction should be situated beyond the circle of 
 .Wilhs. Observation verifies tliis presumption, and the 
 obliterations of the internal carotid, for instance, have 
 not the effect, unless the clot should have prolonged 
 itself by successive deposits beyond the arterial 
 hexagone : when this prolongation has not taken place, 
 the cure may be complete and rapid. This condition 
 applies equally to thrombosis and to embolism ; but 
 whilst the former has no situation it specially prefers, 
 the second is more frequent in the left Sylvian artery 
 than anywhere else. Cohn pretends even that the 
 obstruction only occupies the right Sylvian artery in 
 the cases where the embolus does not come from the 
 heart, but from the brachio-cephalic trunk, or from 
 the right carotid. This assertion is too absolute ; for 
 in the table of Meissner I find eight cases of right 
 embolism in which tlie heart was tlie sole cause . 
 In obstruction of the Sylvian artery, the infarctus 
 generally occupies the median spots of the corpus 
 striatum ; the region of tlie liemispliercs under the
 
 1
 
 E.L.Fox.M.D. 
 
 Plate 5^
 
 DEGEXERATIONS. 10 i 
 
 immediate control of tlie collateral circulation remains 
 intact. When the choroidal artery is obstruc^tcd, the 
 softenino; is situated in the white substance of the 
 hemispheres. The obliteration of one vertebral only 
 has no effect, because of the afflux through the trunk of 
 the basilar ; but the infarctus remains persistent when 
 the basilar or the posterior cerebral is the seat of the 
 obstruction. In one case of Brunnicke, the occlusion 
 occurring in the trunk of the basilar, the softening 
 occupied the pons and the optic thalamus. In a case 
 of Bennett, with thrombosis of the same artery, the 
 necrosis was confined to the jions. In a case of 
 Cohn, where the posterior cerebral was occluded, the 
 infarctus occupied the optic thalamus, and did not 
 reach the corpus striatiun. 
 
 The case from which plates 5 and 6 were taken 
 was this : — 
 
 WiUiam G., aged 30. lias a tuberculated syphi- 
 litic rash all over the body, and ulcers on the legs. 
 Partial right hemiplegia, but no impairment of speech. 
 Soon after admission his intellect beo-an to be im- 
 paired and his speech thick. Later he became 
 temporarily hemiplcgic on the left side, this symptom 
 lasting only a few days. About two months ago he 
 suddenly became blind, and this amaurosis lasted for 
 several days, and then passed off. The right hemi- 
 plegia continued. Some paralysis of bladder. A state 
 of stupor very gradually came on, which terminated in 
 deatli. 
 
 P. M. Ex. Broca's spot and every part of both 
 cerebral hemispheres quite healthy. The pons was
 
 1Q2 DEGENERATIONS 
 
 the seat of softening over a space the size of a filbert, 
 occupying rather more of the left half than of the 
 right, but passing a good deal over the middle line on 
 the right side. The nervous tissue was here quite 
 dehquescent. The vessels of the circle of Willis a 
 little fatty. All the other organs healthy, except that 
 in part of the left lobe of the liver there were 
 regions of yellowish discolouration. On microscopical 
 examination, after preparation, the blood-vessels were 
 the only structure left, except a few nerve-cells and 
 fibres atrophied and isolated by the disease. But 
 there were also found some strange round bodies, 
 about YoVo of ^^^ i^^'^^i i^^ diameter, that seem to be 
 conglomerate cells, Plate 6. 
 
 Obliteration of the Capillaries. — This subject is 
 very imperfectly known, for the question of the 
 pathological anatomy is alone ehicidated. The ob- 
 struction of the capillaries is spontaneous or embolic. 
 The former — capillary thrombosis — is connected with 
 lesions slow and gradual in their progress, which have 
 been carefully studied since the first works of Paget 
 and Robin. The chief of these lesions are the deposit 
 of fattv o;ranulations in the walls ; in aged individuals, 
 moniliform dilatations and atheromatous and calca- 
 reous incrustations of the small cerebral arteries. 
 As to dissecting aneurism, we look upon it as a 
 secondary lesion, consecutive to necrobiotic softening, 
 and not as the primary pathogenic condition of the 
 alteration of the nervous tissue. Whatever be the 
 preliminary lesions of the capillaries, they have for 
 their elTect retardation, and then arrest of the course
 
 Serj'iiU.Litii, 
 
 Bajiks Sc Go , Edm^ 
 
 CELLS FROM SOFTENED PONS.
 
 DEGENERATIONS. 103 
 
 of the blood ; and, finally, the ischa3niic softening of 
 tlie histological territory fed by the diseased vessels. 
 The initial characteristics of these softeninos are not 
 known. Tlie spots are small and multiple in direct 
 ratio witli the diffusiou of the lesions. The course of 
 tlie process, always slow, differs absolutely from the 
 embolic necrobiosis described above, and is rather 
 related to softening by disseminated thromboses. It is 
 seldom that the spots are situated in those cerebral 
 regions which, impatient of all lesion, show the least 
 alteration by symptoms clearly appreciable. It is in 
 tlie white mass — in the cortical layer of the hemi- 
 spheres — it is in the centre of the corpus striatum, 
 that we most generally meet with them ; and unless 
 the spots of softening are numerous, the lesion remains 
 without symptom, and is recognised only post mortem. 
 The obstruction by embohsm forms two classes, 
 according to the natm-e of the embolus. The one 
 class act only mechanically, merely as obstructing 
 bodies, and producing only the ordinary lesions of 
 ischa3mic necrobiosis ; the other (specific embolisms) 
 owe to their original seat specific properties that tliey 
 transport with them, so that wherever they are 
 arrested they provoke lesions of the same nature as 
 those of the primary spot. It is not yet well estab- 
 lished that simple or mechanical embolism may be 
 effected by pieces of granular or fibrinous material 
 originating from clots in process of breaking down ; 
 consequently, this first class of embolisms should be 
 limited to three varieties, which are pigmental, calca- 
 reous, and fatty embolisms.
 
 104 DEGENERATIONS. 
 
 The pigmental emlDolism can only be produced 
 when the blood contains an abnormal quantity of 
 pigmental corpuscles ; that is to say, in the state known 
 under the name of melansemia. This state has so far 
 only been seen in persons affected at the time, or who 
 have been previously attacked with intermittent fever. 
 These fevers are the sole cause both of the melanasmia 
 and of pigmental embolism. It is of no great im- 
 portance at the moment whether the pigmental 
 corpuscles with which the blood is then charged 
 originate exclusively in the spleen, or also in the 
 liver. What is certain is, that these cellular or cylin- 
 drical granulations may accumulate in the cerebral 
 capillaries, and produce obstruction in them, either 
 directly or by the coagulation of blood they induce. 
 This obliteration prefers as its seat the cortical layer of 
 the hemispheres. When it is general, the change of 
 colour which it produces may be appreciated by the 
 naked eye. The substance is of a dull grey, and the 
 consistence is diminished. It is only exceptionally 
 that we find grey tracts in the white substance. Small 
 capillary hsemorrhages coexist sometimes with this 
 obstruction, and in two cases Frierichs has observed a 
 meningeal haemorrhage. Latent as regards symptoms 
 when it is very limited, pigmental embolism reveals 
 itself in other cases at the beginning by headache, 
 hallucinations, delirium, convulsions ; that is to say, by 
 the phenomena of excitation, and, eventually, by a 
 coma more or less profound. Paralysis is extremely 
 rare ; it may be partial, or hemiplegic, or paraplegic 
 in form. These symptoms have nothing characteristic
 
 DEGENERATIONS. 105 
 
 of themselves ; they only acquire significance by tlie 
 knowledge of tlie antecedents of the patient, by the 
 swelling of the spleen or of the liver, and by the 
 greyish brown colour of the external integument. 
 It would be an error to refer constantly to a pigmental 
 obstruction, the cerebral symptoms of the intermittent 
 fever called ' accompagnee cephalique.' Even when 
 this form of fever is very clearly characterised, the 
 capillary embolism may be wanting. It was absent, 
 indeed, six times in twenty-eight cases observed by 
 Fricrichs. On the otlier liand, tliough the cerebral 
 accidents are vigorously intermittent, it is very difficult 
 to attribute them to a fixed lesion of the same kind 
 as that which occupies us. Sulphate of quinine in 
 large doses, cold applications to the head, cutaneous 
 revulsions, are tlie basis of treatment ; but the prog- 
 nosis is always serious. 
 
 Calcareous embolism is characterised by a calca- 
 reous incrustation obliterating the capillaries. The 
 cerebral tissue resists when cut, and the vessels appear 
 on the surface of the sections rigid, like the hairs of a 
 brush. This alteration, always limited to the smallest 
 vessels, often coincides with similar lesions in the 
 lungs and the mucous membrane of the stomach. 
 According to the theory of Virchow, I place this 
 obliteration among the embolisms, and not among the 
 spontaneous obhterations. According to him, we have 
 to do here A\nth calcareous metastases. The reabsorp- 
 tion which takes place in the bones throws into the 
 blood these mineral elements, which, in consequence of 
 unknown causes, are deposited in the parenchyma of
 
 106 DEGENERATIONS. 
 
 organs, instead of being eliminated by the organs of 
 secretion. Over and above this, nothing is known 
 touching the effects of this obstruction. It is probable 
 by analogy that it also provokes small centres of 
 softening, but it is all obscure. The same thing may 
 be said for fatty embolism, which is demonstrated as a 
 fact by some observations, but the anatomical and 
 clinical facts of which are wholly unknown. 
 
 In the specific alterations the embolus is formed by 
 pus or by the debris of organic matters in decom- 
 position carried from gangrenous, putrid, or purulent 
 centres. Virchow admits that these debris, once 
 arrested, produce by catalysis some modifications 
 similar to those which go on in the original centre. 
 Panum believes rather that the decomposition of these 
 debris continues after their arrest, and that the products 
 of this decomposition are a cause of irritation to the 
 contiguous tissues ; whence inflammation, suppuration, 
 and sometimes gangrene. Whether one adopts the 
 idea of the similar production, or that of irritation of 
 the neighbouring parts, the chief fact is tliis : the 
 embolisms are tlie causes of the spots and of the 
 abscesses called metastatic. For the particular case 
 of the brain, see what takes place. Some fragments 
 detached from a putrid or a purulent centre arrive in 
 the capillaries (or the smallest arteries), obstruct them, 
 and provoke lesions and symptoms which have been 
 described as the cerebral accidents of the putrid or 
 purulent infection. I do not pretend that it is not so, 
 but I believe that we must observe that the embolus, 
 when it does not come from the lung, passes through a
 
 DEGENERATIONS. 107 
 
 course truly enormous. If the primary centre is in 
 the spleen (of whicli tliere huve been examples), "\ve 
 must admit that the embolus traverses the liver, the 
 right side of the heart, the pulmonary artery, the 
 lung, the pulmonary veins, the left side of the heart, 
 the carotid, to escape at last, after so many peregrina- 
 tions, in the cerebral capillaries. The thing is possible, 
 but it ' demands a little complaisance,' the more so 
 that here the mechanism invoked cannot be demon- 
 strated by fitting together the two fragments of the 
 clot, as in the ordinary embolism, so that we must 
 adnnt many lesions at one and the same time, without 
 reciprocal mechanical relations ; lesions governed and 
 provoked all of them by the general morbid disposition. 
 As the observations are not sufficiently clear to dissipate 
 all these doubts, an absolute solution is not possible. 
 Already 0. Weber, whilst admitting these diffused 
 capillary embolisms, rejects the conclusions of Virchow, 
 Panum, and Cohn on their specific nature, and only 
 attributes to them a mechanical role. 
 
 Obliteration of Venous Sinuses. — The primary oblite- 
 ration is generally situated in the superior longitudinal 
 sinus, and thence extends symmetrically into the neigh- 
 bouring sinuses (the lateral, &c.) ; if it is secondary, 
 it naturally occupies the sinus nearest to the pathogenic 
 lesion. The sinus is turgid, tense, and filled wdth a 
 fibrinous clot ; this clot is resisting, homogeneous, non- 
 adherent, formed of concentric layers, if it is not old ; 
 later it is softened in the centre, where one finds a 
 puriform ' bouilli,' Avhich for a long time was taken 
 for pus, and which is composed of fat, Ijreaking down
 
 108 DEGENERATIONS. 
 
 granulations and leucocytes. Unless the clot should 
 be of inflammatory origin, the adhesion to the wall is 
 slow ; if it results from the formation of connective 
 tracts, the membranes of the vessel are intact. In 
 secondary thrombosis, which most frequently succeeds 
 to caries of the cranial bones (30 times in 39 cases of 
 Lanceraux), the walls of the sinus are altered at the 
 level of the diseased bones ; they are thickened, friable, 
 with small resistance ; sometimes even tliey are 
 destroyed ; the coagulum is not always composed of 
 pure fibrin ; it contains besides some pus and debris 
 of false membranes 
 
 The cerebral lesions produced by obliteration of 
 the sinuses result from the increase of pressure in the 
 capillaries and tlie afferent veins, or rather also from 
 the arterial ischtcmia, caused by the venous stasis ; these 
 are capillary hasmorrhages, interstitial or meningeal, 
 oedema of the cerebral tissues, and of the pia mater, 
 with or without dropsy of the ventricles and superficial 
 centres of softening, which occupy symmetrically the 
 surface of the middle lobes, and are found especially in 
 the grey substance. Some lesions, piu-ely inflammatory, 
 of the meninges (false membranes, pus) often coincide 
 with thrombosis from caries of bone. 
 
 Depots of softening, which lie within the hemi- 
 spheres, cannot be obliterated, because their walls can- 
 not collapse, and thus arises a cyst. Near the surface, 
 however, cither of tlie brain or a ventricle, there may 
 be a 'slight depression of the separating layer, and the 
 Liyer of softening is completely obliterated (its place 
 being taken by cerebro-si)innl fhiid). Eokitansky
 
 DEGENERATIONS. 109 
 
 nioiUions a special form of yellow softening, consisting 
 of sharply circumscribed spots, in wliicli the cerebral 
 substance is connected witli a very moist, tremulous, and 
 occasionally gelatinous pulp, of a straw-yellow colour ; 
 the expressed fluid is acid. He thinks it is a peculiar 
 chemico-pathological transformation of brain substance 
 in which the liberation of an acid, phosphoric, or one 
 of the fatt)^ acids may be considered to be the impor- 
 tant phenomenon. 
 
 Calmeil records a very interesting series of cases of 
 cerebral softening from various causes, under the title 
 of chronic cerebral softening, or clironic local encepha- 
 htis, without clots of blood. 
 
 Of 27 cases, in 6 the cranial bones appeared injected, 
 in 1 perforated, in 1 with exostosis. 
 
 In 4 the cerebral dura mater was injected, in 5 
 strongly soldered to the bony tissife, in 2 altered by 
 accidental products. 
 
 In 6 the cavities of the cerebral arachnoid contained 
 serum, in 3 the cavity of the right arachnoid contained 
 false membranes, in 2 some kind of plastic plug, in 1 a 
 cyst lilled with blood. 
 
 In 7 the pia matei- of the right cerebral lobe was 
 injected, in 13 infiltrated with serum, in 4 thickened, in 
 8 adherent to the convolutions locally inflamed. 
 
 In 9 the pia mater of the left cerebral lobe was 
 injected, in 15 infiltrated with serum, in 3 thickened, in 
 5 partially adherent to the subjacent substance. 
 
 In G the convolutions of the riu'ht cerebi'al lobe 
 showed spots disintegrated and i)ulpy, in 5 s])ots disin- 
 tegrated with mixture of cellulosity, in 3 spots indurated
 
 110 DEGENERATIONS. 
 
 and shrivelled, in 3 faded and atrophied cores, in 4 
 false membranons spots of orange colour, in 2 spots of 
 ecchyinosis. 
 
 In 4 the convolutions of the left cerebral lobe 
 showed spots in a state of ecchymosis of a strawberry 
 colour, in 4 spots disintegrated and pulpy, in 3 spots 
 disintegrated with a mixture of cellulosity, in 3 false 
 membranous spots of an orange colour with softening, 
 in 3 without softening, in 5 spots indurated, faded, and 
 shrivelled. 
 
 In 3 there were in the depth of the right cerebral 
 lobe spots of softening in a creamy state, in 1 spots 
 softened and mixed with cellulosity, in 3 spots with 
 cellular bands, in 1 cavities with softened walls, in 1 
 with consolidated walls, in 2 spots of a raspberry colour. 
 The white substance was often injected, sometimes yel- 
 low, sometimes firm and resisting. 
 
 In the depths of the left cerebral lobe there were 
 foimd in 4 local softened spots, in 5 spots filled with 
 cellular band-like products, in 1 hollow spots with 
 cellular walls. In 10 the white sul^stance of this lobe 
 was found injected, in 3 generally indurated. 
 
 In 3 the right corpus striatum was found faded and 
 shrivelled, in 5 locally softened, in 3 hollowed with 
 cellular cavities. 
 
 In 1 the left corpus striatum appeared stunted, in 
 2 softened locally, in 3 red-coloured in places, in 4 
 traversed by cellular bands. 
 
 In 1 the right and left optic thalamus were stunted 
 and indurated, in 1 disintegrated at their surface. 
 
 In 4 tlie lateral ventricles were distended by serum ;
 
 DEGENERATIONS. Ill 
 
 their walls were traversed by vascular arborizations of 
 great intensity in 3 ; in 4 indurated, in 2 disintegrated 
 and softened. 
 
 In 3 the central parts, especially the septum of the 
 ventricles, were softened, in 5 indurated, and as it were 
 atrophied. 
 
 In 4 the pia mater of the cerebellum adhered to the 
 surface of the hemisplieres of the cerebellum, in 6 it was 
 injected. 
 
 In 6 the superficial grey matter of the whole cere- 
 bellum was softened, in 4 very red-coloured, in 2 yellow. 
 
 In 1 the two lobes of the cerebellum were atrophied, 
 in 1 there existed on the right side a spot of ecchy- 
 mosis, in 1 a false membrane, in 1 a spot of softening, 
 in 1 on the left side a hollow spot with soft walls. 
 
 In 2 the pons showed in its centre a spot or several 
 spots in a cellular state, in its right half a cellular spot 
 once. 
 
 In 3 it was injected, in 1 soft, in 2 hard, in 1 
 shrivelled. 
 
 In 1 the medulla oblongata was diminished in firm- 
 ness, in 1 it was too firm, in 1 pierced with small cellular 
 spots. 
 
 In 4 the spinal cord was thin and indurated, in 1 
 softened and disintegrated, in 1 of a violet colour. 
 
 In 14 a microscopical examination was made, botli 
 of the products contained in the cavities of tlie cerebral 
 arachnoid, and of the products contained in the different 
 spots of local encephalitis. 
 
 Softening of the spinal cord is due to injury, or 
 inflammation, or to the pressure of a tumour. Softening
 
 112 DEGENERATIOXS. 
 
 is sometinies of the whole extent, generally of some 
 spot, or of several spots with healthy spaces between, 
 especially of the posterior columns. The affected parts 
 may be swollen or atrophied. There is no special 
 alteration of the arteries. 
 
 The grey and white matter seem to be blended 
 homogeneously, as Hammond says, and the double 
 crescentic arrangement of the grey matter is lost. 
 
 Microscopically, the nerve-tubules are broken up ; 
 oil globules and granule masses (the constituent of which 
 is fat) have taken their place. In the grey substance 
 the nerve-cells are destroyed, and oil and fat appear in 
 large amount. Even the neuroglia exhibits a similar 
 disintegration and regressive metamorphosis. 
 
 The areas of softening, due to a kind of disseminated 
 myelitis, are sometimes well seen in fatal cases of para- 
 plegia after small-pox. 
 
 Grey Degeneration. — The terms grey degeneration 
 and sclerosis are used variously by different wi'iters. 
 To some they express different ideas ; to others they are 
 one and the same thing. It is certain that the connec- 
 tion between them is very close. The colour is more 
 or less common to both, and is due to the loss of the 
 sheath of the white substance of Schwann on the part of 
 the nerve-fibres. Eindfieisch indeed classifies both under 
 one heading, speaking of grey degeneration as taking two 
 forms — 1, simple non-inflammatory, grey degeneration 
 proper ; and 2, indurating inflammatory form, sclerosis. 
 
 In a similar manner also Gintrac speaks of patches 
 of grey or amber-yellow colour, a sort of half trans- 
 parency of the affected [)arts, and says that the diseased 
 portions may be indurated or softened.
 
 DEGEXEKATIONS. 113 
 
 It may aflbct various points or regions in the brain 
 and spinal cord, or tlie cord only, the lateral and 
 anterior columns, or the posterior columns of the cord, 
 the most frequent seat of this lesion. Tlie breadth of 
 the disease is generally greater than its deptli. 
 
 It may extend the ^vhole lengtli of the cord, or it 
 may be interrupted by portions of liealtliy spinal cord 
 tissue. The posterior roots of the spinal nerves are 
 very often implicated ; they are atrophied, and are 
 themselves in a state of grey degeneration. 
 
 Microscopically we fnid amorphous matter, finely 
 granular, between the nerve-tubes, disappearance or 
 atropliy of the latter, numerous nuclei of connective 
 tissue, amyloid bodies, and fatty granulations. 
 
 Eindfleisch says the first factor of this grey degene- 
 ration is an increase of the interfibrillar connective sub- 
 stance of the white fibres ; the second factor, the dis- 
 nppearance of the nerve-iibres in the attacked colunms 
 (probably by atrophy caused by pressure of the in- 
 creased connective tissue); the third factor, increased 
 connective tissue surrounding the small vessels, with 
 fatty and pigmental granules on them, and a lustrous 
 condition of the vascular walls; the fourth factor, 
 corpora amylacea, the nature of which is unknown. 
 They aie probably due to an amyloid infdtration of 
 sound neuroglia cells. 
 
 The disease is either due to a chronic irritation or 
 to a perversion of nutrition, causing a loss of the 
 normal condition of the nerve-tubes. The tubes 
 perish, and their place is taken by hyperplasia of 
 connective tissue and these corpora amylacea. These 
 
 I
 
 114 DEGENERATIONS. 
 
 amyloid bodies exist in far larger amount than in true 
 sclerosis, whilst the hyperplastic condition of the con- 
 nective tissue is much less marked than in the latter 
 lesions. Still the difference is very little more than one 
 of degree, and the two lesions can scarcely be separated 
 pathologically. Whilst, however, the distinction be- 
 tween them pathologically is difficult to draw, there is 
 certainly a difference, on microscopic examination, 
 between a well-marked instance of grey degeneration 
 and one of complete sclerosis. 
 
 Plate 7 is a tolerably good example of grey de- 
 generation affecting the cord. In this case the whole 
 of the cord was more or less affected, and in its whole 
 length. But the posterior columns and a small por- 
 tion of the grey matter were chiefly disintegrated, and 
 that mainly at the cervical and lumbar swellings. 
 
 Plate 8 represents the large amount of amyloid 
 bodies found in this lesion, and shows also some increase 
 of the connective tissue. 
 
 Grey degeneration, of the cervical swelling specially, 
 of the cord is sometimes accompanied by progressive 
 atrophy of the muscles, a loss of their transverse stria3, 
 with granulations and fatty globules, and a recent 
 connective tissue. 
 
 When the lesion is located in the posterior columns 
 of the cord, it is associated with loss of co-ordinatiuf? 
 power. This condition is very often accompanied also 
 witli a similar degeneration of tlie opti(^ tract or centre. 
 A condition standing mid-way between grey degenera- 
 tion proper and sclerosis is sometimes found in the cord, 
 depending on atheroma of the capillaries. There is
 
 E.L.Foi,M. D. 
 
 Plate 7. 
 
 • Beriea'a.Litli Ba^^^s 8, Co.Edm-'. 
 
 GREY DEGENERATION OF CORD.
 
 E.L.Fox.M.D 
 
 C. Berifcei-uti. Banks &- Co.. Edin'' 
 
 GREY DEGENERATION AMYLOID BODIES.
 
 DEUEXEKATIO.N'S. 115 
 
 degeneration and atrophy of a greater or less number 
 ■of nervous filaments, the formation of granular ror- 
 ])uscles in the degenerated tissue, and proliferation of 
 the connective tissue which takes the place of nerve- 
 tubes. In these cases grey degeneration, sclerosis, 
 and softeninn- of cord seem almost to mero-e one into 
 the other. 
 
 Sclerosis. — Speaking in general terms, sclerosis, 
 wherever met with, is composed of two conditions, the 
 latter of which depends on the former ; the first being 
 the abnormal development of the connective tissue, the 
 second the compression and gradual destruction of the 
 tissue of the part by the pressure and contraction of this 
 proliferated connective tissue. Although the patho- 
 logical anatomy of this morbid condition is tlie same, 
 however it be distributed in the nervous centres, it is 
 convenient to speak of it as taking three forms : 1, 
 general sclerosis, seldom affecting the brain, but not 
 unusually affecting large tracts of the cord ; 2, 
 disseminated sclerosis, ' sclerose en plaques,' which is 
 found both in the brain and spinal cord ; and lastly, 
 a form which may be only a variety of disseminated 
 sclerosis, the miliary sclerosis, described by Ivesteven, 
 Tuke, Eutherford, and other ]]ritish observers. 
 Benedikt, however, says tliat it is an error to speak of 
 ' sclerose en plaques,' since it has been established by 
 Bourneville's researches that the disease is not limited 
 to foci, but that even the apparently healthy interstitial 
 parts are diseased. We have, lie says, in reality, to deal 
 with a diffuse neuritis, whicli derives its character, at least 
 
 so far as regards its spinal symptoms, from a coml)i:iation 
 
 I 2
 
 116 DEGEXEliATlOXS. 
 
 of disease of the anterior or lateral columns. Before we 
 come to the distribution of this abnormality, it is only 
 fair to tell you that pathologists di3er as to the inter- 
 pretation of the first element of sclerosis, because 
 physiologists differ as to the existence of connective 
 tissue at all in the nervous centres. Some physiologists, 
 such as Virchow, assert the existence of a tissue of this 
 kind, which they call the neuroglia. In health it is 
 so fine that its demonstration is almost impossible. 
 Analogy is certainly in fav;uu' of its existence. It can 
 be demonstrated in the liver, spleen, kidney, mucous 
 niembrane of the stomach, &c., to say nothing of 
 many tumom^s. To those who believe in its existence, 
 sclerosis is in its first element a simple hyperplasia. To 
 those who will not acknowledge that neuroglia is a 
 healthy constituent of nervous-centre tissue, sclerosis is 
 a new formation. Out of a good deal of controversy, 
 in which various opinions have been held by Virchow, 
 Bidder, Henle, Stilling, Deiters, Kolliker, Boll, Jac- 
 cobouritz, &c., to say nothing of British observers, 
 it seems now to be pretty generally allowed that there 
 is in the nervous centres an element that answers to a 
 connective tissue ; though whether this is formed by 
 the union of the processes of the spider-web cells of 
 Deiters and Eindfleisch, or in some other way, is still a 
 matter of controversy. But whether this nerve-cement, 
 as it has been called, is nominally finely granular or 
 finely fibrillated — and each view has strong and learned 
 adherents — it is certain tliat the first step in sclerosis is 
 the transformation of this cement into a finely-meshed 
 network. The only anatomical distinction that can be
 
 DEGEXEKATIOXS. 117 
 
 drawn between sclerosis and grey degeneration is 
 in tlie greater or less proliferation of this fibrous 
 network, and the laet of the presence of corpora 
 amylacea in gi'ey degeneration. It is wholly a question 
 of degree, and I am loth to assent to the one being 
 inflammatory and the other not. It is probable that 
 both are of inflammatory origin. 
 
 Eindfleisch, speaking of the grey foci from which 
 sclerosis starts, and the smallest of which are about the 
 size of a pin's head, says that an attentive examination 
 of the smallest of these grey foci leads to the curious 
 discovery that they have all got a red spot or line in 
 their centre, a distended blood-vessel cut across trans- 
 versely or obliquely. The microscope shows that all 
 these vessels, together with their finer ramifications, are 
 in a state which we should not scruple to call one of 
 chronic inflammation. He says that in these altera- 
 tions of individual vascular tufts is the first anatomical 
 element of the disease, the second consisting in a fibroid 
 metamorphosis and overgrowth of the neuroglia. 
 
 Van der Kolk thouo-ht that sclerosis was due to 
 repeated congestions, which lead to the exudation 
 of an albuminous fluid. 
 
 It may affect the brain in a variety of ways. 
 Gintrac speaks of it as affecting several parts of the 
 brain at once, or one cerebral hemisphere, or the 
 anterior lobes of the brain, or the posterior or the 
 middle, or the corpora striata, optic thalami, and 
 cornua Ammonis, or the cerebellum, or the pons and 
 tlie medulla oblongata, or various parts of the spinal 
 cord, or very rarely the nerves. The optic nerVe is
 
 lis DEGENERATIOXS. 
 
 more liable to tliis lesion tlian others ; and in specimen 
 765 of the Oxford Pathological Museum may be seen 
 the trunk of the facial nerve as hard as cartilage. There 
 was ulceration round it in the internal ear, and at its 
 exit from the bone it came to an end in consequence of 
 the ulceration, so that all communication with the face 
 was cut off. 
 
 Not unfrequently the sclerosed regions will lie sub- 
 jacent to the ependyma of the ventricles, and then the 
 ependyma will be thick and indurated ; and the walls 
 of the ventricles beneath the ependyma may be rugose 
 and full of small projections of indurated cerebral 
 tissue ; and ranch fluid will be found in the ventricles. 
 It may occur coincidently with softening, or be produced 
 round an old spot of ha3morrhage, or coexist with a loss 
 of substance of the brain, more or less considerable. 
 
 Pinel states that it does not invade the grey matter 
 of the brain, but this is certainly a mistake. Kot to 
 mention all the authorities quoted by Jaccoud, this 
 condition has been found in one case in the hemispheres, 
 centrum ovale, arbor vita3 of cerebellum, pons, and 
 anterior and lateral columns of the cord ; also in the 
 superior and inferior marginal convolutions and the 
 borders of the fissures of Sylvius on both sides, with 
 disseminated amyloid degeneration in the anterior 
 and lateral columns, and proliferation of the connective 
 tissue in the spinal ganglia and the cervical cord of the 
 sym]:)athetic ; also in the cortical and medullary sub- 
 stance of the hemispheres, the corpus callosum, fornix, 
 optic llialanii, corpora striala, })ons, crura cerebri, 
 cereljelhun, medidla oblongata, lateral and anterior
 
 DEGEIS^ERATIOXS. 119 
 
 columns of the cord, and a little in llie posterior 
 colunms ; also considerable induration of one hemi- 
 sphere. Again, in a case mentioned by Hirsch, there 
 "Were twenty spots on the left side, forty on the right 
 in the medullary substance of tlie hemispheres, with 
 the ])ons, medulla oblongata, optic thalami, and much 
 of the grey matter of the cord similarly affected ; whilst 
 in a case mentioned by Liouville both substances of the 
 hemispheres, the corpora striata and optic thalami, 
 cerebellum, crura cerebelh, corpora mamillaria, pons, 
 all the right olivary body, the olfactory nerves, the 
 optic, the motores ocuh, the left fifth, the left facial, 
 and the spinal nerves were all in a state of sclerosis. 
 
 Is it ever general over the whole brain ? 
 
 Dr. Quain has informed me of a case he had seen 
 in which the patient, a young lady, fell into a state of 
 quiet hebetude, and in which at the autopsy there was 
 found great increase of the cerebro-spinal lluid and 
 atrophy of the whole brain, with a very well-marked 
 indm-atiou of all the brain-substance, both grey and 
 white matter. ISlo microscopical examination was 
 made. But a case recorded in Bright's Medical Eeports 
 makes this point tolerably certain : ' A little girl, for 
 the last twelve months of her life, became stiff and 
 incapable of the slightest effort. The thumbs were 
 drawn in and the feet stretched out. There was diffi- 
 culty of swallowing, and apparently the power of vision 
 was gone, and she became quite imbecile. The skull 
 was well formed. On removini>- the dura mater about 
 live ounces of fluid escaped, but it was impossible to 
 say whether it was external or beneath the arachnoid
 
 ] 20 DEGENERATIOXS. 
 
 (probably the latter). Xo deposit on the dura mater, 
 and the arachnoid not thickened. The whole volume 
 of the brain was contracted ; on making a horizontal 
 section, the knife met with remarkable resistance as 
 soon as it had passed through the cortical substance, 
 as if cutting soft cartilage. The section was very re- 
 markable-looking. The corticle part was thick and 
 pulpy ; the medullary part was hard, constricted, and 
 shrunk, so that it seemed to enter the cortical substance 
 like white bands. It could not be scraped as an 
 ordinary brain. The margin around it was more 
 prominent and whiter than the rest. When pressed on 
 externall}^, the grey matter gave way, and the con- 
 volutions of white matter were felt beneath, like an 
 irregular hard body, and by a stream of water the 
 grey matter could be "slashed off, leaving the medullary 
 convolutions exposed, like the rugose stomach of 
 animals ; it appeared indeed more like a wax model 
 of a brain. The ventricles were moderately distended 
 and open, as if moulded in wax. The cerebellum had 
 its cortical substance soft, but the medullary was hard, 
 like the other ; but the corpus rhomboideum was soft, 
 so that a cavity could be washed out of it. The 
 medulla oblongata nnd spinal cord, as for as taken 
 out, also hard,' Dr. Bright adds, this hardening w^as 
 probably the result of chronic inflammation. 
 
 Perhaps the best description of sclerosis has been 
 given by Dr. Batty Tid^e, when speaking of this morbid 
 condition as it is found in the brain and spinal cord of the 
 insane. The microscopic appearances are as follows : 
 
 General Sclerosis. — Increase of granular material
 
 DEGEXERATIOXS. 121 
 
 of the outer layer of the grey matter of the brain. 
 Normal condition of tlie two inner layers. Irregularity 
 of tlie cells of the intervening layers as regards their 
 number, shape, size, and distribution. Thickening and 
 displacement of the nerve-fibres of the white matter. 
 Increase of the neuroo;lia. Proliferation of the nuclei 
 of the neurooflia and blood-vessels. Dr. Tuke ^ives a 
 case in which there was hypertrophy of tiie right 
 hemisphere depending on this condition, with atrophy 
 of the left limbs. 
 
 Disseminated Sclerosis. — Tliis Dr. Tuke woidd con- 
 sider a synonym for grey degeneration. I have already 
 told you that I believe grey degeneration and dis- 
 seminated sclerosis vary only in degree; that in one 
 the connective tissue proliferation is more than in the 
 other; and that each owns an inflammatory origin of a 
 low type. Dr. Tuke finds it among the cases of chronic 
 insanity ; most frequently in the white matter of the 
 corpora striata and optic thalami in scattered patches 
 of various size ; less commonly in the white matter of 
 the hemispheres, but, when there, in larger tracts. In 
 general paralysis and in epilepsy this variety is often 
 found in the medulla oblongata and the spinal cord, and 
 frequently in an extreme form. The nerve-fibres are 
 atrophied partially or completely ; in transverse sec- 
 tions the axis cylinders and sheaths are destroyed, and 
 the field is occupied by finely molecular and fibrillated 
 material imbedded in a cloudy homogeneous plasm. 
 In this matrix the proliferated nuclei exist, somewhat 
 enlarged, sometimes slightly granular in appearance; 
 but around the implicated spot they are to be seen in
 
 122 DEGENERATIONS. 
 
 much greater quantity, and not actually diseased. No 
 fatty degeneration. The morbid plasm is probably 
 modified neuroo-lia. 
 
 See Plate 9, in which the posterior columns show 
 the chief increase of the connective tissue. 
 
 Miliary Sclerosis. — There is not necessarily any 
 proliferation of nuclei. This condition is no way con- 
 nected with blood-vessels. It is a disease of the nuclei 
 of the neuroglia. It is common in both brain and 
 spinal cord in the insane, especially in general paralysis 
 and epilepsy. It may be described in three stages : 
 1st. A nucleus becomes enlarged and throws out a 
 homogeneous plasm of a milky colour, displacing the 
 nerve-fibres. In the centre of these semi-opaque spots 
 a cell-like body is seen with a nucleus, being the 
 original dilated nucleus of the neuroglia. The patch 
 may be unilocular or multilocular. 2nd. The morbid 
 plasm becomes distinctly molecular and permeated 
 by fibrils. Further displacement of the contiguous 
 tissues takes place, shown by induration of the com- 
 pressed fibres and blood-vessels curving round the 
 diseased part. After preparation in chromic acid the 
 white matter shows a number of opaque spots, irre- 
 gularly distributed, a molecular material with a stroma 
 of exceedingly delicate colourless fibrils. They can 
 be separated from the tissue and analysed ; they are 
 rendered transparent by strong nitric and sulphuric 
 acid, the acid rendering the molecular matter fluid. (Sec 
 Plate 15.) 3rd. The molecular matter becomes more 
 opaque, and contracts on itself", the boundaries become
 
 Plate 9. 
 
 C. Berjeau.Lith. 
 
 Baclcs Sc Co., Edm^ 
 
 CLE RO SI S
 
 DEGENERATIOXS. 3 23 
 
 puckered and irregular in outline, and the material 
 often foils out of the section, leavino; rao:2;ed holes. 
 
 Wliat Dr. Tuke has thus graphically described as 
 sclerosis foinid in the nervous centres of tlie insane 
 can be seen to exist in a large numljer of cases in which 
 the mental faculties have scarcely suffered at all — in 
 spinal cord disease, not at all. It is seen in cases of 
 myelitis in which life has been preserved for a few 
 weeks. In a case in wliich the symptoms consisted 
 mainly of intense neuralgic pain in the spine and 
 hmbs, whilst only very partial paralysis supervened 
 towards the close of life, a longitudinal section of the 
 cord showed in the grey matter some multipolar cells 
 remaining, with the debris of tubes and broken-up 
 tissue and many holes. The white matter was still more 
 degenerated. Miliary sclerosis may be extremely nnil- 
 ti[)le. Kesteven found spots of this degeneration in the 
 brain of an idiot to amount to 25,000 to a square inch 
 of surface. It is associated with amyloid and colloid 
 bodies, and yet must be distinguished from them. The 
 distinction is thus draw^n by Dr. Tuke and Mr. Kesteven. 
 ]\Iiliary sclerosis is distinguished from amyloid bodies 
 by the polariscope, whic]], in the former case, will give 
 neither the concentric rings nor the black cross of 
 amyloid bodies, whilst it renders evident the molecular 
 character of the degeneration. Colloid bodies (see 
 Plate 18) may be distinguished by their clearly defined 
 margins (miliary sclerosis presenting more or less irregu- 
 lar borders from the broken ends of fibrils, vessels, &c., 
 encroaching on their space), and from tlieir clear homo- 
 geneous translucent contents, which do not take tlie
 
 124 DEGENERATIO^'g. 
 
 carmine colouring. In extreme cases the appearance 
 of sections containing colloid bodies may best be com- 
 pared to a slice of sago pudding, for they exist in such 
 large numbers as almost completely to fill the field 
 of the microscope, separated slightly from each other 
 by a fine granular material. They do not undergo the 
 same gradation of development as miliary sclerosis, 
 nor push aside the fibres, nor can they be removed as a 
 separate substance from the dried section in which they 
 exist. 
 
 Mr.Kesteven expresses surprise that the same lesion, 
 miliary sclerosis, can be found in so great a variety of 
 diseases. He has seen it in acute meningitis of cord, 
 abscess of brain, locomotor ataxy, idiocy, leuksemia, 
 chorea, tetanus, subacute myehtis, pseudo-muscular 
 hypertrophy, paralysis with aphasia, hydrorachis interna, 
 progressive muscular atrophy, apoplexy with ha3mor- 
 rhagic softening, infantile convulsions, dementia, general 
 l)aresis, malignant disease of the cord, glioma of the 
 pons, internal haemorrhage, and puerperal mania. In 
 many of these conditions, however, there was inflam- 
 mation, and in other instances the diseases were of im- 
 portance, not so nmch qua lesion, but qua the seat of 
 lesion; the physiological phenomena varying according 
 to the part of the nervous centre attacked. 
 
 So little is definitely knoAvn about sclerosis, although 
 its presence is now readily recognised after death, that 
 I have thought it might help you to have a very brief 
 analysis of Bourneville's and Guerard's observations on 
 tliis morbid affection. They describe it as it affects the 
 spinal cord alone, and the spinal cord with the brain ;
 
 DEGENERATIOXS. 125 
 
 and although thek cases are not very numerous, their 
 observations make a valuable addition to our know- 
 ledge of the subject : — 
 
 1. The Spinal Form. — Symptoms: debut sudden or 
 gradual, generally gradual ; ushered in by feelings of 
 weight, formication, increasing weakness in one or both 
 lower limbs. 
 
 1st period. The feebleness ' paresis ' further attacks 
 the upper extremities. This may show remissions and 
 exacerbations. Progress painful. Help needed in 
 walking. The patient staggers like a drunkard. After 
 a variable time there are rhythmical tremors in the 
 upper and lower limbs, only accompanying acts of 
 voluntary movement. No tremor during repose. Sen- 
 sation retained. No disturbance in the functions of 
 nutrition, respiration, or circulation. 
 
 2nd period. To the paresis succeeds paralysis, which 
 becomes more and more complete. Aggravation of all 
 preceding symptoms. Soon rigidity and contraction of 
 all the paralysed limbs, and attacks of tonic convulsion 
 of the rigid limbs, especially the lower. The lower 
 limbs are also the seat of spasmodic rigidity witli inter- 
 missions of relaxation. The contraction affects first the 
 lower limbs, then the upper, then the trunk. 
 
 3rd period. Motor power vanishes. Contraction is 
 permanent. The patient becomes bed-ridden. Sen- 
 sation generally good. Keflex power diminished or 
 lost. Nutrition interfered with. Emaciation. Bed 
 sores. Intelligence preserved all through. 
 
 The Cerehro-SpinalForm. — Debut sudden or gradual ; 
 either by sudden or progressive feebleness of one or
 
 126 DEGENERATIONS. 
 
 both lower limbs ; or by this feebleness accompanied 
 by cerebral or ocular phenomena ; or by cerebral or 
 ocular phenomena, followed by feebleness of the lower 
 limbs. 
 
 1st period. Motor phenomena as in the spinal form. 
 Feebleness of sight. Diplopia. Vertigo. Headache. 
 Embarrassment of speech. Transitory apoplectiform 
 attacks without loss of consciousness. After a variable 
 time, tremor of the lower limbs, then of the upper, then 
 of the head, then of the eye, oscillation ' nystagmus,' 
 then of the tongue. The nystagmus is generally 
 binocular, but may be monocular. 
 
 2nd period. Aggravation of previous symptoms ; 
 then rigidity, or contraction, and convulsion, especially 
 of the upper limbs, usually tonic, sometimes clonic, 
 sometimes atrophy of papilla in retina. Speech worse. 
 Sensation good. Intelligence gradually impaired ; even 
 hebetude sometimes. Eespiration, circulation, and 
 digestion normal, except that there is constipation. 
 Urine healthy. 
 
 3rd period. Increase of spasm, rigidity, contrac- 
 tion, and paralysis. Speech uninteUigible. Intense 
 thirst. Swallowina; difficult. Nutrition interfered with. 
 Emaciation. Death from lung complications. 
 
 Our authors then endeavour to draw distinctions 
 between this disease and some others, and in this attempt 
 I think they fall into error. Their mistakes, however, 
 teach us something. 
 
 Senile Tremhling. — Disease of old ago, whilst scle- 
 rosis is of middle age. Tremors almost permanent. 
 Begins in head, tlien li|)s, cliin, longue, limbs.
 
 DEGENERATIONS. 127 
 
 Alcoholic Tremor. — At intervals ; worse in tlie 
 morning than in tlie evening, diminishing after a close 
 of alcohol. Begins in hands, then arms, legs, tongue, 
 lips. Speech hesitating, but not stuttering. Vertigo, 
 insomnia, hallucinations, amblyopia, weakened intelli- 
 gence. 
 
 Mercurial Tremor. — Only in workers in mercury. 
 Vibratory movements. All the limbs attacked at once. 
 No nystagmus. Tremor constant. Cure tlie rule. 
 
 Paralysis Agitans. — Debut often sudden. Tremors 
 incessant. No nystagmus. Tremor begins in the upper 
 limbs, then descends. Locomotion slow at first, then 
 becomes running, as if the patient were always running 
 after his centre of gravity. Intelligence preserved. 
 Very peculiar shape of the hand. No post-mortem 
 appearances known. 
 
 (In this our anthors are quite mistaken, as reference 
 to Lecture 10 will show.) 
 
 Sclerosis Cerehro-Spinal. — Debut generally gradual. 
 Tremor following on paresis. Tremor only on inten- 
 tional movements. Nystagmus. Tremor first in lower 
 limbs, and ascends. Locomotion uncertain, ' titabout,' 
 perhaps from the tremor. Hebetude. Distinct lesions 
 found ]}0st mortem. 
 
 Sclerosis Spinal. — Uncertainty of walk, due to feeble- 
 ness and paresis of the lower limbs, the initial symptom. 
 Motor troubles due to paresis or paralysis. Locomotion 
 feeble. Vertigo. No loss of equilibrium on shutting 
 the eyes. Sensation normal. Contraction present. 
 Pain in the lower limbs rare. Slight disturbance of 
 sight. Diplo})ia. Embarrassed speecli. Ilcadarhe. 
 Speech stuttering, never voluble.
 
 128 DEGENERATIONS. 
 
 Locomotor AtcLvy. — ■ Iiieoordmatioii, preceded by 
 pain in the back, and sometimes by paralysis of some 
 of the nerves of the orbit. No paralysis of Hmbs, only 
 incoordination. Locomotion disordered. Equilibrium 
 lost if the patient shuts his eyes. Muscles strong. 
 More or less antusthesia. Peculiar sensation of the soles 
 of the feet, as if the ground were cotton-wool. It is a 
 disease of adult age. Contraction only present in those 
 cases in which the posterior columns have been attacked 
 by sclerosis, and it is a late symptom. Pain in lower 
 limbs usual. Vertigo uncommon. Feebleness of sight, 
 amblyo[)ia, or amaurosis, at iirst temporary, then per- 
 manent ; or paralysis of the muscles of the eye, e.g. 
 ptosis, external strabismus at intervals. Dilatation of 
 pupils. 
 
 Chorea. — Jactitation, not only of voluntary move- 
 ments, but often involuntary. Paresis following jacti- 
 tation. Begins first in the arms, then face, trunk, lower 
 limbs. Walking in irregular jumps. Irritability of 
 temper. A disease of childhood. 
 
 General Paralysis. — Arrest of speech in the middle 
 of a word, but the patient is voluble. He has no know- 
 ledge of anything being wrong, and it irritates him to 
 tell him of it. Tremor continuous. General paralysis 
 and sclerosis may coexist. 
 
 Pathological Anatomy. — 1. Lesions visible to the 
 naked eye. Grey circumscribed patches or islets, of 
 greater or less size and depth, expanded without order 
 on the different columns of the cord, or on various 
 regions of the brain. These patches have irregular, 
 but pretty well defined contours. Their dimensions are
 
 DEGEXERATIONS. 129 
 
 very variable, tlic smallest being almost linear ; the 
 largest may measure three to four centimetres in 
 length and two to three in widtli. Their number is 
 generally pretty considerable. 
 
 On touch, they have a consistence firmer than that 
 of surrounding tissue. Sections show that they extend 
 more or less deeply, in the form of nodules or of 
 cones, with badly-delined limits. At the periphery of 
 the cord they are generally rather below the level of 
 cord — sometimes they project. Colour deeper than 
 that of the grey matter of the brain. In chromic 
 acid they are yellowish, then white and opaque, con- 
 trasting with the greenish grey colour of healthy nerve 
 substance in chromic acid. 
 
 As to distribution, it seldom attacks the grey 
 cortex of the brain. It is sometimes found on the 
 limits of the white and grey, intruding into each. 
 Pretty often it is seen in the walls of the lateral 
 ventricles. It may be in the centrum ovale ; in the 
 crura cerebri, looking like secondary degeneration ; 
 but in secondary degeneration the lesion has a regular 
 form, and extends from one extremity to the other ; 
 whilst in disseminated sclerosis the lesion is irreo-ular, 
 very limited, and coloured hke the neighbouring parts. 
 The pons is often attacked by sclerosis. Grey spots, 
 more or less deep, appear on its lower surface. In the 
 medulla oblongata, the olivary bodies are frequently 
 attacked, or one of them ; but the pyramids and the 
 other columns may be. In one case the aqueduct of 
 Sylvius was surrounded by a large patch of sclerosis, 
 whence sprang prolongations to the medulla oblongata
 
 130 DEGENERATIONS. 
 
 and towards the fourth ventricle. The cerebellum is 
 seldom attacked at its circumference. Patches may be 
 visible in its white matter on section, and more espe- 
 cially in the rhomboidal body. In the spinal cord 
 grey spots are seen beneath the pia mater, elongated 
 patches terminating in a point, more symmetrical 
 than in the brain, occupying two opposite columns 
 or several columns on the same side. All the regions 
 of the cord are liable to it. The cranial nerves are 
 usually free ; but Cruveilhier found the roots of the 
 hypoglossal, glosso-pharyngeal, and pneumogastric 
 nerves grey ; Skoda, the optic nerves hard and flat- 
 tened ; Vulpian, the olfactory and optic, with very 
 apparent patches of sclerosis ; Ordenstein, the hypo- 
 glossal and motor oculi extei'nus of the left side 
 sclerotic. The spinal nerves are not affected, and 
 may spring quite healthy from the centre of patches 
 of sclerosis. Membranes generally healthy. Muscles 
 often fatty. 
 
 (Other observers, however, ]iave sometimes found 
 the spinal nerves sclerotic.) 
 
 Microscopically, their observations arc very similar 
 to those recorded above ; and they come also to similar 
 conclusions — that proliferation of the nuclei and con- 
 comitant- hyperplasia of the reticulated fibres of the 
 neuroglia are the initial and fundamental facts. De- 
 generative atrophy of the nerve elennents secondary 
 and consecutive. 
 
 Whilst these observations are useful up to a certain 
 point, it must be remembered that the aggregate of 
 symptoms does not depend on the special form of 
 
 A
 
 DEGENERATIONS. 131 
 
 invasion of the disease, but on the foci which are 
 attacked ; and when we come to speak of other 
 diseases, you will find there is in many cases no broad 
 line of demarcation between them and cerebro-spinal 
 sclerosis. 
 
 Consult — 
 
 Giutrac. Op. cit. 
 
 Jaccoud, * Pathologie Interne.' 
 
 Hammond, ' Dis. of Nervous System.' 
 
 Wilks, ' Path. Anatomy.' 
 
 Rindfleisch, 'Path. Histology.' 
 
 Rokitansky, 'Path. Anatomy.' 
 
 Reynolds, ' System of Medicine.' 
 
 Bucknill and Tuke, ' Psychol. Medicine.' 
 
 Calmeil. Op. cit. Vol. ii. pp. 200, 418. 'Softening.' 
 
 ' Med. Record,' vol. i. .39. Westphal. 
 
 'West Riding- Asylum Rep.,' vols. ii. and iii. Dr. Herbert Major. 
 
 ' Med. Record,' vol. i. 830. Palmerini. 
 
 ' Med. Record,' vol. i. 728. Dr. Batty Tuke. 
 
 Bourneville & Guerard, ' De la Sclerose.' 
 
 ' Med. Chir. Rev.,' April 1873. 
 
 ' Guy's Hosp. Rep.,' vol. xvii. 185^ 190. 
 
 'Med. Chir. Rev.,' July 1874. 
 
 ' Med. Record,' vol. ii. 128. Benedikt. 
 
 ' Med. Record,' vol. i. 258. Boll. 
 
 ' Med. Record/ vol. i. 466. Deiters. 
 
 K 2
 
 132 
 
 LECTUEE V. 
 
 TUMOURS. 
 
 I^^OTHING is more difficult than to form a tolerably 
 reasonable classification of tumours of the nervous 
 system. We might take each envelope and each por- 
 tion of the brain and cord, and mention the tumours 
 that are found in each situation, but such a classification 
 would involve much tautology. Or we might form 
 divisions according to the characters of the tumours 
 themselves, or dependent on the tissues from which 
 they spring. All classifications must be more or less 
 artificial ; all are open to objection. 
 
 Jaccoud, closely followed by Hammond, divides all 
 tumours of the brain into four varieties : — 
 
 1. Vascular, including Aneurisms and Erectile 
 Tumours. 
 
 2. Parasitic, including Echinococci and Cysticerci. 
 
 3. Diathetic and constitutional, including Cancer, 
 Tubercle, and Syphilitic growths. 
 
 4. Accidental and non-vascular, including — 
 i. Fibroplastic, or Sarcomata. 
 
 ii. Tumeurs a myelocytes, 
 iii. Cholesteoma. 
 iv. Cranial exostoses.
 
 TUMOURS. 133 
 
 V. Lipoma, 
 vi. Cysts, which may be simple, compuimd, or 
 
 containing hair, 
 vii. Enchondroma. 
 viii. GUoma. 
 ix. Gho-Sarcoma. 
 X. Cyhndroma. 
 xi. Myxoma. 
 He classifies Uimours of the cord as — 
 
 1. Syphilitic, either osseous or periosteal. 
 
 2. Cancer, including Colloid, Melanic, Sarcoma, and 
 Cysto-Sarcoma. 
 
 3. Tubercle. 
 
 4. Fibroma. 
 
 5. Parasites. 
 
 This list is a sufficiently good one, looked at as a 
 mere enumeration, but it is defective as a classification. 
 For instance, aneurisms would come better under 
 lesions of vessels ; parasites can hardly be said to form 
 a tumour at all in the brain and cord ; to class cancer 
 and tubercle under the head of diathetic tumours, is 
 to make an assertion as to the nature of those lesions 
 that many observers consider as still unproved ; whilst 
 it seems scarcely advantageous to make a separate 
 heading of cylindroma, which is an instance of mucous 
 degeneration of a fibroma or a sarcoma. 
 
 Gintrac simply enumerates various forms of tu- 
 mours under the heading of degenerations, and mentions 
 tumours as amyloid, fatty, cholestearic, and hasmatic 
 (the latter, by the bye, seeming to be merely old extrava- 
 sations partially reabsorbed and surrounded by a cyst-
 
 134 TUMOURS. 
 
 wall) lime concretions, bony productions, encliondro- 
 mata, fibromata, and fibroplastic tumours. 
 
 Dr. John Ogle, in ' The British and Foreign Med. 
 Cliir. Eeview,' is not so much attempting a classification 
 of tumours as illustratinfj; certain well-known forms 
 from the resources of two important museums ; and 
 with this purpose he speaks of scrofulous deposits, 
 purulent deposits, cancer, fibrous and allied forms of 
 tumour, calcareous and osseous deposits, tumours of 
 uncertain nature, and cysts including hydatids. 
 
 It seems, however, more reasonable that, as Eind- 
 fleisch says, the most important consideration should be, 
 not the individual species of tumours, but their seat, 
 the tissue from which they proceed. 
 
 He divides tumours into three varieties ; viz. : — 
 
 1. Tumours which proceed from the free surfaces 
 of the envelopes and interior cavities of the nervous 
 system. 
 
 2. Tumours Avhich proceed from the sheaths of the 
 vessels. 
 
 3. Tumours which have their origin from the 
 neuroglia. 
 
 Under the first heading, tumours which jiroceed 
 from the free sm^faces of the envelopes and interior 
 cavities of the nervous system, he classes : 
 i. Pacchionian granulations, 
 ii. Spindle-celled Sarcoma. 
 iii. Myxoma, 
 iv. Psammoma. 
 V. Lipoma. 
 Under the second heading, tumours which proceed 
 from the sheaths of the vessels, he classes :
 
 TUMOURS. 135 
 
 i. Carcinoma cerebri simplex, 
 ii. Fungus of the dura mater, 
 iii. Cliolesteoma. 
 
 iv. Epitlielioma myxomatodes psammosum. 
 V. Papilloma of pia mater and vessels. 
 vi. Papilloma myxomatodes. 
 vii. Gumma syphiliticum.' 
 
 Under the third headmg, tumours which have their 
 origin in the neuroglia, he places : 
 i. Glioma. 
 
 ii. Myxoma of the nerve substance, 
 iii. Tubercle. 
 
 iv. Fibroma, including false neuroma. 
 Following this classification as convenient, though 
 by no means perfect, let us see where these various 
 tumours are situated, and of what elements they are 
 composed. Taking them, then, in the order above 
 mentioned : 
 
 i. Pacchionian granulations of the arachnoid, espe- 
 cially along the longitudinal sinus ; non-vascular groups 
 of papillae, consisting of striped connective tissue, poor 
 in cells, proceeding directly from a thin but a con- 
 tinually renewing layer of sub-epithehal germinal 
 tissue. 
 
 ii. Sarcoma. Less frequent than cancer ; these 
 productions have a variable volume, seldom attaining 
 the size of an apple. Exceptionally they may be 
 developed in the thickness of the nervous tissue, but 
 they generally spring from the dura mater, and more 
 often at the base than tlie convexity. Sarcoma may 
 also spring from the dura mater spinalis. Eokitansky
 
 136 TUMOURS. 
 
 has seen some that liacl originated from the pia mater 
 or the ependyma, but this starting-point is rare. Their 
 consistence varies. In some cases it is nearly aUied to 
 that of fluid tumours ; in others the mass is soft ; it 
 presents a sort of gelatinous transformation ; sometimes 
 it is pitted with small cavities, filled with a clear, 
 yellowisli, non-viscous fluid. These tumours are com- 
 posed of fusiform bodies, nuclei, and vessels ; amorphous 
 matter is also met with, connective tissue, and less 
 frequently fat vesicles. 
 
 iii. Myxoma, generally from tlie convexity of the 
 brain ; the brain accommodates itself to its presence 
 easily. Also from the dura mater spinalis, and here 
 presses dangerously upon the spinal cord. 
 
 Jaccoud speaks of these tumours as having their 
 origin from the spheno-occipital synostosis ; as being 
 very small, attaining the size of a filbert at most, soft 
 and fragile, having a gelatinous aspect. The small 
 mass is attached by a pedicle to a, small cartilaginous 
 excrescence springing from the spheno-occipital suture, 
 appearing free between the dura mater and the 
 arachnoid, or adherent with the arachnoid to the 
 centre of the pons. These tumours are rare. 
 
 iv. Psammoma. A tumour with a connective 
 tissue, or even with a mucoid tissue substratum, which 
 is distinguished by its contents of globular lime con- 
 cretion, as in the pineal gland. These growths have 
 been met with at once in the brain, spinal cord, spinal 
 membranes, and nerves. They are not uncommon in 
 the choroid plexus. They vary in size from a pea to 
 a nut. It is probable that these tumours have always
 
 TUMOURS. 137 
 
 a connective tissue origin, and tliat when they are found 
 with a mucoid tissue substratum tlicy are really exam- 
 ples of mucoid degeneration. 
 
 V, Lipoma. Eare. Small lipomata may be found 
 springing from the inner surface of the dura mater 
 cerebri, and from the ependyma of the ventricles. Dr. 
 Coats of Glasgow has published a case of a fatty growth 
 connected with the pia mater over the corpus callosum. 
 Gintrac speaks of lipoma as a disease generally of foetal 
 or very early life, and especially of the ventricular 
 walls. Later on they may attack the grey matter of 
 the convolutions and the corpora striata, and in adult 
 ao-e the meninges. The fattv matter is often con- 
 tained in a kind of cell, these cells being surroimded by 
 a common membrane or cyst, and provided with 
 vessels. 
 
 The second heading comprises : 
 
 i. Carcinoma cerebri simplex. Most frequent from 
 the under surface of the pia mater. The first link of 
 this process is the formation of larger cell-heaps out of 
 each adventitial cell. The cells at the centre of the 
 ball are globular, at the surface spindle-formed. The 
 spindles of adjacent cell-heaps come together with 
 incomplete fibrous lines, and thus form finer septa, 
 which subdivide the larger alveoli of every carcinoma. 
 In the further increase of the tumour the cell prolifera- 
 tion predominates. The vessels from which the new 
 formation proceeds are in a great measure obliterated 
 to thin lines of connective tissue. This is Eindfleisch's 
 description. 
 
 Cancer may spring from the bones, the meninges,
 
 138 TUMOURS. 
 
 the orbital cavity, or the brain : wlien the brain is the 
 seat of origin, cancer may attack, in order of frequency, 
 the cerebral hemispheres, the cerebellum, the optic 
 thalami, the corpora striata, and the pons. Less 
 frequently are the corpora quadrigemina, the fornix, 
 and tlie medulla oblongata attacked. Cancer of the 
 orbit or of the cranial bones may proceed inwards, 
 and cancer of the brain outwards. The size of the 
 tumours is very variable ; the largest are those which 
 proceed outwards, or which occupy the cerebral hemi- 
 spheres. 
 
 When cancer is primary, which in tlie brain is 
 generally the case, it is mostly single ; if it is secondary, 
 or if it coincide with cancer of viscera, it is often 
 multiple, and then may be perfectly symmetrical. 
 
 Unless it proceeds externally, cerebral cancer 
 undergoes no ulceration or sanious softening ; indeed 
 it may partially retrograde, its elements becoming 
 atrophied or fatty, and the tissue is transformed into a 
 compact homogeneous caseous mass, in wiiich the vessels 
 are destroyed. The stroma may beincrusted with lime 
 deposits. 
 
 The principal varieties of cancer are encephaloid, 
 much the most common, then scirrhous, and colloid. 
 Ogle gives ten instances of cancer springing from the 
 external cerebral membranes, two from tlie ependyma, 
 twenty-two occupying some part of the cerebrum, three 
 having their origin in the bones of the skull, two in 
 the cerebellum, and two in the medulla oblongata. 
 
 ii. run2!;us of tlie dura mater. It arises from the 
 side of tlie dura mater turned to tlie bone, penetrates
 
 TUMOUES. 139 
 
 with the vessel into the compact substance, destroys 
 the vitreous table, thereupon spreads out somewhat 
 more easily in the diploe ; finally breaks the external 
 compact lamella of the cranial bones to lift up the 
 integuments of the cranium as a fungoid proliferation. 
 
 In the catalogue of the Pathological Department of 
 the Oxford Museum, Van der Kolk makes some interest- 
 ing remarks with reference to specimen 803, three 
 so-called fungi of the dura mater. These tumours 
 were supposed by Wenzel to spring from the dura 
 mater ; by Walther, from the diploe of the cranium ; 
 by Chelius, sometimes from the dura mater, sometimes 
 from the diploe, sometimes from the periosteum. To 
 settle the point, he says, I injected the middle 
 meningeal artery on either side, and found that the 
 injection passed freely into the fungi, thus showing that 
 they grew from the dura mater itself. But the outer 
 of the layers of which the dura mater is composed is 
 nothing but periosteum, and therefore these fimgi are 
 diseases of the periosteum. 
 
 iii. Cholesteoma. Pearl cancer. It unites the 
 structure of an epithelial carcinoma with the inuocuity 
 of a wart. It is a pavement epithelium, whose cell 
 cyhnders have been entirely converted into a mass 
 of pearly globules, shining like satin, most frequent 
 at the base of the brain, and occasionally as large as 
 a walnut. It is covered upon its surface by the 
 arachnoid, and evidently springs from the vessels of 
 the pia mater. Sometimes it is found in the centre of 
 the brain substance, having its origin in the lymph 
 spaces and slie:iths of vessels. Some observers say that
 
 140 TUMOURS. 
 
 a tumour of this kind may contain a good deal of 
 cholesterine and stearine. It may be connected with 
 the meninges, the brain, the cerebellum, and the spinal 
 cord. Its form is irregular, with an envelope of a 
 certain fibrillar arrangement, and with the parenchyma 
 of the tumour disposed in connective layers ; both 
 envelope and parenchyma are nearly non-vascular. 
 
 iv. Epithelioma myxomatodes psammosimi. It is 
 very doubtful whether it is scientific to draw any line 
 of demarcation between this tumour and the preceding. 
 It is closely allied to it. It consists of epithelial cell- 
 cylinders and nodules imbedded in a very voluminous 
 stroma of mucoid tissue. It seems really to be an 
 instance of mucoid degeneration of pearl cancer, with 
 the addition of lime concretions. It is rare. It has 
 been met with in the third ventricle. 
 
 Perhaps this form and the two following might be 
 included under tlie cylindroma of Jaccoud. 
 
 On looking back upon a case I saAv a good many 
 years ago, I believe it was an instance of this disease : 
 
 Man, aged 52. Calvaria very dense. Dura mater 
 adherent along the supeiior longitudinal sinus. Brain 
 itself rather soft, especially the crura cerebri. Cere- 
 bellum very soft. Pituitary gland very jirominent. 
 Beneath it and all round, the dura mater was detached 
 from the bone, and there -was a soft feeling beneath it. 
 On section this was found to depend upon a mass of 
 soft colloid-looking material, which was united to the 
 pituitary gland, and occupied the site of nearly all the 
 body of the sphenoid bone, which it had destroyed, 
 part also of the ethmoid, and the basis of each orbit,
 
 TUMOURS. 141 
 
 with the nerves entering each orbit. The colloid mass 
 was the seat of small haemorrhages. Under the micro- 
 scope it was composed of granular cells of very various 
 shapes. The disease had attacked the dura mater 
 lying over it. 
 
 V. Papilloma of the pia mater and vessels. This 
 tumour is reddish-grey, transluceut, tremblingly soft. 
 It breaks up into a mass of reddish branched papillai, 
 each of which has a central vessel, very little connec- 
 tive tissue, and a doubly stratified epithelial mantle. 
 The stroma of the papilke is connected with the blood- 
 vessels. 
 
 vi. Papilloma myxomatodes mostly occurs multiple 
 in the brain. It is distinguished from simple papilloma 
 by the abundant production of mucus at the surface of 
 the papilla'. The epithelium consists of very large 
 well-formed cylindrical cells, which secrete the mucus. 
 
 vii. Syphiloma of the nervous centres. Syphiloma 
 of the nervous centres exists sometimes in the state 
 of diffuse infiltration, but most generally it forms a cir- 
 cumscribed swelling, a true tumour. It is situated in 
 the meninges alone, or rather in these membranes and 
 in the cortex ; it rarely occupies the nervous tissue 
 alone. Syphiloma is never encysted, and even when 
 it appears to constitute a well-limited tumour, it is 
 really diffused at the circumference, and penetrates for 
 a certain distance into the normal tissue ; the volume 
 is very variable, but in the brain it never attains tlie 
 considerable dimensions that it sometimes presents in 
 the lung or the liver. The tumour appears as a soft 
 homogeneous mass of reddish-grey, sprinkled with
 
 142 TUMOURS. 
 
 bloody puiicta in certain cases ; this substance furnishes 
 no juice, or rather it gives out a juice hmpid and 
 opalescent, and, as it were, mucous. These productions 
 are essentially composed of nuclei and cells ; these latter 
 occupy sometimes the centre of the mass, whilst the 
 nuclei are at the circumference ; the nuclei, which 
 generally contain a very visible nucleolus, present 
 besides nothing particular ; the cells are like the white 
 globules of the blood with a single nucleus ; these 
 elements, with which we sometimes find some bodies of 
 a doubtful cellular nature (the protoplasms of Wagner), 
 occupy the meshes of a connective network of new 
 formation, and from the reciprocal relations of the cells 
 and the stroma there results a finely alveolar texture. 
 
 The most frequent further transformation is atrophy 
 of the cells and of the nuclei, either simple atrophy, or 
 combined with a fatty degeneration of greater or less 
 extent. 
 
 The point of origin of syphiloma is generally the 
 normal connective tissue; but for the brain and all the 
 organs poor in tissue of this kind Wagner is led to 
 admit that the cells and the nuclei proceed from the 
 multiplication of the nuclei of the capillaries, and 
 that the stroma is formed by the further fibrous meta- 
 morphosis of the wall of the vessel. This process is 
 not constant, and in a good number of cases there is 
 really a new formation of connective tissue. 
 
 Dr. Broadbent has lately given an exhaustive 
 account of syphilitic lesions of the nervous centres. 
 He says that, generally, a small part of the organ is 
 attacked, and the remainder is left quite free. The
 
 C. Berjeau.lith.. 
 
 Banks Sc Co. Edxa' 
 
 SYPHILIS OF BR,AIN,
 
 TUMOUES. 143 
 
 disease is strictly localised in the spot it alTects. The 
 outer part is composed of librous tissue, whicli can be 
 seen to represent the natural fibrous supporting elements 
 of the part in a state of augmentation, while the func- 
 tioning elements of the [)art liave dwindled away. It 
 is a local sclerosis. See plate 11, in which this fibrous 
 condition is beautifully seeii in a concentric arrange- 
 ment. Dr. Moxon's plate of syphilis of the spinal cord 
 in ' Guy's Hosp. Eeports,' vol. xvi., is somewhat similar. 
 
 The central part of the syphilitic nodule sliows 
 the caseous or gummatous iaint yellowish matter of 
 more and more elastic consistence, and less and less 
 friability and curdiness, generally rather sharply dis- 
 tinguished from the fibrous outer part, and sometimes 
 softening down or calcifying. There are signs of more 
 acute inflammation in tlie immediate neighbourhood, 
 showing lymph or adhesions to the part aroimd. 
 
 Dr. Moxon says that syphilis attacks the surface 
 of the brain and its membranes ; it attacks them in 
 limited spots, and it spreads slowdy. The morbid 
 changes are, on the one hand, adhesions of the mem- 
 branes to each other and to the surface of the brain, 
 by means of an adventitious material of firm consist- 
 ence and yellow colour, which may be called lymph, 
 but is liarder, tougher, and mere opaque. This exu- 
 dation may be found at any part of the surface ; it 
 invades and destroys the grey matter, interferes with 
 the supply of blood, and, wlien it occupies the mem- 
 branes at the base of tlie brain, surrounds and involves 
 the nerves in the intracranial part of their course. 
 
 Locomotor ataxy is not directly caused by syphilis ;
 
 144 TUMOURS. 
 
 but it is easily conceivable that in multiple syphilitic 
 deposits in the cord a sufficient number might be 
 situated in the course of the posterior white columns 
 and grey matter to impair spinal coordidation. Acute 
 general or local myelitis may be caused by syphilis, 
 especially in the secondary stage, inflammatory soften- 
 ing being set up round a small gumma. Spinal menin- 
 gitis may also be due to syphilis. Small syphilitic 
 tumours may exist both in the pons and the medulla 
 longata, and the cerebellum may probably be affected 
 in a similar manner. The habit of locality of the 
 tumours, as well as of the diffused exudations, is to 
 affect the surface, although gummata may be found, in 
 the substance of the brain ; usually, however, in the 
 more vascular parts, the grey matter of the corpora 
 striata or thalami. In the diffuse form we may have 
 the membranes adherent to each other and to the con- 
 volutions by means of firm plastic material ; and, as a 
 result, the vessels of the pia mater are occluded, the 
 supply of blood to the peripheral grey matter is dimi- 
 nished, and this undergoes atrophic change of some 
 kind ; or small indurations may invade the nervous 
 structures and the membranes. 
 
 The following case showed some of the usual 
 appearances : — Woman, aged 50. The dura mater rather 
 roughened on its inner surface, over the space of a five- 
 shilling piece, on the upper surface of the middle 
 lobe of the right hemisphere. At this spot all the 
 membranes were adherent to the brain. At this spot 
 also the brain itself was very hard, but smooth, and 
 there was no appearance of convolution here. On
 
 TUMOURS. 145 
 
 section vertically, a small tumour was cut through, 
 hard and yellow, like tliose of syphilitic origin. It was 
 the size of a small walnut. The grey matter imme- 
 diately around it was indurated ; all the rest of the 
 grey matter was healthy. The white matter was uni- 
 versally soft in this hemisphere, almost diffluent in 
 some places, and totally without bloody puncta. The 
 septum was entirely gone, and only the fine membrane 
 left. No fluid in the ventricles. Arteries healthy. Left 
 hemisphere healthy. 
 
 Convulsions depending upon epilepsy may be pro- 
 duced by tumours growing either from the bones or 
 dura mater, or in the pia mater, or in tlie substance of 
 the hemispheres, where the tumours reach the suriiice ; 
 or by diffused exudation in the pia mater, or by throm- 
 bosis at the time of its occurrence and during the 
 consecutive changes ; or by slighter changes affecting 
 tlie nutrition of the hemispherical grey matter. 
 
 Speaking generally, and still drawing much from 
 Dr. Broadbent's experience, paralysis of cranial nerves 
 and of the limbs, gradual in its mode of access, is 
 characteristic of disease about the base of the brain ; 
 convulsions and mental affections of disease of the 
 convex surface of the hemispheres. No strict line of 
 demarcation can be drawn between cases in which 
 there is extensive exudation in the membranes and 
 those in which the morbid process results in the 
 formation of distinct tumours. In the former, the 
 deposit frequently here and tliere takes the form of a 
 nodule, which projects into the l)rain .substance ; and 
 a syphiloma is accompanied by or sets u[) clianges 
 
 L
 
 146 TUMOURS. 
 
 in the adjacent part of tlie meninges. Gros and 
 Lanceraux give one case in which the entire mass 
 was infiltrated ; in another, disseminated exudations 
 existed in diflferent parts ; in six, tumours were found 
 in the anterior lobes ; in three, in tlie middle lobes ; 
 in three, in tlie corpora striata ; in three, a great part 
 of the hemisphere was involved. 
 
 Double optis neuritis is said by some observers to 
 be an important symptom of these and other cerebral 
 tumours. I have no doubt that the ophthalmoscope 
 gives important aid in determining the condition of 
 syphihtic meningitis or of syphihtic tumour. If the 
 latter is present, and is not complicated with meningitis, 
 its effect on the retina is to produce choked disc, as 
 the result of pressure interfering with the venous 
 reflux from the retina. On the other hand, if basilar 
 meningitis of the anterior lobes is present, we may 
 have true optis neuritis from the spreading downward 
 along the nerve of the meningeal inflammation. This 
 is usually a gradual process, and more likely to follow 
 syphilitic than any other variety of meningitis. The 
 real difficulty lies in the fact that syphilitic tumour is 
 not unfrequently associated with a certain amount of 
 meningitis. Cerebral disease in infantile syphilis may 
 be mistaken for tuberculous meningitis. In Dr. Broad- 
 bent's case there was lesion of the left occipital lobe, 
 which was hard and shrunken. The induration 
 involved the cuneiform lobule. The pia mater was 
 adherent and almost black. The grey substance was 
 atrophied ; and the white, firm and tougli, like leather. 
 The posterior corner of the lateral ventricle was 
 
 I
 
 C Berjeau.Lith 
 
 Banks &: Co.Edia' 
 
 GLIOMA 1'' B KA I N
 
 Banks 8c Co., Edm'.' 
 
 CtLioma diseased vessels,
 
 TUMOUKS. 147 
 
 inclosed by this indurated wlnte substance. There 
 was also superficial induration of the posterior part of 
 the left optic tlialamus, and some induration of the 
 superficial transverse fibres of the pons. 
 
 Tlie arteries of (lie brain in syphihs are frequently 
 attacked with inflammation, usually beginning in the 
 outer coat. This may lead to thrombosis, which cuts 
 off the supply of blood, and produces the results now 
 known to follow this event. The effects are first an 
 accumulation and stagnation of blood in the capillaries 
 in the area of distribution of tlie vessel blocked ; and 
 unless collateral circulation con be established, tliere 
 will be subsequent softening. 
 
 Tlie Third Form. — Tumours wliich proceed from 
 the neuroglia. The cells of tlie neurosflia are the 
 starting-point. 
 
 i. Glioma. An abnormal development of con- 
 nective tissue, more usually found in the posterior 
 cerebral lobes. It may be as large as an orange. It 
 is of two kinds — one soft, of the consistence of brain 
 substance ; the other much harder. It consists of 
 cells and nuclei, but never contains any of the nervous 
 elements. It is practically a neoplasia of the neuroglia ; 
 and, on minute examination, is seen to consist of cells 
 of connective tissue, of vessels, and of cells resembling 
 amyloid bodies, but which give rise to no iodine 
 reaction. 
 
 Plate 12 is an example of glioma of the brain. 
 
 Plate 13 is a second specimen of the same, showing 
 that the vessels are much implicated, being specially 
 thickened. 
 
 L 2
 
 148 TUMOURS. 
 
 Dr. S. Smith's account of the microscopical appear- 
 ance of the vessels in his case, reported in the ' British 
 Medical Journal,' June 6, 1874, is, that in the mem- 
 brane surrounding the tumour, but not in the substance 
 of the tumour itself, the vessels were all surrounded by 
 a cellular infiltration of the intervening tissues, and the 
 perivascular lymphatic sheaths were much distended 
 by epithelial proliferaticju from their walls : the calibre 
 of the vessels was much diminished by the surrounding 
 cell-growth. Small masses of red corpuscles were 
 seen, surronnded by a cell-growth, extending to as 
 much as twelve times the diameter of the calibre of the 
 vessels, the growth being of a fibronuclear structure, 
 arranged in a concentric manner around the calibre of 
 the vessels, and limited externally by a finely fibrous 
 investing membrane, no muscular coat being visible. 
 
 ii. Myxoma of the nerve substance. More com- 
 mon in the spinal cord than in the brain, and more 
 common on the peripheral nerves than in the spinal 
 cord. The myxoma proceeds from a hyperplasia of 
 the nerve-connective substance, and uniformly extends 
 by infiltration in all directions. The fibres of the 
 spinal cord or of the peripheral nerves are crowded 
 asunder and partially perish. On the nerves myxoma 
 presents itself as a spindle-formed tumefaction. 
 
 It forms a variety of neuroma. 
 
 Genuine neuroma contains pre-eminently newly- 
 formed nerve-fibres. Another form of neuroma 
 possesses no new nerve-fibres ; it is really a fibroma in 
 the substance of a nerve, and is produced by a local 
 new formation from the interstitial connective tissue ;
 
 E.L.rox.M.D, 
 
 Plate 14. 
 
 Banks 8c CcEdm"" 
 
 FIBROMA OF ^^= CERVICAL NERVE
 
 TorouRs. 149 
 
 this interstitial proliferation has most frequently the 
 libroid character, more rarely that of myxoma, or the 
 softer forms of lipomatoiis sarcoma. 
 
 Plate 14 is an example of the fibroid form of false 
 neuroma, from the Oxford Museum. 
 
 The specimen was from a girl, aged 24, who 
 had long complained of pain in the left scapula and 
 shoulder. To this succeeded numbness of the left arm 
 and foot, and then paralysis of these parts, with violent 
 attacks of pain and tetanic spasms in all the limbs. 
 
 The neuroma is covered by a thick fibrous capsule; 
 it has stretched and elono-ated in a remarkable manner 
 the root of the fourth nerve, so that the posterior root 
 of the nerve seems to have been injured by it ; it is 
 contained or shut in the sac of the dura mater. At 
 the posterior surface of the medulla are abundant false 
 membranes, which have glued together the medulla 
 and the dura mater. 
 
 iii. Tubercle. Tubercle prefers the hemispheres 
 and the cerebellum ; it is seldom found in the 
 optic thalami and corpora striata, and is only ex- 
 ceptionally met with m the pons and the medulla 
 oblongata. 
 
 Oo:le has found a scrofulous mass on the dura 
 mater, coverinii; the rif>ht lobe of the cerebellum, and 
 implicating the brain at the same time ; twice the 
 tentorium cerebelli was affected ; twenty-three times 
 the masses were connected with the pia mater, of 
 which in two cases the choroid plexus was affected ; 
 in one the velum interpositum, and in one the 
 ependyma of the ventricles was the seat ; twenty-seven
 
 150 TUMOUES. 
 
 times the tuberculous masses were found in tlie sub- 
 stance of the cerebrum itself ; twenty-eight times in the 
 cerebellum ; once in tlie left crus cerebelli ; four times 
 in the medulla oblongata, in one of which a similar 
 mass was found in the substance of the sixth cranial 
 nerve ; and five times in the pons. It is scarcely 
 necessary to say that in many of tliese cases the 
 scrofulous masses were multiple, and existed in various 
 organs of the encephalon at one and the same time. 
 
 Gintrac has found tubercle in all portions of the 
 meninges, in the brain, especially in the cortical sub- 
 stance, in several situations at once, in the cortical 
 substance only, in the middle lobes, in the anterior and 
 the posterior, in the optic thalami, generally solitary in 
 this situation, and in the pituitary gland ; in the cere- 
 bellum, its right lobe, its left, and both lateral lobes, 
 in the central region of the cerebellum alone, and in 
 this situation as well as the lateral reo;ion. He finds 
 it generally solitary in the mesocephale, especially in 
 the crura cerebri ; but it may coexist in the mesoce- 
 phale and the brain ; in the mesocephale and the 
 cerebellum ; in the mesocephale, the cerebellum, and 
 the brain ; and the mesocephale, the cerebellum, the 
 brain, and the meninges. It is also generally solitary 
 in the medulla oblongata, but has been found coinci- 
 dently in the medulla oblongata and the brain, the 
 medulla oblongata and the cerebellum, and the me- 
 dulla oblongata and the mesocephale ; whilst the 
 same rule obtains in tubercle of the spinal cord, 
 although it may exist at once in the spinal cord and 
 the brain,
 
 E.L.Fox.M.D. 
 
 Plate 10. 
 
 Berjeaij.Litli, 
 
 Ba-nis & Co,E4m'' 
 
 FIBROID OF C CRD
 
 TUMOURS. 151 
 
 Eindfleiscli considers that the so-called tubercle 
 of the brain occurs under two forms ; one a fibroma, 
 non-tuberculous, in which it is seen that the number 
 of cellular elements in the nervous substance always 
 increases the nearer we approach the zone of prohfera- 
 tion, and that a layer of round-celled germinal tissue is 
 at the same time the matrix of the tumour and the 
 l^roduct of the cerebral substance, and that there is a 
 transformation of the germinal tissue into fibres, and 
 that there are no slirivelled cells. 
 
 The second form, tlie caseous nodule, often mul- 
 tiple and smaller, not homogeneous, but composed 
 of round portions, will agree in form and size 
 with miliary tubercle. The caseous nodule contains 
 dead, the grey proliferating zone still living, miliary 
 tubercles. 
 
 This seems to me to be the weakest point in 
 Kindfleisch's classification. Whatever may be true as 
 to the starting-point of these small fibromata, the seat 
 of origin of tubercle in the nervous centres is probably 
 always, or at least most generally, the vessels. What 
 can be seen to be the case in the minutest point of 
 tubercle is most probably the case in the caseous 
 nodule, which is simply an agglomeration of miliary 
 tubercles. 
 
 Plate 10 is an example of a small fibroid tumour, 
 non-tuberculous, implicating the spinal cord, 
 
 I much prefer Jaccoud's account of these tubercles. 
 They occupy the wliite and the grey substance equally, 
 and present themselves under the form of small isolated 
 circumscribed masses, varying in number from one to
 
 152 TUMOURS. 
 
 twenty, and seldom exceeding the latter. Their volume 
 is in inverse ratio to their number. Pretty often they 
 are the size of a cherry ; at other times they scarcely 
 exceed the size of a grain of wheat. As to the colossal 
 masses, which attain to the magnitude of a hen's egg, 
 they result from the confluence and fusion of several 
 spots originally distinct. 
 
 These tumours are of a greenish-yellow colour. The 
 small tumour is only a mass of caseous deposits, which 
 are most frequently encysted by a layer of connective 
 tissue, which quite separates them from the nervous tissue. 
 
 According to the observations of Cornil, these yellow 
 nodosities are generally made up of two very distinct 
 parts, which appear on their surface on section ; one 
 central, oj^aque, and yellow, dense, hard, dry, deprived 
 of juices and of vessels visible to the naked eye ; the 
 other, peripheral, semi-transparent, less dense, more 
 succulent, and allowing one to see with the naked eye 
 some few red lines indicating vessels. At the point 
 where the vessel penetrates into this semi-transparent 
 zone, the aspect of the elements which surround it 
 changes completely ; the small cells or the nuclei, ag- 
 glutinated one to the other by a granular mass, fill the 
 space between the lymphatic sheath and the muscular 
 layer, and the cavity of the vessel, instead of being per- 
 meable and free, is filled with coagulated fibrine. The 
 coagulation and impermeability are absolutely constant 
 in the opaque and yellow central mass of these tumours. 
 This character distinguishes tubercles from the ' tumeurs 
 k myelocytes ' of Robin, in which the vessels remain 
 permeable. These deposits are sometimes encrusted
 
 TU.AfOURS. 153 
 
 with salts of lime, l)ut tliey liave little tendency to dif- 
 fluent softening and su})pui'ation. 
 
 Fereol, Med. Eecord, v. 1, 566, reports a case of 
 confluent tubercle of the pons varolii just at the nucleus 
 of origin of the left sixth nerve, the phenomena having 
 been paralysis of the left sixth nerve, and conjugate 
 inaction of the internal rectus of the right eye. 
 
 Syphilitic tumours may become caseous, and must 
 be distinguished from tubercle. 
 
 This classification of Eindfleisch takes no direct 
 notice of Cysts of the nervous centres. A proliferation 
 of tlie connective tissue round liosmorrhages, collections 
 of pus, and various growths, cannot be spoken of under 
 the name of tumour. But other cysts are met with of 
 more or less independent origin ; cysts, for instance, from 
 the internal surface of which hair has been secreted, or 
 thick honey-like fluid, or fibrinc. It is not certain that 
 tlie two latter varieties may not have been formed 
 originally round a haemorrhage ; but the cysts containing 
 hair are certainly of a different nature. They are very 
 rare. Serous cysts, moreover, are met with connected 
 vascularly with tlie neighbouring parts. They are 
 attached to the cranial and spinal meninges, especially 
 the pia mater ; in the cerebral ventricles, especially 
 attached to tlie choroid plexus ; they are met with in 
 the brain, cerebellum, and mesocephale. They are 
 generally solitary. They are composed of two or three 
 layers of serous, fibrous, or cartilaginous tissue, and are 
 made up of connective tissue, fibrous and fibi'o-plastic 
 elements, and contain in their structure or on their 
 internal surface amyloid bodies, cholesterine and crystals
 
 154 TUMOURS. 
 
 of triple phosphate. The interior may be hnecl with 
 an epithehal expansion. For arachnoid cysts see 
 Lectnre 7. 
 
 Dr. Ogle speaks of five cases he has found in the 
 museums of cysts connected with the dura mater, nine 
 with the pia mater, thirty-two occupying some part of 
 the brain, of which one was connected with the pineal 
 gland ; two of these, however, were most probably 
 hydatid cysts ; in five the cyst was situated in the cere- 
 bellum, in one in the medulla oblongata, and in one in 
 the pons. 
 
 Parasites. — Hydatids occur in the nervous centres in 
 various situations. 
 
 a. Developed outside the meninges in connection 
 
 with the cranial bones. 
 h. In the meninges. 
 
 c. In the brain ; in the cerebral substance ; in 
 
 ventricles and the choroid plexus. 
 
 d. In the spinal canal, generally attached to the 
 
 meninges. 
 Cysticerci. — More rare; not found connected with 
 the cranial bones, nor in the spinal canal. 
 
 a. Developed in the meninges of the brain. 
 
 b. In the substance of the brain and cerebellum. 
 
 c. In the ventricles and the choroid plexus. 
 
 Von Grafe once observed a Coenurus in the 
 encephalon. 
 
 Consult — 
 
 Hammond, 'Dis. of Nervous System.' 
 .Taccoud, ' Path. Interne.' 
 Wilks, ' Path. Anatomy.' 
 
 i
 
 TUMOURS. 155 
 
 Gintrac. Op. cit. 
 
 Rindfleisch, * Path. Histology.' 
 
 Ogle, ' Brit, and For. Med. Chir. Review,' 68, 70, 71, 72. 
 
 Broiidbent, ' Brit. Med. Jour.,' 74, vol. i. 
 
 ' Guy's Hosp. Rep.,' vol. xvii. ' Syph. of Brain.' Dr. Moxon. 
 
 'Guy's Hosp. Rep.,' vol. xvi. ' Syph. of Cord.' Dr. Moxon, 
 
 ' Guy's Hosp. Rep.,' vol. xvii. * Strumous Tumours.' Dr. 
 
 Habershon, 
 Lanceraux, ' Treatise on Syphilis.' 
 ' Jour, of Mental Science,' April 73 and J an. 73. Dr. Boyd. 
 
 * Jour, of Mental Science,' July 72. Dr. Clouston. 
 'St. George's Hosp. Rep.,' vol. iv. Dr. AUbutt. 
 
 * Lond. Hosp. Rep.,' vol. iv. Dr. Hughlings Jackson. 
 ' Brit. Med. Jour.,' 74, vol. i. Dr. S. Smith. 
 
 < Brit. Med. Jour.,' 74, vol. ii. Dr. Coats. 
 
 ' Med. Record,' vol. i. p. 105. Becoulet & Giraud. 
 
 * Med, Record,' vol. i. p. 566. ' Tubercle of Pons.'
 
 156 
 
 LECTUEE VI. 
 
 DELIEIUM. 
 
 Acute Delirium. Postponing for tlie moment the 
 consideration of cUlire aigue of French anthors, acute 
 delirimn is met with under very varied conditions of 
 blood supply. It is not by any means associated in all 
 cases with hyperasmia of the brain. On the contrary, 
 all medical men will recognise in their experience the 
 truth of Dr. Bucknill's statement, that the fact that all 
 the symptoms of acute mania frequently arise and con- 
 tinue throughout the course of an exhausting bodily 
 disease, which leaves every individual organ, the brain 
 included, in an ill- nourished and anaemic state, afibrds 
 irresistible evidence that the phenomena of acute in- 
 sanity must in many cases coexist with a state of the 
 cerebral organs the very reverse of hyperaamia. Graves 
 records a case where a patient, though violently deli- 
 rious and unmanageable, on tlie borders of frantic 
 madness, had a pulse almost uncountable from quick- 
 ness, and exceedingly weak, with cold extremities. 
 Closely connected witli this point is the condition of 
 the urine in acute delirium. If there were a constant 
 hyper-secretion of ])hosphates in all cases of acute 
 delirium, we shoidd be nearer a reasonable explanation.
 
 DELIRIUM. 157 
 
 Acute delirium, iu fact, would be a syuiptom of exces- 
 sive brain action. But this is far from beino' the case. 
 In one form of the disease, delirium tremens, in which 
 {it times the delirium is most acute and vii^lent, the 
 phosphates are generally diminished very considerably ; 
 and it is not even proved s:itisfactorily that acute deli- 
 rium, with manifest hyperemia of brain, is in all cases 
 accompanied or followed by abnormal increase of 
 phosphoric acid in the urine. This amemic acute 
 delirium is seen sometimes at the end of exhausting: 
 diseases, or after severe haemorrhage, as flooding after 
 parturition. A condition not dissimilar is seen in 
 superhictation ; or, again, some days after the birth of 
 a child acute delirium may supervene, and may have 
 its origin either from exhaustion or from septicaemia. 
 The thermometer here is a great aid. 
 
 Next to the anaemic form we meet with acute deli- 
 rium depending upon toxaemia. We see this condition 
 from the exhibition of certain substances, such as alcohol, 
 sulphuric ether, belladonna, datura stramonium, &c. It 
 is this form that we find at the commencement of acute 
 diseases, inflammation of any kind, fevers, &c. This 
 form obtains also in rheumatic pericarditis, although it 
 is thought by some that this delirium was an anaemic 
 kind, due to the interference with the heart's action. 
 It is worthy of note that true rheumatic meningitis is 
 generally accompanied by a low muttering delirium. 
 It is this form that we meet with at the close of 
 phthisis, due to the circulation in the brain of morbid 
 blood. In some few cases the presence of an abnormal 
 amount of carbonic acid in the blood <nves rise to
 
 158 DELIRIUM. 
 
 acute delirium. This seems to be the rationale of the 
 mental phenomena of delirium tremens, and it is some- 
 times seen in fatal cases of pneumonia. In erysipelas 
 the morbid blood is again the cause of the delirium. 
 It is a difficult question to decide whether the delirium 
 is caused in these diseases by a blood rendered impure, 
 or by the heat of the blood. At any rate, it is re- 
 markable how anything that reduces the heat of the 
 blood seems to relieve the delirium. 
 
 It is not easy to say what is meant by excitability 
 of brain, apart from the calibre of vessels. Let it be 
 granted that there is no abnormal increase or deficiency 
 in the amount of blood in the brain, and that the blood 
 is not morbid in quality, can any condition of brain 
 exist that will oive rise to acute delirium ? No doubt 
 this state of delirium may come on after shock of any 
 kind, but it is doubtful whether shock can affect the 
 brain except through its vessels. 
 
 The whole subject is full of difficulty. The use of 
 the word ' polarity,' as applied to the brain cells, is no 
 real explanation of any known condition. It is a 
 mere hypothesis from analogy. It may be true that 
 the brain is made up of a series of batteries, but it is 
 far from being a proved fact. On the one hand, the 
 known convulsive phenomena and loss of consciousness 
 consequent on arterial spasm, the fact of the regions 
 of epileptic discharge being governed by the distribu- 
 tion of vessels, and the morbid cerebral phenomena 
 occasionally met with immediately after an epileptic 
 fit ; and on the other hand, the lesions found in the 
 cells themselves in all cases of prolonged abnormal
 
 DELIRIUM. 159 
 
 cerebral phenomena, such lesions being constantly due 
 to previous alterations of blood supply, make it diffi- 
 cult to realise the existence of acute delirium, the cells 
 being healthy, except under one or other abnormality 
 of vascularity, expressed l)y the varieties of ana3mia, 
 toxasmia, or hypera^mia. So far we see anaemia, 
 toxaemia, heat of blood, and perhaps shock, as condi- 
 tions under which acute delirium may be a prominent 
 phenomenon. Dr. Handheld Jones considers that in 
 many instances the excitation of the tissue is the 
 primary change, and the vascular repletion is secondary 
 and varying. 
 
 My own belief is that delirium is in all cases an 
 expression of functional inactivity or perverted activity, 
 accompanied or caused by deficient blood supply ; in 
 anaemia from deficient circulation ; in toxa3mia from 
 the circulation of the blood, part of which, at least, is 
 unfit for functional pm^poses, and therefore useless ; in 
 hypera3mia, because from the very pressure upon the 
 vessels the due interchange between tissue and nutritive 
 material is rendered abnormally difficult. 
 
 It stands to reason, therefore, that, except in tJie 
 latter condition, the post-mortem appearances will be 
 few. The brain may be abnormally pale in aniemia, 
 and if it has been of long duration, we may find either 
 slight partial softenings, or slight atrophy of brain and 
 CBdema of the pia mater, or at least very empty vessels. 
 But on this point it must be remembered that, owing 
 to the facility with which the cerebral vessels empty 
 themselves, considerable hyperasmia of brain may have 
 existed and yet leave no trace behind, unless it has
 
 160 DELIRIUM. 
 
 been very prolonged. In toxsemia there may be spots 
 of local congestion or of pigmentation, but in most 
 cases the post-mortem appearances will be simply 
 none. 
 
 In hypergemia, however, the case is different. It 
 may be we find a brain abnormally red, and showing 
 on section many puncta vasculosa. Or part of the 
 brain may exhibit the cribriform condition already 
 allnded to, due to the pressure the tissue has undergone 
 from dilated vessels ; or the vessels themselves may be 
 dilated, as in some cases of epilepsy, and a vast amount 
 of hypersemia of the brain and so-called congestion is 
 subsequent to an epileptic attack ; or, if the hypera3mia 
 has been of long duration, the muscular coat of the 
 vessels becomes hypertrophied. 
 
 In other cases a pigmental condition of the walls of 
 the vessels is observed, and the smaller arteries will be 
 found aneurismal or tortuous, or here and there per- 
 manently dilated. In some cases the altered vessels 
 will have given way, and the results of the hgemorrhage 
 (crystalline hasmatoidine, &c.) may be recognised. 
 
 Acute delirium is a common symptom of acute 
 meningitis, though probably not of the meningeal 
 lesion proper. Meningitis is so intimately allied with 
 lesion of the brain, so much so, indeed, as to induce 
 Trousseau to call this malady by the name of cerebral 
 fever, that it would be difficult to say which symptoms 
 are caused by the inflammation of the meninges, which 
 by the inflannnation of the brain. Most probably tliese 
 phenomena are directly associated with the hyperosmia 
 of the convolutions so constantly found in this malady.
 
 DELIRIUM. IGl 
 
 111 such cases there Avill be all the special lesions of 
 meiiiuo;itis. 
 
 In many cases the cerebral congestion is of tem- 
 porary duration, and does not lead to inflammatory 
 lesion. 
 
 In some few cases the extreme hypero3mia has 
 seemed to have been the commencement of local spots 
 of encephalitis. Calmeil gives many such cases in his 
 first volume, and it is likely that it is always a very 
 early phenomenon in such cases, though it may not be 
 the primary one. 
 
 Acute delirium may accompany periencephalitis in 
 insidious forms. Calmeil gives 19 cases in which this 
 was the case. In 9 the tissue of the cranial ])ones was 
 notably coloured red. In 8 the vessels of the cerebral 
 dura mater were red and arborescent. In 2 cases the 
 cavities of the cerebral arachnoid contained a certain 
 amount of purulent liquid ; in 3 of serous. 
 
 In 4 the cerebral pia mater was infiltrated with 
 serum ; or with a liquid of a plastic appearance in 
 8 cases, with pus in two. 
 
 In 3 it was separated with difficulty from the 
 nervous substance beneath it. In 7 it adhered inti- 
 mately in spots to this substance. 
 
 In 18 its folds were red, its network more or less 
 rugose by injected vessels, sometimes of considerable 
 calibre. 
 
 In 18 effusions of blood had occurred in its thickness. 
 
 In 7 the convolutions of one hemisphere, or both, 
 or of certain spots of the brain were swollen, and more 
 or less aucfmented. 
 
 M
 
 162 DELIRIUM. 
 
 Ill 1 tliey were tinted brown by contact with pus. 
 
 In 18 the cortex was red, rose, or violet colour, 
 either externally or in its thickness ; in 9 it was of too 
 little consistence ; in 1 it contained a small centre of 
 tubercle ; in 1 a small centre filled with cholesterine. 
 
 In 14 the vessels of the wdiite matter were in- 
 jected ; in 4 this substance was loose and of a white 
 consistence ; in 1 totally softened. 
 
 In 7 the grey substance of the corpora striata was 
 of a violet or raw-flesh colour ; in 2 that of the optic 
 thalami was red. 
 
 In 2 the walls of the large ventricles were rugose 
 by vascular expansions ; in 1 they, as well as the 
 central parts of the brain, were soft. 
 
 In 1 the pia mater of the cerebellum was infiltrated 
 with pus ; in 10 notably injected ; in 5 it adhered to 
 the surface of the hemispheres of the cerebellum. 
 
 In 4 the substance of the cerebellum appeared 
 diminished in firmness ; in 16 it was coloured lilac or 
 violet. 
 
 The rhomboidal spaces were fibrous, and encrusted 
 with lime salt in 1 ; in 10 the grey substance of the 
 pons was a violet colour. 
 
 In 1 the spinal dura mater was covered with an 
 extravasation of blood ; in 3 the sinuses of the spinal 
 cavity were much congested ; in 1 the spinal prolonga- 
 tion was atrophied and disintegrated. 
 
 In 8 microscopical examinations were made. 
 In two, the web of the cerebral pia mater contained 
 many pus glolules and pyoid elements ; in another, it 
 contained amorphous granular elements, or small
 
 DELIRIUM. 163 
 
 granular cells in course of formation. In tlie greatest 
 number of cases the grey substance was not disinte- 
 grated ; it was sometimes moist, and easy to spread out. 
 It generally contained a more or less considerable 
 ramification of vessels ; almost always the external walls 
 of tlie vessels were, as it were, sprinkled with greyish 
 granules, or spotted with small finely granular cells. 
 Sometimes the formation of these small cellules com- 
 menced in the very midst of the grey substance, where 
 many small pointed spheres, like the eggs of insects, 
 could be distinguished. 
 
 Delirium Tremens. — It is probable that the great 
 differences of opinion that exist as to the proper 
 treatment of this condition are due to the fact that we 
 habitually use the term too generally, and as inclusive 
 of morbid states only loosely connected together by the 
 element of a common alcoholism. 
 
 M. Laval, liowever, in his study of delirium tremens, 
 has arrived at the following conclusions : — 
 
 ' I. All delirium is due to a pathological process 
 carried on in the intimate structure of the cerebral 
 cell, starting with irritation, and leading to steatosis of 
 the histological elements. 
 
 ' 2. Alcoholic delirium, improperly called delirium 
 tremens, only differs from delirium in general by its 
 first cause, alcohol ; seeing that the mechanism of its 
 production, its symptomatology, its complications, its 
 diagnosis, obey wholly the general laws which regulate 
 other species of delirium. 
 
 ' 3. Finally, digitalis, opium, chloroform, are no 
 more specifics for delirium tremens than for other
 
 164 DELIRIUM. 
 
 delirious manifestations, and in all cases recourse must 
 be had to a rational treatment. The patient, and not 
 the disease, must be treated, the author reorardino; 
 delirium tremens as not being a morbid entity.' 
 
 With the great diversity of views respecting this 
 condition, it will be necessary to say a few preliminary 
 words before speaking of the patliological anatomy. 
 
 Alcohol, when it morbidly affects the nervous 
 centres, may do so in one or other of several ways. 
 
 1. It may do so with the phenomena of a fit of 
 drunkenness, of which tlie symptoms differ in different 
 individuals ; in some, never amounting to excitement, 
 the patient only becoming more and more stupid until 
 he flills into a state of hebetude or even coma ; in 
 others, alcohol will induce the most frantic delirium, 
 sometimes only for a few moments, at other times for 
 many hours (delirium e potu). There are, of course, 
 iniinite shades of variety between these two states. 
 
 2. It may affect the patient periodically with the 
 phenomena of a fit of dipsomania. In some people 
 the tendency to drink to excess is persistent, in many 
 others it is strictly periodic. I have a lady now under 
 my care who has this tendency only during the cata- 
 menial period. The s3miptoms of this attack vary as 
 much as those of ordinary intoxication. 
 
 3. The patient may manifest tlie symptoms of 
 chronic alcoholism with indefinite cerebral phenomena, 
 such as a tendency to emotional weakness, the being 
 easily startled, a certain want of purpose in all the 
 concerns of life, diminution of intellectual power, the 
 impression of fear, certain morbid sensory phenomena,
 
 DELIRIUM. 1G5 
 
 excessive tremor at times almost simulating paralysis 
 agitans, and often towards the close of life some motor 
 paralysis. In some cases insanity supervenes. 
 
 4. Delirium may occur also in persons who, having 
 been habitual drunkards, liave been subject to some 
 great shock, some accident or operation. This condi- 
 tion, called traumatic delirium tremens, may be ana3mic 
 dehrium, or it may be reflex delirium, the alcohol only 
 playing the indirect part of rendering the nerve centre 
 more sensitive to excitation from a distant origan. At 
 any rate it is certain that this traumatic delirium tremens 
 may occur where there has been no indulgence in 
 intoxicating liquors. Dr. Ilandfield Jones mentions 
 several examples ; and he deduces from these examples 
 the opinion that the peculiar morbid state (in delirium 
 tremens) is not necessarily one of poisoning at all. 
 The distinction between this nervous disorder and true 
 delirium tremens is the more important that the two 
 conditions often demand a diametrically opposite 
 treatment. 
 
 5, We get true delirium tremens, manifested by 
 various symptoms and various phj^sical signs, but never 
 manifesting itself by any intensilication of pleasurable 
 emotions. Tlie emotions excited seem always to be 
 either horror, or fear, or melancholy. iStill I doubt 
 whetlier the commission of suicide in delirium treniens 
 is ever the result of melancholy. It is probably 
 always an im reasoning attempt to avoid present horrors, 
 such as the hallucinations of sight, constantly present 
 to the view of the patient. 
 
 I am not i^oino- to £five you all the svm])toms of
 
 166 DELIRIUM. 
 
 delirium tremens. Suffice it to say, that the tremor 
 varies immensely in different cases ; that the patient 
 often at the beginning of his illness seems preter- 
 naturally busy ; that though the attempt to be busy 
 passes away, the delirium all through the patient's 
 illness may keep upon the ordinary avocations of his 
 life ; that the horrors may be completely absent, and 
 all the hallucinations of sio-ht and hearinsf be connected 
 with the common business of life ; that, on the contrary, 
 in many, if not in most cases, the delirium will be 
 connected with scenes of terror, the hallucinations 
 with loathsome reptiles, the ideas (in Protestant 
 countries particularly) with a present or a coming 
 hell. One more point with reference to the mode of 
 attack. It has formerly been taught that these pheno- 
 mena occurred in habitual drunkards from a depriva- 
 tion of the accustomed stimulus, and no less an 
 authority than Dr. Handheld Jones, basing his opinion 
 on observations and statistics of Dr. Marston, considers 
 this former teaching to be the right one. 
 
 Dr. Marston showed that delirium tremens comes 
 on in soldiers commonly from the first to the seventh 
 day after the privation of liquor, and this in men who 
 had not suffered from it before. The statistics of 
 prisons, whose occupants are largely drawn from the 
 class of habitual drunkards, go far to disprove this 
 theory, as also does the observation of many cases in 
 which the attack comes on during the fidl indul<2jence 
 in alcohol. It is certain, however, that the phenomena 
 either commence or are greatly intensified many hours, 
 in some cases several days, after the deprivation ; but
 
 DELIRIUM. 167 
 
 I think it is in accordance with observation to say that 
 they are not caused by tlie deprivation. The effects 
 of alcohol vary in different individuals. Perhaps no 
 two persons absorb it with equal rapidity ; still less do 
 they agree in the time necessar}^ for its oxidation. 
 We shall see directl}^ that it is not alcohol itself that 
 causes tlie morbid phenomena so much as its chemical 
 products ; and Avhen these are formed they will act 
 upon the nerve-cells in different individuals with 
 greater or less rapidity. It is perfectly easy to under- 
 stand that in two people the alcohol will be broken 
 up quickly in one and slowly in the other, and the 
 products exercise a rapid action on one brain, a slower 
 one on the other. 
 
 These few words seemed necessary before speaking 
 of the pathological results in this disease. And here, 
 as in insanity, and probably in other nervous disorders, 
 the post-mortem appearances are not the only, if they 
 are the main, test of the lesions. Here, too, as in 
 insanity, the sphygmograph has proved of service, and 
 the tracings show a close similarity to what is seen 
 in fevers and inflammation of a typhoid type, and are 
 especially remarkable for the prominence of the 
 phenomenon called ' Dichrotism.' This is interesting 
 in connection with Dr. Johnson's assertion of the 
 frequent presence of fatty degeneration of the heart in 
 these patients. 
 
 Dr. Fraser gives the following post-mortem appear- 
 ances in fifteen cases of idiopathic delirium tremens : — 
 Head- 
 In 8. Ventricular and arachnoid serous effusion.
 
 168 DELIRIUM. 
 
 In 1. Sanguineous arachnoid effusion. 
 
 In 1. Subarachnoid gelatinous effusion. 
 
 In 2. The scalp and dura mater deeply injected. 
 
 In 2. The brain and membranes much injected, 
 and of a rosy hue throughout. 
 Lungs — 
 
 In 1. Emphysematous. 
 
 In 2. Gorged with pus. 
 
 In 7. Gorged with blood. 
 
 In 1. Tuberculous. 
 Heart — 
 
 In 3. Dilated. 
 
 In 1. Hypertrophied. 
 
 In 3. Fatty. 
 
 In 1. Effusion of blood in the pericardium. 
 
 In 1. Fibrinous clot in the joulmonary artery. 
 Liver — 
 
 In 7. Enlarged. 
 
 In 1. Fatty. 
 
 In 2. Cirrhosed. 
 Stomach — 
 
 In 5. Congested. 
 Kidneys — 
 
 In 1. Disorganised. 
 And he says there is no special appearance in 
 either the brain, spinal marrow, or the membranes 
 which can be placed as a constant effect of this disease ; 
 for all the conditions which have been seen by the 
 many observers have been noticed when there had 
 been no delirium tremens, and all of them have been 
 absent under the most aggravated and flxtal cases of 
 this disease.
 
 DELIRIUM. 169 
 
 I add tlie following cases, illustrating various post- 
 mortem appearances : — 
 
 Case 1. Man, aged o3. Died rather suddenly after 
 twenty-four liours of intense delirium. Treatment, 
 dio;italis. 
 
 No congestion of brain. All the encephalon rather 
 pale. Brain wet. A good deal of subarachnoid fluid 
 botli on tlie convexity and at base. No iluid in the 
 ventricles. Septum lucidum, pons, and cerebellum 
 very soft. Arteries iiealtliy. Both lungs very dark 
 from congestion, ])ut crepitant. Heart rather large. 
 Several old white spots on right ventricle. Hardly 
 any blood in the heart. Pulmonary and aortic valves 
 with aorta and internal surface of left ventricle 
 deeply stained. Walls firm. Valves healthy. Very 
 little atheroma of the aorta. Liver large, ]iard, 
 bloodless, and waxy. Gall-bladder full of bile. Spleen 
 rather large. Kidneys healthy, except that the capsule 
 of the right kidney did not peel readily. Internal 
 surface of the stomach highly congested, and covered 
 with ecchymoses. 
 
 Case 2. Man. Dehrium tremens four days. Beer 
 and opium treatment. Head : much sub-arachnoid 
 fluid both of convexity and at base of tlie brain. Veins 
 of hemispheres rather full of blood. The brain wlien 
 taken out fell apart, most of the central white matter 
 being very soft. The fornix, corpus callosum, and 
 boundaries of the lateral ventricles were hardly of 
 greater consistence than cream. No fluid found in the 
 lateral ventricles, but it may have escaped when the 
 brain was being taken out. Corpora striata and optic
 
 170 DELIRIUM. 
 
 thalami soft. Soft commissure, almost liquid. A little 
 white thickening of the arachnoid at the base of the 
 cerebellum. Pons and medulla oblongata healthy. 
 Vessels of the base healthy. Thorax : heart with a 
 good deal of fat externally ; and the walls of the 
 ventricles were partly encroached upon by, and partly 
 converted into, fat. Walls of right ventricle very thin. 
 A little atheroma round base of aortic valves. No 
 clots anywhere. Fluid blood in both ventricles and 
 in pulmonary artery. Lungs intensely engorged with 
 blood ; otherwise healthy. Abdomen : liver healthy, 
 except that on convex surface there was a little cyst, 
 the size of a filbert, full of bile. Kidneys healthy, 
 except that the capsules split up, one layer adhering to 
 the organ. Suprarenal capsules and spleen healthy. 
 
 Case 3. Man. Many attacks of delirium tremens ; 
 died in epileptic fit. Head : vessels of the dura mater 
 and the brain much injected. Brain firm. Lateral 
 ventricles enormously distended. The fluid they had 
 contained had been let out in the process of getting 
 out the brain. Kidneys healthy. 
 
 Case 4. Man, aged o2. Had delirium tremens for 
 four days. Many epileptiform attacks, one every ten 
 minutes during the last twenty-four hours of life. 
 Head : dura mater healthy. Chronic thickening of 
 the arachnoid over convex surface of both hemispheres, 
 with opaque spots and plates. Much subarachnoid 
 fluid. Brain somewhat atrophied ; otherwise healthy. 
 Kidneys and liver healthy. 
 
 Case 5. Man, aged 48. Tremor. Sleeplessness. 
 Dehrium. Almost fatuity. Head: all the vessels of
 
 DELIRIUM. 171 
 
 the brain engorged with black blood, both arteries and 
 veins. No softening of brain. A little finid in left 
 lateral sinus. Much subarachnoid fluid. Arteries at 
 base of brain rather atheromatous. Thorax : a spot 
 of grey hepatization in lower lobe of right lung, about 
 the size of the palm of a hand. It was perfectly 
 circular. The rest of both lungs healthy. A little 
 adhesion of both lungs to thorax. Heart covered with 
 fat. Very little remains of muscular wall of right 
 ventricle. Abdomen. Liver fatty. Kidneys rather 
 granular ; the capsules do not peel readily. Pelves of 
 kidneys full of fot. 
 
 The presence of the fluid under the arachnoid, 
 and perhaps even in the ventricles, is in consequence 
 of the atrophic condition of the brain itself. This is 
 one of the most frequent post-mortem appearances, 
 the commencement of shrinkino- of the convolutions, 
 due probably to insufficient nutrition by the alcoholised 
 blood. Alcohol has been sometimes found free in the 
 fluid in the lateral ventricles. The whole mass of 
 the brain wastes. This takes place sometimes by 
 way of fatty degeneration, at other times by gradual > 
 atrophy of the elements of nervous tissue. 
 
 The delirium cannot depend upon the arachnitis. 
 The thickening of the arachnoid is generally so chronic, 
 whilst the cerebral phenomena are so recent, that there 
 cannot well be any connection between them. Besides 
 which extreme chronic arachnitis may persist, without 
 any cerebral phenomena whatever. The thickening 
 of the arachnoid seems related to that gradual develop- 
 ment of fibrous tissue that one sees in delirium tremens,
 
 172 DELIRIUM. 
 
 sometimes in the lungs, sometimes in the hver, or the 
 kidneys, or the larger arteries, and occasionally in 
 many organs together. 
 
 But post-mortem records point to more than the 
 results in the brain. They not only sliow that these 
 appearances are of an atrophic character, but they 
 absolutely demonstrate the condition of blood that 
 must lead to this atrophy. It is dark in all the vessels, 
 and in some cases stains the endocardium as it does in 
 some of the blood diseases. Now, Prout and Vierordt 
 have proved tliat even a moderate use of alcoholic 
 liquors causes botli an absolute and a relative diminu- 
 tion in the amount of carbonic acid excreted. The 
 increased excretion of carbonic acid wliich accompanies 
 digestion is considerably checked by the use of spirits. 
 If this is the effect of small doses of alcohol, what will 
 be the effect of large doses taken dail}-, without any 
 interruption or opportunity for more efficient decar- 
 bonization. The constant diminution in carbonic acid 
 excreted gradually causes a sure augmentation of 
 carbon in the blood ; so that this fluid will sometimes 
 contain as much as thirty per cent, more of this matter 
 tlian in healtli, and will in some cases assume an oily 
 or even a milky appearance. Tlie renewed supplies of 
 alcohol, creating an artificial stimulus to the motions 
 of the heart and the frequency of the respirations, will 
 add still more to the baneful carbonaceous accumula- 
 tion. This fatty carbonaceous blood, unfit for the 
 nutrition of any organ, is especially unfit for the due 
 performance of those regulated physical conditions of 
 osmosis in so fatty an organ as tlu^ brain. It must also 
 lead to con2;estion of the internal viscera.
 
 DELIIUUM. 173 
 
 We see by this stateiiieut how fai' we can agree 
 with Dr. Haudfield Jones's statement, that deUriuni 
 tremens, except in cases of acute occasional excess, is 
 much more than alcohohc poisoninn-. Without bindiuG; 
 ourselves too closely to humouralist views, it is only a 
 fair result of observation to acknowledge that the 
 direct and indirect effect on the blood of undue imbi- 
 bition of alcohol is to load this fluid with a proportion 
 of carbonic acid that not only alters its appearance, but 
 materially modifies its nutritive powers and impedes 
 the circulation. And this morbid blood may not only 
 induce congestions of the internal viscera, or even low 
 inflammation of some of them, such as tlie aracluioid, 
 the lungs, the liver, the spleen, or the kidneys, but by 
 its innutritions character impresses that atrophic modi- 
 fication on the brain, that is shown post mortem, leading 
 to the compensating increase of the subarachnoid fluid. 
 
 In addition to these lesions the arteries of the base 
 of the brain are sometimes found atheromatous, and 
 with such alteration in the lumen of the vessels that 
 thrombosis is easy, and softening as a necessary con- 
 sequence. ]S!"or are other changes altogether wanting. 
 Small granular kidney is not a very unusual concomi- 
 tant of delirium tremens, and the vessels of the brain 
 may therefore have to bear the additional pressure of 
 the lesions consequent on deficient excretion of tlie 
 urinary constituents. 
 
 Dr. Fraser makes another suo;2;estion as to the mode 
 of blood-poisoning in this disease. He says : ' Alcoliol 
 is said to take the oxygen of the blood (which would 
 otherwise liave gone to the normal oxygenation of the
 
 174 DELIRIUM. 
 
 various tissues of the body), and thus to stop the 
 ordinary waste of material, while its carbon and 
 hydrogen are given off as carbonic acid and water. 
 Why, then, if the action of alcohol merely stops waste, 
 should its action be so injurious ? Because the arrest 
 of this waste throws into the circulation an abnormal 
 amount of nitrogenous matter. The resemblance 
 between the convulsions attending delirium tremens 
 and those attending ura3mic poisoning is close, and 
 arises either from a similarity of action of the alcoholic 
 and uraimic poison on the nervous centres, or from a re- 
 tention of urea during the delirium tremens, such as 
 happens in true urasmia. 
 
 Observations are wanting on the spinal cord in this 
 disease. It is impossible, with this atrophic modifica- 
 tion of the brain, but that something similar should 
 obtain in the spinal cord. That such lesion is of no 
 great severity is rendered certain by the absence of all 
 paralysis in most cases, and by the subsidence of tremor 
 after prolonged sleep. But the explanation of the 
 tremor is yet wanting. It cannot depend on sclerosis 
 of any portion of the encephalon, or it would not dis- 
 appear so rapidly. It must probably be fi'om the 
 malign influence of, or the negative fact of, mal-nutri- 
 tion by the carbonaceous blood of some of the motor 
 centres, either some of the external cerebral convolu- 
 tions, or some large organs at the lower part of the 
 brain, or the great cells of the grey matter of the 
 spinal cord. 
 
 Whatever may be the true explanation of this motor 
 phenomenon, it is to alcohol and its effects on the brain
 
 DELIRIUM. 175 
 
 itself, witli the secondary results of tlie circulation of 
 this innutritions fluid through the brain, that we must 
 look for the pathological lesions of delirium tremens, 
 and the evils of this impure blood are in many cases 
 intensified by the concomitant lesion of fatty degenera- 
 tion of the heart. 
 
 Consult — 
 
 Foedere, ' Traite du Delire.' 
 
 Calnieil, vol. i. 237, op. cit. 
 
 Graves, ' Clin. Lectures.' 
 
 Handfield Jones, * Functional Nervous Disorders.' 
 
 Reynolds, * System of Med.' 
 
 ' Med. Chir. Trans.,' vol. xlviii. Dr. Weber. 
 
 Wilks, ' Path. Anatomy.' 
 
 Dr. Peddie on ' Pathology of Delirium Tremens.' 
 
 * Lond. Hosp. Rep.,' vol. iii. Dr. Fraser. 
 
 'Med. Record,' i. 296. M. Laval.
 
 176 
 
 LECTUEE VII. 
 
 INSANITY. 
 
 It has been said by no less distinguished an ahenist 
 physician than Griesinger that ' if we examine the 
 great mass of uncertain records, and except the cases in 
 which tlie insanity was cured before death, there still 
 remains a number of cases, reported by careful ob- 
 servers (and which may be confirmed in any asylum), 
 where the cranial cavity and its entire contents pre- 
 sented altogether normal relations.' 
 
 In a vast number of cases of insanity there may 
 be found recognisable lesions. The more precise our 
 methods of investigation become, the better are we 
 able to appreciate the finer structural changes in the 
 nervous centres. But even when the microscope has 
 done all that we can expect of it, there still remain, 
 and there always will remain, instances in which, while 
 the symptomatic phenomena are most intense and 
 startling, yet it is impossible after death to discover 
 structural alteration. Are these cases instances of 
 functional disease ? Well, that leads me to ask a 
 question peculiarly important in the consideration of 
 nervous diseases ; is it possible that any symptom can 
 occur without organic change ; or is so-called func-
 
 LN'SANITY. 177 
 
 tional disease a condition that merely leaves no appa- 
 rent alteration of structure post mortem. Even in 
 these nervous diseases, and they are the most dilFicult 
 of all, you will be right in assuming that morbid 
 phenomena are invariably associated with organic 
 change, but that in a number of cases this organic 
 change is not of a nature to persist after death. 
 
 There are, at least, four conditions that may induce 
 very serious cerebral symptoms, and yet leave little or 
 no change of structure to be recognised after death : 
 1, a condition of the blood itself, as in uraemia, 
 spanasmia, phthisis, &c. ; 2, a variation in the normal 
 blood supply to the brain ; 3, reflex irritation, though 
 this perhaps might be classed under the second head, 
 as irritation radiating from some distant organ would 
 be likely to induce, by reflex action, contraction of the 
 arteries ; 4, shock. Each of these, if long continued 
 or frequently repeated, will induce structural lesion that 
 can be recognised after death ; each of them may be 
 the starting point of phenomena of a severe character, 
 and if the duration of the attack be not protracted, 
 will leave no post-mortem appearance. Still the lesion 
 is present during life. It may be a condition of blood 
 Avholly unfavourable to osmosis ; it may be a transitory 
 congestion, or an ana3mia, partial or complete, from con- 
 traction of the arteries ; it may be a total paresis of 
 absorption. 
 
 Dr. Thompson, of the Bristol Borough Lunatic 
 Asylum, has done some good work here by means of 
 the sphygmograph. He finds by observation on the 
 pulse tracings of general paralysis that this condition is 
 
 N
 
 178 INSANITY. 
 
 marked in very early stages by persistent spasm of the 
 vessels ; that this persistent spasm will lead to changes 
 in the component elements of the vessels, especially in 
 the muscular substance ; and further, that tlie sphygmo- 
 graph, by indicating the true nature of the disease at 
 a period when it could barely be suspected by other 
 symptoms, affords an opportunity of applying remedies 
 — the calabar bean, for instance, — when mere function 
 is disturbed, before actual change has begun, and when 
 the remedial means can be of the most avail. 
 
 This is an illustration of a morbid condition that 
 at first would leave no recognisable structural results ; 
 but it would be wrong to say that the early symptoms 
 of general paralysis were not connected with organic 
 change. The organic change is in the diminished 
 calibre of the vessels, which not only persists, if left 
 untreated, but will lead to further lesions ; whilst, if 
 recognised early, it is amenable to remedial means, at 
 least for a time. 
 
 It is certain that the same may be said of the early 
 stages of mania and melancholia. The true patho- 
 logical anatomy of these first beginnings of mental 
 disease is to be sought for during hfe, and most of the 
 structural lesions found post mortem are secondary 
 results ; secondary, that is, not to the morbid mental 
 phenomena (such a statement, though it has been made, 
 is eminently ridiculous), but secondary to the early 
 organic changes that are only of temporary duration. 
 
 It having, then, been insisted on that the early 
 phenomena of several varieties of msanity depend upon 
 lesions always present, yet transitory in their duration.
 
 INSANITY. 179 
 
 often amenable to treatment, and from their very 
 nature not recognisable after death, it remains to study 
 the coarser structural changes induced by their earlier 
 lesions. 
 
 The majority of post-mortem examinations of the 
 insane show anatomical changes of some kind or other ; 
 and, as Griesinger says, there are certain structural 
 diseases of the brain which always cause considerable 
 anomalies in the mental functions, even insanity. A 
 diffuse inflammation of the grey substance, extending 
 over a number of convolutions, has never been observed 
 without profound mental disturbance ; extreme menin- 
 gitis of the convex surface (in previously robust indi- 
 viduals), considerable acute oedema of the greater 
 hemispheres, rapid bilateral atrophy of the convolu- 
 tions, a deeply penetrating alteration of the ventricular 
 surface of any extent, were never observed without 
 psychical disturbance, particularly mental weakness. 
 
 The examination of a brain should always be 
 made, first, in the fresh state, and afterwards from 
 hardened sections. 
 
 It may be convenient, first, to touch upon the 
 alterations found in the various elements of the nervous 
 tissue, the vessels, the cells, the neuroglia, mentioning 
 the morbid conditions of the cranium and the mem- 
 branes ; and secondly, to pass in brief review the most 
 common lesions found in mania, melanchoha, dementia, 
 general paralysis, and idiocy. 
 
 Although we may somewhat cavil at tlie universality 
 of Rindfieisch's dictum, tliat we must concentrate our 
 attention almost entirely on a chronic hypertcmia of
 
 180 INSANITY. 
 
 the cortical substance as the common foundation of all 
 further mischief, yet a very considerable amount of 
 recognisable lesion in insanity is connected with the 
 vessels. Abnormal dilatation and abnormal contrac- 
 tion may exist during life, and leave no mark behind. 
 More commonly the vessels of the membranes, or of 
 the brain, and often of both, show very definite lesion. 
 The larger vessels of the membranes and the vessels 
 at the base of the brain are often atheromatous and 
 calcareous ; but it must be remembered that many of 
 the autopsies in asylums are held on aged persons, in 
 whom this kind of degeneration is common, and that 
 this condition has more to do with asfe than with 
 insanity. Atheroma is seldom found in the vessels of 
 the cortex at the upper portion of the brain. The 
 vessels of the pia mater are not only very frequently 
 congested, but have been the seat of inflammation ; 
 and a low form of meningitis, involving the cortical 
 layer of the brain, is not unusually met with. 
 
 But whether this hypertemia has gone on to inflam- 
 mation or not, it will, if frequently repeated, have left 
 its marks both on the vessels and on the brain. 
 
 The changes that occur have been recorded in a 
 masterly sketch by Dr. Batty Tuke, from whose ob- 
 servations I gather much for the present Lecture. He 
 calls attention to a fact already recognised, that this 
 hypercemia, leading to dilatation of vessel, causes ex- 
 pansion of its surroundings. When the vessel is 
 relieved from pressure it contracts to its original 
 calibre, and leaves a space. This had been already 
 alluded to under ' hyperasmia ' in Lectures IL and
 
 IXSANITY. 181 
 
 III. ; and it was there stated that little pits or holes, 
 tl'tat crible, were often found, caused by condensation 
 of brain tissue, due to the pressure of the dilated vessel 
 and subsequent exudation. This space may become 
 the receptacle of lymph thrown out in subsequent 
 congestions ; and evidences of this exudation are found 
 in a thickened condition of the hyaline membrane, an 
 evident induration of the contiguous brain, and con- 
 siderable deposit on the adventitia. 
 
 The thickened condition of the hyaline membrane, 
 the hyaline-fibrosis of Drs. Gull and Sutton, is a lesion 
 of common observation, and wholly irrespective of 
 chemical re-agents in the preparation of the micro- 
 scopical specimen. It is, however, not by any means 
 specially connected with venal disease ; it is a condi- 
 tion often found in old age, and seems to depend 
 on previous dilatation of the vessel and exudation 
 from it. 
 
 Deposits on the tunica adventitia are also found 
 after prolonged hyperasmia. Dr. Sankey first described 
 a pecular molecidar material, not unlike oil in appear- 
 ance, but not answering to the chemical tests for fat. 
 Dr. Batty Tuke has found this material in every brain 
 of sane or insane persons that he has examined, but 
 much more largely in the insane, and especially in old 
 cases. It is probably the result of transudation. Be- 
 sides this material, crystalline masses of hasmatoidine 
 are found, especially in the angles of bifurcation of 
 the vessels, in all forms of insanity. Minute extrava- 
 sations of blood are frequently found, and depend upon 
 a variety of causes. In some cases minute aneurisms
 
 182 INSANITY. 
 
 have been seen, and Eindfleiscli states that these punc- 
 tiform haemorrhages generally are due to aneurisms of 
 the smallest veins. But extravasations occur from the 
 giving way of the distended vessels in various states of 
 disease, fatty degeneration, atheroma, &c. I believe 
 aneurism of the pia mater to be more common than 
 of the vessels in the interior of the brain ; but Dr. 
 Tuke has found no less than five aneurisms in the right 
 corpus striatum, immediately underlying the epithelium 
 in one case. 
 
 We also meet with a chang;e of the extravasated 
 blood or of the ha3matine into pigment, the colouring 
 matter being deposited outside the vessels. 
 
 Fatty degeneration of the capillaries is an occa- 
 sional but not a constant lesion in insanity. 
 
 Hypertrophy of the muscular coat is met with pretty 
 frequently, and it has been variously interpreted. Dr. 
 Sankey believes it is due to increased exercise of the 
 vessels in consequence of an impure state of the blood. 
 Dr. Tuke sug-g-ests that the decfcneration of the cells of 
 the sympathetic ganglia, so constantly noted in cases 
 of chronic insanity, is more likely to be indicative of 
 this change. It is not really the result of an attempt 
 on the part of the distended vessels to contract on 
 their contents. 
 
 It is interesting to note that hypertrophy of the 
 muscular coat is always accompanied by the hyaline- 
 fibrosis just spoken of, although this latter condition 
 often exists independently of any hypertrophy of the 
 muscular coat. 
 
 And lastly we have some alterations in the direction
 
 IXSANITY. 183 
 
 of the vessels ; undue straiglitness due to the distension ; 
 tortuosity or kinking caused by the witlidrawal of the 
 strain. 
 
 Taking next tlie membranes, we fuid in tlie dura 
 mater evidences of old inflammatory processes, 
 thickening of the dura mater, and partial or complete 
 adhesion of it to the bones of the skull. In the 
 arachnoid we meet with the same difficulty in insane 
 persons as in other morbid conditions of this membrane, 
 viz., that it is so intimately connected with the dura 
 mater and the pia mater. It is frequently opaque and 
 thickened in all forms of insanity, or adherent to the 
 dura mater, or to the pia mater, or with bony plates on 
 its surface, or with fine granulations on the external 
 surface, or on the ependyma of the ventricles, evidences 
 of chronic inflammatory action. In addition to these 
 lesions, small ecchymoses are found in the cavity of the 
 arachnoid, and Virchow says pseudo-membranes, though 
 these have been explained by other observers as extra- 
 vasations of blood with absorption of the ha^matine. I 
 have no doubt the former explanation of Virchow is the 
 true one. The most peculiar affection of the arachnoid 
 in the insane is seen in the haemorrhages into its sac 
 and their residts. These may be seen in their recent 
 condition, and will then be simply masses of blood, of 
 greater or less extent, compressing the brain, and 
 causing abnormal separation between the layers of the 
 arachnoid, though generally the haemorrhage is slow 
 and gradual. Very soon, however, these masses of 
 blood undergo change. Some of the fluid part is 
 absorbed, and the lymph forms a cyst-like wall adherent
 
 184 INSANITY. 
 
 to the layers of the arachnoid, being firmly united to 
 them, and becoming organised, enveloping either a clot 
 or serum, or small accumulations of blood globules, 
 and forming what are known as arachnoid cysts. Dr. 
 Sutherland says the cysts may take the form of a small 
 sheath, not unlike the finger of a glove in size and 
 shape, or may consist of two large flat walls of organised 
 lymph, which may be thick or thin, and divisible or 
 not into laminae. The cysts may be so soft that they 
 cannot be removed without tearing, or of such strength 
 and toughness that they will bear rough handling, or 
 can be filled with water and suspended by a cord with- 
 out their walls giving way. They are generally thick 
 in the middle ; but become more attenuated towards 
 the edges, where the two walls adhere to one anothei-, 
 forming an acute angle. They are found on both 
 hemispheres, and generally, but not always, on the 
 upper surface. They are often due to blows on the 
 head, but may form, without previous accident, from 
 hypera3mia of the meningeal vessels, with weakness of 
 the vessels themselves, and probably impoverishment of 
 the blood. Idiocy, dementia, and general paralysis 
 are the forms of disease most usually associated with 
 these cysts of the arachnoid ; but, like many other 
 cerebral lesions, they are found in persons who have 
 not been insane. 
 
 It is a moot point whether the external layer forming 
 the cyst wall is the peripheral layer of the coagulated 
 fibrine, or the fibrinous exudation of an inflammation 
 originating secondarily around the clot. Most commonly 
 I believe the cyst wall is formed by the coagulated 
 fibrine itself.
 
 INSANITY. 185 
 
 Dr. Bright gives a beautiful plate of one such cyst 
 which contained half a pint of serous fluid. 
 
 In the pia mater we may find active hypericmia of 
 the vessels, and dilatation of the vessels in mania com- 
 pared with the normal size ; haemorrhages of various 
 amounts, frequently punctiform, due, as in the case of 
 the cerebral vessels, to small aneurisms, to atheroma, to 
 fatty degenerations, &c., all the various changes in the 
 structure of the vessels that have been mentioned as 
 occurring in the vessels of the brain ; a special con- 
 gestion connected with the larger veins, leading to 
 thickening and cedema of the pia mater; sometimes a 
 very anaemic state of the pia mater as part of a general 
 anaemia ; and a thickening of the Avhole membrane 
 from inflammation, which generally involves some of 
 the outer layers of the cortex of the brain, so that in 
 attempting to strip off the pia mater the external layer 
 at least of the brain's substance comes with it. This 
 condition as it affects the brain will be spoken of 
 immediately. Deposits of crystals of phosphate of lime 
 have been found by Dr. Tuke in one case, the subject 
 of acute melancholia due to great brain exhaustion ; 
 and lastly the same observer has met with two cases, 
 in which there were lymph deposits between the pia 
 mater and the substance of the spinal cord. 
 
 The ventricles are often found dilated, doubtless a 
 secondary lesion consecutive to atrophy of the brain. 
 Of very little importance also are the alterations in the 
 shape of the ventricles from partial contractions and 
 shortening and adhesions of their surfaces. Bergmann 
 observed adhesion of the posterior cornua in several
 
 186 INSANITY. 
 
 hundred cases, and considered this condition to be the 
 special pathological lesion in chronic dementia, but it 
 is not unusually met with in the brains of sane persons. 
 
 Vascularity, and even inflammation of the pineal 
 and pituitary glands, have been met with, and we shall 
 see by-and-by that a morbid state of the latter organ 
 has been found in many cases of epilepsy ; but obser- 
 vations on these glands seem to have no definite 
 relation wdth the phenomena of mental alienation. 
 
 I have already mentioned many of the changes the 
 neuroglia undergoes in the insane while speaking of 
 the various forms of sclerosis, Lecture IV. 
 
 General sclerosis may be met with congenitally, or 
 in some cases of idiocy, or in a mental condition that 
 can only be described as one of liebetude. It is not 
 common. 
 
 Disseminated sclerosis is very constantly found in 
 general paralysis, and in many cases of chronic insanity 
 of various forms. It may occur as true sclerosis, or as 
 grey degeneration with corpora amylacea. 
 
 Miliary sclerosis is also common in general paralysis. 
 The neuroglia, too, is much atropliied in cases of 
 atrophy of the nervous centres depending on impaired 
 nutrition, due to atheroma of the vessels. In this 
 morbid state all the elements of the tissue are seen to 
 be diseased, cells, nerve-tubes, and neurogha. 
 
 Another form of disease of the neuroglia is colloid 
 degeneration. 
 
 It is not associated with proliferation of the nuclei, 
 but is a form of degeneration of the nuclei of the 
 neuroglia.
 
 INSANITY. 187 
 
 It is found in cases of chronic insanity, and is most 
 marked in the white matter. Gricsinger speaks of the 
 colloid masses and corpora amylacea being one aiid the 
 same thino;. The difference of their behaviour with 
 carmine shows some distinction between them. The 
 parts affected in. each case are the nuclei of the 
 neurooiia, but the form of defeneration is different in 
 the two cases. 
 
 The condition of the cells may vary according to 
 the special disease. It is at present difficult to deter- 
 mine, whether any abnormality of cells can be the 
 primary lesion in mental disease. Most probably all 
 alteration in their number and condition is secondary 
 to the vascular abnormalities previously referred to. 
 Still, as secondary lesions, the alterations in the cells are 
 very noticeable. These lesions consist of atrophy of 
 cells, especially in the external layer of the cortex, 
 diminution in their number, or even in spots, entire 
 absence. Drs. Tuke and Eutherford, and after them 
 Dr. Herbert Major, have described considerable enlarge- 
 ment of the cells of the inner layers of the cortex, 
 where the cells of the outer layer were affected by 
 degeneration. In senile insanity, old dementia, and 
 especially in general paralysis, the cells are found 
 pigmental and granidar. In other cases there is com- 
 plete degeneration of the cell-wall, with a setting-free 
 of the nucleus. 
 
 Speaking more generally of lesions in the insane, 
 we sometimes find an apparent hypertrophy of brain ; 
 it being impossible, when the skull-cap is removed, to 
 get the brain back again into its normal cavity. It is
 
 188 INSANITY. 
 
 very rare, and, as was said in Lecture IV., it is not due 
 to general hypertrophy of all the elements of brain 
 tissue. Still, when it is associated with a dry condition 
 of membranes, anaimia of the whole brain, and some 
 flattening of the convolutions, with empty ventricles, 
 the increase in volume ]nust be due to abnormal 
 increase of some portion or other. 
 
 The cases are so rare, that it is mere hy[)othesis to 
 su2^<T:est that in all such instances this increase is due to 
 great proliferation of the neuroglia nuclei, but this is 
 the lesion that has been found in the hypertrophy of 
 brain in children. 
 
 Atrophy is extremely common in chronic cases, 
 and it is impossible by the naked eye alone to distin- 
 guish between senile atrophy and the form that follows 
 very acute disease. In both the membranes may be 
 thickened ; in both there is great oedema of the pia 
 mater, varying in exact pi'oportion to the atrophy of 
 the convolutions ; in both the sulci are w^ide and 
 distended with this fluid, and the brain as a whole 
 smaller than natural. 
 
 The shrinking of the convolutions may be universal, 
 or more in one part than in another, of one hemisphere, 
 or of one convolution. Partial atrophy, however, is 
 far more common as the result of previous disease 
 (chronic mania, dementia, &c.) than of old age. 
 
 I refer to the remarks on atrophy. Lecture IV., for 
 an explanation of the causes of this lesion ; but partial 
 atro])hy is fi'cquently associated with sclerosis, or is 
 due to the absorption of spots of haemorrhage or 
 softenino;.
 
 INSANITY. 189 
 
 Without giving you all tlic conflicting observations 
 as to the weight of the brain in the insane, it may suffice 
 to point out these results : — 
 
 1. The weight of the whole brain (cerebrum, cere- 
 bellum, pons, and medulla oblongata) is somewhat less 
 in the insane than in the sane, regard being paid to 
 the age of each. This is particularly seen in chronic 
 cases. 
 
 2. The w^eight of the cerebellum, pons, and medulla 
 oblongata is rather more in insane males tlian in the 
 sane. 
 
 3. Therefore the loss of weight of the brain in in- 
 sane males is at the expense of the cerebrum proper. 
 
 4. The weight of the brain does not always bear 
 any exact proportion to the intellectual power. 
 
 5. In brains, whose weight is not above the average, 
 the depth of the grey matter may account for the intel- 
 lectual power. 
 
 6. With the exception of idiocy, no particular 
 mental disease is associated with a small or a light 
 brain. Thus in Dr. Claphani's cases the maximum 
 male brain was found in connection Avith senile de- 
 mentia, and the mininuun with dementia; the maximum 
 female brain occurred in acute forms, the minimum 
 in epileptic insanity. 
 
 7. Dr. Bucknill finds an average lower specific 
 gravity in the brains of the insane. He even thinks 
 there is a kind of atrophy of the brain in mental 
 disease, which manifests itself solely by diminution of 
 the specific gravity, a kind of fatty degeneration of the 
 cerebral substance without diminution in volume.
 
 190 
 
 INSANITY. 
 
 Mr, W. G. Balfour has collected from the records of 
 the Montrose and Fife and Kinross Asylums, and from 
 observations of his own at Colney Hatch, the post- 
 mortem appearances (not microscopical) in 700 insane 
 cases. I cannot give you a better idea of the most 
 usual lesions than by quoting these results : — 
 Number of cases, 700. 
 
 Calvarium abnormally thickened 
 „ „ thin 
 
 „ dense 
 „ loose in texture 
 Caries and perforation 
 Membranes. Dura Mater : 
 Adherent to calvarium 
 Abnormally thickened 
 Calcareous deposit 
 Abnormally thin 
 Ossification of . 
 Timiours attached to . 
 Arachnoid : 
 
 Effusion of blood into sac of 
 „ „ serum 
 „ pus . 
 False membranes in sac of . 
 Sanguineous cysts 
 Crystalhne granulations 
 Opacity of ... 
 
 Adhesion of surfaces of 
 Pi a Mater : 
 
 Marked injection of vessels . 
 Local bulke of fluid in meshes 
 
 in 
 
 112 
 
 ?5 
 
 59 
 
 5) 
 
 12 
 
 ?5 
 
 9 
 
 ?i 
 
 1 
 
 ?? 
 
 74 
 
 5? 
 
 76 
 
 ?? 
 
 1 
 
 55 
 
 1 
 
 ?5 
 
 7 
 
 ?5 
 
 10 
 
 5) 
 
 27 
 
 '5 
 
 125 
 
 5? 
 
 2 
 
 ?5 
 
 38 
 
 5 
 
 o 
 O 
 
 55 
 
 19 
 
 55 
 
 294 
 
 55 
 
 6 
 
 55 
 
 53 
 
 55 
 
 61
 
 INSANITY. 
 
 191 
 
 Sanguineous efiiision into nicslies . 
 Tumours attached to . 
 Brown gelatinous deposit . 
 Adhesion to surface of grey matter 
 
 Blood vessels of brain : 
 
 Atheroma of arteries .... 
 Aneurismal dilatations 
 Marked injection of . 
 
 Grey substance : 
 
 Abnormalities in thickness of 
 
 „ „ colour 
 
 Gelatinous softening of . . . 
 Effusion of blood into 
 Granulations of surface of convolutions 
 Acute inflammation of 1 
 Local atrophies of J * ' 
 
 Wliite substance : 
 Induration of 
 (Edema 
 Softening . 
 Effusion of blood into 
 Excessive shrinking of 
 Marked injection of . 
 Cysts in . 
 
 Optic Thalami and Corpora Striata 
 Sansjuineous effusion into 
 Softening of 
 Tumours in 
 Cysts in . 
 Cicatrices in 
 
 in 
 
 41 
 
 ?? 
 
 3 
 
 ?? 
 
 24 
 
 It 
 
 G3 
 
 •)•> 
 
 108 
 
 5? 
 
 3 
 
 ?1 
 
 50 
 
 ?5 
 
 35 
 
 55 
 
 79 
 
 ,*? 
 
 10 
 
 55 
 
 G 
 
 n 
 
 o 
 O 
 
 10 
 
 
 )5 
 
 39 
 
 
 ?5 
 
 75 
 
 
 55 
 
 31 
 
 
 55 
 
 15 
 
 
 55 
 
 30 
 
 
 55 
 
 64 
 
 
 55 
 
 G 
 
 triata : 
 
 
 
 
 55 
 
 19 
 
 
 55 
 
 25 
 
 
 55 
 
 o 
 O 
 
 
 55 
 
 l 
 
 
 55 
 
 G
 
 192 
 
 IXSANITY. 
 
 Cerebellum : 
 
 Adhesion of membranes to 
 Effusion of blood into pia mater of 
 
 „ „ serum „ 
 Haemorrhage into substance of 
 Softening of . . . 
 
 Cysts in . 
 
 Ventricles : 
 
 Excessive serous fluid in 
 Sanguineous effusion into 
 
 Opacity of . . . 
 Softening of floor of . 
 Cysts in choroid plexus 
 Tumours in choroid plexus 
 Earthy deposit in choroid plexus 
 
 Pons : granulations on free surface of 
 
 Corpora Quadragemina : Softening at fis- 
 sure of Eolando on left side 
 
 in 
 
 3 
 5 
 1 
 
 2 
 1 
 1 
 
 353 
 
 20 
 68 
 
 4 
 70 
 
 2 
 12 
 
 1 
 1 
 
 Marked difference in size of the two 
 
 hemispheres .... 
 Apparently normal brains . . . ,, GO 
 
 It is to be remarked in this, as in all similar 
 collections of cases, that tumours are seldom found in 
 the brains of the insane. Here they have been found 
 three times m connection with the pia mater and 
 twice in the choroid plexus, ten times connected with 
 the dura mater, and only three times in the optic 
 thalami and corpora striata ; whilst apart from these 
 organs the grey and white substances of the brain have 
 wholly escaped. The proportion of cases is no larger
 
 INSANITY. • 193 
 
 than would probably be Ibiiiid in uii equal number of 
 sane persons. 
 
 Dr. Boyd states that, during his residence in the 
 St. Marylebone Infirmary, in three years and a half 
 there were in 1,039 post-mortem examinations twenty- 
 two cases of tumours in the brain ; one of these was 
 transferred to the insane ward, and two were in a 
 state of fatuity, leaving nineteen, or at the rate of 
 about 18'3 per 1,000, in whom no mental derangement 
 was observed. Whilst he was at the Somerset County 
 Lunatic Asylum, in 875 post-mortem examinations 
 there were fourteen cases of tumours of the brain and 
 membranes, or at the rate of IG per 1,000. 
 
 Whilst it would not be scientific to speak of 
 syphilitic insanity as a variety of madness, yet it is 
 certain that morbid mental phenomena coincide with, 
 if they do not depend on, syphilis. Thus headache, 
 sleeplessness, with the symptoms of progressive de- 
 mentia, with epileptiform or apoplectiform attacks, 
 sometimes preceded by a period of maniacal excite- 
 ment, sometimes devoid from the first of all excite- 
 ment, but taking the form of melancholia and hypo- 
 chondriasis, and especially of syphilophobia, and 
 accompanied in its later course with paralysis of one 
 or more of the cerebral nerves, and even with general 
 diminution of the motor power, are phenomena that 
 are very usually associated with syphilis. 
 
 Nor do these symptoms necessarily occur at a long 
 date from the primary infection. They are known to 
 have occurred within a month from the primary in- 
 fection. It is on this account that Dr. Wille has con- 
 

 
 194 INSANITY. 
 
 sidered these morbid symptoms may in some cases 
 depend on anaemia rather than on any structural 
 lesion. He would distinguisli the following forms of 
 mental disorder due to syphihs : — 
 
 1. Irritative forms based upon cerebral anaemia 
 following syphilitic infection even from its commence- 
 ment. 
 
 2. Simple inflammatory forms due to meningitis 
 and inflammatory softening of the cerebral substance. 
 
 3. Neoplastic forms proceeding from cerebral or 
 meningeal gummata. 
 
 I doubt whether any form of meningitis can by 
 its appearance alone be accurately deemed specific, 
 without the presence of gummata. Griesinger declares 
 a partly diffuse, partly circumscribed thickening of the 
 arachnoid to be specific ; while Maudsley and others 
 regard as specific the diffuse exudation glueing the 
 membranes to each other, to the cerebral substance 
 on the one hand, and to the skull on the other. It is 
 probable, however, that the meningitis of syphilis 
 cannot be distinguished from that accompanying rheu- 
 matism or other morbid states. It is evident, when 
 meningitis is accompanied by paralysis of any of the 
 cerebral nerves, that it is of the base of the brain ; and 
 it may reveal its presence by the effects on the optic 
 disc. See Lecture XIV. 
 
 Syphilitic meningitis is sometimes secondary to 
 caries of the cranial bones. In this ease it is generally 
 very partial. 
 
 Much that belongs to syphilis affecting the nervous 
 centres has been said in Lecture V. upon tumours ;
 
 INSANITY. 195 
 
 but we should notice a peculiar form of syphilitic 
 encephalitis congenital and associated with mental 
 phenomena. It probably begins as an inflammation of 
 tlie neurogha, either solely or coincidently with the 
 connective tissue of the capillary vessels ; and if life is 
 prolonged, it may lead to general sclerosis of the whole 
 brain, or of one hemisphere, &c. 
 
 Many of the morbid cerebral symptoms seem to be 
 connected with the presence of gummata, or of small 
 local softenings dependent on syphilitic thrombosis ; 
 but gummata may exist in the brain without giving 
 rise to any mental symptom, or indeed to any pheno- 
 mena except pain, and I have elsewhere in these 
 lectures recorded such an instance. 
 
 It remains only to say a w^ord about the cranium. 
 
 Almost every malformation of the cranium may be 
 associated with idiocy, but microcephalous heads are 
 most commonly found with this disease. In cases of 
 chronic insanity the skull-cap is often thickened and 
 indurated. Sometimes the bones are very thin, espe- 
 cially where they have been pressed against by a 
 gradual accumulation of fluid in the ventricles. They 
 may be carious from struma or syphilis, or they may 
 be the seat of nodes externally or internally, of exos- 
 toses, spiculai, &c. ; and lastly, many injuries to the 
 cranial bones have been known to have been the 
 starting-point of morbid mental symptoms. Various 
 abnormalities of the spinal cord are found in chronic 
 insanity ; myelitis, grey degeneration, disseminated and 
 miliary sclerosis, &c. Such lesions are accompanied 
 by ataxic or paralytic symptoms. 
 
 2
 
 196 
 
 LEOTUEE VIII. 
 
 INSANITY {continued). 
 
 Mania. It is not easy to draw pathologically accurate 
 distinctive lines of demarcation between the various 
 forms of insanity. Between mania and melancholia, 
 especially, the pathological difference may be very slight. 
 It is only possible, therefore, to give the most common 
 appeai'ances, whilst we acknowledge that much of the 
 lesion we point out as belonging to mania obtains also in 
 melancholia. The clinical history of each form of disease 
 shows also that in many cases the lesions on which the 
 symptoms depend are transitory, and not persistent. 
 Not only do many patients recover both from melan- 
 cholia and from mania, but in recurrent mania the 
 attacks are separated by intervals, of variable duration, 
 of perfect health ; and in some cases the patients 
 themselves can foresee the recurrence of the mental 
 phenomena by their own cerebral sensations. Clinical 
 observation, therefore, as well as pathological research, 
 leads us to consider lesion of the vessels as at once the 
 })rimary and the most important of all the cerebral 
 chang;es in mania. 
 
 Tlie post-mortem manifestations of cerebral hyper- 
 ncmia are often not readily recognisable. The empti-
 
 mSANITY. 107 
 
 ness of the capillaries, as we have already said, is no 
 proof they have not been distended during life, as the 
 cerebral vessels are able to empty themselves with such 
 facility. It is this capillary distension, this hyperasmia 
 of the cortical substance of the brain, that is the chief 
 lesion in acute mania. This hyperremia will generally 
 affect the pia mater, and, I believe, specially the pia 
 mater of the convexity. Eindfleiscli says that this 
 cortical hypero3mia will here cause a sort of stasis ; 
 this, again, leads to over-distension, then to atony of 
 the vessels. A return to the normal calibre of the 
 vessels is at first only a question of time ; it is only 
 when the distension has become habitual that corre- 
 sponding changes are set up in the walls of the 
 vessels, and the return to the normal calibre becomes 
 impossible. 
 
 I must risk the danger of being charged with repe- 
 tition if I again remind you that this hyperasmia of 
 the pia mater and the cortex may be shown merely in 
 a slight tinge of redness ; more frequently, however, 
 its previous presence is manifested by its results. These 
 are extravasations, diffuse encephalitis, affecting spe- 
 cially one layer of the cortex, and pigmentation ; and if 
 the hyperjBmia has been long continued or has frequently 
 recurred, further changes are found to have taken place 
 in the vessels themselves. The extravasations may take 
 the form of punctiform haamorrhages, but more usually 
 the extravasation has not absolutely reached the brain 
 matter, but exists in the form of dissecting aneurisms of 
 the small veins. Besides these minute aneurisms Ave find 
 various dilatations of the smallest vessels, causing altera-
 
 198 INSANITY. 
 
 tions of shape of variable intensity. Dr. Bucknill thinks 
 that in acute mania extravasations of blood are chiefly in 
 the pia mater. Greding states tliat the choroid plexus 
 was healthy in only 16 out of 216 cases of insanity, and 
 that out of 100 maniacs 96 showed a choroid plexus 
 that was either thickened or full of hydatids ; by 
 hydatids he doubtless means serous cysts. The in- 
 flammatory condition met with in mania is usually 
 confined to the middle layer of the cortex ; the external 
 layer is occasionally affected, this layer of the cortex 
 coming off in patches when the pia mater is re- 
 moved, and leaving the appearance of ragged ulcera- 
 tions of the external portion of the brain. The 
 internal layer is scarcely ever affected in mania. 
 These three layers correspond to the arrangement 
 of the vascular branches in the cortex. The middle 
 layer is in a state of red softening, and when it 
 is thus affected the removal of the pia mater will 
 often bring away the external layer pretty much as a 
 whole, its cohesion with the softened middle layer being 
 destroyed. I speak of three layers with a knowledge 
 that Lockhart Clarke has divided the cortex into eight 
 layers. For practical purposes, and especially as a 
 basis for pathological observation, the smaller number 
 will suffice, even though each one of these three layers 
 may be further minutely subdivided. It must, how- 
 ever, be remembered that this important lesion, the 
 softening of the middle layer, is not universally met 
 witli in acute mania. Were it so, we might be tempted 
 to look at lesion of this middle layer as causing an 
 ataxy of the brain corresponding to locomotor ataxy
 
 INSANITY. 199 
 
 of the muscles, the thoughts being there, but the power 
 of conibiiiatioii bein<f absent. We often iXQt in acute 
 mania an overwliehning richness and flow of ideas ; 
 the brain may react on the external stimulus with a 
 marvellous quickness and ability, or it may be so taken 
 up with its fulness of ideas that external stimuli pass 
 wholly unnoticed. What is wanting is sequence, or at 
 least such sequence of ideas as can be recognised. 
 Much of the so-called incoherence of acute mania is 
 no more than a rapid jumping from a first idea to a 
 second and third, the first and third being put into 
 words, the second, the connecting link, being passed 
 over in silence. If a perfectly sane man, with his 
 brain in full activity, were to put into words each idea 
 as it arose, or still more, if he were to put into words 
 every alternate idea, his speech would frequently simu- 
 late pretty closely the incoherence of acute mania. 
 Inordinate richness of idea, ^\^thout a sequence that can 
 be appreciated by another person, may be considered 
 one of the most important symptoms of acute mania ; 
 and this symptom may be connected with the hypertemia 
 of this middle layer of the cortex before further 
 degenerative change has passed upon it. 
 
 But although this may be the case roughly, patho- 
 logical histology will demand greater accuracy. It is 
 not enough to localise the lesion in the middle layer, 
 even if this were always the part affected. This middle 
 layer itself contains no less than three varieties of cor- 
 puscles, viz., neuroglia corpuscles, small finely granular 
 bodies having nuclei, and the pyramidal nerve-cells. 
 In disease, not only does the proportion of these bodies
 
 200 INSANITY. 
 
 vary, but their outline and appearance ; and it is on 
 their normal proportion and freedom from all lesion 
 that clearness of thought and systematic sequence of 
 idea probably depend. 
 
 Pigmentation is a proof of chronicity to a greater 
 o.r less extent. Tlie blood corpuscles or the hasmatine 
 extravasated either beyond the vessels or between the 
 coats of the vessels is changed into pigment and connec- 
 tive tissue, and the part so affected is somewhat firmer 
 than in health, but also stained a brownish colour. 
 
 And finally, in acute mania, where the symptoms 
 have recurred often or have extended over some time, 
 the distension of the vessels leads to still further 
 changes, and there occurs fatty degeneration of the 
 capillaries. It is not met with universally in these 
 cases, but, when there, it imports an element of chro- 
 nicity, or more or less of hopelessness of cure, on the 
 case. It is doubtful whether capillaries can ever 
 become normal in which oil globules collect to a con- 
 siderable extent round the nuclei, such oil globules not 
 being derived from the fatty portion of the brain itself, 
 but being a sign of degeneration due to the long-con- 
 tinued distension of the capillary walls. 
 
 Melancholia. — The post-mortem appearances of 
 acute melancholia are in many cases the same as in 
 acute mania, viz. : dilatation of vessels, extravasation, 
 subacute inflammation, and pigmentation. Extrava- 
 sations occur more frequently in the pia mater than 
 in the cortex. In a large number of cases the lesion is 
 simply dilatation of the vessels. We judge so by the 
 constant return to health of melancholiacs.
 
 INSANITY. 201 
 
 The symptoms of unreasoning depression, however, 
 may coincide with very various lesions of the brain ; 
 with tumours, witli syphilis, with the circulation of 
 impure blood in the brain, with anscmia as a sequence 
 of epilepsy, and even witli the gradual formation of 
 cerebral abscess. 
 
 Mania and melancholia may merge into each other. 
 Many cases commence with symptoms of melancholia, 
 at first gentle and quiet, then suicidal, which will 
 afterwards advance to acute mania, with homicidal 
 phenomena. In such cases it would be impossible to 
 draw any pathological distinction between diseases that 
 differ only in name. 
 
 In chronic melancholia, however, we often meet 
 with further disease of the vessels ; either tlie fatty 
 degeneration of chronic mania or ossification of 
 arteries. An anaemic condition of the brain is very 
 common ; and Griesinger mentions a consistence of 
 the cerebral substance abnormally great, witli more or 
 less serous infiltration. 
 
 In very chronic cases, however, we may meet with 
 the lesions of brain-wasting, large sulci, much cerebro- 
 spinal fluid over the cortex, with the alterations both 
 of vessels and of cells that will be mentioned below. 
 
 Chronic Insanity, Dementia. — We find thickening 
 and opacity of the membranes the result of chronic 
 stasis and slow inflammatory action. The dura mater 
 may be adherent to the skull ; and there is often 
 serous infiltration of the pia mater and dropsy of the 
 ventricles. There is sometimes superficial induration 
 and adhesion of the pia mater : but this lesion is not
 
 202 INSANITY. 
 
 found in senile atrophy. We meet als(j with anasmia, loss 
 of colour, and atrophy of the convolutions, a widening of 
 the sulci between the convolutions, pigmentation of the 
 external layer of the cortex, with sometimes induration 
 of the cortical or of the medullary substance. 
 
 The minute changes causing some of the coarser ones 
 are, according to Eindfleisch, an increase in the amount 
 of the perivascular protoplasms, appearance of a num- 
 ber of fine feebly-refracting processes of protoplasms, 
 giving the vessel a curious thorny appearance. Some 
 atrophy of the ganglion cells is found ; brownish dis- 
 colouration of them, due to the imbibition of hsematine. 
 Sometimes fatty degeneration of these cells. Fission 
 of the neuroglia nuclei is found in all the layers of the 
 cortex. Connected with this, and leading to the in- 
 duration above mentioned, forming the most important 
 lesion in chronic mania, is the interstitial growth of 
 the connective tissue of the cortex. 
 
 Frequently also we meet with a granular condition 
 of the ependyma of the ventricles ; and occasionally 
 some of the spinal lesions above mentioned, haemor- 
 rhage, myelitis, sclerosis, &c. 
 
 Dr. Crichton Browne says of senile dementia, that 
 there is thickening of the vessels of the cortex by 
 fibroid degeneration, and atheroma of the arteries at 
 the base in some cases ; whilst cerebral wasting is the 
 true anatomical basis of the fatuity of old age. The 
 coarse changes in the brain discernible with the naked 
 eye correspond with the more intimate alterations in 
 its structure. The microscope shows degeneration and 
 softening. The cells of the grey matter are compara-
 
 INSANITY. 203 
 
 lively few in number and small in size, as if shrunken ; 
 or, on the other hand, they contain molecular fat and 
 pigment in an advanced stage of the disease ; aggre- 
 jTjation of granules remain as the debris of distinct cells. 
 The vessels traversing the grey matter are studded 
 Avitli fatty granules and large compound corpuscles, 
 and the neuroglia pervading it also shares in the fatty 
 cliange. The fibres of the medullary substance also 
 undergo some degree of fatty metamorphosis. 
 
 General Paralysis. — The commencement of this 
 disease, like some other forms of insanity, is connected 
 with no lesion that can be recognised after death. 
 Dr. Thompson's valuable observations with the sphyg- 
 mograpli have been already referred to in Lecture VII. 
 He proves tliat general paralysis of the insane may 
 be presumed to be owing, to a considerable extent, to 
 persistent spasm of the vessels, and that this spasm 
 leads to cliange in the component elements of the 
 vessels, especially in the muscular substance. It is only 
 the secondary effects, therefore, that we see post niorteni. 
 
 But what causes the spasm? Observations such as 
 these of Dr. Thompson are most important as carrying 
 us one step further back towards the origin of the 
 disease ; but this origin is not yet reached. It is all 
 hypothesis that blood in a particular state has some 
 effect on the vaso-motor nerves that we caU ' irritation,' 
 and that this irritation causes spasm. We do not know 
 for certain that the blood has anything to do with it. 
 "We have not the slightest idea of what irritation is. 
 It is a convenient word by which to formulate our 
 ignorance, and that is all.
 
 204 INSANITY. 
 
 As far, therefore, as our present knowledge carries 
 us, we find first tJiis spasm of vessels ; but we know 
 that beyond this abnormal condition there is something 
 on which the spasm depends. It is not unlikely, from 
 the observations of Poincare and Bonnet, that this 
 lesion is to be found in disease of the cervical, and 
 perhaps other ganglia of the sympathetic. 
 
 The recognisable lesions in general paralysis vary 
 according to the intensity of the disease, the time at 
 which death has occurred, and the portions of the 
 nervous system affected. The great disagreement be- 
 tween observers is due to the fact that the post-mortem 
 appearances are sequences of the original lesion, and 
 also that in some cases this, in others that element of 
 the disease is more strongly developed. 
 
 The naked-eye appearances are as follows, always 
 remembering, as we must, that in no case can all the 
 lesions mentioned be found : — 
 
 1. Great oedema of membranes ; adhesions of the 
 closest nature of the pia mater to the subjacent cortex ; 
 meningeal apoplexy ; degeneration of the cerebral 
 arteries, such degeneration being fatty in only some 
 few cases ; thickening and nodulation of the ependyma 
 of the ventricles. 
 
 2. Changes in the cortex ; greyish-red softening 
 most frequently found in the middle layer of the cortex, 
 and proceeding later to induration. I presume it is this 
 lesion that explains the frequent association of mania- 
 cal symptoms with general paralysis. Induration of 
 the most superficial layer, which probably had been 
 previously softened ; atrophy of the whole brain ;
 
 
 -K^. 
 
 
 ^i 
 
 fit> 
 
 C. Berjeau, Lith., 
 
 MILIARY SCLEROSIS 
 
 Banks & CcEdm'^
 
 INSANITY. 205 
 
 induration also of the wliite matter ; dikitatiou of the 
 ventrieles. 
 
 3. Induration and atrophy of the spinal cord, or 
 of spots in it ; on more minute examination, tlio 
 vessels are seen to be dilated without any thickening 
 of their coats ; much liaamatoidine in the hyaline 
 sheath all over the vessels ; increase of connective 
 tissue and destruction of nervous elements ; the 
 atrophied appearance depends partly on this destruc- 
 tion of the nervous elements, partly on the imperfect 
 mitrition of the brain ovv'ing to the diseased vessels ; 
 this increase of the connective tissue is also found in 
 the white substance, either diffused throughout or 
 Hmited to certain portions. 
 
 Plate 15 represents miliary sclerosis in a case of 
 general paralysis. It had affected many portions both 
 of the brain and sjnnal cord. 
 
 Fat granules and granule cells have also been ob- 
 served in the posterior and lateral columns of the cord 
 in general paralysis, but they seem to bear no relation 
 to the clinical symptoms. They are dependent upon 
 fatty degeneration of the walls of the vessels, and Dr. 
 Huguenin gives them the excellent name of ' the 
 visible form of physiological death.' 
 
 Dr. Herbert Major mentions a case in which careful 
 examination showed all the layers of the cells of the 
 cortex healthy, except that they were very pigmental, 
 and that there existed nerve-cells of immense size, 
 situated about midway in tlie depth of the cortical 
 layer, irregular in contour, with large and numerous 
 branches, these cells beino- most numerous in the
 
 206 INSANITY. 
 
 parietal region, then in the occipital, and most rarely 
 in the frontal lobes. He states also that the neuroglia 
 cells were not so niuiierous as in brain-wasting. 
 
 Calmeil's name will always be so closely associated 
 with general paralysis of the insane, his observations 
 having; been the means of attracting the attention of 
 English pathologists to this disease, that a resmne of the 
 post-mortem appearances in some of his cases will 
 not fail to be of interest. He gives 37 cases of this 
 disease, the main lesion being diffuse chronic peri- 
 encephalitis in a simple state. 
 
 In 10 the tissue of the cranial bones was notably 
 red ; in 6 the vessels of the cerebral dura mater were 
 injected. 
 
 In ] 5 the cavity of the cerebral arachnoid contained 
 serosity, in 3 false membranes, in 1 coagulated blood. 
 
 In 31 the vascular web of the pia mater was red and 
 injected, in 1 infiltrated with pus, in 20 infiltrated with 
 serosity, in 7 thickened, in 9 roughened with opahne 
 lines. 
 
 In 35 it adhered more or less intimately to the 
 surface of the cerebral hemispheres. 
 
 In 34 the cortical substance of the cerebral hemi- 
 spheres was red, rose-coloured, or violet, or consider- 
 ably injected with blood ; in 7 it was yellowish, in 1 
 slate-coloured. 
 
 In 14 it seemed to be abnormal by a want of con- 
 sistence, in 5 by excess of resistance and firmness ; in 
 4 it seemed atrophied. The white substance which 
 constitutes the greater part of the cerebral mass was 
 injected with blood in 23 cases ; in 13 it was too firm
 
 INSANITY. 207 
 
 cUilI iudunited ; in 3 too lax and of too little con- 
 sistence. 
 
 In 14 the optic thalami were remarkably red, in 
 3 yellow or orange ; in 7 tlieir consistence was too 
 great, in 1 too little. 
 
 In 18 the corpora striata were Hesh-colonred or 
 violet, in 4 orange-coloured, in 1 indurated, in 1 too 
 soft. 
 
 In 4 the w\alls of the lateral ventricles were in- 
 jected, in 5 covered with miliary vesicles, in 6 bathed 
 in serosity, in 2 too soft, in 2 too firm. 
 
 In 3 the septum lucidum, fornix, and corpus cal- 
 losum appeared indurated, in 2 diminished in con- 
 sistence. 
 
 In 9 the pia mater of the cerebellum was red and 
 injected, in 1 slate-coloured ; in 12 it adhered to the 
 surface of the cerebellum. 
 
 In 17 the cortical substance of the cerebellum was 
 injected at its circumference, in 10 extremely so, in 5 
 yellow or orange, in 8 diminished in firmness, in 1 too 
 firm. 
 
 In 14 the pons was red or rose-coloured in its centre, 
 in 3 it was orange. 
 
 In 1 the pons appeared atrophied, in 1 it was too 
 soft, in 1 too firm, in 1 it contained a small cicatrix. 
 
 In 11 the medulla oblongata was of a rose or 
 strawberry colour, in 1 of a nut colom\ 
 
 In 1 it appeared atrophied, in 2 indurated, in 1 too 
 soft. 
 
 In 1 its peculiar membrane was surrounded by coa- 
 gulated fibrine.
 
 208 INSANITY. 
 
 In 1 the spinal cord was slender, in 4 indurated, in 
 1 diminished in firmness, in 4 rose-coloured or injected, 
 in 1 soot-coloured, in 1 surrounded by a plastic 
 coagulation. 
 
 The number of brains examined by the microscope 
 was 12. This examination was held in one case in 
 which the delirium presented the characters of mania, 
 in 2 of melancholic delirium, in 1 of ambitious delirium, 
 in 1 of variable delirium, in 3 of dementia with 
 delirious ideas, in 3 of simple dementia, in one where 
 the patient was epileptic. 
 
 It is difficult to make a resume in figures of the 
 number of microscopical alterations which have been 
 noted in these twelve cases of diffuse chronic perien- 
 cephalitis; nevertheless we may easily be sure that 
 certain alterations are almost constantly found. 
 
 Of this number are the serous infiltration of the 
 cortex of cerebral hemispheres, its state of separation, 
 of bloody injection, its mixture with granular elements, 
 either on the walls of the vessels or on the surface of 
 the large nerve-cells, the state of injection of the vessels 
 of the white matter, the development of the corpora 
 striata, the presence of molecular granules and collec- 
 tions of small cells in the midst of the grey matter in 
 the same bodies, the dilatation of the vessels of the cere- 
 bellum and of the pons, the formation of granular 
 products on the vessels or in the grey substance of 
 these same regions ; finally, the dilatation of the vascular 
 net-work of the pia mater, and its infiltration, either 
 serous or sero-sanguinolout, with the formation of 
 granular elements.
 
 INSANITY, 209 
 
 He also o'ivcs an account of 45 ijaticnls of aeneral 
 paralysis, with clirouic dilllisc periencephalitis in a state 
 of complication. 
 
 Of these, in 13 the diploe of the cranial bones was 
 coloured by ha^matosine and blood. 
 
 In 17 the dura mater was injected externally. 
 
 In 34 the cavity of the arachnoid contained false 
 membranes or cysts ; in 3 the false membranes were 
 vascular; 12 times they were situated in the right 
 cavity of the arachnoid, 9 times in the left. 
 
 In G the cysts were vascular, in 8 they contained 
 blood, in 5 serosity. 
 
 In 20 there was clear serosity in the cavity of the 
 arachnoid, in 7 purulent, in 3 sanguinolent. 
 
 In 5 these cavities contained blood, free or scarcely 
 coagulated — once this has been found in the arachnoid 
 surrounding the cerebellum. 
 
 In 32 the vascular network of the cerebral pia 
 mater was red and much injected ; in 8 it was tinted 
 besides with large suffusions of blood. 
 
 In 8 the web of this pia mater was thickened ; in 
 19 infiltrated with serum, in 1 with pus. 
 
 In 39 the internal surface of this membrane was as 
 if it were soldered to the cerebral convolutions over a 
 variable, and sometimes considerable, extent. 
 
 In 31 the superficial cortical substance was tinted 
 violet, rose, or red; in 4 yellow. 
 
 In 10 it seemed softened, in 3 hard, in 4 atrophied. 
 
 In 12 it showed one centre, or many, of inflam- 
 mation. 
 
 In 25 the white substance was injected and more or 
 
 p
 
 210 INSANITY. 
 
 less tinted by the coluuring matter of the blood, hi 7 
 indurated, in 2 somewhat suifused. 
 
 In 5 it contained localised inflammatory spots, in 
 1 pus in cysts. 
 
 In 6 the central parts of the brain were found 
 separated. The ventricular walls were often covered 
 with small vesicular projections, causing irregularities 
 on that surface ; they were often roughened by large 
 expansions of vessels. 
 
 In many cases the cavities of all the principal ven- 
 tricles contained a certain amount of serum. 
 
 In 5 the optic thalami were red, in 1 yellowish. 
 
 In 3 they were deficient in consistence, in 1 they 
 contained cicatrices. 
 
 In 16 the colour of the corpora striata verged on 
 violet, or a more or less intense red ; in 5 on a more 
 or less intense orange yellow ; in 3 these bodies were 
 soft, in 2 they contained cicatrices. 
 
 In 10 the pia mater of the cerebellum was red and 
 much injected, in 2 reddened by extravasations of 
 blood, in 6 adherent to the nervous substance. 
 
 In 23 the grey matter of the cerebellum was coloured 
 violet or red, in 8 it was soft, in 1 too hard. 
 
 In 10 the interior of the pons was of a remarkable 
 violet or amaranth tint, in 2 it was deficient in con- 
 sistence. 
 
 In 5 the spinal sinuses were engorged with blood ; 
 this blood sometimes formed infiltrations. 
 
 In 2 there were deposits of blood outside the spinal 
 dura mater, in 2 beneath it. 
 
 In G the figure of the spinal cord was red-coloured,
 
 INSANITY. 211 
 
 111 5 of little iinimcs.s, in 2 too firm, in 1 nuu']i injected 
 and atrophied locally, in 4 softened. 
 
 Almost always most of the above-mentioned altera- 
 tions were found united in the same patient. 
 
 Thirty-seven brains were examined microscopically. 
 
 In 1 these investigations were made on the brain 
 of a patient who had succumbed to an attack of 
 intercurrent congestion of the brain ; in 2 on subjects 
 who showed simple false membranes in the cavity of the 
 arachnoid ; in 1 case on a subject who had cysts filled 
 with blood on the surface of the brain ; in 1 where the 
 cysts were filled with serum. Once these investigations 
 were carried on on purulent fluids, in 4 on interstitial 
 centres in a state of inflammation, once on a spot of 
 central softening, once on a spot of inflammation with 
 induration, twice on imflammatory spots containing 
 cellular fibres in a state of division, once on an 
 inflammatory spot containing the lamellar tissue of 
 cicatrices, twice on cases of softening of the spinal 
 cord. 
 
 Finally, the result of all these investigations is that 
 the cerebral capillaries in subjects attacked with difiuse 
 chronic periencephalitis are diseased in various ways ; 
 that abundant extravasations of fibrine are often found ; 
 and that many secondary products are met with, 
 especially in that form of disease that is complicated 
 with phenomena of an apoplectic or convulsive form. 
 I append a case that died of general paralysis after 
 many years' illness. 
 
 Man, aged 50. A large quantity of fluid under 
 the dura mater and under the arachnoid, filling up the 
 
 p 2
 
 212 INSANITY. 
 
 space in tlie skull left vacant by the shrinking of the 
 brain. Brain small and shrunken. Surface of cerebrum 
 very vascular, and convolutions shallow and flat. 
 Surface of cerebellum very pale. There appeared to 
 be a small quantity of grey matter relatively ; ven- 
 tricles very large, containing much fluid. Substance 
 of brain firm. Pons and medulla oblongata on section 
 appeared almost fibrous. Spinal cord remarkably 
 small. In the dorsal and cervical regions it was soft. 
 A great deficiency of grey matter throughout, and the 
 cornua seemed unequal in size and shape. 
 
 I cannot close the resume of the lesions found in 
 general paralysis of the insane without mentioning the 
 conclusions to which Poincare and Bonnet have come, 
 
 1. In general paralysis there is sometimes prolifera- 
 tion of the cellular tissue about the vessels, but it never 
 advances so far as to diminish, still less to completely 
 efface, the calibre of these vessels. Consequently, w^e 
 cannot attribute the functional and material alterations 
 of the nervous tissue, properly so-called, to a want of 
 blood supply. In one word, there is no sclerosis of brain. 
 
 2. The principal and constant alteration of the brain 
 consists in the change of shape and the fatty degenera- 
 tion of the cells. We find besides, but less frequently, 
 fat globules free in the midst of the granular matter, 
 sometimes isolated, sometimes agglomerated ; masses of 
 granulations of a ferruginous tint not surrounded by 
 a common envelope ; pigment and hasmatosine in 
 the walls of the vessels and of the fatty granules. 
 Sometimes fatty granulations form vast agglomerations 
 at the circumference of the vessels. We often perceive
 
 INSANITY. 213 
 
 enormous globules of fat free or mingled with blood 
 globules. The tubes are always intact. 
 
 3. We have found no other modifications in the 
 cord, except a greater abundance of ferruginous granu- 
 lations in the cells next the ependyma. 
 
 4. The cells of the whole chain of the great sympa- 
 thetic are coloured by brown pigment much more 
 intensely than in other patients, whatever their disease 
 may be. In the ganglia of the cervical regions, and 
 often in the ganglia of the thoracic region, there is 
 evidently substitution of cellular tissue and fat cells 
 for the nerve-cells, which appear relatively much less 
 frequently. Everything leads us to think here is found 
 the anatomical point of origin of the affection, and that 
 the alterations of the brain are only the consequence 
 of the disturbance that this sclerosis carries in its train 
 on the cerebral circulation by paresis of the cervical 
 ganglia. There is always a w^ell-marked pigmentation 
 of the spinal ganglia, and of those connected with the 
 cranial nerves. The fat cells which are substituted for 
 the nerve-cells in the ganglia of the great sympathetic 
 often show a deep colour, that may even be black. 
 
 5. All the alterations we have described cause dis- 
 turbances of nutrition in most of the organs, disturbances 
 which are on the vei'ge of fatty degeneration, or some 
 other modification of their elements ; and are manifested 
 physiologically by ataxy at first, and afterwards by 
 enfeeblement of the functions of the life of relation and 
 of ve2;etative hfe. 
 
 Plate 15, however, shows that sclerosis does exist in 
 the brain in general paralysis. In many cases too in
 
 214 INSANITY. 
 
 wliicli no microscopical examination has been made we 
 have records of induration. 
 
 Idiocy. — This disease has been divided and sub- 
 divided in a manner that only leads to confusion. Dr. 
 Ireland in his excellent article upon it divided it into 
 ten groups : 1, hydrocephalic idiocy ; 2, eclamptic 
 idiocy ; 3, epileptic idiocy ; 4, paralytic idiocy ; 5, 
 inflammatory idiocy ; 6, traumatic idiocy ; 7, micro- 
 cephalic idiocy ; 8, congenital idiocy ; 9, cretinism ; 
 10, idiocy by deprivation, that is, by the loss of two or 
 more of the senses. I prefer to follow Griesinger in 
 speaking of two chief varieties, complete idiocy or 
 fatuity, and weakness of mind or imbecility. We may 
 range cretins under both these heads, as the mental 
 power of cretins varies exceedingly. 
 
 The objections to this more simple classification are 
 twofold : one, that imbecility is often used as applied 
 to subjects of chronic insanity who have drifted into 
 dementia after acute conditions of disease ; and the 
 other, that the gradations in mental power in idiots 
 between fatuity and mere weakness of mind are 
 infinite. 
 
 I mean by idiocy a state of mental weakness which 
 has existed from birth or early infancy. 
 
 In my first lecture on congenital abnoi^malities I 
 mentioned several conditions of the brain and mem- 
 branes with whicli mental deficiency is necessarily 
 associated. In some few cases, and these exceptional, 
 the configuration of the child is perfect externally, the 
 head well shaped, tlie limbs well formed, the face in 
 due proportion to the cranium, It is by no means
 
 INSANITY. 215 
 
 true that the skull of an idiot is always small. Out of 
 338 cases, the measureineiit of which is given by the 
 Massachusetts Commissioners, only 99 had diminished 
 brains. On the other hand, the flat-headed Indians 
 of the Columbia river, whose heads by a mechanical 
 contrivance in infancy have been deformed, so that a 
 depression of the forehead and consequent elongation 
 of the whole head is induced, are not inferior to their 
 round-headed nei<?hbours. 
 
 A considerable number of cases seem to owe their 
 origin to falls on the liead. One observer alone met 
 with 48 cases in which the idiocy was ascribed to a fall 
 on the head from a height. 
 
 Arrest of development, the important lesion in 
 idiocy, may be primarily of the brain, and secondarily 
 of the cranium, or mce versa. 
 
 We may meet with local thinning of the cranial 
 bones or local thickening; syphilitic exostoses are 
 sometimes seen, and there is one case on record in 
 which with this lesion iodide of potassium cured the 
 child. The thickenini^ of the cranial bones is some- 
 times very extreme in microcephalous idiots. 
 
 I refer you to Griesinger's work for a minute 
 account of the cranial abnormalities in idiots. The 
 main points he insists upon are these : the sutures may 
 close too soon, or unequally at the two sides. From 
 whatever cause they become occluded, there is inter- 
 ruption of the growth of the bones at that spot, 
 narrowing of the cranium at that point, and, Avhen 
 considerable, the influence is extended to parts at a 
 distance. In some cases, however, of premature
 
 216 INSANITY. 
 
 ossification of the sutures, corresponding dilatations are 
 found in other parts of the cranium, with the effect of 
 limiting the evil of the contraction, but increasing the 
 deformity. Very seldom are the compensations suffi- 
 cient for satisfactory and complete cerebral development. 
 The varieties are these : — 
 
 a. True raicrocephalus would depend upon early 
 closure of the sutures, with early ossification of the base 
 of the skull also, with great interference with the due 
 growth of the brain. 
 
 b. If compensation occurs from growth at the base 
 of the brain, we have the Aztec type of idiocy, though 
 in many of these cases idiocy would be a harsh name. 
 There is merely weakness of intellect in certain direc- 
 tions. In several cases that have been examined the 
 cranium was small, the bones thick, and synostosis 
 of the arch had occurred. The basis cranii, on 
 the contrary, was very shghtly ossified ; the basilar 
 portion almost quite cartilaginous ; the petrous portion 
 and ethmoid bone were rather larger than normal; 
 the space for the cerebellum was enormous in all 
 directions. 
 
 c. Too narrow crania, shortening of the transverse 
 diameter, caused mainly by early ossification of the 
 sagittal sutures. 
 
 d. Too short crania, caused often by early ossifica- 
 tion of the lambdoidal suture, generally with compen- 
 sating development of the region of the anterior 
 fontanelle ; or by extended ossification of the frontal 
 with the parietal bones. 
 
 e. Too low crania, caused by ossification of the
 
 INSANITY. 217 
 
 wings of the splieiioid. with the frontal bone and the 
 squamons portion of the temporal bone. 
 
 f. Unsyrametrical obhqncly narrow crania, caused 
 by unilateral ossification, either of one half of the 
 coronal suture, or of one half of the lambdoidal suture, 
 with compensating extension towards the opposite 
 side. 
 
 9. The sinosto-basilar form ; cretinism in the proper 
 sense of the term, though cretins exist without this 
 abnormaUty. This form is due to premature ossification 
 of the base, ossification of the synchondrosis between 
 the sphenoid and tlie basiLar portion, whicli in the 
 normal state does not occur until the fifteenth year, 
 and sometimes not till the twentieth year. This 
 shortening of the base of the cranium causes a ejreat 
 curvature upwards of the base of the cranium, a small 
 angle at the point of union between the sphenoid and 
 the basilar portion, and a steep clivus, with a condition 
 of face that is called prognathism. Dr. Stahl, finding 
 this abnormality frequent in cretinism, examined the 
 condition of the clivus. In 104 insane patients, he 
 found it only in three, one of whom had previously 
 been imbecile. 
 
 When we proceed to a resume of the lesions of the 
 brain, Ave meet with a greater variety of conditions. 
 
 1. The brain may be symmetrical, and simply very 
 small. 
 
 2. The arrest of development may be shown not 
 only in a small size of brain, which, however, may be 
 symmetrical, but in deficiency of the grey matter of the 
 convolutions. Thus, Dr. Merjeiensky mentions an idiot.
 
 218 INSANITY. 
 
 fifty years of age, who had had the capacity of a child 
 a year and a half old. The size of the head was about 
 that of a child of one year old. The encephalon 
 weighed 369 grammes ; the cerebellum, pons, and me- 
 dulla oblongata were about the usual size, the deficiency 
 being in the cerebrum ; the corpus callosum was only 
 one-third of the usual length ; the convolutions were 
 simple and undeveloped, the grey matter deficient. 
 
 3. Inequality in the size of the two hemispheres, 
 owing to atrophy of the smaller ; this atrophy either 
 from arrest of development due to stenosis of that side 
 of the cranium, or from sclerosis, the sequence of some 
 form of encephalitis. This encephalitis may have 
 existed during foetal hfe, or in the early months of 
 infancy. The sclerosed portion of brain is often also 
 pigmental. Atrophy sometimes occurs from sclerosis 
 round an old apoplectic clot. 
 
 4. A want of symmetry of the cerebellum, the pons, 
 and the medulla oblongata, sometimes existing alone, 
 sometimes in connection with a want of symmetry of the 
 brain proper. This abnormality of the pons and the 
 medulla oblongata is often found to depend on the 
 spheno-basilar synostosis before mentioned. 
 
 5 . A stunting of both anterior lobes with defective 
 development of the olfactory bulbs, or of the posterior 
 lobes. Examples of the former abnormality have been 
 reported by Dr. Cramer of Soleure. He has shown the 
 brains of three microcephalous cases. The dimension 
 of the smallest amounted to 360 cubic centimetres. In 
 all these brains the island of Eeil was left uncovered, 
 owing to tlie defective development of the frontal and
 
 INSANITY. 219 
 
 parietal gyri. In the case of an imbecile woman, 
 reported by Dr. T. H. Simon, tlie convolutions were 
 more simple than usual, and those of the island of Eeil 
 were replaced by a smooth layer of grey matter. 
 
 6. Absence of the upper convolutions of the brain, 
 disclosing the ventricle ; tliis absence of the convolu- 
 tions being generally rather a result of disease than an 
 arrest of development. 
 
 7. Congenital or early hydrocephalus of chronic 
 form ; sometimes the sole lesion, and accompanied by 
 great thickening of the ependyma, sometimes only secon- 
 dary to the want of development in the brain. The 
 brain in these cases is often abnormally small. 
 
 8. An abnormal amount of the grey matter in pro- 
 portion to the white, or an unusual distribution of the 
 grey matter in regions where it generally has no place. 
 
 9. Absence or deficiency of many of the special 
 parts of the encephalon. Thus, the cerebellum may be 
 absent, or the pineal gland. The fornix may have a 
 very deficient formation, or the olivary bodies, the crura 
 cerebri, the corpora mamillaria, the optic thalami, or 
 the corpora striata. There may be considerable bilateral 
 atrophy of the optic or the auditory nerves, or more 
 commonly this may be unilateral ; and lastly, the corpus 
 callosum is sometimes absent, or only represented by a 
 very thin baud of fibres ; and this latter abnormality is 
 found to be accompanied with some weakness of intellect 
 rather than complete idiocy. 
 
 10. In a few cases there is found a peculiar condi- 
 tion, the presence of a fifth ventricle in the olives of the 
 cerebellum, a co:idition that exists in the brain of birds.
 
 220 INSANITY. 
 
 11. Lastly, various abnormalities of the pituitary 
 body. This brief resume of the lesions of idiocy would 
 be incomplete, unless we mention the occasional ab- 
 normal narrowness of some of the cerebral arteries from 
 contraction of the foramina of the skull. In many idiots, 
 not only is there much deformity of face, but of the 
 whole body. They are frequently dwarfed, with a 
 thickness and heaviness of all the limbs. In cretins the 
 cerebral weakness is constantly accompanied by goitre, 
 and a great fulness of the throat is to be found in many 
 idiots. I have now under my care a man of nearly 
 40 years of age, with the mental capacity of a child of 
 live, very sweet-tempered and religious. In him the 
 fulness of the throat amounts distinctly to goitre, and 
 occasions him some difficulty in deglutition. 
 
 Slowness in the development of the teeth is also seen 
 in cretins and in many idiots, and in both the teeth are 
 apt to decay early. A keel-shaped palate is very com- 
 mon in congenital idiocy. Cleft palate is not very 
 unusual. 
 
 The development of the sexual organs is often 
 arrested in idiots. In advanced cases of cretinism, and 
 in many complete idiots, the organs are quite unfit for 
 generation. 
 
 In semi-cretinism unfortunately this function is not 
 wholly lost, and the disease may be transmitted from 
 parent to child. 
 
 But recent pathological research, and still more the 
 results of treatment in modern times, have shown that 
 the state of mental deficiency in idiots bears no defi- 
 nite relation to the cerebral lesion. We can form no
 
 INSANITY. 221 
 
 reasonable prognosis on these cases without taking into 
 consideration tlie medium iu which they live, including 
 the food, the air, the comforts of life, and especially the 
 moral and intellectual surroundino;s. 
 
 Consult — 
 
 Blandford, ' Insanity and its Treatment,' 
 Bucknill and Tuke, ' Psychological Medicine.' 
 Rindfleisch, * Path. Histology.' 
 
 Reynolds' ' System of Med. Art' ' Insanity.' Dr. Maudsley. 
 Calmeil. Op. cit. 
 Griesinger, on ' Mental Diseases.' 
 Poincare and Bonnet, on ' General Paralysis.' 
 < Brit. & For. Med.-Chir. Review,' April 1873. Dr. Tuke. 
 'Jour, of Mental Science/ Oct. 1872. Dr. Ireland. 
 ' Jour, of Mental Science,' Jan. 1873. Dr. Wille and Dr. Boyd. 
 'Jour, of Mental Science,' July 1S73. Dr, Stahl, &c. 
 *Jour. of Mental Science,' April 1874. Dr. Balfour and Dr. 
 Wilks. 
 
 * West Riding Asylum Rep.,' vol. i. 58. Dr. Thompson. 
 'West Riding Asylum Rep.,' vol, i. 258. Dr. Mayhew. 
 
 ' West Riding Asylum Rep.,' vol, i. 219. Dr. Sutherland, 
 'West Riding Asylum Rep.,' vol. ii, 41, Dr. Herbert Major. 
 
 * West Riding Asylum Rep.,' vol, iii. 285, Dr. Clapham, 
 
 ' West Riding Asylum Rep.,' vol. iii. 124. Dr, Fothergill, 
 'Brit. Med, Jour.,' vol. i. 1874. Dr, Crichton Browne. 
 ' Guy's Hosp. Rep.,' vol. xvi. Dr. Wilks. 
 ' Med. Record,' vol, i. 134. Dr. Wolf, on ' Monomania,' 
 
 * Med. Record,' vol, i, 130, Dr, Wille, on ' Syphilitic Insanity.' 
 
 ' Med. Record,' vol. i. 290. Von Rabeuau, on ' Myelitis in the 
 Insane.'
 
 222 
 
 LECTURE IX. 
 
 APHASIA. 
 
 For the expression of ideas in speech there are three 
 requisites: 1. The memory of words. 2. The remem- 
 brance of how to say them. 3. A proper condition of 
 health of the external organs of voice and articulation 
 with their muscles and nerves. A want of action, 
 however, in these latter, though it would prevent 
 speech, would not be aphasia. 
 
 Aphasia is of three kinds : 1. Amnemonic or 
 amnesic aphasia, the loss of memory of words. 2. The 
 more common form, the loss of memory of how t(j say 
 words. The seat in the brain of the first faculty, the 
 memory of words, has never, I think, been quite made 
 out. It may exist in many parts of the brain, as well 
 as in Broca's spot. The seat of the second faculty, the 
 remembrance of how to say words, has been located by 
 Broca and others in a particular spot in the brain. 
 3. The loss of speech consequent on the third form 
 of aphasia is due to the want of co-ordinating power 
 over the muscles of articulation. 
 
 Dr. Bartholow says the existence of a distinct 
 centre of the faculty of language, although not abso- 
 lutely proven, a number of facts render exceedingly
 
 APHASIA. 223 
 
 probable. The precise liinitution to the third left 
 frontal convolution attempted by Broca, or to the walls 
 of the left sylvian fissure as suggested by Meynert, 
 may not, in the present state of our knowledge, be 
 considered anything more than plausible conjecture. 
 It were better, probably, to hold with Hughhngs 
 Jackson, that the district of cerebral matter supplied 
 by the left middle cerebral artery is most intimately 
 concerned in the function of language ; for this will 
 mclude all that region of the anterior and middle 
 lobes which has from the time of Gall been supposed 
 to be the seat of this faculty. It is obvious, he says, 
 that three forms of loss of the language faculty may 
 exist : Amnesic aphasia, paralytic aphasia, ataxic 
 aphasia. In amnesic aphasia, the defect must be 
 strictly limited to the vesicular matter in which the 
 memory for words is situated. All other forms of 
 expression may be retained, the mental conception 
 may be accurately defined, but the store of words for 
 giving vocal form to the ideas has been obliterated. 
 It is rare indeed to find a perfect case of amnesic 
 aphasia, for the destruction of the one faculty is 
 usually associated with more or less impairment of 
 the others. The cases of paralytic aphasia are very 
 numerous. These arise from embolism of the middle 
 cerebral artery, apoplectic extravasations in the white 
 matter and in the corpus striatum, and tumours, such 
 as aneurism, glioma, gummata, and other forms. The 
 very common association of right hemiplegia and 
 aphasia is now perfectly well known. In these cases 
 an interruption exists in the communication between
 
 224 APHASIA. 
 
 the language centre and the vocal apparatus. In the 
 ataxic form of aphasia there is no disorder of the 
 language centre, nor in the transmission of the motor 
 impulse through the motor channels to the olivary 
 bodies ; but owing to disease of this part of the cord, 
 the muscles concerned in the production of articulate 
 language cannot be combined to execute the varied 
 movements necessary. As Schroeder van der Kolk 
 supposed that the olivary bodies were intimately con- 
 cerned in the function of spoken language, he has been 
 interpreted to mean that this is the real language 
 centre. Undoubtedly he did not refer the idea or 
 mental conception and the memory of words to the 
 olivary bodies, but only the mechanism of vocal 
 expression. 
 
 Broca finds, and his views and observations have 
 been confirmed in the main (with the exceptions to be 
 mentioned further on), that the seat of lesion in cases 
 of aphasia is the posterior part of the third left frontal 
 convolution. In Broca's description of this portion 
 of the brain, the third frontal convolution presents a 
 superior or internal border adjoining the tortuous 
 border of the middle convolution, and an inferior or 
 external border, the relations of which differ according 
 as they are examined before and behind. In its 
 anterior half this border is in contact with the external 
 border of the most external orbital convolution. In 
 its posterior half, on the contrary, it is free, and 
 separated from the temporo-sphenoidal lobe by the 
 fissure of Sylvius, of which it forms the superior border. 
 The inferior border of this fissure is formed by the
 
 APHASIA. 225 
 
 superior convolution of the teniporo-splieiioidal lobe. 
 When the two marginal convolutions, the superior 
 and the inferior, are drawn away from the fissure of 
 Sylvius, there appears a large and slightly prominent 
 eminence, from the summit of which five small, simple 
 convolutions, or rather five straight folds, radiate in a 
 fan-like manner. It is the lobe of the insula, which 
 covers the extra-ventricular nucleus of the corpus 
 striatum, and which, rising from the bottom of the 
 fissure of Sylvius, is found to be structurally continuous, 
 by its cortical layer, with the deepest or most deeply- 
 seated part of the two marginal convolutions above- 
 named (forming the superior and inferior borders of 
 the fissure), and by its medullary layer with the 
 extra- ventricular layer of the corpus striatum. The 
 result of these structural relations is, that a lesion 
 which propagates itself continuously from the frontal 
 lobe to the temporo-sphenoidal lobe, or vice versd^ will 
 pass almost necessarily hj the insula, and that from 
 thence it will most probably extend to the extra- 
 ventricular nucleus of the corpus striatum, since the 
 proper substance of the insula, which separates this 
 nucleus from the surface of the brain, forms only a 
 very thin layer. 
 
 In considering, however, the close relation of the 
 corpus striatum with this third frontal convolution, 
 and the important part it plays in being what Dr. 
 Broadbent calls ' a way out for words,' it is necessary 
 to remember that it is not quite the only way out. 
 The fibres of the corpus callosum apparently connect 
 symmetrically corresponding convolutions of the two 
 
 Q
 
 226 APHASIA. 
 
 hemispheres ; and it is far from improbable tliat in 
 lesion of the left corpus striatum the right corpus 
 striatum may form the channel for the transmission 
 outwards of words. These few preliminary observa- 
 tions were necessary before the pathological anatomy 
 of this disease was entered upon. 
 
 In a very large proportion of cases of aphasia, the 
 loss of speech has coincided with right hemiplegia. 
 This is not only the case when lesion has occurred after 
 biith, but in the few cases on record of congenital 
 aphasia the right limbs have suffered. 
 
 Thus Waldenburg reports Ji case of a child in 
 whom, shortly after birth, the parents observed partial 
 paralysis and wasting of the right side of the body. 
 As it grew older, and up to six years, the child had 
 given little evidence of speech. He was not deaf, and 
 was quite intelligent. The child, with only slight 
 interference with the motion of the tongue, did not 
 even try to bring forth articulate sounds. The case is 
 the more interesting in that the mother, when three 
 months pregnant with this child, was seized with right 
 hemiplegia and loss of speech. She improved slowly, 
 but six years afterwards, when first seen by Dr. Wal- 
 denburg, there remained a certain weakness in the right 
 extremities, and lier speech was not only somewhat 
 thick, but she had difficulty in expressing herself 
 properly. Dr. Waldenburg believed the child's con- 
 dition to be congenital, caused by an intra-uterine 
 affection. Here tlie left hemisphere was affected before 
 the child had arrived at the natural age for commencing 
 to speak, but the right or healthy hemisphere did not 
 meet the want.
 
 APHASIA. 227 
 
 The cases luituially divide themselves into two 
 classes of lesions : one ot" Broca's spot, and the other 
 of the way out from it towards the nerves used in 
 articulation. Theory is of very little use in deter- 
 mining the question. It is only by numerous observa- 
 tions of symptoms and of the exact seat of lesion that 
 we can arrive at any intelligent understanding of the 
 matter. 
 
 Now the kinds of lesions met with are manifold : 
 Thus Case 1. Eight hemiplegia. Aphasia. A little 
 thickening of the pia mater and arachnoid over the 
 convex surface of cerebrum. A spot of softening, the 
 size of half-a-crown, exactly in Broca's spot. 
 
 Case 2. Girl, aged 13. Eight hemiplegia. Aphasia. 
 A little discolouration at the posterior portion of the 
 third left frontal convolution. Much black discoloura- 
 tion along the fissure of Sylvius on tlie left side. 
 Beneath this latter region was an old clot, partially 
 discoloured, with creamy tissue all round it, extending 
 slightly into the anterior lobe, but mostly into the 
 middle lobe, and implicating the left corpus striatum, 
 except the upper layer of it, which forms part of the 
 floor of the ventricle. This clot was the result of a 
 ruptured middle cerebral artery. Just at the com- 
 mencement of the fissure of Sylvius the artery was 
 enlarged to the size of a small haricot bean. This 
 aneurism had given way. No embolism. The lesion 
 immediately causing death was the rupture of a small 
 vessel in the left lateral ventricle, on the outer and 
 upper side of it, just above the corpus striatum. The 
 whole of the left lateral ventricle was full of clot, which 
 
 a 2
 
 228 APHASIA. 
 
 filled all the corniia, and had found its way, to a small 
 extent, into the right lateral ventricle. The posterior 
 portion of the third left frontal convolution at the seat 
 of discolouration was stained to about a fifth of an inch 
 in depth, and sensibly softened over a space the size of 
 a walnut. 
 
 Several of Dr. Hughlings Jackson's cases were living 
 when he wrote his paper in the London Hosp. Reports 
 on aphasia, and we are deprived, therefore, of the 
 accuracy of post-mortem records. From the manner 
 in which the morbid phenomena occurred, and their 
 coincidence with valvular disease, or some other abnor- 
 mality of the heart, there seems no doubt that the 
 lesion was embohsm. In his Case 10, death occurred 
 from rupture of an aneiu^ism of the middle cerebral 
 artery. In his Cases 27 and 28, syphilis seems to have 
 given rise to the lesion. Several others of his cases 
 were probably due either to small hcemorrhages or to 
 very localised softenings. 
 
 Darx recorded 140 cases of disease of the left hemi- 
 sphere, accompanied with aphasia and right hemiplegia, 
 and concluded that the faculty of language must be 
 connected with tlie left liemisphere. 
 
 Trousseau so far corroborated this experience by 
 finding in 134 cases of aphasia disease of the left hemi- 
 sphere in 124, while 10 cases were contradictory of 
 Darx. 
 
 Darx, Junior, placed the organ of the manifestations 
 of thought by s])eech at the point of union of the 
 middle with the frontal lobe of tlie left hemisphere. 
 
 In his clinical lectures. Trousseau mentions a case of
 
 APHASIA. 229 
 
 aphasia and right hemiplegia in which tliere was found 
 at the autopsy yellow softening on the left side of the 
 lower marginal convolution of the lower portion of the 
 transverse parietal convolution, and of the convolutions 
 of the insula. At first sight, the irontal lobe seemed 
 to have escaped ; but on drawing away the edges of 
 the Sylvian fissure, the softening was seen to extend 
 from the convolutions of the insula to the lower portion 
 of the transverse frontal convolution ; and, moreover, 
 the third frontal convolution was itself softened in its 
 posterior portion, that is, in tJie part nearest the sulcus 
 of Rolando. 
 
 Cases as definite as this are given by M. Broca him- 
 self, and can be added to by most hospital physicians. 
 Dr. Charcot exhibited to the members of the Biological 
 Society several brains removed from old women who 
 had died in the Salpetriere, and who had, for a variable 
 period dining life, suffered from loss of speech. In 
 most instances the lesion was complex, as in Broca's 
 first case. Thus there had generally been paralysis as 
 well as a])hasia, and the second and third frontal con- 
 volutions were not the only spots where there was 
 softeninii or haimorrhaGje ; but the lobule of tlie insula 
 and temporo-sphenoidal lobe were also the seats of an 
 anatomical lesion, which had ])robably occurred simul- 
 taneously everywhere, or which had resulted from the 
 extension of softening by continuity of tissue. 
 
 In Broca's second case, in which there was aphasia 
 without paralysis of limbs, and the patient liad suddenly 
 lost his speech since a fit of apoplexy which he had 
 eighteen months before his death, the posterior third
 
 230 APHASIA, 
 
 of the second and third left frontal convolutions was 
 alone destroyed, over a space of about 15 or 18 millo- 
 meters. The transverse frontal convolution was normal, 
 whilst inferiorly the lesion extended as far as the lobule 
 of the insula, but without involving it. The result of 
 this loss of substance was a cavity full of serosity, and 
 closed externally by the pia mater. The walls of this 
 cavity were firm, and on them were small spots of an 
 orange-yellow colour, proved afterwards to be of a blood 
 origin. This was, therefore, an old haemorrhagic cyst. 
 
 I will not take up your time by multiplying in- 
 stances of this nature. Some are recorded in St. 
 George's Hosp. Eeports, Vol. 2. They are numerous, 
 and would be conclusive if there were no exceptions. 
 Still, in recording the pathological anatomy of aphasia, 
 it is necessary to note the exceptional cases also. 
 
 These are of two kinds: (1) those instances of 
 aphasia occurring with left hemiplegia ; and (2) grave 
 lesions of Broca's spot without loss of speech. To 
 these may be added also those instances of aphasia 
 with lesion on the left side, but of some other portion 
 of the brain, and not of Broca's spot. 
 
 Of the first kind of exceptions there are not many 
 examples on record. Let us take a few in order : — 
 
 1. Trousseau mentions the case of a patient, named 
 Marcou, affected with hemiplegia and aphasia. The 
 lesion was probably of a syphilitic nature, as the patient 
 improved in all respects very much under mercury and 
 iodide of potassium. 
 
 2. Case 18 of Dr. Hu2;hlin2s Jackson : 
 
 Mrs. B., aged 32, after a natural labour, was sud-
 
 APHASIA. 231 
 
 denly seized with complete paralysis of the left side, 
 and was perfectly unable to talk. Of course, it is 
 possible in this case that there was disease on each side 
 of the brain, but the left hemiplegia and the aphasia 
 occurring simidtaneously and instantaneously renders 
 the idea of a double lesion difficult. 
 
 3. Case 19 of Dr. Hus^hlinsjs Jackson: 
 
 Man, aged 49, suddenly complained of severe head- 
 ache, and left his work at 7 p.m. ; after a walk he sat 
 down and became s}K'echle.ss, and by the time he was 
 got to bed he had lost the use of the left arm and leg. 
 He did not speak at all for six weeks, except to say 
 'Yes' or 'No.' 
 
 4. Case 38 of Dr. Huohlino-s Jackson : 
 
 A gentleman, who fourteen years before had a bad 
 fall from his horse, was suddenly taken with loss of 
 consciousness without convulsion. The result of this 
 fit was entire paralysis of the left side, and for eighteen 
 months total loss of speech. There was ptosis of the 
 left eyelid. He lingered for five years and a half, the 
 paralysis continuing up to the time of his death. After 
 the first eighteen months he seemed to be recovering 
 his words and could enunciate parts of them only, 
 but these in no way corresponded to his seeming inten- 
 tions ; his ideas being imperfect, and his speech both 
 confused and ataxic. For a httle while there was 
 paralysis of the bladder ; but the tone of that viscus 
 soon returned. There was no autopsy. 
 
 Besides these, there are a few more cases on record, 
 scarcely a dozen in all, in some of wliich there is no 
 post-mortem record.
 
 232 APHASIA. 
 
 Dr. W. A. F. Browne speaks of the numerous cases of 
 left hemiplegia with aphasia, of which not less than six 
 have been noticed in this hospital (the Crichton Eoyal 
 Institution), He states that BaiUarger, in like manner, 
 records 155 cases of hemiplegia, of which only ten were 
 upon the left side, from which it would appear that in 
 aphasia right is to left hemiplegia at 15 to 1. I believe 
 the proportion of right hemiplegia to left in aphasia is 
 enormously larger than this where the aphasia and 
 the hemiplegia were coincident in point of time, and 
 not due to lesions occurring at different periods. 
 
 The second class of exceptions includes those in 
 which there was lesion of the posterior portion of the 
 third left frontal convolution, but no loss of speech. 
 
 Case 1. Not a satisfactory one, reported by Pro- 
 fessor Velpeau : 
 
 The patient, a hair-dresser, was admitted into the 
 Charit<^ Hospital, suffering from incontinence of urine. 
 He was an extremely tiresome talker, and died three 
 weeks after admission, without having presented any 
 symptom of cerebral disease, any difficulty of articula- 
 tion, or defect of speech. On dissection there was 
 found hypertrophy of the prostate, stricture of the 
 urethra, and old disease of the mucous membrane of 
 the bladder. The dura mater was found to be firmly 
 adherent to the mass of the brain. The right anterior 
 lobe of the brain was completely destroyed by a volu- 
 minous tumour having all the characters of scirrhus. 
 The left frontal lobe also had been encroached upon, 
 and was to a great extent destroyed. This description 
 is not sufficiently exact to enable us to form an opinion 
 as to whether Broca's spot was much injured.
 
 APHASIA. 233 
 
 Case 2. The next case was observed by M. Aug. 
 Berard : 
 
 The patient, a miner, was injured by tlie explosion 
 of a mine. He cUd not lose consciousness: managed 
 to creep out of his hole, and asked to be taken to 
 M. Berard's house. The whole frontal reirion was laid 
 open, the integuments hung in sJn-eds, the bones were 
 splintered and in detached fragments, and the brain was 
 exposed. Both anterior cerebral lobes were completely 
 destroyed, and in their stead was a mixture of blood, 
 of bony splinters, and of brain substance. In spite of 
 this frightful accident the man could relate, in all its 
 details, how the accident had occurred. 
 
 Case 3. Dr. Batty Tuke's and Dr. Fraser's case : 
 
 The history of this case is that of an apoplectic 
 seizure eleven years previous to the date of observa- 
 tion. Her friends affirm that she was insensible for 
 some weeks. No amount of cross-examination of her 
 sister, with whom she resided at this time, could ehcit 
 any evidence of paralysis; there was no distortion of the 
 face, no lameness or want of power in either hand, but 
 complete speechlessness existed for some time. From 
 this, however, she nnist have totally recovered, for pre- 
 vious to her admission she seems to Iiave been rather 
 talkative. She died of paraplegia consequent on 
 atrophy of cord, Avith caries of the vertebraa. On 
 stripping off the dura mater on the left side, some slight 
 adliesions were found between the layers of the arach- 
 noid. These were easily detached, and exposed an 
 excavation of the brain substance at the postero-infero- 
 external part of the left frontal lobe. Its outline was
 
 234 APHASIA. 
 
 irregular, its cavity filled with serum, and narrow 
 white bands sprang from its sides. The serum was 
 opalescent, but otherwise normal, and it was held in by 
 the visceral arachnoid. On emptying the cavity, its 
 dimensions were found to be as follows : In its long 
 axis, from before backwards, parallel to the fissure of 
 Sylvius, two and a quarter inches obliquely, vertically 
 one and three-sixteenths of an inch ; in its deepest part 
 it was three-quarters of an inch, but generally only half 
 an inch. This lesion had destroyed posteriorly the 
 inferior fourth of the ascending parietal convolution, 
 leaving a small posterior portion of the knuckle in 
 which this gyrus ends, the inferior third of the ascending 
 frontal, the inferior margin of the second frontal, and 
 the posterior half of the third frontal convolution. At 
 the inferior margin there was a narrow ridge of slight 
 eminence, which might have been the remains of the 
 inferior border of the third. With these exceptions, 
 the destruction of the posterior half of this convolution 
 was complete, both as regards its grey and white 
 matter. Its inferior boundary was the superior mar- 
 ginal convolution. The bottom seemed to be an 
 anatomical limitation, as it was smooth, rounded, and 
 presented no evidence of morbid action. Incision 
 proved it to be the extra-ventricular nucleus of the 
 corpus striatum. Tlie edges of this lesion, implicating 
 the convolutions, were ragged, which was suggestive of 
 erosion ; but there was no indication, by induration, 
 softening, or thickening of the membranes, of inflam- 
 matory action. Microscopical appearances : chiefly 
 those of fatty degeneration and amyloid bodies. It is
 
 APHASIA. 235 
 
 true that this case was objected to by Dr. Wilks, on the 
 ground that the patient did not use nouns correctly. 
 The woman liad the ftxculty of speech intact, but had 
 forgotten certain words. 
 
 Case 4. My own case : 
 
 Henry E. had been under treatment for some time 
 for syphihtic node on the left side of the forehead. It 
 disappeared to a great extent under treatment, and he 
 left the Bristol Infirmary, but was readmitted in a few 
 Aveeks with very distressing pain in the left side of the 
 head anteriorly. He died comatose, but was able to 
 talk to me within a few hours of his death ; and he had 
 not the slightest loss of speech all through. Coma, 
 lasting only a few hours, came on rather suddenly. 
 The frontal bone was somewhat thickened just above 
 and to the left of the left orbit. Beneath this spot the 
 dura mater was firmly adherent to the bone, and also 
 to the parts beneath it, so that it could scarcely be 
 separated from the other membranes of tlie brain 
 without tearing them. The brain at this spot was 
 hard, and felt as though a hard tumour was contained 
 in its substance. It was yellowish externally, and was 
 so placed that the lower portions of all the frontal 
 convolutions on the outside of the anterior lobe of the 
 left hemisphere were imphcated in the mass. On 
 section, the mass was found to be hard and of a 
 yellowish- white colour, surrounded by congested ves- 
 sels. It extended to the posterior border of the 
 anterior lobe, and about half an inch into the middle 
 lobe, and was tlie size of a small hen's egg. Between 
 the two portions of the tumour iu tlie anterior and
 
 236 APHASIA, 
 
 middle lobes the artery was compressed, so that its 
 canal was almost wholly blocked up and rendered 
 useless. Almost all the central white substance of the 
 middle lobe and of the left corpus striatum was 
 diffluent. A little clear fluid was found in the lateral 
 ventricles. 
 
 In connection with this particular point, a case 
 recorded by Dr. Bristowe is important, as showing 
 that the corpus striatum is not the only way out 
 from the third convolution. The left corpus striatum 
 Avas entirely destroyed, but the power of speech had 
 returned in three or four weeks after the apoplectic 
 attack. 
 
 The third class of exceptions will include those 
 in which aphasia has occurred, and some other 
 portion of the brain besides either the left or the 
 right third frontal convolution has been the seat of 
 lesion. 
 
 1. Dr. Charcot's case. Woman, aged 49. 
 
 She had become hemiplegic on the right side, and 
 aphasic since an apoplectic fit which she had had eight 
 months previously. Intellect and memory seemed to 
 be preserved, but her power of articulate language 
 was restricted to tlie utterance of the monosyllable ' ta,' 
 which she habitutdly repeated, with very great rapidity 
 and distinctly, four or five times in succession, whenever 
 she attempted to answer a question or to communicate 
 her own ideas. Tlie tongue moved freely and in all 
 directions. An examination of the brain showed that 
 there was softening (1) of the so-called lower marginal 
 convolution in all its extent, and of a portion only of
 
 APHASIA. 237 
 
 tlio SL'COud temporal convolution of the temporal lobe ; 
 (2) of the lower extremity of the two posterior 
 convolutions of the insula of Ileil. In deptli, the 
 softening extended in tlic direction of the corpus 
 striatum ; llie whole of the extra-ventricular nucleus 
 and the posterior half of the intra-ventricular nucleus 
 were also softened. The thalamus opticus was normal. 
 Tlie transverse parietal and transverse frontal convo- 
 lutions, the three anteroposterior frontal convolutions 
 were examined thoroughly, one after another, with the 
 greatest care, in M. Broca's presence. Even micro- 
 scopically Dr. Charcot and M. Broca considered that 
 there was no lesion in them. 
 
 Case 2. Dr. Yulpian's case. Woman, aged 73. 
 Aphasia, and later on riglit hemiplegia. 
 
 Dr. Vulpian says : ' Dissection did not disclose the 
 lesion, which I fidly expected. I found a broad patch 
 of softening of apparently recent date in the posterior 
 half of the white supra-ventiicular nucleus of the left 
 cerebral hemisphere, and no trace of disease in the 
 frontal or other convolutions. Old lesions, slight in 
 degree, lacuna?, were seen in the corpus striatum and 
 optic thalamus on the same side, and an analogous 
 lesion, of still smaller extent, but of as old a date, in 
 the right corpus striatmn. Both middle cerebral 
 arteries were very atheromatous ; but whilst the right 
 artery was still pervious to tlie blood, tiie lei't one was 
 completely or almost completely plugged up in two 
 places, separated by an interval ofal)out one centimetre 
 from one another, owing partly to the atheromatous 
 thickening of its walls, and partly to an indurated
 
 238 APHASIA. 
 
 fibriiioLKs deposit of manifestly old date. This deposit 
 seemed to have been the result of thrombosis rather 
 than of embolism. 
 
 Cruveilhier has brought forward several curious 
 instances in which the loss of speech was a prominent 
 symptom, while the disease was not found in the 
 anterior lobe, but in some other part of the brain. 
 
 Andral has recorded 37 cases of cerebral ha3- 
 morrhage, observed by himself or by others, in which, 
 whilst the morbid condition occupied one or both of 
 the anterior lobes, the power of speech was ajQfected 2 1 
 times and unaffected 16 times. On the other hand, he 
 has collected 14 cases in which the power of speech 
 was lost, yet no alteration had taken place in the 
 anterior lobes. In 7 of these 14 cases the lesion was 
 situated in the middle lobes, and in the other 7 in 
 the posterior lobes of the brain. 
 
 Case 3. Man, aged 48. Admitted into the Bristol 
 Infirmary, and died the same night. Tlie wife states 
 that eighteen months ago he lost his speech altogether 
 for four months, without any paralysis of the limbs. 
 Nine months ago, and therefore five months after the 
 recovery of his speech, he had loss of motion and 
 sensation on the right side, with some muffling of 
 speech, but no aphasia, and never recovered from this 
 condition. He died in a third attack. A clot of 
 considerable size occupied the middle portion of the 
 right hemisphere, reaching from the external border of 
 the right corpus striatum to the lateral surface of the hemi- 
 sphere, through which the clot protruded on the slightest 
 pressure. The cerebral substance around the clot was
 
 APHASIA. 239 
 
 uli brokcu up iiuel cicuiuy. The right kiteriil ventricle 
 itself healthy. The left optic thalamus was partially de- 
 stroyed, its seat being occupied by a depression stained 
 yellow, the floor of which was very soft. This condition 
 extended some way also into the crus cerebri of that 
 side. This was evidently the seat and formed the remains 
 of an old clot. Broca's spot was perfectly healthy. It 
 certainly was no softer than the otlier healthy parts of 
 tlie brain. There was no lesion that accounted for the 
 first loss of speech for 4 months. Cerebral vessels fairly 
 healthy, and the rest of the cranial contents. Small 
 granular kidneys. 
 
 Case 4. Man, aged 30. Syphilitic. Aphasia and 
 right hemiplegia for six weeks. Admitted into Bristol 
 Infirmary, March 1873. Broca's spot and every part 
 of both hemispheres quite healthy. Pons, the seat ot 
 softening, the size of a filbert, occupying rather more of 
 the left half than the right, but passing a good deal 
 over the middle line. The nervous tissue were here 
 quite deliquescent. Vessels of the ckcle of Willis a little 
 fatty. Both these latter cases may have been instances 
 of lesion of parts concerned in the way out from the 
 anterior portion of the brain. 
 
 It is difficult, if not impossible, to reconcile all these 
 exceptional cases with Broca's law. We must either 
 admit that the seat of the faculty of speech is located in 
 several portions of the brain, or that lesions of otlier 
 parts cause paresis of the faculty either by pressure or 
 by reflex irritation, or at least that a corresponding- 
 portion of the right anterior lobe is or may be the seat 
 of this faculty. Xor do the pathological observations,
 
 240 APHASIA. 
 
 which show that lesion of the corresponding spot in the 
 right hemisphere has not been accompanied by aphasia, 
 mihtate entirely against this latter view. It is recognised 
 pretty generally that right-handedness depends on the 
 earlier and more complete nutrition of the left side of 
 the brain. Even if Gratiolet's statement is incorrect, 
 that the anterior convolutions of the left side are earlier 
 developed than those of the right, yet, at any rate, 
 according to Broca, in forty brains the left frontal lobe 
 was found to be on an average heavier than the right ; 
 and a similar assertion with respect to the weight of the 
 entire left half of the cerebrum has been made on the 
 basis of very numerous observations by Dr. Boyd. 
 
 This more complete nutrition is due partly to the 
 somewhat greater size of the left carotid, mainly, pro- 
 bably, to the fact that the blood enters the brain on the 
 left side much more directly than on the right ; that 
 in fact it has not the temporary obstruction to contend 
 with that it has on the right side in its course from the 
 aorta to the innominate, and from the innominate to the 
 carotid. 
 
 It is only reasonable to believe that in the case of 
 left-handed persons the ordinary nutrition of the two 
 sides of the brain has been reversed, and that the right 
 side has been better and earlier nourished. In a very 
 interesting paper on left-handedness Dr. Pye Smith 
 calls attention to two cases of aphasia occurring in left- 
 handed persons, recorded by Dr. Hughlings Jackson 
 and Dr. Ogle. In both these patients there was para- 
 lysis of the left side ; so that it seems likely that in 
 these two left-handed people the right half of the brain
 
 APHASIA. 241 
 
 had the hiiictioiis, if not the structure, wliich ordinarily 
 belongs to the left. In Dr. Wadliam's case also a 
 ])artially left-handed lad was attacked with left hemi- 
 plegia and loss of speech ; he had partly recovered at the 
 time of his death twelve months later, and then the 
 right insula and adjacent parts were found softened. 
 Bearing on this subject it is well to notice that in two 
 brains of left-handed persons examined by Dr. 
 Broadbent and Dr. William Ogle the ordinary con- 
 ditions of the two hemispheres were reversed, the 
 greater complexity of convolution occurring in both on 
 the right side, and not on the left ; and there is no 
 reasonable doubt but that right-handedness and left- 
 handed ness are associated with more highly developed 
 frontal convolutions, in the one case on the left, in the 
 other on the rig;ht side. 
 
 It may well be that Broca's spot and the corre- 
 sponding portion of the right hemisphere are seats 
 of the faculty of speech ; that the spot on the left side 
 of the brain, being more highly nourished, either takes 
 in the whole faculty, there being no need in most cases 
 for the right side to be called into use, or that the left 
 side may be the seat of the higher faculty, the right of 
 the lower; that, in other words, and those Dr.Hughhngs 
 Jackson's, the left is the leading side of the brain, the 
 right the automatic. Dr. Jackson beheves that the 
 involuntary utterances of aphasic patients are the result 
 of action of the right side. 
 
 What I have said, however, may give you some 
 idea of the pathological anatomy of aphasia, whatever 
 may be the true pathology. 
 
 R
 
 242 APHASIA. 
 
 To sum up iu a few words : 
 
 1. The posterior portion of the third left froutal 
 convolution is the main seat for the faculty of speech. 
 
 2. That it is not the only seat seems proved by 
 three classes of exceptional cases, viz., those in which 
 aphasia has occurred coincidently and synchronously 
 with left hemiplegia; those in which Broca's spot has 
 been the seat of grave lesion without aphasia; and those 
 in which aphasia has occurred without lesion of Broca's 
 spot, but with lesion of some other portion of either 
 left or right hemisphere. 
 
 3. Some of the instances of aphasia with left 
 hemiplegia have been met with in left-handed people, 
 and therefore in persons with the right anterior lobes 
 presumably or certainly developed with a complexity 
 of convolutions that is generally only found on the left 
 side of the brain. 
 
 4. To use Dr. Broadbent's words, ' The left third 
 frontal gyrus being the outlet for expression, the left 
 corpus striatum necessarily takes the lead in the pro- 
 duction of spoken words ; but a way round exists, pro- 
 bably from the left to the right third frontal gyrus, 
 by the corpus callosum, and thence to the right corpus 
 striatum. Thus speech, though temporarily embar- 
 rassed by damage to the left corpus striatum, is re- 
 covered ; whereas if the cortex of the left third frontal 
 convolution is damaged, or its fibres, both to the corpus 
 striatum and to the corpus callosum, cut through, speech, 
 having no other outlet, is lost.' 
 
 Glosso-Laryngeal Paralysis. — In uncomplicated
 
 GLOSSO-LARYNGEAL PARALYSIS. 243 
 
 cases tlie disease is maui Tested by paralysis of swal- 
 lowing, of speech, of phoiiatioii. The lips, the tongue, 
 the larynx, the pharynx, are all more or less paralysed. 
 There is paralysis of all the parts employed in talking. 
 There seems to be a great tendency in the paralysis to 
 become general ; but at present we will confine our- 
 selves to the uncomplicated disease. 
 
 Deglutition is difficult, the patient being only able 
 to take liquids ; certain words are especially difficult ; 
 the patient cannot pronounce the vowels o and u, 
 nor the consonants p, b, m, n, k, c, t, which require 
 the intervention of the tongue and lips. This condi- 
 tion is different from the mumbling articulation of 
 cerebral paralysis with partial implication of the facial 
 nerve ; still more does it dill'er from the loss of memory 
 of words, or of the power of articulating them, we meet 
 with in aphasia. The voice is often either feeble or 
 absolutely whispering, a phenomenon depending on 
 lesion of the spinal accessory nerve. This feebleness 
 of voice also is due in some cases to weakness of expi- 
 ratory effort, when the spinal roots from which the 
 phrenic nerve derives its nervous influence are coinci- 
 dently affected. The saliva constantly dribbles from 
 the mouth, as the patient is unable to retain it by 
 means of the lips. This flow of saliva is not only due 
 to the labial paralysis and loss of power of swallowing. 
 The quantity and quality of the saliva are altered, as 
 a direct result of the disorder of innervation. Schulz has 
 shown in one case that galvanization of the facial nerve 
 has caused the disappearance of the abnormal secretion. 
 
 The food collects between the cheeks and the 
 r2
 
 244 GLOSSO-LARYNGEAL PARALYSIS. 
 
 teeth. The muscles of the soft pahxte hang down, and 
 if the patient opens the mouth and takes a deep inspi- 
 ration the pahite is not elevated as it is in health, 
 and the posterior nares cannot be closed. 
 
 The post-mortem examinations on such cases have 
 been very few. The disease is rare in itself, and often 
 so gradual in its progress that cases will not remain 
 in hospital until the fatal event occurs. Still, there 
 are some few on record, and it is necessary to call your 
 attention to them. It is remarkable that of those few 
 the disease is, in several instances, associated with pro- 
 gressive muscular atrophy. It will be my duty to call 
 your attention to this connection by-and-by. 
 
 In the first of Trousseau's cases the post-mortem 
 examination was entirely negative as regards the ana- 
 tomical lesion ; perhaps, as he himself says, because it 
 was incomplete. 
 
 In the second case there was found very marked 
 atroj^hy of the roots of the hypoglossal nerve, without 
 any alteration of the muscular fibres themselves. The 
 medulla oblongata was apparently also of greater con- 
 sistence than normal. 
 
 In Trousseau's third case there was found well- 
 marked thickening and grey discoloration of the dura 
 mater on a level with the medulla oblongata, and as 
 ftir down as the roots of the fourth cervical pair. This 
 thickening was due to a considerable increase in the 
 amount of fibres of connective and fibro-elastic tissue, 
 and seemed to result from a chronic congestive process, 
 as shown by the great number of capillaries and of 
 deposits of ha3matinc external to them. The roots
 
 GLOSSO-LARYXOEAL TARALYSIS. 245 
 
 of the hypoglossal and spinal accessory nerves were 
 atrophied, and reduced in several places to the neuri- 
 lemma ; and at the spot where the spinal accessory was 
 in contact wdtli the dura mater there was adhesion of 
 the neurilemma to the librous envelope of the cord, 
 and a deposit of a nucleus of connective tissue the 
 size of a pea. A gx)od many motor roots in the cer- 
 vical region were thinner than natural, from partial 
 disappearance of the nerve-tubes. With the aid of the 
 microscope, the neurilemma was seen to preponderate 
 everywhere over the nerve-tissue properly so-called, 
 and notable hyperasmia could be detected everywhere, 
 together with greyish discoloration of the neurilemma. 
 The cord itself, at the upper paj-t of the anterior 
 columns, was as congested and of the same colour as 
 the posterior columns are found to be in cases of pro- 
 gressive locomotor ataxy. The fibres of the palsied 
 muscles of the tongue, soft palate, lips, chin, and 
 cheek were unaltered. There was diminution of size and 
 incipient fatty degeneration of some of the muscles of 
 the right leg, especially of the peroneus longus, tibialis 
 anticus, and quadriceps femoris. Here, as in the two 
 following cases, the special lesion was complicated with 
 progressive muscular atrophy. 
 
 Dr. Dumenil's case showed atrophy of the hypo- 
 glossal, facial, and spinal accessory nerves ; complete 
 motor paralysis of the tongue, incomplete of the face ; 
 integrity of the muscles of the tongue and the face : 
 atrophy of the anterior spinal roots ; incomplete 
 paralysis of the limbs ; incipient muscular atropliy. 
 
 Dr. Wilks' case showed no nodes or other sisns of
 
 246 GLOSSO-LARYNGEAL PARALYSIS. 
 
 disease of the cranial bones. Tlie brain was tough 
 and hard. There were no signs of formative disease : 
 the changes required to be looked closely for. But on 
 opening up the visceral arachnoid, there was a most 
 obvious atrophy of the roots of the hypoglossal nerve, 
 wdiich had quite lost the natural white opaque appear- 
 ance of nerves, and were thin little gelatinous threads 
 as they crossed the corpora olivaria. In the same 
 condition Avere the inner roots of the spinal accessory, 
 and also very markedly the whole of the anterior roots 
 of the spinal nerves, especially the cervical ; and the 
 sacral least. The anterior view of the cord was re- 
 markable ; the outer aspect was flat, not round ; yet, it 
 was harder than natural, so that mere flaccidness was 
 not the cause of this ; the anterior roots also came 
 from a line nearer the middle line than is natural. On 
 section, the anterior half of the white matter was 
 atrophied ; it was white, harder than natural, and on 
 the section it stood out, while the grey matter receded ; 
 the latter was larger than natm^al, it was darker, con- 
 taining obvious vessels, and at the lower part of the 
 cervical cord it was double the natural size, and showed 
 a red colour finely mingled with yellowish white ; this 
 part, so affected, was not of great length ; generally 
 the redness and largeness of the grey part, and the 
 thin liard shell or coat-like layer of white matter, 
 made the pathological state of the spinal cord. In the 
 medulla oblongata, as seen from the front, nothing 
 diseased was visible, except the state of the nerve- 
 roots, as before stated. But opening up the arachnoid 
 over the fourth ventricle, and drawing down the
 
 GLOSSO-LARYNCiEAL PARALYSIS. 247 
 
 medulla oblongata to look at the fourth ventricle, there 
 was a very striking diseased appearance, without 
 obvious derangement of anatomical position ; there 
 was a red grey change of the calamus scriptorius, so 
 that the nib of this was quite involved, and from the 
 nib upwards and outwtirds for half an inch there ran 
 this change. 
 
 The lining membrane of this ventricle and its 
 choroid plexus were of a deeper colour than usual. 
 
 Muller gives a case in full detail, and considers that 
 the real seat of the disease is in that part of the en- 
 cephalon, which regulates the articulation of words and 
 the voluntary part of swallowing. 
 
 A large number of cases are on record that are 
 wanting in completeness from the absence of post- 
 mortem examinations. In some the orbicularis oris 
 w^as paralysed, but not the buccinator ; and the nerves 
 affected show every degree of abnormality. 
 
 Closely connected with these cases are those in 
 whicli one or more of these nerves are affected. I was 
 lately asked to see a man who had had hemiplegia for 
 some time. The day before I first saw him he had 
 another fit, and in addition to the loss of motor power 
 in the limbs he lost the power of swallowing. To a 
 great extent he was able to speak, and he moved his 
 tongue with ease. He died of exhaustion consequent 
 on the impossibility of deglutition. 
 
 In a case recorded by Mr. Henry Taylor, a man 
 after a fall complained of great pain over tlie left side 
 of the occiput, and in a few days' time found lie had 
 entirely lost the power of deglutition. He complained
 
 248 GLOSSO-LARYXGEAL PARALYSIS. 
 
 of numbness of the right arm and leg, but had perfect 
 motion. The pupil of the right eye was dilated, but 
 sensible to light. He expressed himself as feeling 
 quite well, only very hungry. He made the most de- 
 termined efforts to swallow, but the fluid always 
 returned by the nose. He sank from exhaustion. On 
 removing the brain at the necropsy, that organ was 
 found perfectly healthy, with the exception of the left 
 v.etebral artery, which was entirely filled up with an 
 embolic clot. 
 
 Lichtenstein records three cases in which what he 
 calls laloplegia or glosso-plegia was the most pro- 
 minent symptom, two of them recovering before long 
 completely, and one dying. He believes that it may 
 occur as a temporary affection from mental emotion, 
 or as a permanent one from some exudation at the 
 site of the nervous centres which preside over speech. 
 This he locates at the upper part of the medulla 
 oblongata, near the origin of the vagi, which are 
 often involved to some extent at some period of the 
 affection. 
 
 A somewhat anomalous case bears upon this 
 subject : — 
 
 A boy, five years old, bright and intelligent in 
 mind, but having always been extremely delicate, and 
 liable to faint away on the least exertion, is the subject 
 of the following symptoms : — He has never been able 
 to swallow anything solid since his birth. He swallows 
 liquids well. Tlie palate is equal, and is moved on 
 inspiration. He protrudes the tongue well and straight. 
 He cannot pronounce D or K, There is a little
 
 GLOSSO-LARYNGEAL PARALYSIS. 249 
 
 diminution of tlie motor power of the right facial 
 muscles. No others are paralysed. Septum nasi is 
 pushed over towards tlie left side, and nearly fdls up 
 the left nostril. Cries, laughs, and coughs much as 
 other children. 
 
 The intimate relation between the nuclei of the 
 nerves generally implicated in glosso- laryngeal paralysis 
 explains anatomically tlie most usual association of 
 symptoms. 
 
 Lockhart Chirke has demonstrated a close anato- 
 mical connection between the nuclei of tlie hypoglossal, 
 vagus, spinal accessory, facial, and trigeminal nerves. 
 He says there is a column of cells forming the nuclei 
 of these nerves which supplies all the parts used in 
 speaking. The whole of this group of cells being 
 diseased, we get loss of deglutition, loss of voice, loss 
 of speech m great measure, especially of labials, loss of 
 motor power in the lips, tongue, and palate. 
 
 Part of the group only being affected, we get partial 
 symptoms, loss of deglutition associated with the power 
 of protruding the tongue, loss of phonation with com- 
 parative preservation of the motor power of the lips, &c. 
 
 The afTection is distinguished from paralysis of the 
 soft palate succeeding to simple or diphtheritic angina 
 by the lips and tongue not being involved in the latter ; 
 from double facial paralysis by the electric sensibility 
 being lost in this affection, and not in glosso-laryngeal 
 paralysis ; from general paralysis of the insane in that 
 in this latter disease there is no special difficulty in 
 articulating certain letters, and the movement of the 
 tongue is quite free.
 
 250 GLOSSO-LARYNGEAL PARALYSIS. 
 
 What then is the special lesion ? It is in the nerve- 
 roots, an absolute or partial disappearance of the nerve- 
 tubes, the neurilemma being left, though in some 
 cases stained and altered. In Dr. Wilks' case the 
 roots of the hypoglossal and spinal accessory nerves had 
 lost their natural white opaque appearance, and had 
 become little thin gelatinous threads. The particular 
 lesion of the nerves in this form, called by Jaccoud 
 ' atrophic spontanee,' consists not in a purely fatty 
 degeneration, but in a fibrous fatty degeneration. In 
 his plates he portrays a very considerable growth of 
 fibrous tissue ; the whole lesion being made up of 
 steatosis and proliferation of connective tissue. In 
 one of Trousseau's cases there was seen in the midst 
 of the elements of the neurilemma a fatty substance, 
 irregularly scattered in granules. The fibres of the 
 connective tissue were markedly developed, and were 
 mixed up with a good many elastic fibres. This form 
 of degeneration may be due to inflammatory action; 
 that is, it may be the latest development or sequence 
 of slow inflammation, or it may be a purely passive 
 process. When it does not depend on inflammation, it 
 probably owes its origin to grey degeneration, or true 
 sclerosis, of the group of cells forming the nuclei of 
 these associated nerves. I say probably, because ilie 
 absolute lesion has yet to be demonstrated micro- 
 scopically, althougli in Dr. Wilks' case the medulla 
 oblongata liad a diseased appearance even to the naked 
 eye. This is the more probable from the connection 
 of this disease with ])rogressive muscular atrophy. 
 In several of tlie cases recorded the two conditions
 
 GLOSSO-LARYNCiEAL PARALYSIS. 251 
 
 were associated. In the former the paralysis is the 
 first symptom, and muscular atrophy when it is met 
 with is only towards the close of the disease ; in the 
 latter the muscular atrophy is the first symptom, and 
 the paralysis seems generally to be in direct proportion 
 to the loss of muscular tissue. 
 
 Duchenne considers that these two diseases are only 
 associated accidentally. Still it is difficult, when they 
 coexist in the same individual, to believe in a difference 
 in the nature of the lesion. The atrophy of the motor 
 roots may exist in each disease ; in each there may be 
 sclerosis of some portion of the nervous centres, of the 
 medulla oblongata in the one, of the anterior columns 
 and the grey matter of the cord in the other. The 
 probable explanation of the connection is that the 
 atrophy of the muscles depends on some lesion of the 
 sympathetic that may or may not be present in 
 glosso-laryugeal paralysis. 
 
 This is all that is known of the pathological 
 anatomy of this disease, and the key-note of its simpli- 
 fication is in Lockhart Clarke's demonstration of the 
 associated nuclei of these several nerves. 
 
 But still the question is not invariably so simple, 
 since Voisin has recorded a case of glosso-labio- 
 laryngeal paralysis without sclerosis of the medulla 
 oblongata ; and Jaccoud in his latest work says, ' II 
 n'est done pas possible de faire de cette paralysie une 
 entite morbide veritable, puisqu'elle n'est uniform e ni 
 dans ses symptomes ni dans ses lesions : il y a Ih, 
 simplement deux modalites topographiques de la 
 paralysie des ncrfs bulbaircs ; au surplus, cette paralysie
 
 252 FACIAL PAEALYSIS. 
 
 SOUS Oil sus-bulbaire n'est pas toujours isolee ; on I'a 
 vue coincider avec la paralysie des nerfs oculo- 
 moteiirs, avec I'atropliie musciilaire progressive, eniiii, 
 avec line paralysie plus ou moins marquee des membres 
 thoraciques.' 
 
 Facial Paralysis. — It is one of the inconveniences 
 of speaking of diseases in this special way, that we have 
 in talking of facial paralysis to include in it a great 
 variety of morbid conditions. 
 
 In order that you may understand pretty easily the 
 abnormalities to wliicJi the facial nerve is subject, it will 
 be well to remind you briefly of its origin and its course. 
 Here we ao-ain owe our thanks to Stillino- and Lock- 
 hart Clarke for the discovery of the relations of the 
 nucleus of the facial with the nuclei of other nerves. 
 The hypoglossal, the vagus, the spinal accessory in part 
 at least, the facial, and the fifth, all have nuclei closely 
 associated with each other in the lower part of the 
 medulla oblongata. Besides these, close to the olivary 
 bodies, the sixtli nerve arises from the same nucleus as 
 the facial. 
 
 The nucleus of this nerve, therefore, is on the floor 
 of the fourth ventricle, but some of its fibres are de- 
 rived from the ])ons, even if a few do not come from 
 an origin as high as the corpus striatum, or at any rate 
 as high as the crus cerebri. In some of the lower 
 animals, however, and to some extent even in man, 
 some of the fibres of the facial nerve do not spring 
 from the facial nucleus, but ])ass through the raphe of 
 the medulla oblongata to the columns of the spine,
 
 FACIAL I'AEALYSIS. 253 
 
 Avliilst those fibres, in man the most numerous, whicli 
 spring from the nucleus, send radiating libres across 
 the raphe to the nuclaiis of tlie otlier side, so tliat in 
 the medulla itself there is a double decussation. This 
 decussation is somewhat higher than that of the motor 
 fibres to the limbs. 
 
 The facial and auditory nerves appear together 
 on each side of the posterior margin of the pons, 
 opposite to its junction with the middle peduncles 
 of the cei'ebellum. The facial is nearer the median 
 line, and in its course with the auditory lies in a 
 groove on the upper surface of that nerve. It runs 
 outwards with the auditory to the internal auditory 
 meatus, and at the bottom of the meatus enters the 
 aqueduct of Fallopius, and follows the winding of that 
 canal to the surface of the skull. At the bend, the 
 nerve presents a reddish gangliform enlargement, which 
 marks the junction of several nerves. These nerves 
 are a large superficial petrosal from the Vidian nerve, 
 a filament from the small superficial petrosal derived 
 from the tympanic nerve, and the external superficial 
 petrosal from the sympathetic accompanying the middle 
 meningeal artery. Xear the exit from the aqueduct 
 of Fallopius it is joined by a few filaments from the 
 auricular branch of the pneumogastric. In this osseous 
 canal the chorda tympani is given off from the facial, 
 supplying the membrana tympani, &c., and ultimately 
 is inclined forwards to the gustatory nerve, cndimx in 
 the submaxillary ganglion. Opposite the pyramid the 
 facial nerve is arched downwards behind the tympanum 
 to the stylomastoid foramen, by which it leaves the skull.
 
 254 FACIAL PARALYSIS. 
 
 Outside the skull tlie facial nerve gives off branches 
 in the following order : (1) The posterior auricular ; 
 
 (2) the digastric and stylo-hyoid arising together ; 
 
 (3) the temporo-facial, splitting up into temporal, 
 malar, and infra-orbital branches ; and (4) the cervico- 
 facial, passing through the parotid gland towards tlie 
 angle of the lower jaw, and terminating in buccal, 
 supra-maxillary, and infra-maxillary branches. 
 
 The lesions of the facial nerve are often divided 
 into lesions inside and those outside the stylo-masto'id 
 foramen. But the symptoms vary very much according 
 to the position of the lesion in or near the nucleus, and 
 in each part of its course. 
 
 Jaccoud's division is more in accordance with 
 clinical observation. He would divide the causes of 
 the paralysis of this nerve into cerebral and peripheral, 
 and the peripheral are separated into basilar, inter- 
 stitial, and superficial lesions. 
 
 Let me remind you that, whilst in facial palsy, from 
 lesion of the portio dura, the orbicularis palpebrarum is 
 almost invariably paralysed, in the great majority of 
 cases of cerebral hemiplegia of the face, the orbicularis 
 palpebrarum is not materially affected ; the act of wink- 
 ing and of voluntary closure of the eyes continues on 
 the paralysed as on the sound side, with the single 
 exception that the voluntary closure is usually weaker 
 on the palsied side. These symptoms indeed, as Dr. 
 Sanders remarks, form one of the best diagnostic marks 
 between centric and peripheral paralysis of the face : 
 the hanging cheek, with wide-open, staring, unwinking 
 eye, denotes lesion of the portio dura ; the flaccid face,
 
 FACIAL PARALYSIS. 255 
 
 with tlie iiiituml position and motions of the eyehcls, is 
 a sign of cerebral lesion, and indicates a more serious 
 disease. 
 
 Central lesions, confined to the nuclei of the nerve, 
 are extremely rare. Iltemorrhage into that portion of 
 the medulla oblongata would be very rapidly fatal. 
 Still, judging by the analogy of glosso-laryngeal paralysis, 
 a lesion that implicated these nuclei may exist. If the 
 nucleus be affected it is almost certain that the sixth 
 nerve, springing as it does from the same nucleus, will 
 be affected also, and the j^atient will have converging 
 strabismus. 
 
 Complete paralysis of the nerve has been known 
 to coexist with hemiplegia of the same side. The 
 explanation is difficult, and Dr. Brown-Sequard has 
 suggested that the facial paralysis in these cases was 
 due to reflex irritation. 
 
 In a few cases there is a cross paralysis seen, the 
 facial nerve being paralysed on one side, the limbs on 
 the other. This is invariably due to disease of the 
 pons, and is easily intelligible anatomically. The wonder 
 is that, with hasmorrhage into the pons, it is not more 
 frequent. That it is not so is simply because a lesion 
 to produce these symptoms must be in a very limited 
 portion of the pons. In Dr. Hughlings Jackson's words : 
 ' Since the nerve-fibres for the limbs cross below the 
 pyramids, those of the left arm and leg will pass in 
 the right side of the pons, on their way to the higher 
 parts of the motor tracts. But the facial nerve of the 
 right side runs through the lower part of the right 
 side of the pons to its nucleus on the fioor of the
 
 IJob FACIAL PARALYSIS. 
 
 fourth ventricle. So tliat a clot which damages the 
 right facial nerve damages also the motor fibres which 
 have come over fi'om the left arm and leg.' 
 
 The morbid conditions that may influence the func- 
 tion of the nerve in the pons or the medulla oblongata 
 are heemorrhages, inflammations, softening, sclerosis, and 
 tumours. 
 
 Disease of the motor tract above the pons varolii 
 causes a facial paralysis very limited in extent and very 
 slight in degree ; and the facial paralysis is, under these 
 circumstances, always on the same side as the paralysis 
 of the arm and leg. 
 
 Disease in the crus cerebri will cause hemiplegia 
 and facial paralysis on the side opposite to the lesion, 
 and if the disease extends to the nucleus of the third 
 nerve in the crus, there will be paralysis of the third 
 nerve on the same side as the lesion, and therefore 
 on the opposite side to the hemiplegia and facial 
 paralysis. 
 
 Lesion above this spot will implicate the facial 
 nerve very slightly, and the facial paralysis may be 
 therefore rapidly and almost completely recovered from. 
 In disease, indeed, above the crus only a small part of 
 the face, notably the levator anguli oris, levator labii 
 superioris, and the zygomatici, will be paralysed, and in 
 many cases not wholly so ; always, however, on the 
 same side as the limbs, that is, on the side opposite to 
 the lesion, showing not only that a few fibres of the 
 facial exist above the crus, but that the fibres that are 
 found higher up decussate eventually. 
 
 We may easily conceive that this very partial affec-
 
 FACIAL P.mALYSIS. 257 
 
 tiou of the facial in lesion of parts above the cms cerebri 
 is owing to the very limited number of fibres of the facial 
 to be found above this ])oint. A more elaborate expla- 
 nation lias been given, however, by Dr. Sanders, with 
 tlie idea of showing why the orbicularis palpebrarum 
 escapes, or at least is so very slightly affected, in ordinary 
 hemiplegia. He says : ' In examining this question it 
 is necessary to remember that one reason why the 
 action of the orbicularis palpebrarum is not arrested in 
 cerebral hemiplegia is, because ordinary winking is a 
 reflex and not a voluntary act. When the motor 
 influence of the brain is withdrawn from a part, the rule 
 is that the voluntary movements cease, but the reflex 
 actions persist. Winking continues therefore in cerebral 
 hemiplegia of the face after the mobility of the features 
 has ceased, for the same reason that the respiratory 
 movements of the intercostals and diaphragm are pre- 
 served in the cerebral hemiplegia, which deprives the 
 limbs of voluntary power. On the other hand, both 
 voluntary and involuntary closing of the eyelids is pre- 
 vented, and the orbicularis palpebrarum and other 
 muscles are completely paralysed, in lesion of the portio 
 dura, because the efferent conduction of all motor 
 influence, reflex and voluntary alike, is then interrupted. 
 In the same way spinal hemiplegia is distinguished from 
 cerebral by the muscles of the thorax being paralysed 
 in conjunction with those of the limbs, because in 
 the spinal disease the tracts for reflex action are injured 
 simultaneously with the conduction of vohtion. This 
 explanation, which accounts for part of the phenomena, 
 may be extended, however, beyond the simple reflex 
 
 s
 
 258 FACIAL PARALYSIS. 
 
 action, as follows : — The facial motor or portio dura of 
 the seventh pair, considered as a musciilo-motor nerve, 
 contains within its common trunk fibres serving different 
 purposes, and provided, therefore, with different 
 capacities of action. These fibres may, for our present 
 inquiry, be divided into — 1, voluntary motor fibres, by 
 which the voluntary movements of the features are 
 performed, and by which, especially, labial and buccal 
 speech and mastication are accomplished ; 2, emotional 
 fibres, by which the features express the passions more 
 or less involuntarily ; 3, reflex motor fibres, which are 
 involuntary, for the act of winking, and for the move- 
 ments of the nostrils in respiration. According to the 
 principles of physiology, these different sets of fibres 
 derive their peculiar functions, not from any special 
 properties of the nervous fibres themselves, but solely 
 from the nature of their origin or central connections 
 in the brain or the medulla oblongata. Thus, although 
 anatomy cannot yet trace individual fibres to their 
 primary source, there is good reason to believe that the 
 voluntary motor fibres originate from a cerebral centre 
 of conscious volition ; those for expression must be con- 
 nected with the cerebral organs of the emotions ; while 
 those for reflex action arise, more or less independently 
 of the cerebral hemispheres, from the medulla oblongata, 
 in connection (inter alia) with the sensory branches of 
 the fifth pair, with which they are associated in the act 
 of winking. The symptoms therefore will vary with 
 the special seat of the central disease.' 
 
 I doubt, however, whether the phenomena demand 
 so ingenious an explanation.
 
 FACIAL PAEALYSIS. 259 
 
 The lesions tlieu in tlio bniiu itself affecting any 
 portion of the portio dura directly must be in the 
 medulla oblongata, the pons, the crura cerebri, the optic 
 thalami, or the corpora striata. But any lesion of the 
 cerebral hemispheres that causes either pressure or irri- 
 tation of the corpora striata may indirectly induce slight 
 paralysis of some fibres of the portio dura. 
 
 The nerve has, however, a short free course from 
 the lower part of the pons, where it leaves the nervous 
 centre, to its entrance into the petrous portion of the 
 temporal bone. During this course it maybe injured. 
 Dr. Ogle has seen a case where the nerve was paralysed 
 by being stretched by an aneurism of the anterior cere- 
 bellar artery. It may be injured by accident, such as 
 fracture of the skull, by being pressed upon by menin- 
 geal hasmorrhage, or by tumour at the base of the 
 brain, or by being imbedded in lymph from meningitis. 
 In the Oxford Museum there is a specimen of a facial 
 nerve as hard as cartilage. The disease was probably 
 due to very gradual inflammation, secondary to ulcera- 
 tion in the internal ear. At the stylo-mastoid foramen 
 the nerve came to an end, so that all communication 
 with the face was cut off. The facial paralysis, however, 
 would have been caused by the sclerosis of the nerve, 
 even had not the peripheral destruction occurred. But 
 injury or disease of the nerve in this short [)assage 
 within the cranium is rare. 
 
 It is not, however, very unusual to meet with para- 
 lysis of the portio dura from disease in its course through 
 the petrous portion of the temporal bone. The lesions 
 are most commonly osteitis or caries of the pars petrosa, 
 
 s 2
 
 260 FACIAL PARALYSIS. 
 
 otitis of the middle or of the internal ear, haemorrhages 
 in the aqueduct of Fallopius, and fracture of the tem- 
 poral bone. In the majority of cases the portio dura 
 will only be affected secondarily, the inflammation 
 attacking the auditory filaments first and travelling 
 backwards to affect the portio dura ; the occurrence of 
 deafness affordino- aid to tlie diaQ;nosis. 
 
 In otlier cases, especially where suppuration com- 
 mences in the middle ear, we often find the membrana 
 tympani destroyed, and discharge taking place from 
 the external meatus. Not only do two filaments pass 
 from the portio dura into the middle ear, but the 
 whole relation of this portion of the auditory apparatus 
 with this nerve is so close that disease of the middle 
 chamber would seem to be particularly likely to cause 
 facial paralysis. Still, as a matter of clinical observa- 
 tion, disease of this part is frequently met with without 
 any facial paralysis. Deafness, followed later by facial 
 paralysis, would suggest disease of the middle or 
 internal ear, spreading afterwards to the portio dura. 
 Deafness and facial paralysis occurring simultaneously, 
 and unaccompanied by other paralysis, should suggest 
 lesion of the two nerves as they enter together the 
 pars petrosa; and such a lesion would probably be 
 either haemorrhage or fracture of bone. 
 
 Anatomically, we should expect that lesion 
 attacking the nerve during its progress through tlie 
 bone would be evidenced by some paralysis of the 
 chorda tympani, as this branch is only given off a very 
 short distance above the stylo-mastoid foramen. It 
 passes through the short ' canal behind the tympanum,
 
 FACIAL PARALYSIS. 20 1 
 
 enters the tympanum, crosses it to the membrana 
 tympani and the liandle of the malleus, and emerges 
 at the opening at tJie inner side of the Glasserian 
 fissure ; then lies beneath the external pterygoid 
 muscle, and is inclined obliquely forwards to the 
 gustatory nerve, a branch of the fifth, ending in the 
 submaxillary ganglion. Observation seems rather to 
 contra-indicate that the sense of taste is impaired in 
 cases where the facial is seriously injured above the 
 point of going off the chorda tympani. But, of course, 
 we are almost wholly in the dark as to what part the 
 chorda tympani takes in intensifying the action of the 
 gustatory branch of the fifth. At any rate, it does 
 not give us any definite aid in determining the seat of 
 lesion of the facial nerve. 
 
 Jaccoud speaks of lesion to the nerve in its transit 
 through the bone as evidenced by paralysis of the 
 branches given off by the facial in the aqueduct of 
 Fallopius ; these phenomena being deviation of the 
 tongue and difficulty in turning the point upwards, 
 from paralysis of the branches to the digastric and 
 stylo-glossus, and of the hngual branch ; diminution 
 of taste, from paralysis of the lingual branch and of the 
 chorda tympani, the erector nerves of the papillai ; 
 the exaltation of hearing, especially for the lower and 
 highest notes of the scale, from paralysis of the small 
 superficial petrosal, which supplies the internal muscle 
 of the malleus ; diminution of the salivary secretion 
 and dryness of the mouth, from paralysis of the chorda 
 tympani running to the submaxillary ganglion, and of 
 the small petrosal going to the parotid ; and lastly, tlic
 
 262 FACIAL PARALYSIS. 
 
 alteration in shape of the velum of tlie palate, from 
 paralysis of the large superficial petrosal nerve. This 
 deformity consists in a deviation of the uvula, which 
 sometimes is turned wholly towards the healthy side ; 
 sometimes its point deviates towards the paralysed 
 side, whilst its base is turned towards the other. At 
 the same time, the velum palati is enfeebled and 
 flabby on the diseased side. 
 
 I can only say that English observers have been 
 very much alive to these points, and have found taste 
 frequently unaffected ; and many of them believe, 
 with Dr. Todd, that the affection of the palate is of 
 very rare occurrence, and then only as a coincidence ; 
 but Dr. Sanders describes a case in which this con- 
 dition of the palate coexisted with facial paralysis, and, 
 as he thinks, depended upon lesion of this nerve. 
 
 Lastly, we come to affections of the nerve after it 
 has emerged from the stylo-mastoid foramen. This is 
 what is generally understood by true facial paralysis ; 
 and the abnormal condition is generally very complete, 
 involving the filaments that supply the orbicularis 
 palpebrarum quite as much as those which supply the 
 muscles round the mouth. The electric contractility 
 of the nerve is in complete abeyance. 
 
 The kinds of lesion are manifold : — 
 1. Injuries to the nerve by various accidents or by 
 surgical operation. Before Sir Charles Bell's beautiful 
 elaboration of the various nerves of the face, section of 
 the facial had been attempted for the cure of tic. The 
 nerve may easily be injured by operation, even the 
 most careful, fo]' tlie removal of tumour in the neigh-
 
 FACIAL PARALYSIS. 263 
 
 bourliood of the styloid process. There have also 
 beeu instances in which the nerve at its exit has been 
 injured by the forceps of the accoucheur in a tedious 
 birth, though this accident is nuich more likely to 
 affect some branch of the temporo-facial termination 
 of the nerve. 
 
 2. Swelling of the parotid gland, or tumours in its 
 immediate neighbourhood. Part of the difficulty of 
 opening the mouth in ordinary mumps is due to the 
 pressure exercised by the gland on a portion of the nerve. 
 
 3. Syphilis. In this case the })aralysi3 is generally 
 very localised from the pressure upward on the nerve 
 in spots where it is very near bone. 
 
 4. Exhaustion. Dr. Todd mentions this as an 
 occasional cause. It ought, perhaps, to be placed 
 among the central lesions ; as also may the next, to 
 which, again, Dr. Todd lias drawn the attention of the 
 profession. 
 
 5. Paludal poison : the motor power of a motor 
 nerve being affected by marsh-rniasm, and paralysis 
 induced, just as neuralgia is caused by the action of the 
 same poison on a sensory nerve. Still, neither exhaus- 
 tion nor paludal poison can be supposed to act only on 
 the peripheral portion of a nerve ; they must act by 
 causing anaemia of the nucleus. 
 
 6. Eheumatism or gout, as distinguished from the 
 impress of cold ; that is, paralysis of the facial nerve 
 due to the rheumatic diathesis. Here, again, it is 
 perhaps hardly fair to s})eak of this as being a cause of 
 peripheral paralysis. Dr. Todd's case 10 is an example 
 of this.
 
 264 FACIAL PAEALYSIS. 
 
 7. Cold. Tlie most frequent of all causes ; so 
 much so, that peripheral facial paralysis has been called 
 a disease only of the northern climates. Sometimes the 
 paralytic condition comes on quite suddenly, after the 
 patient has been exposed to great cold, especially to 
 the influence of a cold draught impinging immediately 
 on the trunk of the nerve as it emerges from the 
 stylo-mastoid foramen. In this case the nerve trunk is 
 simply much congested. At other times the paralytic 
 symptoms come on more gradually, and the interior of 
 the nerve in that case is the seat of an exudation of 
 serum or of lymph ; in a Avord, it is an instance of 
 neuritis. 
 
 If the paralysis persists, we either get a condition of 
 sclerosis of the nerve — the result of low subacute 
 inflammation — or more or less atrophy of the nerve, 
 due partly to the pressure of the exudation, partly to 
 disuse of the nerve itself. 
 
 It is in such cases, where the nerve has undergone 
 persistent degenerative changes, that we may meet 
 with contraction of the paralysed muscles, the spas- 
 modic tic of Marshall Hall. 
 
 A few cases have been recorded of double facial 
 paralysis. Very seldom are both the muscles affected 
 simultaneously. If they are, we may expect the lesion 
 to be an aneurism of the basilar artery, or central 
 hcemorrhage of the lower part of the pons, or an 
 accident causing fracture of each pars petrosa. The 
 double paralysis is sometimes seen when the lesion 
 is in the temporal bone, being then attended with 
 deafness. Cases have been met with depending on
 
 FACIAL PARALYSIS. 265 
 
 rheumatism or on S3'[)liilis, and in each case affecting 
 only tlie peripheral ])ortion of the nerve. Dr. War- 
 bnrton Begbie has seen one example of double facial 
 palsy occurring in a ])litliisical patient, who subse- 
 quently died of Avhat appeared to be strumous 
 meningitis ; but no autopsy was permitted. 
 
 Consult, for Aphasia — 
 
 Trousseau, ' Clinical Lectures.' 
 
 Jaccoud, ' Path, interne.' 
 
 Hammond. Op. cit. 
 
 Reynolds, * System of Med.' Dr. Huglilings Jackson. 
 
 ' Med.-Chir. Trans.' vol. liv. Dr. W. Ogle. 
 
 ' Med.-Chir. Trans.' vol. Iv. Dr. Broadbent. 
 
 ' St. George's IIosp. Ifep.,' vol. ii. Dr. W. Ogle. 
 
 * Lond. Hosp. Rep.,' vol. i. Dr. Hughlings Jackson. 
 'West Riding Asylum Rep.,' vol. ii. Dr. W. Browne. 
 ' Guy's PIosp. Rep.,' vol. xvi. Dr. Pye Smith. 
 
 ' Guy's IIosp. Rep.,' vol. xvii. Dr. Wilks. 
 
 ' Jour, of Mental Science,' April and Oct. 1872. Drs. Tuke and 
 Frazer. 
 
 * Med. Record,' vol. i. 107. Waldenberg. 
 ' Med. Record,' vol. i. 5.33. Bartholow. 
 
 Consult, for Glosso-laryngeal Paralysis — 
 Jaccoud, ' Path, interne,' 
 Duchenne, ' De I'electrisation localisee.' 
 'Guy's Hosp. Rep.,' vol. xv. Dr. Wilks. 
 
 'New Sydenham Soc. Year-Book, 1802.' Miiller, Lichten.^tein. 
 'Brit. Med. Jour.,' vol. ii. 1871. Mr. Taylor. 
 
 Consult, for Facial Paralysis — 
 
 Romberg, ' Dis. of Nervous System.' 
 
 Trousseau, ' Clinical Lectures.' 
 
 Todd's ' Clinical Lectures.' 
 
 Jaccoud, ' Path, interne.' 
 
 Reynolds, ' System of Med.' Dr. Warburton Begbie. 
 
 ' Lancet,' 18G.5. Dr. Sanders. 
 
 ' Lond. Hosp. Rep.,' vol. i. Dr. Hughlings .lackson. 
 
 Van der Kolk, on ' Medulla Oblongata.' New Syd. Soc.
 
 266 
 
 LECTUEE X. 
 
 PEOGRESSIVE MUSCULAR ATROPHY. 
 
 Ever since this disease has been recognised there have 
 been diverse views as to its pathology ; some observers 
 considering the degeneration of muscles the main, and 
 sometimes even the sole lesion, others finding it in some 
 portion of the nervous system. Since Lockhart Clarke's 
 observations, however, most authorities unite in con- 
 sidering the nervous system to be the seat of primary 
 lesion, but there is no complete agreement as to the 
 portion of the nervous system affected. 
 
 Still, taking mto consideration the comparative 
 agreement of a majority of recorded cases, and the 
 probability of imperfect observation of some other, it 
 may be said that the most usual, I cannot say the 
 universal, lesion is atrophy of the anterior grey cornua. 
 
 The lesions that liave been observed in the spinal 
 cord are mainly these : softening of the centre of tlie 
 grey matter in the cervical and dorsal regions ; atrophy 
 of the grey matter with amyloid deposits and granular 
 bodies ; this atrophy has been found to extend to the 
 anterior cornua, to the posterior, to both at one time, 
 to the posterior commissure, to the central part itself,
 
 PROGRESSIVE MUSCULAR ATROPHY. 267 
 
 which may have been already encroached upon by 
 enlargement of the central canal. Lockhart Clarke 
 has found changes in the grey matter. Round or at 
 the sides of bloodvessels spots were seen differing from 
 proper grey matter, and composed of a substance 
 which had a delicate transparent and very finely 
 granular aspect. A considerable deposit of corpora 
 amylacea existed round the central canal.- These 
 appearances, however, also existed in parts of the cord, 
 from which the nervous influence was derived to 
 perfectly healthy muscles. Lastly, grey degeneration 
 of the posterior col inn ns with amyloid bodies, under 
 which circmnstances the symptoms of locomotor ataxy 
 and progressive muscular atrophy are found combined. 
 In many cases, lesions of the anterior nerve-roots have 
 been found, and this lesion consists in a diminution of 
 volume caused by the disappearance of a certain 
 number of the nerve-tubes. This alteration may be 
 more or less seen in various parts of the cord, but 
 especially in the cervical region. It is important to 
 remember that these roots contain, besides the motor 
 filaments, some filaments of the sympathetic. Before 
 I say anything about the sympathetic, let me point out 
 to you that the above-named lesions are very diverse, 
 and seem to deny to the anterior cornua any specialty 
 as the seat of lesion. 
 
 Besides which the fact observed by Dumenil and 
 the more recent observations of Bamberger seem to 
 refute it ; in these cases the cord was examined micro- 
 scopically by liecklinghausen, and was found com- 
 pletely healthy. In one of the cases, tlie anterior roots
 
 2G8 PROGRESSIVE MUSCULAR ATROPHY. 
 
 were alone diseased ; in the other, in which the 
 atrophy of the muscles was less advanced, these roots 
 were quite normal, but in the most altered muscles he 
 found degeneration of some of the nerve-filaments. 
 The result of these two post-mortem examinations was 
 such that Bamberger concluded from them that in 
 progressive muscular atrophy the process begins by 
 deo-eneration of the muscles, and that the alteration of 
 the peripheral nerves and of the anterior roots are 
 secondary lesions. That the disease of nerve-root might 
 be secondary, depending on the disease of the muscles 
 it supplies, is only analogous to what is seen in the 
 body. The optic nerve will become atrophied when 
 the eye is lost, and in some cases, at least when a limb 
 is lost, the nerve atrophies also. 
 
 The examples of lesion of the sympathetic in this 
 disease amounted to six up to the date of the publica- 
 tion in 1873 of ' Jaccoud's Volumes on the Pathology 
 of Internal Organs.' The first in date was that of 
 Schneevogt ; the two following were observed by 
 Jaccoud in 1864 ; two belonged to Dumenil, and the 
 last was observed by Swarzenski in French's clinique. 
 In Schneevogt's case, the fatty degeneration of the 
 sympathetic occupied the cervical and dorsal cords ; in 
 Jaccoud's cases, there was a fibro-fatty degeneration 
 of the sympathetic cord in the neck of the superior 
 cervical ganglion, and (in one of them) of the branches 
 that unite this ganglion and the spinal cord. In these 
 three cases, atrophy of the anterior root existed in 
 various degrees, but the spinal cord was healthy ; in 
 Dumenil's observation he found a sclero-fatty atrophy
 
 PROGRESSIVE MUSCULAR ATKOrilY. 269 
 
 of the cervico-doisal sympatlietie, and a granular fatty 
 alteration of the lumbar sympathetic, coincident with 
 atrophy of the roots, and with many lesions of the cord, 
 and even of the intervertebral ^ano'lia. Swarzenski 
 states that in his case the two superior ganglia of the 
 sympathetic were much ihittencd and of a livid colour, 
 but no microscopical examination was made. The 
 explanation of tliis lesion in its relation to progressive 
 muscular atrophy is thus given by Jaccoud : ' In- 
 dependently of the motor and sensitive filaments, the 
 muscles receive by the nerves that emanate from the 
 cord sympathetic or trophic filaments, which maintain 
 and rule their nutrition ; complete inertia of a nerve, 
 therefore, has necessarily as its effects tlie loss of inc)tioii, 
 the loss of sensation, and insufficient nutrition (atrophy). 
 In the trunks of the nerve the three filaments are closely 
 grouped together ; tliey cannot be attacked in an 
 isolated way, so that the complete lesion of such a 
 nerve has always the triple result I have indicated ; 
 but if there is a point at which these various elements 
 can be separately altered, the effect Avill be simple 
 instead of being complex ; this will be, according to 
 the case, either a loss of motion alone, or a loss of 
 sensation alone, or, lastly, an alteration of nutrition, an 
 atrophy alone.' 
 
 Now this region of isolation really exists ; for the 
 motor filaments, it is the anterior spinal system and the 
 anterior roots as far as the intervertebral ganglia ; for 
 the sensory filaments, it is the posterior spinal system and 
 the corresponding roots ; for the trophic filaments, it is 
 the whole tract they pass through before their fusion
 
 270 PROGRESSIVE MUSCULAR ATROPHY. 
 
 with the peripbenil nerve-trunk — that is to say, the 
 grey substance of the cord, wherever they take their 
 origin, the anterior and posterior roots by which tliey 
 leave the spinal axis, the anastomosing branches which 
 connect the cord with the sympathetic, the sympathetic 
 cord itself, and the branches which spring from it. In 
 all these points the lesions of nerves may be isolated, 
 and in this case it has for its sole consequence in- 
 sufficiency of nutrition : if, further, this lesion is exten- 
 sive or progressive, the greater part of the animal 
 muscular system is attacked with atrophy without 
 primary or contemporaneous paralysis either of motion 
 or of sensation. This is precisely the clinical charac- 
 teristic of the disease, the anatomical and pathological 
 condition of which is a lesion of the sympathetic or 
 trophic system. 
 
 The state of the muscles is one either of fatty or 
 granular degeneration, and of these the latter may be 
 only a first stage of the former. We observe at first a 
 disappearance of the transverse and longitudinal striae, 
 whilst at the same time the contents of the sarcolemma 
 present as it were a granular segmentation ; they are 
 replaced by opaque granulations of a nitrogenous 
 nature, which are dissolved for the most part in acetic 
 acid, and are not modified either by ether or by alcohol. 
 The muscular bundles then undergo a considerable 
 diminution in volume. Later on these granulations 
 undergo the fatty transformation, and some fat is also 
 deposited in the muscular interstices, constituting what 
 is called interstitial fatty degeneration, as opposed to 
 parenchymatous degeneration. Even if we look at
 
 PROGRESSIVE MUSCULAR ATROPHY. 271 
 
 these two lesions as distinct and isolated, or as neces- 
 sarily succeeding each other, we have just the same 
 reason for recognising in muscular atrophy two dis- 
 similar alterations, the granular and the fatty, this latter 
 presenting two forms generally combined, the parenchy- 
 matous and the interstitial form. 
 
 Finally, atrophy, the disappearance of the contrac- 
 tile element, may still be produced by another 
 mechanism, that is, by the proliferation of the connec- 
 tive elements which enter into the composition of the 
 muscle. Wlien this substitution is complete the mus- 
 cular fibres are transformed into true fibrous cords. 
 This lesion may coincide with fiitty degeneration in the 
 same subject, but it may also exist alone. This muscular 
 sclerosis appears to correspond with the third form of 
 atrophy, described by Professor Eobin as a whitish 
 transformation. It is of great importance to recognise 
 this special lesion ; and Jaccoud believes that it enables 
 us to conceive the possibility of permanent muscular 
 retractions in progressive atrophy, and furnishes a 
 satisfactory interpretation of this symptom. Dr. 
 Bazire, in a note to Trousseau's article on this disease, 
 says that in his opinion it is still an open question 
 whether this atrophy is an idiopathic affection of the 
 muscles themselves, or whether it is dependent on 
 structural alterations of the spinal cord. He states that 
 Dr. Meryon, who holds the former opinion, has sup- 
 ported it by the results of two carefully made micro- 
 scopical examinations of the cord in undoubted in- 
 stances of the disease, and even cites a case in wliich the 
 bones seemed to participate in the inadequate nourish-
 
 272 PROGRESSIVE MUSCULAR ATROPHY. 
 
 ment of the muscles. lu 105 cases collected by Dr. 
 Eobei'ts, iu his essay on wasting palsy, the cord v/as ex- 
 amined in 13 and found altered in 4 only. But Dr.Eoberts, 
 in a later article in ' Keynolds's System of Medicine,' 
 gives a very different relative proportion of cases in 
 which the cord was affected. He says, ' The condition 
 of the spinal cord and of the spinal nerves has been 
 examined in thirty-five cases, of which thirty-four have 
 been tabulated by Bergmann.' The results of the in- 
 vestigation have not been by any means uniform. In 
 sixteen cases the cord and the nerves were pronounced 
 healthy, and in six of these the parts were examined 
 microscopically. In six cases the cord itself was found 
 healthy, but there was marked atrophy of the anterior 
 roots of a certain number of spinal nerves. In one 
 case both the spinal cord and nerves were healthy, but 
 there existed disease of the medulla oblongata. In six 
 cases the cord was found diseased, when examined 
 microscopically, though it appeared sound, or nearly so, 
 to the naked eye. Lastly, in several cases the cord 
 appeared to the unaided senses palpably softened and 
 disoro-anized. Dr. Bazire thinks that the total absence 
 of all visceral disorders in this complaint is a fact not 
 easily reconcilable with an affection of the sympathetic, 
 and he says, ' It is a remarkable circumstance that pale 
 unstriated muscular fibres escape in progressive mus- 
 cular atrophy, and that the heart, the walls of which 
 consist of striated fibres, is not affected. But this is 
 only in accordance with the capriciousness of the line 
 of attack, which is a striking characteristic in this 
 disease.'
 
 PROGRESSIVE MUSCULAR ATROPHY. 273 
 
 When we consider the difficulty of examining every 
 portion of the spinal cord in any one case, and the 
 frequency with which lesions have been found in this 
 organ, I believe the seat of lesion must be placed in 
 the cord itself. Still, it need not be at first such as 
 would cause paralysis, either of motion or sensation, 
 Mr. Lockhart Clarke, speaking on this point, says, 
 ' There may be very obscure structural changes in the 
 grey substance of the cord, or perhaps only in the 
 ganglia or the posterior roots of the nerves, that may 
 affect the nutrition of the parts to which they are sub- 
 servient, without interfering with the functions either 
 of sensation or motion ; and in cases where the lesions 
 occur in small isolated spots, the limitation of disease 
 to particular muscles, or even to particular fasciculi of 
 any one muscle, could be explained, I think, by the 
 particular nerve-fibrils within the grey substance.' 
 This abnormality of the trophic nerves, or of the 
 trophic centres, will cause atrophy of some kind or 
 other of the muscles ; this atrophy, leading to disease, 
 causes, or may cause, atrophy of nerves or nerve-roots, 
 in accordance also with the chnical observation that tlie 
 paralysis follows the loss of muscular substance, and is 
 always in direct ratio with such loss. Further loss of 
 power will also be induced by extension of original 
 lesion in the cord to those portions of the grey matter 
 that rule motion, or to the anterior columns, as the 
 tract by which the orders of will are transmitted down- 
 wards. It is only by further extension of the same 
 lesion to the posterior columns that we meet with the 
 
 T
 
 274 PROGRESSIVE MUSCULAR ATROPHY. 
 
 combination of the symptoms of locomotor ataxy with 
 progressive muscular atrophy. 
 
 M. Gombault has recorded a case of this disease, 
 accompanied by glosso-labio-laryngeal paralysis. In 
 this case the nerve-cells of the hypoglossal nucleus in 
 the medulla oblongata were found to have undergone 
 considerable pigmentary degeneration, to have lost 
 their angular appearance and some of their processes ; 
 whilst in the spinal cord both the antero-lateral column 
 and the grey substance were considerably altered by 
 disease. 
 
 Locomotor Ataxy. — It may be well, as an aid in 
 understanding the pathological anatomy of this disease, 
 to mention briefly its most important symptoms : — 
 
 1 . Certain affections of the eyes ; diplopia, strabis- 
 mus, partial loss of sight, complete amaurosis, and 
 contraction of pupils. AU these ocular symptoms 
 may be absent or intermittent ; or they may occur 
 and vanish, and not recur again. A man lately in the 
 Bristol Eoyal Infirmary with locomotor ataxy had com- 
 plete amaurosis for ten days, and entire recovery from it. 
 
 2. Neuralgic pains of very severe character, espe- 
 cially in the limbs about to be affected. These pains 
 are often afterwards followed by a corresponding 
 numbness. 
 
 3. Want of coordination in the muscles of the limbs, 
 with all the varied phenomena consequent on this 
 condition. 
 
 4. Sometimes, but very rarely, affection of the 
 special senses other than sight, especially taste and smell.
 
 LOCOMOTOR ATAXY. 275 
 
 5. Towards the termination of the disease certain 
 paralyses affecting the sphincters, the muscles of the 
 limbs, particularly of the legs. 
 
 It is scarcely necessary to refer you to my Lectures 
 of the Winter Session, in order to remind you of the 
 differential points between tliis disease and chorea on 
 the one hand, and disease of the cerebellum on the other. 
 Suffice it to say, that there are most important points of 
 difference between these three morbid conditions. 
 
 The morbid appearances are, lesion of the pos- 
 terior columns, of the posterior roots of the spinal 
 nerves, and probably of the posterior cornua. Dr. 
 Axenfeld's account of the lesion (quoted by Trousseau) 
 is as follows : — ' In the white matter of the posterior 
 columns, which has now become yellowish or grey, 
 are seen scattered nerve-tubes, pale, shrunken, or 
 varicose, sometimes reduced to their nemrilemma 
 only, or filled with granular contents, a few still retain- 
 ing their axis cylinders. On the other hand, the con- 
 nective transparent substance, the blastema in which 
 these tubes are imbedded, has become fibrillated, and 
 presents, amidst a large quantity of amorphous granules, 
 a smaller quantity of elongated nuclei, and a smaller 
 one still of cells (perhaps the nuclei, or at least most 
 of them, belong to the nerve-sheaths). Corpora 
 amylacea also are met with in variable quantity, dis- 
 tinguishable by their usual reaction with tincture of 
 iodine. Lastly, the blood-vessels are considerably 
 developed, and their thickened walls, composed of 
 several layers, are incrusted with a deposit of fatty 
 granules. In the posterior cornua of the grey matter 
 
 T 2
 
 276 LOCOMOTOR ATAXY. 
 
 the same alterations are found, but less markedly. 
 The reddish tint of this part is due to the injection of 
 its capillary network, and occasionally its tint is darker, 
 blackish, owing to the presence of numerous granules 
 of pigment. The nerve-tubes in these cornua are 
 sometimes destroyed, and the nerve-cells altered in 
 shape, although in general both the tubes and cells are 
 normal. The changes noticed in the posterior roots are 
 the same as those of the corresponding columns ; and 
 they are the same again in the diseased portions of the 
 bulb, the pons, and the optic nerves.' 
 
 Lockhart Clarke's account is still more circumstan- 
 tial : ' The morbid anatomy of locomotor ataxy consists 
 chiefly of a certain grey degeneration and disintegra- 
 tion of the posterior columns of the spinal cord, of 
 the posterior roots of the spinal nerves, of the pos- 
 terior grey substance or cornua, and sometimes of the 
 cerebral nerves. A variable number, and frequently, 
 in the latter stages of the disease, nearly all the fibres 
 of the posterior columns and posterior roots fall into 
 a state of granular degeneration, and ultimately dis- 
 appear. Usually the posterior columns retain their 
 normal size and shape in consequence of hypertrophy 
 of connective tissue, which replaces the lost fibres. In 
 this tissue, at wide but variable intervals, lie imbedded 
 the remaining nerve-fibres, with the debris of their 
 neighbours in different stages of disintegration. In 
 some places they are severed into short portions, or 
 into rows of globular masses, formed out of their 
 medullary sheaths or white substance, which has been 
 stripped from their axis cylinders. In other places
 
 LOCOJIOTOR ATAXY. 277 
 
 they have fallen into smaller fragments and granules, 
 which either lie aggregated in the line of the original 
 fibres, or are scattered at irregular distances. Corpora 
 amylacea are usually abundant, and oil-globules of 
 different sizes are frequently interspersed among them, 
 and collected into groups of variable shape and size 
 around the blood-vessels of the part. I am inclined 
 to believe, from my own investigations, that in the 
 course of the disease the posterior cornua of grey sub- 
 stance are more or less affected ; and it appears to me 
 to be a question whether they are not the first parts, 
 or at least among the first parts, that are morbidly 
 changed. I have also shown that in some cases the 
 deeper central parts of the grey substance are more or 
 less injured by areas of disintegration. These latter 
 lesions, however, are not essential to the production 
 of locomotor ataxy, the peculiar symptoms of which 
 depend solely on lesions of the posterior columns, of 
 the posterior nerve-roots, and probably of the posterior 
 cornua. The cases in which they occur may be con- 
 sidered as mixed cases, partaking of the nature of 
 locomotor ataxy and common spinal paralysis.' 
 
 The lesion is grey degeneration, or a more intense 
 form of sclerosis. (See plate 7.) Now, these lesions 
 seldom affect the whole length of the cord, but tliey 
 may do so. Generally only a hmited portion of the 
 cord is affected, and that most usually the dorso- 
 lumbar, and very rarely the cervical portions. 
 
 In a case under my own care, however, the whole 
 length of the cord was affected, but the cervical portion 
 not so intensely as the lumbar and lower dorsal. The
 
 278 LOCOMOTOR ATAXY. 
 
 patient had symptoms of locomotor ataxy for some 
 years, and eventually a certain amount of paralysis. 
 There was great diminution of the multipolar cells of 
 the grey matter. The white matter, especially of the 
 posterior columns,was almost wholly gone, its place being 
 taken by many amyloid bodies, granular matter, and a 
 considerable growth of the very finest connective tissue. 
 
 There are a few other points that demand remark. 
 Thus the spinal membranes in some cases show marks 
 of inflammation. In one of Trousseau's cases, the dura 
 mater spinalis was very vascular in its whole length, 
 and of a dark red hue ; it was also very markedly 
 thickened in its upper portions, and somewhat 
 (Edematous. There was no trace of old exudations. 
 The spinal pia mater was also abnormally injected, 
 more especially over the lower third of the cord and 
 along its posterior columns. 
 
 In these points, in fixct, it strongly adhered to the 
 posterior column, and like them had a yellow tint. It 
 could not be separated from the cord without tearing 
 away some of the nerve- substance. 
 
 Again, the atrophy of the nerve-roots bears no 
 accurate relation to the lesion of the posterior columns. 
 The columns may be in a very distinct state of grey 
 degeneration, and yet the nerve-roots connected with 
 them be healthy. 
 
 Again, the course of the lesion seems to be different 
 according as it attacks the cord or the brain. In the 
 cord the central portions seem to be the first attacked, 
 and the disease radiates towards the circumference ; 
 in the brain we find just the reverse ; the periphery of
 
 LOCOMOTOR ATAXY. 270 
 
 the nerves suffers first, then tlie body of the nerve, and 
 then the centre from which it springs, as from the optic 
 nerve to the corpora geniciilata. 
 
 Again, when sight is lost or gravely impaired, there 
 is a gradual whitening of the optic disc, without any 
 diminution in the size of the retinal arteries and veins. 
 
 The lesion of the optic nerve is a progressive grey 
 induration, and differs from optic neuritis. 
 
 The ophtlialmoscopic characters correspond with 
 what is understood as progressive atrophy of the papilla. 
 It is a very interesting observation of Charcot's that 
 the great majority of women who are admitted into the 
 wards of the Salpetriere suffering from amaurosis 
 present sooner or later after their admission more or 
 less marked symptoms of locomotor ataxy. 
 
 The form of sclerosis found in this disease, and 
 called grey degeneration, has been termed by Rind- 
 fieisch non-inflammatory. The spinal meningitis which 
 accompanies this sclerosis of the posterior columns, and 
 which is usually limited to those parts, would seem to 
 render it very probable that the disease has an inflam- 
 matory origin. Besides which, one part of the cord 
 may be in a state of this grey degeneration, and another 
 in a condition of the so-called inflammatory sclerosis. 
 
 It is not very likely that the origin of the lesion 
 will be inflammatory in one part of the cord and non- 
 inflammatory in another part. 
 
 Again, Charcot and Vulpian have pointed out that 
 in general locomotor ataxy a degeneration of a special 
 portion of the posterior columns is the characteristic 
 and essential lesion. It is known that in cases of this
 
 280 LOCOMOTOR ATAXY. 
 
 kind, there are to be observed, in addition to the 
 sclerosis of the fillets of Goel, which is almost always 
 present, two slender grey bundles. These, viewed on 
 the surface of the cord, appear to occupy the posterior 
 lateral fissures, and the most internal sensory roots 
 appear to emerge from them. Degeneration of these 
 bundles is then the special characteristic of the disease 
 under consideration. 
 
 Another point in the pathological anatomy of this 
 disease is w^ith reference to general paralysis of the 
 insane. Quite apart from the special mental difficulties 
 in cases of the latter disease, of which exaggerated 
 optimism is perhaps the most frequent, the muscular 
 trembling, especially of the lips and tongue, the hesita- 
 tion and mumbling of speech, with a peculiar unsteady 
 gait quite different from the loss of coordination in 
 locomotor ataxy, will suffice to separate the two con- 
 ditions. But I cannot remind you too often that 
 nature constantlj^ shows us disease in a complex form. 
 You have already seen that locomotor ataxy may, 
 toward the end of its course, come to be mixed up 
 with spinal paralysis, from extension of this lesion into 
 the thickness of the grey matter of the cord. This 
 mingling of two pathological conditions may be seen 
 also in general paralysis of the insane ; and Dr. Patrick 
 Nichol has reported several cases in which the two 
 states were coexistent. At the autopsy of one of them 
 were foimd lesions characteristic of the two conditions : 
 ' The pia mater thickened and white over the whole 
 brain, but most so over the anterior and middle lobes. 
 Four ounces of fluid escaped during removal ; the con-
 
 LOCOMOTOR ATAXY. 281 
 
 volutions much wasted. A pale pinkish tinge in the 
 grey matter ; puncta vasculosa numerous ; brain sub- 
 stance watery ; ventricles very large and filled with 
 clear fluid ; the ganglia which project into the lateral 
 ventricle liave lost their fulness and roundness ; 
 numerous small holes visible to the naked eye in the 
 substance of the corpora striata. On removal of the 
 spinal cord, and opening of the sheath of dura mater, 
 the arachnoid was found to be much thickened, and of 
 a milky-white appearance. At the cauda equina, and 
 over the lumbar enlargement, there are several dilated 
 vessels gorged with blood. Extending up the posterior 
 columns there was a softish white substance passing 
 irregularly from side to side, commencing over the 
 lumbar enlargement, being thickest throughout the 
 dorsal region, and becoming thinner again in the 
 cervical. It seemed to be under or in the visceral layer 
 of the arachnoid, and resembled a streak of thick 
 arrowroot-milk in appearance. There seemed to be 
 some dilatation of the vessels on each side of it, and 
 especially in the neighbourhood of the origin of the 
 posterior roots of the nerves. The ligamenta dentata 
 were thickened, whitish, and opaque. Microscopically, 
 the lesion, grey degeneration, was seen to involve the 
 posterior columns, and to reach the grey commissure, 
 and partly to involve it, and also most of the rootlets 
 of the posterior roots. 
 
 Dr. Crichton Browne has made the remark that in 
 all the cases of locomotor ataxy with mental derange- 
 ment that have fallen under his observation, and in 
 which there was optimism, the optimism has been 
 invariably tinctured with suspicion. It is probable that
 
 282 LOCOMOTOR ATAXY. 
 
 general paralysis is not the only form of mental disease 
 with which locomotor ataxy may be associated. 
 
 In connection with this subject a very interesting 
 point is the existence of cases which recover, cases 
 therefore in which we may presume no grey degenera- 
 tion has taken place in the posterior columns or the 
 posterior cornua. 
 
 What is the lesion here ? Excluding simulation 
 and hysteria, are the ataxic symptoms due to rellex 
 action, the irritation being in some distant organ ; or 
 are the phenomena due to anaemia of the cord of a 
 temporary nature ; or are they dependent on an 
 exhausted state of the nervous centre, irrespective of 
 blood supply, and leaving no recognisable lesion 
 behind ; or are they due to syphilitic lesion that may 
 be cured ? The great improvement that occasionally 
 takes place, even where the cord is disorganised, in 
 certain symptoms of ataxic patients, as for instance in 
 the sight, or in the power of retaining the urine after 
 there has been incontinence of urine for some time, 
 seems to point to some non-persistent condition of these 
 centres as sometimes occurring. Trousseau gives a 
 case of this disease in which the most careful micro- 
 scopical examination of the cord failed to disclose any 
 lesion. Dr. Wilks reports three cases in which im- 
 provement was so marked under treatment as to 
 amount to recovery. Are not such cases examples of 
 what we see in many diseases of the cord and of the 
 brain, the latter especially, that the pathological 
 anatomy of many maladies of the nervous system exists 
 only during the life of the patient.
 
 INFANTILE PARALYSIS. 283 
 
 Infantile Paralysis. — Here also, as in other morbid 
 conditions of the nervous system, the pathological 
 anatomy is twofold. In one set of cases, that do not 
 improve under treatment, lesions are found of a very 
 definite nature. In others, that completely recover, the 
 temporary lesion is believed to be spinal congestion. 
 The reasons for this belief are : (1) that an imperfect 
 and curable form of paralysis does occur from spinal 
 congestion. (2) That the symptoms of paralysis from 
 spinal congestion and infantile paralysis are very 
 similar. In both the paralysis is partial, in both 
 sensation is exaggerated rather than dulled in the 
 paralysed parts, in neither are the sphincters affected, 
 in both the paralysed muscles are limber, not rigid, in 
 both recovery more or less complete is the rule, in both 
 head symptoms are at any time exceptional phenomena. 
 
 Dr. Hillier has tabulated the lesions that may be 
 found, or may be supposed to exist, in this paralysis of 
 children : — 
 
 1. It may be caused by an organic change in the 
 muscles, as in inflammation of the muscles, and possibly 
 in progressive muscular atrophy. 
 
 2. By an organic change in the conductors of 
 motor impulse, as of the nerves supplying the muscles, 
 or part of the cord, or of the brain ; either of these 
 may be affected by inflammation, haemorrhage, or 
 degeneration. 
 
 3. By an organic change in that part of the brain 
 which is the organ of will; this and the preceding 
 usually go together. 
 
 4. By a morbid change in the blood, as in typhoid, 
 scarlatina, measles, diphtheria, or anaemia.
 
 284 INFANTILE PARALYSIS. 
 
 5. By a reflex influence transmitted from afierent 
 to eflerent nerves, and thence to muscles, or from some 
 part of the brain or cord which is tlie seat of irritation. 
 4 and 5 are often combined. 
 
 This differs from cerebral paralysis in hemiplegia 
 being rare, and in the absence of muscular rigidity, 
 which often attends cerebral paralysis. The disease to 
 which we give the name of infantile paralysis is wholly 
 dependent on the s|)inal cord. Tliere may be hj'-per- 
 ajmia of the spinal meninges, though this is often absent. 
 The fulness of vessels is seen much more in the grey 
 matter than in the white ; if only slight, it cannot be 
 recognised except by careful measurement of the capil- 
 laries under the microscope ; if intense, it is easily seen 
 with the naked eye ; when it afiects the whole length of 
 the cord, it does so with unequal intensity ; the cervical 
 and lumbar swellings are most likely to be found 
 especially hypersemic. If the congestion has been of 
 long duration or frequently repeated, it will leave 
 persistent capillary dilatation, and, as in other 
 morbid conditions, may become the point of departure 
 for grave alterations of tissue, myelitis, sclerosis, &c. 
 It is with this more serious disease that we find easily 
 recognisable lesions. Cerebral abnormalities are seldom 
 met with ; wlien they are, they are probably more by 
 way of accidental complications. There is certainly no 
 special lesion of the brain in these cases. Still Laborde 
 found in two cases a small quantity of reddish serosity 
 in the lateral ventricles, and Vul[)ian a slight softening 
 witli adhesion of the pia mater in the neighbourhood of 
 the fissure of Sylvius, coinciding with haemorrhage of the
 
 INFANTILE PAKALYSIS. 285 
 
 corpus striatum and optic thalamus of the left hemi- 
 sphere. 
 
 Medulla Oblongata. — -There maybe cellular atrophy- 
 in the pyramids and on the floor of the fourth ventricle 
 at the level of the pons. 
 
 Spinal Cord. — The spinal meninges may be very 
 vascular or slightly opaline, with a little thickening. 
 The volume of the cord is variable. There is some- 
 times atrophy of the lumbar swelling, either when the 
 cervical swelling is normal, or with a diminution in 
 volume of the whole cord. Sometimes there is atrophy 
 of the dorsal and lumbar regions in the antero-lateral 
 columns on both sides, or on one ; or there may be indura- 
 tion of the lumbar swelling, or an alteration of colour of 
 the medullary tissue. The anterior roots are sometimes 
 healthy, but they are generally atrophied, and unequally, 
 according to the regions from which they spring. 
 Sections of cord show to the naked eye in some cases 
 the transparent gelatinous colour peculiar to sclerosis 
 of the nervous centres, or a distinct brown tint of the 
 two anterior cornua, with marked softening. Sometimes 
 the atrophy of the grey matter of the anterior cornua 
 or of the antero-lateral columns can be thus seen. 
 
 Under the microscope we find a dissemination of 
 lesions in the various regions of the cord. These lesions 
 are situated in the anterior cornua of the grey matter, 
 sometimes in the posterior commissure, but very rarely 
 in the posterior cornua. The main lesion is a striking 
 diminution in the volume of the anterior cornua of the 
 grey matter, especially transversely. The groups of 
 large motor cells in the anterior cornua have disappeared,
 
 286 INFANTILE PARALYSIS. 
 
 especially the internal group. The motor cells which 
 remain are altered. Their dimensions are reduced 
 in every way ; the prolongations of the cells being gone, 
 some cells have no nucleus, or one smaller than normal. 
 The nucleolus is not always present, and its colour is 
 often changed. Between the nucleus and the walls of 
 the nerve corpuscles there is often a mass of ochrey 
 pigment. 
 
 The neuroglia is often condensed, but it may be in 
 just the opposite condition, or else the reticulum is 
 crowded with nuclei, which are much more numerous 
 than in the parts that have remained healthy. 
 
 The vessels may not be appreciably altered, or else 
 the lymphatic sheath of the vessel may be the seat of 
 proliferation of the nuclei, or of crystals of haamatoidine 
 and masses of granular bodies. On sections the lumen 
 of the small arteries may be seen to be obstructed by 
 many granular bodies. These granular bodies may be 
 numerous when the cells are little altered, or, on the con- 
 trary, very few may be seen when the cells of the anterior 
 cornua are gone. Spots of softening are sometimes 
 found near the vessels ; the myeline may be broken up 
 in a state of small globular masses. The consistence of 
 the tissue is variable. The granular bodies of ordinary 
 softening are seldom found. These spots are never 
 surrounded by any thickened wall or limiting membrane, 
 as is often seen round spots of inflammatory softening. 
 Some observers have remarked spots of red softening 
 due to real myelitis surrounded by sclerosed tissue. 
 
 Hasmorrhagic spots or pigment, the result of old 
 haemorrhage, are occasionally among the medullary
 
 INFANTILE PARALYSIS. 287 
 
 lesions of infantile paralysis. Sometimes in the pos- 
 terior cornua there is a partial or complete disap- 
 pearance of the cellular group that constitutes the 
 vesicular columns of Lockhart Clarke, either in the 
 cervical or in the dorsal and lumbar regions. 
 
 The posterior commissure is sometimes traversed 
 by a dense fibroid tract. In the white matter there may 
 be an atrophy of the antero-lateral bundles only, either 
 partial or general, due to sclerosis ; but sclerosis may 
 occur here without any atrophy. Or atrophy may be 
 caused by extreme diminution in the volume of the 
 axis cylinders. The nerve-tubes which go from the 
 anterior cornua, and traverse the white bundles to 
 become the anterior roots of the spinal nerves, may be 
 attacked by sclerosis ; and many amyloid bodies are 
 found about these tubes. 
 
 The granular bodies and the alterations of the 
 vessels described as existing in the grey matter are 
 here met with equally. 
 
 The anterior roots have been found healthy ; or 
 they may be reduced to the axis cylinders, the myeline 
 having disappeared ; or the thin nerve-tubes may be 
 separated by spaces filled with connective tissue. 
 
 Other lesions are found in the body. 
 
 1. The bones. There may be considerable diminu- 
 tion in their length and volume. The femur may be 
 only the size of the humerus in the same subject. Luxa- 
 tions are common. The extremities of the limbs are 
 pretty often considerably deformed. The cartilages 
 lining the joints may be rough and granular. The 
 epiphyses are of small volume, owing to arrest of
 
 288 INFANTILE PARALYSIS. 
 
 development. The atrophy of the bones bears no neces- 
 sary relation to the extent of the muscular paralysis. 
 
 2. The muscles are generally in a state of fatty 
 atrophy, or even of simple atrophy ; or they may be 
 granular and fatty, or with proliferation of the nuclei 
 of the myolemma. The atrophy may not be imme- 
 diately apparent, because the aponeuroses may be 
 distended by fat. The muscles, on the other hand, may 
 be healthy. When muscular disease is met with, the 
 most common seat is of the antero-extensors of the 
 leg, seldom of the foot ; the thigh is affected less often 
 than the leg ; when it is, the muscles of the anterior 
 region are chiefly attacked. Sometimes the psoas and 
 iliacus, the intercostals, and the muscles of the trunk 
 may be implicated ; very seldom the muscles of the 
 neck. The temporal muscle on one side of the face 
 has been affected, but this is rare. In the upper 
 extremity the extensors of the arm are generally first 
 attacked, especially the deltoid, but sometimes the pec- 
 torales, the triceps, and the muscles of the thenar and 
 hypothenar eminences. 
 
 3. The vessels that run to the atrophied part are 
 sometimes diminished in volume, and occasionally 
 sclero-atheromatous. 
 
 4. The peripheral nerves show some rarefaction 
 of the nerve-tubes and increase of the connective 
 tissue, or atrophy of the fibres, with proliferation of 
 nuclei in the midst of these fibres. 
 
 The weight of authority is now tolerably united on 
 the lesions of the spinal cord in infantile paralysis. 
 
 Heine (1840) and Duchenne (1855) referred its 
 origin to the spinal cord, though they had no patho-
 
 INFANTILE PARALYSIS. 289 
 
 logical evidence of disease in tlie latter. Boiicliut, 
 however, placed the anatomical seat of the lesion in 
 the muscles, and the disease among the muscular 
 paralyses. Cornil, in 1863, and with Laborde in the 
 following year, gave the residt of their anatomical in- 
 vestigations ; their example ^vas followed by Prevost 
 and Vulpian in 1865, Olivier in 1869, Charcot and 
 Joilroy in 1870, and Parrot in 1871. Later still 
 Damaschino and Eoger have recorded tliree cases with 
 autopsies. They state that the changes in the muscles 
 were of the ordinary character, consisting of fatty and 
 fibroid degeneration of the fibrillar. In the spinal 
 cord they found the same lesions of the grey sub- 
 stance and the anterior and lateral columns differ- 
 ing in the three cases only in its seat ; in the first 
 case lesions existed in two places, the cervical and 
 lumbar enlargements ; in the second, chiefly in the 
 latter position ; and in the third case, in the same 
 region, but on both sides. The microscope revealed 
 changes in the vessels, thickened walls, proliferation of 
 their nuclei, atrophy of the ganglion cells and their 
 processes, as well as of the nerve-fibres. There was 
 also thickening of the connective tissue, especially 
 marked in the third case. These facts lead these 
 observers to the conclusions that the lesion of the 
 spinal cord is essential and primary, and that the 
 pathological appearances found justify their use of 
 the term spinal infantile paralysis. The lesion they 
 consider to be a myelitis, especially of the anterior 
 grey substance, of which tlie atrophy of the nerves and 
 muscles is the consequence. Einecker gives the autop- 
 
 u
 
 290 INFANTILE PARALYSIS, 
 
 sies of two cases. In the second of the two. the ante- 
 rior and lateral columns, as well as the nerve-fibres 
 and gangha, were atrophied, and in both the peri- 
 pheral nerves. Rosenthal, instead of looking upon the 
 atrophy of the nerve-cells as the primary cause, con- 
 siders the dilatation and thickening of the vessels 
 which he has observed, and which are the signs of an 
 active participation of the latter, as a pathological 
 process, which results further in secondary growth and 
 destruction of the grey substance. 
 
 Feeling convinced, as I do, that infantile paralysis 
 is due to lesion of the spinal cord, it is only fair to 
 state that cases are on record in which no lesions can 
 be found. Dr. Carl Ketli gives the history of a child 
 who died of small-pox six months after the onset of 
 paralysis. Professor Schenthauer undertook the micro- 
 scopical examination of the spinal cord, which he found 
 to be perfectly natural. Dr. Elischer examined the 
 paralytic muscles Avith the following results : They 
 showed two forms of pathological change, namely, fatty 
 degeneration and a change which came nearest to 
 colloid degeneration. The sarcolemma and nerves were 
 not altered. In the striated muscles, instead of the 
 single normal cell-nucleus, there were seen three or 
 four granular cell-nuclei, which seemed to be at the 
 same time enlarged, and contained two, three, or even 
 more nucleoli. The contractile material was diminished, 
 so that it did not fill out the sheath, but drew away 
 from it. This atrophy was so great that at the upper 
 and under part of the spindle-shaped cell-nucleus of 
 the sheath there was hardly to be found a breadth of
 
 INFANTILE PARALYSIS. 291 
 
 •002 milKmetre of cross-striped contractile muscular 
 substance. Ketli thinks that these appearances point 
 to an idiopathic muscular lesion, to peripheral and not 
 central changes, as being the cause of the paralysis. 
 
 This and similar cases, however, may be explained 
 on the view that the structural lesions were not found 
 because they had not yet been formed. The child 
 died of small-pox after having only for six months 
 been subject to the paralysis. The lesions would very 
 likely have only been dilatations of vessels, even if the 
 child had not decidedly improved before it was taken 
 with small-pox, of which we have no record. 
 
 Paralysis Agitans. — Although I have somewhat 
 recently lost a case of paralysis agitans of long stand- 
 ing, death occurring from cerebral hsemorrhage, I have 
 never had an opportunity of post-mortem examination 
 in this disease ; you must trust, therefore, to the obser- 
 vations of others. In some cases, generally those before 
 middle age, recovery has taken place ; and although 
 the symptoms are in most respects similar, the pathology 
 must differ from the cases of paralysis agitans that 
 Trousseau well calls ' senile trembling.' 
 
 Jaccoud's remarks on the pathological anatomy are 
 as follows : ' In certain cases the autopsy has show^n no 
 important alteration of the nervous centres even where 
 there has been microscopical examination ; in other and 
 more numerous cases there has been observed general 
 or diffuse induration (sclerosis) of the medulla oblongata, 
 the pons, the corpora quadrigemina, sometimes also 
 
 V 2
 
 292 PARALYSIS AGITANS. 
 
 of the cervical region of tlie cord, especially of the 
 lateral columns. Various alterations have been met 
 with besides, such as lacimge in the raeso-cephale, 
 softening of the crura cerebri, simple rarefaction of 
 nerve-tubes in the cord. In a case in which the 
 symptoms of paralysis agitans had been confined to a 
 right upper hmb, the left optic thalamus was the seat 
 of a sarcoma the size of a large nut. The inconstancy 
 of these lesions, in the double point of view of their 
 existence and their nature, takes away from them all 
 specific character. Paralysis agitans is certainly a 
 disease of the meso-cephale ; but it is a neurosis, that 
 is to say, a disease without any constant and uniform 
 anatomical characteristics. Practically, however, it is 
 of importance to remember that sclerosis of the 
 meso-cephale is the alteration most frequently connected 
 with this neurosis,' Drs. Murchison and Cayley record 
 a case of paralysis agitans in which the spinal cord was 
 examined after preparation. The cortical and connec- 
 tive tissue layer of the cord appeared thickened, and 
 presented an increased number of nuclei. Irregular 
 tracts and patches of connective tissue, thickly 
 nucleated, passed from the cortical layer into the sub- 
 stance of the cord, the reticulum of which was much 
 thickened. These patches were most frequently met 
 with near the exit of the posterior roots of the nerves, 
 which themselves did not appear altered. The place of 
 the central canal was an oval tract, crowded with cells 
 of various shapes and sizes, the majority having the 
 character of leucocytes, none presenting the character 
 of the normal epithelium of the canal. This oval tract 
 occupied not only the site of the canal itself, but also
 
 PARALYSIS AGITANS. 293 
 
 that of the surrounding central substantia gelatinosa. 
 The capiUaries of the grey matter, and to a less extent 
 of the white, were distended with blood, and here and 
 there were small points of extravasation. Tlu^ougli the 
 whole cord, chiefly in the grey matter, were small de- 
 posits composed of leucocytes or exudation cells. The 
 first three changes were due to a chronic, the last two 
 to an acute process. 
 
 Joffroy's account of the morbid changes in these 
 cases is very similar. In all there was proliferation of 
 the epithelium completely filling up the central canal, 
 great proliferation of nuclei in the neighbourhood of 
 tlie ependyma, pigmentation of the nerve-cells, espe- 
 cially of those of Clarke's columna vesiculosa, and a 
 large quantity of amyloid corpuscles. In the third case 
 there was a sclerotic patch of connective tissue in the 
 neighbourhood of the pons, with dilated vessels. The 
 conclusion to which the writer comes is that the seat 
 of the lesion in paralysis agitans is to be looked for in 
 the cord. 
 
 In Oppolzer's case, quoted by Trousseau, the post- 
 mortem appearances were as follows : — There was 
 pneumonia of the right lung, and it is interesting that 
 in Trousseau's three cases death had occurred from 
 pneumonia. This coincidence is, however, only what 
 is so frequently found in the subjects of chronic 
 cerebral disease. The cranial bones were very thin, 
 and their inner surface was rough. The dura mater 
 was thickened, and adherent, here and there, to the 
 inner table of the cranial vault ; the pia mater opaque, 
 and infiltrated with serosity ; there was also a pretty 
 large quantity of serosity in the subarachnoid cellular
 
 294 PARALYSIS AGITANS. 
 
 tissue. The cerebral convolutions were thinner, the 
 sulci between them seemed deeper than usual, the 
 cortical substance was of a pale brown colour, while 
 the medullary was perfectly white and traversed by 
 dilated vessels ; the cerebral substance was moist and 
 of good consistence. The ventricles contained several 
 drachms of transparent serosity, and the ependyma, 
 principally on a level with the posterior cornua, was 
 granular. In the substance of the right optic thalamus 
 there was an apoplectic cyst of the size of a small 
 bean, the walls of which contained pigment. The 
 pons Varolii and the medulla oblongata were very 
 manifestly indurated. The spinal cord was firm, and 
 the medullary substance of the lateral columns, prin- 
 cipally in the lumbar region, presented opaque grey 
 strio3. On making a microscopical examination, there 
 was found in the substance of the pons and of the 
 medulla oblongata an abnormal production of con- 
 nective tissue, accounting for the induration of those 
 parts. The opaque stria3 in the lateral columns of the 
 cord were due to the presence of connective tissue in 
 process of development. 
 
 Handheld Jones says that Stofella relates the case 
 of a man, aged seventy-nine, who had the affection live 
 years before his death. At the autopsy he found 
 traces of atrophy of the brain, with secondary dropsy 
 of the ventricles and of the cerebral membranes, and 
 an apoplectic cyst the size of a pea in the right optic 
 thalamus; the pons Varolii and medulla oblongata 
 were remarkably stiff; the arteries at the base cal- 
 careous, and the laleial columns of the cord, especially
 
 PARALYSIS AGITANS. 295 
 
 in the lumbar region, traversed by greyish opaque 
 streaks, which, as well as the indurations in the pons 
 and the medulla, resulted from embryonal connective 
 tissue. 
 
 Of two autopsies recorded by Cohn, there was 
 marked cerebral atrophy in one, and in the other 
 wasting of the cord opposite the second cervical vertebra. 
 The ages of the patients were forty-nine and seventy- 
 four. 
 
 In Skoda's case, the brain was tough, the pia 
 mater oedematous, the walls of the ventricles, the 
 fornix, pons Varolii, medulla oblongata, and cord were 
 remarkably stiff; both optic nerves were flattened and 
 stiff. In some opaque reddish spots in the brain, the 
 nerve-tissue was destroyed by embryonal connective 
 tissue, which occasioned also the induration of the 
 pons and medulla. The muscles were very fatty, the 
 neurilemma of the nerves of the upper limbs was 
 thickened. 
 
 It is worthy of remark that the tremor precedes 
 the paralysis in point of time. At first in very many 
 cases there is no absolute loss of motor power. Indeed 
 the muscular power may be considerable. It is only 
 later on that paralysis supervenes. This is important 
 in connection with the observation that before middle 
 life some of these cases are curable, even when not 
 dependent on mercurial poisoning. It is impossible 
 that in such cases sclerosis of any part of the brain or 
 cord can have existed. The symptoms in such cases 
 must be due to some abnormahty of circulation, which 
 may disappear under suitable treatment. Some dc-
 
 296 PARALYSIS AGITANS. 
 
 rangement of the nutrition of the nerve-cells, either 
 from some abnormality of the blood itself or of the 
 vessels, or some condition of the nerve-cells preventing 
 proper assimilation of nutritive material from the 
 blood, must obtain in these cases ; and, as we have 
 seen in other diseases of the nervous system, lesions 
 recognisable after death are only produced by one or 
 more of these abnormalities being prolonged beyond a 
 certain time, and the nutrition being thereby materially 
 and persistently affected. 
 
 That paralysis may depend upon an abnormal 
 condition of circulation in the nervous centres, and 
 may be recovered from when this is removed, is seen 
 in spinal paralysis depending on congestion of the 
 spinal cord ; and tremor is so closely connected with 
 paralysis, and is so often followed by it, that it is not 
 straining analogy too far to believe in a similar cause 
 in varying degree inducing both conditions. 
 
 But in cases that have gone too far for cure we 
 may be pretty sure we shall find sclerosis of the meso- 
 cephale, and generally of some portions of the spinal 
 cord. 
 
 This will probably explain the reason for MM. 
 Bourneville and Guerard drawing the distinctions they 
 do between paralysis agitans and cerebro-spinal sclerosis. 
 A patient may recover from paralysis agitans, or may 
 die with it, and no lesion be found ; but if life is pro- 
 longed, lesions will be gradually induced, and these 
 generally in the form of partial and scattered indura- 
 tions. These observers are, however, right in saying 
 that nystagmus (oscillation of the eyeballs) seldom, if 
 ever, occurs in paralysis agitans.
 
 LEAD PALSY. 297 
 
 Lead Palsy. — In lead-poisoning we may meet with 
 the well-known symptoms of colic, with an aggravated 
 dyspepsia, "svith auasmia, with cerebral phenomena 
 taking various forms, manifesting themselves either as 
 delirium, convulsion, or coma ; neuralgia followed 
 by paralysis of nerves or of parts of nerves, and of those 
 nerves that supply the extensor muscles sooner than 
 those which supply the flexors, as in wrist-drop ; and, 
 as a sequence of this paralysis, considerable atrophy of 
 the muscles themselves. 
 
 In certain cases, before paralysis occurs, we find 
 partial or general tremor, that is, tremor of groups of 
 muscles, or of one limb, and tremor of all the limbs and 
 even of the whole body. 
 
 Sometimes also amaurosis is met with, depending 
 upon optic neuritis, or on atrophy of disc. 
 
 The brain is pale and soft, the convolutions wasted, 
 the sulci wide, with serous fluid distending them, and 
 separating the pia mater and the brain. Sometimes 
 there are patches of white softening in the brain. We 
 meet also with oedema of the brain leading to capillary 
 anaemia from pressure ; though this result is doubtful. 
 There may be some periarteritis. Lead has been found 
 in the brain. 
 
 The ganglia of the sympathetic have been found in 
 a state of sclerosis. The nerves themselves are some- 
 times seen surrounded by small particles of lead, 
 compressed, and with their nutrition interfered with 
 and more or less atrophied. 
 
 I believe the nerves of the limbs are sometimes in 
 a state of neuritis. This condition has been seen in
 
 298 LEAD PALSY. 
 
 the retina in lead-poisoning. Dr. E. Meyer has 
 recorded the cases of two sisters employed at Brussels 
 in bleaching lace with the aid of white lead. In the 
 first case the girl was attacked by colic at the age of 
 nineteen, and afterwards became hemiplegic on the 
 right side. From this she perfectly recovered, but her 
 sight gradually failed, and in the course of four months 
 she became perfectly blind. When the author first saw 
 her the optic discs were in a state of complete white 
 atrophy. The second sister, when twenty years old, sud- 
 denly fell down unconscious, and was convulsed. On 
 recovery her mind was confused and her speech embar- 
 rassed. Another attack occurred a few hours later, and 
 was followed by deep sleep. On awaking she complained 
 of severe headache, and of a constantly thickening mist 
 before her sight. On the day following she described 
 herself as being blind, but when Dr. Meyer visited her 
 two days later she could see the glimmer of a lamp two 
 yards distant. The field of vision, tested by means 
 of two candles, was considerably but irregularly con- 
 tracted. The pupils were largely dilated. The 
 ophthalmoscope showed the optic discs much swollen, 
 elevated, opaque, and of a reddish-grey colour. The 
 retina near the disc was opaque ; the veins were large, 
 fiexuous, and deeply coloured ; the arteries fine. The 
 conditions were those described by Von Grafe as due 
 to neuritis, from obstruction to the circulation by con- 
 striction in the sclerotic ring. 
 
 Kussmaul and Maier have recorded a case of a 
 house-painter who, with many symptoms of chronic 
 lead-poisoning, yet had no paralysis or brain symptoms.
 
 LEAD TALSY. 299 
 
 The post-mortem appearances seen are, however, 
 very instructive: ' General and great emaciation ; marked 
 riijor mortis of the muscles and heart nineteen hours 
 after death ; a certain amount of jaundice ; great 
 catarrh of the stomach, intestines, and ductus chole- 
 dochus ; fatty degeneration of the glands of the stomach : 
 slight fatty change of the muscular walls of the stomach, 
 especially at the pylorus ; atrophy of the mucous 
 membrane of the jejunum, ileum, and upper part of 
 colon, in which both the stroma and glands shared ; 
 atrophy of the intestinal villi, the glands of Lieberkiihn, 
 the solitary glands, and Peyer's patches ; marked 
 development of the submucous tissue of the stomach, 
 and even more so of that of the intestines, from pro- 
 liferation of the areolar tissue, and thickening of the 
 sheaths of the vessels ; this was shown especially in the 
 smaller arteries in the narrowing of their calibre, caused 
 by the large amount of fat cells deposited in the dis- 
 tended network of this layer ; fatty degeneration of the 
 muscles of the intestines, especially in the small intes- 
 tines ; pigmental degeneration of the muscular fibres 
 of the heart. The brain, especially in its cortical 
 substance, showed slight periarteritis ; there was pro- 
 liferation and sclerosis of the connective tissue septa of 
 the small ganglia of the sympathetic, especially the 
 caihac and the cervical ; these glands were hard, and 
 the circulation in them affected, and their nerve-cell 
 elements diminished. The author considered that the 
 changes found in the absorbent apparatus account for 
 the chronic dyspepsia, the anaemic colour, and the mal- 
 nutrition of the patient.'
 
 300 LEAD PALSY. 
 
 These lesions account for many of the ordinary 
 phenomena. 
 
 Besides these lesions, in experimental researches 
 upon dogs, in chronic lead-poisoning the bones con- 
 tained the largest quantity of lead, next the liver and 
 the kidneys. 
 
 Heubel attributes the rapid atrophy of the muscles 
 in lead-poisoning to general interference with nutrition, 
 which lead causes in a marked degree, and partly to 
 the paralysis itself, which he attributes to the direct 
 action of the poison on the intra-muscular ends of 
 the nerves, and not on their central ends. 
 
 A complication not unfrequently met with in lead- 
 poisoning, but only indirectly connected with it, is 
 granular degeneration of the kidney. It is so common 
 an accompaniment that some physicians have con- 
 sidered the cerebral phenomena to depend upon uremia. 
 Still it has been easy to disprove this, since these 
 symptoms have occurred without the presence of albu- 
 men in the urine ; and such cases have shown after 
 death no granular degeneration. But the frequency 
 of the occurrence of this renal disease is very remark- 
 able, and has an important bearing on the true 
 pathology of lead-poisoning. 
 
 I am bound to tell you that the presence of lead 
 in the various organs is not sufficient to account in any 
 direct manner for the phenomena. I have no hesita- 
 tion in saying that the cerebral atrophy, the cerebral 
 auEemia, or the somewhat rare cases of cerebral soften- 
 ing, cannot owe their origin to the presence of lead in 
 the brain. There must be some other cause, some-
 
 LEAD PALSY. 301 
 
 thing more directly affecting tlie nutrition, than such a 
 lesion as this. 
 
 Other phenomena of lead-poisoning point in the 
 same direction. It is well known tliat women who 
 work in lead manifest a great tendency to abort ; and, 
 what is far more remarkable, if a man, the subject of 
 lead-poisoning, begets a child, such a foetus is compara- 
 tively unlikely to arrive at perfection. In fact, the 
 impregnated ovum passes away as an abortion, if either 
 parent is the subject of lead-poisoning. This surely 
 cannot be explained by the mere [)reseuce of lead in 
 this or that organ. Neither can the atrophy of the 
 gastric and intestinal glands be explained on any 
 ground, except that of a deteriorated blood. Still less 
 can the frequent complication of gout. A very large 
 proportion of workers in lead die of kidney disease ; 
 a very large proportion of those who thus die have 
 been attacked with gout. Gout associated with lead- 
 poisoning seems to have a special affmity for the 
 kidneys ; whilst gout associated with alcoholic excess 
 will generally attack the joints. 
 
 The lesions in the brain, therefore, the atrophy of 
 the gastric and intestinal glands, the granular degene- 
 ration of the kidneys, the tendency to abortion, the 
 frequent coexistence of gout, all point to one and the 
 same idea — that the blood is first injured by the lead- 
 poisoning, and that most of the lesions above mentioned 
 are due to abnormalities of nutrition, owing to this 
 alteration of the blood. 
 
 That whicli has seemeil necessary theoretically for 
 the reasonable explanation both of the lesions and of
 
 302 LEAD PALSY. 
 
 the morbid phenomena has received important con- 
 firmation by the observations of M. Malassez. He 
 states that M. Andral long ago pointed out that the 
 blood of patients suffering from lead-poisoning was 
 deficient in red corpuscles. M. Malassez has, how- 
 ever, taken the trouble in eleven instances to count 
 the absolute number of red corpuscles, and he finds 
 that whilst men in good health have on the average 
 4,500,000 and women 3,500,000 red corpuscles in a 
 cubic millimetre of their blood, the number fell in nine 
 men affected with symptoms of saturnine spanasmia to 
 3,700,000, to 3,200,000, and even in one case to 
 2,200,000 ; whilst in two women the numbers were 
 2,900,000 and 2,500,000 respectively. M. Malassez 
 further states that, if the red corpuscles are less nume- 
 rous, they are more voluminous than natural in lead- 
 poisouing, in the proportion of nine to seven. Never- 
 theless he estimates that the increase of volume is not 
 sufficient to compensate for the diminution in number. 
 If the augmentation in the size of the corpuscles has 
 some advantage in compensating to a certain extent 
 for the diminution in number, it has probably the 
 opposite effect of rendering the blood less fluid, since 
 the corpuscles would necessarily pass more slowly in 
 capillaries but little larger than themselves, and would 
 hkewise occupy time in adapting themselves to curves 
 and angles. He sums up the results of his observa- 
 tions : that saturnine intoxication causes a certain 
 number of alterations in the blood, of which the prin- 
 cipal are diminution in the number of the corpuscles, 
 augmentation of their size — such increase being, how-
 
 LEAD PALSY. 303 
 
 ever, insufficient to compensate for their diminution in 
 number — a great fixity of their morphological elements, 
 and finally, very probably a diminution in the circu- 
 latory activity. 
 
 Consult, for progressive muscular atrophy — 
 
 Jaccoud, ' Path, interne.' 
 
 Trousseau, ' Clin. Lect.,' and note by Dr. Bazire. 
 
 Roberts on * Wasting Palsy.' 
 
 Reynolds, ' Syst. of Med.' Dr. Roberts. 
 
 Dr. Duchenne, 'Atlas of Photographs.' 
 
 ' Med. Chir. Trans.,' li. ct Ivi. Lockhart Clarke. 
 
 ' New Syd. Soc. Yearbook,' 18G:.>, p. 103. 
 
 ' Med. Record,' i. 10. M. Gombault. 
 
 Ibid., i. 54. Lockhart Clarke. 
 
 Consult, for locomotor ataxy — 
 
 Trousseau, ' Clin. Lect.' 
 
 Hammond, ' Dis. of Nervous System.' 
 
 Jaccoud, ' Path interne.' 
 
 Reynolds, ' Syst. of Med.' Dr. Radclitfe. 
 
 < St. George's Hosp. Rep.,' v. 1. Lockhart Clarke (and pamphlet). 
 
 * Journal of Mental Science,' Jan. 1874. M. Charcot. 
 
 ' Guy's Hosp. Rep.,' xvii. Dr. Wilks. 
 
 ' West Riding Asylum Rep.,' i. Dr. Nichol. 
 
 'Path. Soc. Trans.,' xxii. 14. Drs. Greenhow and Cayley. 
 
 'Irish Hosp. Gazette,' March 15, 1874. Bouchut. 
 
 Consult, for infantile paralysis — 
 
 Petitfils (monograph). 
 
 Reynolds, ' Syst. of Med.' Dr. RadclifTe. 
 
 Jaccoud, 'Path, interne.' 
 
 Hammond. Op. cit. 
 
 West, ' Dis. of Infancy and Childhood.' 
 
 Hillier, ' Dis. of Children.' 
 
 * New Syd. Soc. Yearbook,' 1871-2, p. 90, Daniaschino and 
 
 Roger. 
 'Med. Record,' i. 102. Vulpian. 
 Ibid., i. 424. Ketli.
 
 304 LEAD PALSY. 
 
 Consult, for paralysis agitans — 
 Trousseau, 'Clin. Lectures.' 
 Jaccoud, * Path, interne.' 
 
 Handfield Jones, ' Functional Nervous Disorders. 
 Reynolds, ' Syst. of Med.' Dr. Sanders. 
 Bourneville and Guerard, ' De la Sclerose.' 
 'Guy's Hosp. Kep.,'xvii. 191. 
 'Path. Soc. Trans.,' xxii. 24. 
 ' New Syd. Soc. Yearbook,' 1871. 98. Jollroy, 
 
 Consult, for lead palsy — 
 
 Hammond, 'Dis. of Nervous System.' 
 
 Reynolds, ' Syst. of Med.' Dr. Sanders. 
 
 Romberg, 'Dis. of Nervous System.' 
 
 Jaccoud, 'Path, interne.' 
 
 ' Lancet,' May 16, 1874. M. Malassez. 
 
 ' New Syd. Soc. Yearbook,' 1871-2. Kussmaul.
 
 305 
 
 LECTUEE XL 
 
 EPILEPSY. 
 
 It was an old saying of Van Swieten : ' Dum viso 
 epileptico tenitns homo corripitur eodem morbo, qiiis 
 definire audebit quid tunc mutatuui fuerit in corpore.' 
 
 With all our better means of research, we must 
 confess at the present moment that the pathology of 
 epilepsy is still very uncertain, whilst the pathological 
 anatomy is simply confusing. Let us try to reach light 
 out of so much obscurity ; and, first, we will mention 
 the lesions that have been found post mortem in 
 epileptics. 
 
 For instance, all parts of the brain have been found 
 to be the seat of lesions of the most varied kind : 
 foreign bodies developed on the meninges, in the ven- 
 tricles, in the cerebral substance ; increase of sub- 
 arachnoid fluid, or distension of the ventricles by 
 serum ; induration, softening, and general swelling of 
 the cerebral mass ; general or partial hypersemia, 
 cysts, tubercles, cancers, exostoses, periosteal growths, 
 thickening, or some change of the arachnoid or the 
 pia mater ; abnormal thickness or abnormal thinness 
 of the cranial bones ; excessive size of head, increase 
 in the volume of the cranial cavity, deformities, or 
 abnormality lu the conformation of this cavity ; canes 
 
 X
 
 306 EPILEPSY. 
 
 of the cranial bones ; pus between the bone and 
 the dura mater ; acute or clironic hydrocephalus ; 
 hydatids ; ossification of the dura mater, tubercle of 
 the dura mater, or pachymeningitis, i.e. inflammation 
 of the dura mater ; abscess in the cerebral tissue, spots 
 or regions of haBmorrhage ; various traumatic lesions ; 
 alterations of the pineal gland ; inequality in weight 
 and size of the cerebral hemispheres ; various lesions 
 connected with blood-vessels, 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 an£emia, &c. &c. Almost every abnor- 
 mality of the viscera in the other cavities of the body 
 have been found in epileptics. They may show after 
 death many lesions of heart and lungs, of tlie digestive 
 and urinary system, and, perhaps, especially of the 
 organs of generation. Every variety of blood may 
 coexist with epilepsy ; sanguineous plethora, gout, 
 ansemia, spansemia, after prolonged discharges, &c. ; and 
 although it may not be recognised post mortem, epilepsy 
 may depend upon malaria, possibly from tlie hydrsemia 
 induced by malaria. 
 
 Dr. Crichton Browne concludes tliat hypertrophy 
 and induration are the characteristic brain changes in 
 epileptic insanity, ' The first effect,' he says, ' of the 
 interrupted pressure which is applied to the brain in 
 epilepsy, appears to be a genuine hypertrophy and 
 augmentation in volume. But hypertrophy is generally
 
 EPILEPSY. 307 
 
 partial, and even when it affects whole organs it is 
 manifested principally in certain textures ; so this 
 hypertrophy of brain in epilepsy is seen chiefly in the 
 connective tissue. A kind of fibroid substitution 
 slowly, but surely, goes on in those parts which are 
 periodically subjected to congestion, and induration, 
 as well as an augmentation in volume, ensues. The 
 skidl becomes thickened, and when it is removed 
 the brain expands, as if relieved from compression, and 
 feels unusually dense and haitl when touched. The 
 specific gravity both of its grey and white matter is 
 greater than in any other class of lunatics, and the 
 absolute weight of the brain is also decidedly higher. 
 The convolutions are flattened, and the sulci are mere 
 lines, and do not gape or contain fluid. The mem- 
 branes show no signs of inflammatory disturbance. 
 When the brain is cut into it is tough and firm, the 
 grey matter being dark, and the medullary white and 
 glistening. The ventricles are of small size. Around 
 the pons Varolii and medulla oblongata, and especially 
 on the floor of the fourth ventricle, redness and vas- 
 cular dilatation are visible, and the vessels when mea- 
 sured are found considerably distended, owing both to 
 increase in their sectional area and thickening of their 
 walls. These are the usual appearances in the brains 
 of persons who have laboured under epileptic insanity, 
 but they are subject of course to numerous variations. 
 Thus a spotty, blotchy, marbled appearance of the 
 medullary substance may be seen when an attack or 
 group of attacks has innnediately preceded death, and 
 some atrophy or wasting, with opacity of the arach- 
 
 X 2
 
 308 EPILEPSY. 
 
 noicl, may be remarked when the disease has been 
 long protracted, and has passed into epileptic stupor. 
 This latter condition of the brain is referable to im- 
 paired nutrition, owing to the thickening of the vessels, 
 or to gradual contraction of the hypertrophied fibrous 
 tissue and puckering of the brain, if it may be so 
 termed.' 
 
 And Dr. Crichton Browne also shows the true 
 part played by pathological anatomy in this disease, 
 when he says : ' With the clue that hes ready at hand 
 in these coarse organic changes, we may proceed back- 
 wards to finer and less perceptible changes connected 
 with earlier stages in epileptic degeneration ; and from 
 these, again, we may cautiously recede to those deli- 
 cate and subtle changes which lie beyond our present 
 means of exploration, and which are contemporaneous 
 with what may be termed the functional epoch in tlie 
 history of the disorder,' 
 
 Plate 16 shows a section of the medulla oblongata 
 in a case of epileptic mania. In part of the field is seen 
 a very dilated vessel. But the main lesion is a saccu- 
 lated lacuna, caused by localized softening and absorp- 
 tion of the softened tissue. 
 
 In the report of the Somerset County Lunatic Asylum 
 for 1864, Dr. Boyd gives the results of his observations 
 upon 53 fatal cases of epilepsy. The shape and form of 
 the skull presented an abnormality only in one case, in 
 which it was thick behind, and the diploe wanting. In 
 nearly one-third there was a difference in the weight 
 between the cerebral hemispheres of from ^ to 6 ounces. 
 Of the males 21 were epileptics only, and in them the
 
 E.L.Fr)x,M,D, 
 
 Plate 16, 
 
 C. Beriea-j. Litii 
 
 B^ji.'i i Co, him' 
 
 MEDULLA OBLONGATA IN EPILEPTIC MANIA,
 
 EPILEPSY. 309 
 
 average weight of tlie brain was 50* 3 ounces ; in 9 
 males who were epileptics and idiots the average weight 
 of the brain was 46*6 ounces ; in 2 only of the latter it 
 was below, but in G above the average. The average 
 weight of the left cerebral hemisphere in the males 
 was £-ounce greater than the right hemisphere. Of 
 the 23 females 20 were epileptics, and 3 epileptics and 
 idiots ; in the 20 epileptics the average weight of the 
 brain was 43'2 ounces, and the right cerebral hemi- 
 sphere was slightly heavier than the left ; in the two 
 idiots the brain was J-ounce less than the average natural 
 weight ; and in the third idiot, who died from cerebral 
 apoplexy, which would add to the weight, the brain 
 was 2 1 ounces heavier. 
 
 In 18 cases Messrs. Bouchut and Cazauvieilh found 
 a true chronic inflammation of the cerebral tissue as 
 the unifoi'Di lesion. 
 
 Wenzel's observations, accompanied by autopsies, 
 amounted to twenty. He said that the pituitary body 
 is invariably found diseased in epileptics, and the 
 morbid condition almost invariably consists in an 
 effusion of lymph which has become more or less 
 indurated at the point of junction of the two lobes. 
 Wenzel's opinion is that the slightest modifications of 
 the pituitary body have the most serious consequences 
 for the animal economy ; and that probably the diseased 
 state of the pituitary body in epilepsy is the result of 
 an inflammatory affection. But other observers have 
 failed to verify Wenzel's observations in most cases. 
 But after all, as Dr. Sieveking says, 'It is rather in its 
 vital relations that the disease deserves to be studied
 
 310 EPILEPSY. 
 
 than in the decad-house '; and here again Dr. Thomp- 
 son's observations of sphygmographic tracings show 
 something of the pathology of the disease. He finds 
 that the sphygmograph shows a lax condition of 
 vessels, just the condition that is shown post mortem in 
 the dilatation of the capillaries, especially in certain parts 
 of the encephalon. It is in this line of work that it is 
 possible to recognise the pathological conditions of 
 epilepsy at what may be called the functional period of 
 the disease. 
 
 Before we speak of the probable pathology of this 
 disease, let us look at the successive phenomena of an 
 epileptic fit. The following is the succession of cause 
 and effect according to Brown-Sequard : 
 
 1. Excitation of certain parts of the excitomotory 
 side of the nervous centre, leading to contraction of 
 the blood-vessels of the brain proper and of the face, 
 and spasm of some muscles of the eye and face. 
 
 2. Contraction of the blood-vessels of the brain 
 proper, leading to loss of consciousness and accumu- 
 lation of blood at the base of the encephalon. 
 
 3. Extension of the first excitation, partly due to 
 accumulation of blood at the base of the encephalon, 
 leading to tonic contraction of the laryngeal, cervical, 
 and thoracic expiratory muscles. 
 
 (Called by Marshall Hall laryngismus and trache- 
 lismus.) 
 
 4. Contraction of the laryngeal and thoracic expi- 
 ratory muscles, leading to crying and stoppage of 
 respiration. 
 
 5. Farther extension of the first excitation of the
 
 EPILEPSY. 311 
 
 nervous centre, leading to tonic contraction, extending 
 to most of the muscles of the trunk and limbs. 
 
 6. Loss of consciousness and tonic contraction in 
 the trunk and limbs, leading to folhng. 
 
 7. Laryngismus, trachelismus, and a fixed state of 
 the chest, leading to asphyxia, ^\dth obstruction to the 
 return of venous blood from the head and spinal 
 cavity. 
 
 8. Asphyxia and accumulation of black blood in 
 encephalon and spinal cord, leading to clonic con- 
 vulsions everywhere, contraction of the bowels, bladder, 
 and uterus ; erection, increase of many secretions, efforts 
 at inspiration. 
 
 9. Exhaustion of nervous power generally, and of 
 the reflex faculty specially, except for respiration, 
 which gradually becomes normal, leading to a cessa- 
 tion of the convulsions, and to coma or heavy sleep, 
 after which the patient complains of extreme fatigue 
 and headache. 
 
 There is some objection to the view that clonic 
 convulsion depends on the asphyxia and the accumula - 
 tion of black blood in the encephalon and spinal cord. 
 Brown- Sequard founds these views on some experi- 
 ments in which clonic convulsions were set up on 
 injecting venous blood into the system. It seems, 
 however, doubtful whether these experiments bear 
 out his conclusions. In Kussmaul and Tenner's ex- 
 periments, the prevention of the entrance of red blood 
 to the brain, when the veins were left perfectly free, 
 induced violent convulsions. Again, in an animal bled 
 to death, and in whom, therefore, no accumulation of
 
 312 EPILEPSY. 
 
 blood can have existed, tlie uterus expelled its contents 
 precisely in tlie same manner as in an animal into 
 whom venous blood had been injected. We would 
 say, therefore, that clonic convulsions depend on the 
 want of arterial blood in the spinal cord, caused partly 
 by the further extension into the spinal cord of the 
 first excitation (contraction of vessels), and partly by 
 the asphyxia inducing a condition of venosity through 
 the whole system. 
 
 If it is allowed that the loss of consciousness is 
 occasioned by arterial spasm in the cerebral lobes, and 
 that tonic rigidity and clonic convulsion are the con- 
 sequence of an arterial spasm, similar in kind, if not 
 in degree, in the medulla oblongata and spinal cord, it 
 is difficult to believe that in the first case the function 
 of the part is temporarily annihilated, whilst in the 
 second it is intensely exalted. It is scarcely reasonable 
 to suppose that the same condition which, when acting 
 on the brain, causes the destruction of all cerebral 
 functions, should, when acting on the spinal cord, cause 
 an intense exaltation of the spinal function ; nor can 
 we believe that a fresh supply of arterial blood, which, 
 acting on the brain, causes it to resume its functions, 
 would, when acting on the spinal cord, almost in a 
 similar ratio, lower and depress the functions of this 
 new centre, as would be the case if the cessation of the 
 convulsion were dependent on exhaustion of nervous 
 power. 
 
 In illustration of the theory that clonic convulsions 
 may be the consequence, not of excitation of a nervous 
 centre by venous blood, but rather of a diminished
 
 EPILEPSY. 313 
 
 supply of arterial blood, I would mention an experi- 
 ment performed by Vulpian, and recorded in liis 
 ' Lemons sur la Physiologie du Systeme Nerveux : ' 
 ' J'ai vu chez un lapin la compression des arteres 
 carotides et vertebrales determiner une suspension des 
 fonctions encephaliques ; mais, chose bien remar-quable, 
 la respiration spontanee continuait, le bulbe rachidien 
 ayant ecliappe plus ou nioins completement a ranasmie 
 encephalique. Les mouvements spontanes et reflexes 
 avaient entierement disparu dans la face et les yeux ; 
 le tronc de I'animal vivait encore en supportant une 
 tete physiologiquement morte. Eli bien, au bout de 
 doux ou trois minutes, les moyens de compression 
 ayant ete enleves, il se produisit d'abord des mouve- 
 ments convulsifs assez violents, qui ne durerent que 
 peu de temps ; puis toutes les manifestations de la vie, 
 tous les mouvements volontaires et autres reparurent 
 peu a peu dans le tete ; Tanimal recommen^a a marcher 
 et revint bientot a son etat normal.' Here tlie convul- 
 sions were the connecting link between apparent death 
 or paralysis of the muscles of the head and face and 
 their restoration to voluntary movement. Entire loss 
 of arterial blood from the part was followed by loss of 
 all movement; the very commencement of restored 
 arterial flow was followed by convulsion before the 
 full circulation was restored ; and a full restoration of 
 arterial circulation was the inunediate precursor of 
 normal life in the part. 
 
 Again, the explanation of these convulsive con- 
 ditions seems peculiarly difficult, if we accept the 
 theory that the accumulation of venous blood at the 
 base of the brain is necessary for their production.
 
 314 EPILEPSY. 
 
 The following case I saw very frequently for two 
 years : — 
 
 E. P., aged 61, a widow. Every day, and many 
 times a day, for six months before I saw her, she 
 suffered from a severe convulsive condition. She never 
 loses consciousness in the least, and does not even feel 
 confused ; but has most violent clonic convulsions of 
 the mouth, jaw, eyelids, and all the facial muscles. 
 The head is shaken from side to side with intense 
 rapidity; the arms and hands are in a similar state of 
 clonic convulsion. The legs are not always affected ; 
 and when they are not she is able to stand through the 
 whole of the attack. In all respects the convulsions of 
 this case closely simulated epilepsy. She had no tonic 
 spasm, no subsequent headache or drowsiness, no loss 
 of memory or of any mental faculty, no paralysis. 
 The absence of headache and sleepiness is a fair test of 
 there having been no venous congestion of the brain, 
 Eiom a condition of ordinary healthy life she was 
 w^ont to be taken with the intense clonic convulsion 
 previously described, and the moment the convulsion 
 ceased she was herself acjain. 
 
 The observation of all such cases seems to point to 
 partial arterial spasm of the spinal cord as the proxi- 
 mate cause of the convulsion. 
 
 Several cases of a similar nature are collected from 
 various sources in Dr. Eeynolds' work on epilepsy. 
 
 It is true enough that some tonic spasm may exist 
 and yet be very difficult of detection, and Trousseau 
 would seem to look upon its non-existence as aai im- 
 possibihty. He says ' the tonic always precedes the
 
 EPILEPSY. 315 
 
 clonic stage ; but the duration and violence of the 
 latter are by no means proportionate to the duration 
 and violence of the former. Thus, very violent clonic 
 movements often succeed a slight tonic contraction, 
 and reciprocally an excessively powerful tonic contrac- 
 tion may be succeeded by very moderate clonic move- 
 ments. Thus the length of the first stage is sometimes 
 so short, and the second stage comes on so quickly, 
 lasting for a more or less prolonged period, that an 
 observer who is not on his guard, or not very attentive, 
 might tliink that the convulsions were clonic at the 
 outset. From what I have said, this remarkable fact 
 follows, that the rigidity seems to be an essential obhga- 
 tory element of all convulsions. It is never absent, and 
 can even be alone present, whether it constitutes the 
 convulsion by itself, as in idiopathic contractions, or 
 whether the convulsion is incomplete, as in eclampsia, 
 where the clonic stage is absent, whereas clonic move- 
 ments never, perhaps, come on from the first.' 
 
 This is a strong statement. In the case before men- 
 tioned the woman has more tlian once been talking to 
 me in the out-patient room when the first symptoms of 
 the attack have commenced in rapid twitching of the 
 facial muscles, followed immediately by clonic convulsion 
 of the limbs ; and with the first twitching she has said, 
 ' Now, sir, the fit is coming on.' 
 
 It is difficult to conceive how any person could 
 speak with any laryngeal spasm sufficient to cause 
 cerebral congestion ; and if this venous blood theory 
 be right, how is it that the tonic spasm and the clonic 
 convulsion do not bear a direct ratio to each other ?
 
 31 G EPILEPSY. 
 
 A slight tonic stage should be followed by slight clonic 
 convulsion, instead of the two stages bearing, as they 
 often do, almost an inverse proportion to each other. 
 How, too, can the period of rigidity exist by itself, 
 unfollowed, as it sometimes is, by clonic convulsions ? 
 
 I would rather repeat my belief that clonic convul- 
 sion is an evidence of partial spasm at the base of the 
 brain and in the spinal cord ; that it plays no part in 
 the causation of the subsequent head-ache and stupor, 
 except by sometimes adding the element of exhaustion 
 when the convulsion has been very protracted ; and 
 that when the convulsion has followed the injection of 
 venous blood, it has been from this venous blood 
 inducing contiaction in the arteries, as the blood in the 
 exanthemata sometimes does. 
 
 Now with such a succession of phenomena, and 
 such an explanation of them, there are three kinds of 
 lesion for which we should search, both during the 
 life of the patient and at the autopsy. 
 
 1. The cause of the abnormal irritability of the 
 excitomotory system of nerves. 
 
 2. The excitants of the fit, which may be centric 
 or eccentric. 
 
 3. Lesions, the results of the fit itself. 
 
 To take this last point first. A very large number 
 of the lesions already mentioned come under this 
 heading, especially those that have been found in the 
 brains of insane epileptics. They may be divided for 
 practical purposes into two classes, viz., lesions that 
 depend on the mal-nutrition of the brain, consequent 
 on constant repetition of arterial spasm and the anosmia
 
 EriLEPSY. 317 
 
 induced by it ; and lesions, the direct result of conges- 
 tion and stasis, caused by the temporary aspliyxia from 
 the closure of the glottis and the tonic spasm of the 
 muscles of respiration. 
 
 Under the first heading we meet with atrophy and 
 white softening, with perhaps some increase of the 
 subarachnoid fluid and some fulness of the ventricles ; 
 under the second we meet with thickeninE^ of the 
 cranial bones, adhesion or ossification of the dura 
 mater ; pachymeningitis ; opacity of the arachnoid ; 
 haemorrhages from the vessels of the pia mater or in 
 various parts of the brain, general or partial induration 
 of the encephalon, absolute sclerosis depending on a 
 very gradual form of cerebri tis and persistent dilatation 
 of vessels. 
 
 The difficult problem to solve in this relation is 
 the reason why some epileptics escape these cerebral 
 lesions for many years. It is quite certain that they 
 may manifest no cerebral phenomena. Thus in a case 
 lately seen by me in consultation, a lady of 27 years 
 of age had had a severe fit almost every day of her 
 life since she was three years old, and yet she w^as able 
 to talk and reason as brilliantly as other people, her 
 memory was good, and she showed no abnormality 
 except irritability of temper. And this bad temper, 
 although it may be due to commencing lesion in the 
 brain, and culminate in a troublesome form of mania, 
 yet in many cases it is only the natural result of the 
 patient having to live so different a life from those 
 around him, and being cut off from a life of useful 
 occupation or anuisement. The variation in point of
 
 318 EPILEPSY. 
 
 time at wliicli such cases manifest cerebral lesion must 
 depend on the greater resilience of arteries in some than 
 in others, the vessel returning more easily and com- 
 pletely to its normal calibre and not becoming 
 persistently dilated so early. 
 
 It is in dkect accordance with the effects produced 
 on the brain by the arterial spasm on the one hand and 
 the temporary asphyxia on the other that we see the 
 different results of the petit mal and the grand mal. 
 In the former the fits may be very frequently repeated ; 
 and their constant repetition, meaning as it does fre- 
 quently repeated arterial spasm of part of the brain 
 and consequent anaemia, will produce a certain mental 
 weakness much more quickly than the ordinary attacks 
 of the grand mal. 
 
 These frequent slight fits interfere necessarily with 
 the nutrition of the brain. But the asphyxia is so 
 slightly marked and of so short a duration that the 
 after effects on the brain, congestion, meningeal, or 
 cerebral hosmorrhage, or inflammation, are absent. In 
 le grand mal, however, all this is changed. The brain 
 not only suffers from the arterial spasm and consequent 
 innutrition, but from the effects of prolonged tonic 
 spasm of the respiratory muscles ; and instead of mere 
 mental weakness we may meet with those cerebral 
 phenomena that are found with hyperasmia of the 
 cortical substance, or inflammation of some one of its 
 layers, or induration. That these results are only 
 induced gradually is because severe attacks of le grand 
 mal are not usually repeated many times in the same 
 day. Tlic attacks, if not more or less periodic, are
 
 EPILEPSY. 319 
 
 generally separated from each other by a definite time 
 — months, weeks, days, or at the least hours — whilst a 
 patient may have several attacks of le petit mal in a 
 single hour. 
 
 2. As to the excitants of the fit. This headincj 
 includes an infinite variety of lesions. It is difficult to 
 say how far abnormalities of the blood should be 
 included under this or under the first division. Ura3mia, 
 paludal poison, icterus, the presence in the blood of the 
 virus of any of the exanthemata may induce the lit. 
 The nutrition change of epilepsy may be a part of some 
 general metamorphosis, such as that present in the 
 several cachexia?, as rheumatism, gout, syphilis, struma ; 
 it may be induced by some circumstances determining 
 a relative excess of change in the medulla oblongata, or 
 perhaps in the cortical substance of the cerebral hemi- 
 spheres, during the general excess and perversion of 
 organic change occurring at the periods of puberty, 
 pregnancy, and dentition. The determining causes are 
 here also probably a lesion of the blood itself. 
 
 It may be induced by anything that either in- 
 creases the amount of carbonic acid in the blood, or, 
 as I think, that diminishes the normal proportion of 
 oxygen, such as various diseases of heart and lungs, 
 alcoholism, pressure on the large arteries that feed 
 the brain, &c. In children the mere presence of 
 an abnormally heated blood in the brain will lead to 
 epileptic phenomena. Undigested food in the stomach 
 or bowels, worms, renal calculus, gallstones, various 
 diseases of the liver, stomach, bowels, bladder, and very 
 specially of the uterus and ovaries, may all act as 
 exciting causes of epileptic phenomena.
 
 320 EPILEPSY. 
 
 Tlie fit may be induced by conditions acting on the 
 nervous centres directly, such as meclianical injuries, 
 overwork, insolation, emotional disturbance, excessive 
 venery, &c. It may be due to diseased action extend- 
 ing from contiguous portions of the nervous centres 
 or their appendages. Thus we find it in meningitis, 
 especially in its chronic forms, in aneurism or embolism 
 of cerebral vessels, in clot in the brain, in any lesion 
 affecting the various parts of the cortical substance. 
 The diseased action may extend from various tumours, 
 and perhaps also from exostoses or spicule of bone 
 from the calvarium. 
 
 All these lesions may act as exciting causes of the 
 phenomena, though several act also as predisposing ; 
 that is, the first and second divisions are much inter- 
 mingled. Two factors at least are necessary for the 
 production of an epileptic attack — the exciting cause, 
 and an impressionable condition of the nervous sub- 
 stance, especially probably of the medulla oblongata. 
 And this leads me to the real difiiculty in the pathology 
 of epilepsy, viz., what is the cause of the impressionable 
 condition of the nervous system. 
 
 That which induces this arterial spasm, or rather 
 that which causes the impressibility of the sympathetic 
 nervous filaments, which rule the cahbre of the arteries, 
 must be the condition of the blood itself. It is from 
 the blood that all the tissues derive the plasma for 
 growth and change, and tlnough the blood alone all 
 remedies are brouglit to bear upon a disease. A 
 morbid condition of this fkiid will induce morbid 
 mental phenomena entirely independent of any arterial
 
 EPILEPSY, 321 
 
 spasm or interference with its full supply. The obser- 
 vation of the many various forms of delirium teaches 
 this most distinctly, that whilst some forms of delirium 
 may depend upon a diminished supply of blood, a 
 large number own as their cause the circulation of 
 blood more or less diseased. 
 
 Twenty years ago, Mr. Harding, writing in the 
 Lancet^ made the following remarks : ' The irregular 
 muscular action of chorea has ever been resjarded as 
 connected with debility ; the bloodless aspect in 
 catalepsy bespeaks too plainly a poverty in life ; the 
 unsuccessful management of epilepsy by depletion led 
 inquiring minds to investigate its pathology, and it is 
 now looked upon as connected with a deficiency, not 
 with an increase, in the amount of stimulus supplied 
 by the blood. 
 
 ' The convulsions of young children occur in weakly 
 not in strong subjects ; and though the pulse may be 
 quickened and congestion take place during the par- 
 oxysm sufficient to justify the application of the leech, 
 it is essentially a disease of irritation as distinguished 
 from inflammation. 
 
 ' If I may be allowed to pursue this reasoning further, 
 let me mention the cramps which take place in elderly 
 people, and where the diminished energy of the digestive 
 power almost forbids the late and hearty meal. Again, 
 the far more powerful and fearful cramp of cholera 
 seems to commence and increase with exhaustion, when 
 the blood has been drained of its watery particles by 
 enormous discharges from the alimentary canal ; and 
 finally, the last act of the muscles commences when 
 
 Y
 
 322 EPILEPSY. 
 
 exhaustion can proceed no more, assuming the cadaveric 
 rigidity of structure when the vital spark has fled.' 
 
 As to the special lesion of the blood that induces 
 this impressibility of the sympathetic or of the medulla 
 oblongata, we are yet in ignorance ; at any rate, we 
 know of no lesion that invariably has this effect. But 
 although the blood seems to be the special organ that 
 induces this impressionable condition on the nervous 
 centre, there are other facts to be considered. The 
 whole question of hereditary influence is a case in point. 
 But we shall probably ever remain in ignorance in this 
 malady, as in gout, in rheumatism, in tubercle, in cancer, 
 and even in syphilis, what this vulnerability means. 
 A parent has a morbid constitution of some kind. He 
 begets a child, and in so doing impresses upon the 
 original germ, from which the child is developed, 
 certain characteristics. Among these characteristics 
 may be the likelihood of his offspring being gouty, but 
 perhaps not till it has lived in the world for forty 
 or fifty years. Or he impresses upon his offspring 
 the peculiar abnormality by which a portion of a nerve 
 centre or a special system of nerves may be morbidly 
 liable to be set in action by almost any excitant, 
 mental or physical. That the blood can have nothing 
 to say to this question of hereditary influence directly 
 is manifest by the anatomical fact that the blood of the 
 child is of course not in existence at the period of con- 
 ception. The impression is made on the cell, and it is 
 only in process of development that it is, as it were, 
 differentiated to the special part, just as any monstrosity 
 may be transmitted from father to child. But, on the
 
 EPILEPSY. 328 
 
 other hand, it is quite as easy to beUeve that this here- 
 cUtary vuhierability to a special disease is differentiated 
 on the blood itself, and that the nervous system only 
 suffers indirectly. And then again the very expression 
 of an abnormality being differentiated on to a special 
 organ is a convenient term by which we endeavour to 
 indicate what later phenomena seem to shadow forth, 
 but of the nature of which, or the mode of action of 
 which, we are absolutely ignorant. 
 
 The blood, in strychnia-poisoning, has been found 
 to be deficient in its power of assimilating oxygen. It 
 is difficult to say whether this peculiarity in the physi- 
 ological state of the blood may have been the cause of 
 the lesions often found in the spinal cord in tetanus, of 
 which I shall speak in another lecture. These lesions, 
 it will be seen, are not constant, and are also found in 
 other diseases in which there is no tonic spasm. It is 
 at least probable that the tonic spasm, or rather the 
 cause of the sympathetic filaments inducing tonic 
 spasm, is this abnormality of blood. Now except in 
 degree, and in the fact that different muscles are mainly 
 attacked, the tonic spasm of tetanus differs in nature in 
 no respect from tonic spasm that is one of the first 
 phenomena of an epileptic fit. 
 
 Again, epileptiform convulsions are seen in people 
 who are bleeding to death, in persons in whom the 
 cerebral circulation is suddenly checked, in persons 
 extremely debilitated by exhausting discharges. Epi- 
 lepsy again has been seen in persons in whom there 
 has been embolism of a middle cerebral artery, and 
 in persons in whom there was aneurism of the same 
 
 T 2
 
 324 EPILEPSY. 
 
 artery, limiting almost equally the supply of blood to 
 that arterial region. All clinical facts seem to me to 
 point to the causation of epilepsy as depending either 
 on a limitation of the supply of blood to some portion 
 of the encephalon, or to an abnormality in the blood 
 itself, and of all abnormalities the most important is 
 the diminution of oxygen. 
 
 Any account of the pathology of epilepsy would at 
 the present day be imperfect without some reference to 
 Dr. Hughlings Jackson's views. Some of these views are 
 necessarily speculative. He has made some observations 
 on epileptic regions, and others as to the nature of the 
 lesion. It is not easy to do full justice to the acumen of 
 these views when stated in a tabulated form. Still it 
 is necessary to make the attempt. Dr. Jackson believes : 
 
 ' 1. That convulsion is a discharging lesion. 
 
 ' 2. That since increase of fimction, even in disease, 
 implies increased nutrition, we infer that the grey cells 
 affected in convulsions store up force in large quantity, 
 and reach a high degree of tension. Further, since 
 they discharge on slight provocation, possibly even in 
 periodical normal changes in the body, when by con- 
 tinuous nutrition a certain degree of tension is reached, 
 we must suppose that they are in a state of highly 
 unstable equilibrium. 
 
 ' 3. That in epileptic discharges the convulsions 
 usually begin in those parts of one side of the body 
 which have the most voluntary uses. The order of 
 frequency in which parts suffer illustrates the same 
 law. Thus fits beginning in the hand are commonest. 
 Next in frequency are those which begin in the face or 
 tongue, and next arc those which begin in the foot.
 
 EPiLErsY. 325 
 
 ' 4. That many cases of epilepsy arc due to some 
 abnormality of the middle cerebral artery (aneurism, 
 embohsm, &c.). 
 
 ' 5. That when epilepsy begins in the hand, and 
 particularly if it frequently occurs in the same manner, 
 and more especially if it sometimes remains localised in 
 the hand and arms, we have every reason for diagnosing 
 a discharging lesion of some part of the superior frontal 
 convolutions of the opposite hemisphere — this has in 
 some cases been found post mortem, 
 
 ' 6. That epilepsy is the name for occasional, sudden, 
 excessive, rapid, and local discharges of grey matter. 
 
 ' 7. That, as any part of the grey matter of the cere- 
 brum may become unstable, there will be all varieties 
 of epilepsy, according to the exact position, or according 
 to the extent of the grey matter altered, and there will 
 be all degrees according to the degree of instability. 
 
 ' 8. That we see externally that the stronger the 
 spasm is, the wider spread it is ; the stronger the internal 
 discharge, the further it will spread. There are two 
 ways of spreading. The discharge will not only explode 
 healthy lower centres, but will probably spread, as it 
 were, laterally, to healthy associated centres in the 
 brain. My speculation is that the latent spreading is 
 by arteries and their vaso-motor nerves ; the spreading 
 is in arterial regions. 
 
 ' 9. That there are two ways in which nutrition may 
 be imperfect, in quantity and in quality. I believe 
 that nerve-tissue in discharging lesions is over-nourished 
 in the former sense, and worse nomished in the latter. 
 In order to make my meaning clearer, I will take 
 chemical illustrations and use chemical nomenclature.
 
 326 EPILEPSY. 
 
 Two bodies may be of the same constitution, but 
 yet of very different composition. For example, the 
 constitution of acetic acid and of the chloracetic acid is 
 the same, but they differ in composition, as in the latter 
 hydrogen has been replaced by chlorine. The structure, 
 however, is unaltered. I believe then that the highly 
 unstable nervous matter of disease (as in a discharging 
 lesion) differs in composition, but not in constitution, 
 from the comparatively stable grey matter of health. The 
 alteration in composition is of com-se such that the ner- 
 vous substance found is more explosive. We must sup- 
 pose that there is some order in this substitution-nutrition, 
 and we must infer that it is in the direction of explosive- 
 ness or instability. The following is a speculation as 
 to the kind of alteration of composition. One striking 
 constituent of nervous matter is phosphorus. It belongs 
 to the chemical class of triads, of which other members 
 are nitrogen and arsenic. My speculation is that in the 
 abnormal nutritive process producing unstable nervous 
 matter the phosphorus ingredient is replaced by its 
 chemical congener nitrogen. There is a substitution 
 compound : the replacement probably occurs in different 
 degrees, as it does in the three differing chloracetic 
 acids. If nitrogen be substituted as supposed, we can 
 easily understand that the substance produced would 
 be more explosive. The supposed value of arsenic in 
 certain nervous affections is significant, and it is another 
 member of the group of triads. The nutrition is there- 
 fore assumed to be defective, not in quantity but in 
 quality, in those functional alterations I call discharging 
 lesions.' These are some of Dr. Hughlings Jackson's
 
 EPILEPSY. 327 
 
 views on epilepsy given partly in his own words. You 
 see they bring us on another ste]) in advance, first by 
 l)roving as a matter of chnical observation that portions 
 of the cortical regions of the hemispheres may be the 
 originating seat of the epilepsy, either solely or primarily, 
 and second, by giving us a valuable speculation, to the 
 effect that the lesion may be an abnormal nutritive 
 process, by which one ingredient of healthy nervous 
 tissue has been replaced by another. We may say in 
 })assing that a substitution could scarcely occur, except 
 from a faidty constitution of the blood itself. 
 
 It is of immense importance to know that some of 
 Dr. Jackson's conclusions have been verified by the 
 experiments of Professor Ferrier. He says not only 
 that ' the anterior portions of the cerebral hemispheres 
 are the chief centres of voluntary motion; but that 
 the proxim.ate causes of the different epilepsies are, as 
 Dr. HughUngs Jackson supposes, discharging lesions of 
 the different centres in the cerebral hemispheres. The 
 affection may be limited artificially to one muscle or 
 group of muscles, or may be made to involve all the 
 muscles represented in the cerebral hemispheres, with 
 foaming at the mouth, biting of the tongue, and loss 
 of consciousness. When induced artificially in animals, 
 the affection as a rule first invades the muscles most 
 in voluntary use, in striking harmony with the clinical 
 observation of Dr. Hughlings Jackson.' 
 
 And Professor Ferrier sums up his views on epilepsy 
 thus : — 
 
 Many of the difficulties in the causation and 
 definition of the epileptic state will disappear, if we
 
 328 EPILEPSY. 
 
 regard the phenomena of this disease or condition as 
 proximately dependent on a local or general abnormal 
 condition of the cerebral hemispheres, characterised 
 by the tendency to recurrent sudden and explosive 
 discharge of the motor centres, with or without func- 
 tional perversion of the centres, which manifest them- 
 selves inwardly in consciousness. We shall thus be 
 enabled to recognise in their true light, and place in 
 their proper relations to the more generally recognised 
 type of epileptic seizure, those forms of epilepsy which 
 commence unilaterally in one or more groups of muscles, 
 and which generally indicate some localised gross 
 lesion of the cerebral hemispheres, while at the same 
 time we shall afford a satisfactory explanation of the 
 phenomena of idiopathic epilepsy, so-called, because it 
 has not as yet been shown to be dependent on any 
 constant discoverable lesion. In the local and uni- 
 lateral attacks we have a successional analysis of the 
 phenomena, which a so-called idiopathic attack presents 
 in too complicated a form for successful diagnosis as to 
 essential nature and causation. But in such cases also 
 there are numerous facts which indicate that the seat 
 of the motor and psychical disturbances of the epileptic 
 attack is above the medulla oblongata, in centres which 
 probably have an intimate relation with each other. 
 And now that the motor signification of the grey 
 matter of the hemispheres is clearly demonstrated, it is 
 not necessary to assume that the medulla oblongata is 
 the primary seat of the motor disturbances, while the 
 psychical symptoms are only subordinate to changes 
 induced in the circulation of the brain by a primary
 
 EPILEPSY. 329 
 
 affection of the medulla itself. When it is said tliat 
 the proximate cause of the epileptic seizure is a con- 
 dition of the instability of the cortical centres, nothing 
 is implied as to the exact physical condition which 
 may exist. It may be established as a hereditary 
 tendency, and it is, we know, capable of being induced 
 by numerous methods of centric or eccentric irritation, 
 both in the indirect experiments of injury and disease, 
 and as the result of direct experiments, such as blows 
 on the head (Westphal), or injuries to nerve-trunks or 
 the spinal cord (Brown-Sequard). To sum up then, 
 in a few words, we may conclude : — 
 
 1. That an epileptic attack is a discharging lesion 
 of some portion of the grey matter of the encephalon. 
 
 2. That a large proportion of lesions found in the 
 brain post mortem are the result of the malnutrition 
 of the brain by oft-repeated arterial spasm, or of 
 congestion and fiu-ther lesion of the brain, due to the 
 spasm of respiratory muscles. 
 
 3. That certain lesions of brain may induce the 
 impressibility of the grey matter, just as a clot rapidly 
 breaking into healthy nervous tissue may sometimes 
 produce convulsion. 
 
 4. That in some cases the cortical substance of the 
 cerebral hemispheres, especially of the anterior lobes, 
 in others the medulla oblongata or the spinal cord, 
 may be the primary seat of the discharging lesion. 
 
 5. That the impressibility of these discharging 
 centres is due to abnormalities of nutrition. 
 
 6. That these abnormalities of nutrition may be 
 from variations in and especially deficiency of blood
 
 330 CHOREA. 
 
 supply, alteration in the character of the blood itself, 
 particularly in its power of carrying oxygen, and 
 perhaps sometimes in the substitution of an abnormal 
 substance for one of the elementary constituents of the 
 nervous tissue. 
 
 Chorea. — Trousseau says that, ' as in the case of 
 other neuroses, pathological anatomy teaches us scarcely 
 anything as to the material alterations of the nervous 
 centres in St. Vitus's dance. If you consult various 
 authors, you will find contradictory facts and opinions. 
 One looks on inflammation or induration of the tuber- 
 cula quadrigemina as the characteristic lesion of the 
 disease ; another regards as such induration or hyper- 
 trophy of the brain or of the spinal cord, or a more or 
 less extensive softening of the cerebro-spinal centres ; 
 a third believes in calcareous concretions of the brain ; 
 a fourth in cysts of the pineal gland, or osteoids of the 
 vertebral canal, and I know not what else. But does 
 not this very diversity of the lesion found after death 
 prove that there is no relation between them and the 
 dynamic phenomena, even if it had not been ascer- 
 tained that in most cases no appreciable anatomical 
 change can be detected in the nerve-centres ? For my 
 own part, in the rare instances in which I have examined 
 the bodies of individuals who had died of St. Vitus's 
 dance, after presenting the most violent symptoms of 
 the disease, I never met with any lesion which seemed 
 to me to be in accordance with the convulsive pheno- 
 mena of chorea.' 
 
 Now, in considering the pathology of this disease, 
 it is necessary briefly to review the circumstances under
 
 I 
 
 CHOREA. 331 
 
 which it arises. These are either moral, such as friglit, 
 conscious or unconscious imitation of another choraic 
 patient, violent excitement such as has been seen in 
 periods of great religious exaltation — as among the 
 flagellants, among some of the subjects of the dancing 
 mania of the fourteenth and fifteenth centuries, in the 
 ranks of the Convulsionaires of France, and in many- 
 religious revivals, especially among the Methodists, in 
 Great Britain and in America — or physical, as chlorosis, 
 or states closely related to it, or pregnancy, or rheu- 
 matism. 
 
 We shall see directly that rheumatism is connected 
 with chorea in a special manner ; that chorea follows 
 it and seldom precedes it, and that in the rare cases in 
 which it seems to precede it there is often evidence 
 during life or after death that some valve or other of 
 the heart has suffered, even though there may have 
 been no manifestation of rheumatism in the joints or 
 elsewhere. 
 
 There have been various statistics of post-mortem 
 results in cases of chorea. Dr. John Ogle found, out 
 of sixteen cases, congestion of brain or of spinal cord, 
 or of both, in six ; in one, actual softening of the 
 spinal cord ; in one, the spinal cord more dull and 
 yellow than usual ; in one, the central parts of the 
 brain much softened ; in ten, granulations on some part 
 of the endocardium. 
 
 Among the records of the Pathological Society we 
 find that fatal cases of chorea have presented the fol- 
 lowing lesions : Chronic disease of the cerebral dura 
 mater, softening of the brain and spinal cord, tumours
 
 332 CHOREA. 
 
 in the centre of the spinal cord, softening of the fornix 
 and of the surface of the third ventricle, softening of 
 the crura cerebri with atrophy of the brain, softening 
 of the central parts of the brain and of the corpora 
 quadrigemina, the specific gravity of the corpus striatum 
 and optic thalamus greater on one side than on the 
 other, spinal meningitis, the arachnoid opaque on the 
 surface of the hemispheres and serum in the ventricles, 
 tubercle of the spinal cord, softening of the cord alone, 
 the medulla oblongata pressed upon by an enlarged 
 odontoid process, and, in chorea combined with 
 paralysis, softening of the occipital cerebral convolu- 
 tions with atrophy and degeneration of the spinal 
 cord. 
 
 Skoda thinks the immediate cause of the disease is 
 an exudation in the spinal cord or in the brain. 
 
 Hammond believes that chorea is either functional 
 or organic ; that in the former there are no post- 
 mortem appearances, whilst in the latter form there 
 maybe — (1) intracranial congestion, softening, opacities, 
 and adhesions ; or (2) congestion or softening of the 
 spinal cord with adhesions and opacities of membranes ; 
 or (3) embohsm of the corpora striata with a beady 
 mitral valve ; or (4) hyperinosis of the blood. 
 
 I have been unable to trace any post-mortem ap- 
 pearance tliat would account for the phenomena in 
 some cases, but in the following case there was evident 
 lesion : 
 
 Girl, aged 17 ; has had rheumatism. Mitral disease 
 evident during life, and the valve found beady after 
 death. She seemed to die of exhaustion, as the choraic
 
 CHOREA. 333 
 
 jactitations were uncontrollable during the whole course 
 of the disease until her death. 
 
 Some clots of blood were found lying outside the 
 brain on the right side in the cavity of the arachnoid. 
 The blood seemed to have come from a small orifice in 
 the right lateral sinus. Many capillary embolisms in 
 both corpora striata. The heart showed no beads of 
 lymph on the ventricular surface of the mitral valve ; 
 but on opening the left auricle the whole circle of the 
 auricular attachment of the valve was surrounded by 
 minute beadings. 
 
 The relations of chorea with rheumatism and heart 
 disease in children have been minutely discussed by M. 
 Roger. He says there is an interdependence between 
 the three conditions. He admits a cardiac chorea, but 
 says the heart disease and the chorea may start together 
 from the same cause, as is the case sometimes with 
 rheumatism and carditis. His cases establish that the 
 heart disease often persists after the cure of the chorea ; 
 and he further shows that chorea may be a cause of 
 heart disease. 
 
 Dr. Murchison records the case of a girl, aged 14, 
 who had for years suffered from chorea with mitral 
 deficiency. While lying in bed she became suddenly 
 unconscious, and had occasional muscular twitchings 
 of the right limbs. The right pupil was contracted, the 
 left dilated, both innnovable. In addition to vegeta- 
 tions on the mitral valve were found embolic masses in 
 the spleen and kidneys, and the left vertebral and left 
 carotic arteries were much distended, hard, and com- 
 pletely blocked by a pale, firm, easily detached clot.
 
 334 • CHOEEA. 
 
 No embolisms of the minute vessels, such as have been 
 described after death from chorea, were found. 
 
 We come then to the pathological theory, only 
 partially as yet proved by post-mortem data, associated 
 especially with the names of Kirkes, Tuckwell, Broad- 
 bent, and Hughlings Jackson, and spoken of on the 
 Continent as the English theory of embolism. 
 
 This theory was shadowed forth by Dr. Kirkes 
 without going much into particulars. His observations 
 in the dead-house taught him that persons dying of 
 chorea often showed on some portion of the endocar- 
 dium, and particularly on the mitral valve, beady vege- 
 tations. Kirkes believed that these vegetations were 
 washed away and carried by the blood to be deposited 
 in some portion of the brain. Beyond this he did 
 not go. 
 
 Dr. Jackson, however, goes further. Founding his 
 views partly on chnical observation and partly on the 
 experience of the dead-house, he suggests that these 
 minute vegetations are indeed carried to the brain, as 
 Kirkes supposed, and are there entangled in some por- 
 tion generally of the middle cerebral artery, blocking 
 up with emboli some one or more of its branches, and 
 affecting therefore either the corpora striata or the 
 convolutions in their immediate neighbourhood. He 
 connects chorea with paralysis in that, whilst an 
 embolus blocking up a large arterial branch will cause 
 the latter, several minute emboli obstructing several 
 small branches in the same situation will induce, not 
 absolute loss of function, but impairment of function. 
 His views are thus spoken of by Dr. Eadcliffe : ' Taking
 
 CHOREA. 335 
 
 chorea of one side of the body, hemichorea, as the 
 simplest form of chorea, and putting it side by side 
 with hemiplegia, the result of embolism, good reason 
 is found for believing that the disorder of movement 
 and the palsy both point to the region of the corpus 
 striatum as the seat of mischief. If this be the seat 
 of mischief in hemiplegia, why not in hemichorea? 
 The muscles most moved in hemichorea are those most 
 palsied in hemiplegia. In hemichorea, as in hemi- 
 plegia, the arm, as a rule, is more affected than the 
 leg. In right hemichorea, as in right hemiplegia, the 
 speech is generally very much affected. Again, hemi- 
 chorea is always more or less mixed up with, and 
 sometimes ends in, hemiplegia ; and, on the other 
 hand, hemiplegia, from various causes, is not un- 
 frequently attended with chorea, or movements of 
 some kind or other. The fact that the face is involved 
 in chorea shows that the seat of the disorder must be 
 above the spinal cord. The facts which have been 
 instanced point to the convolutions near the corpus 
 striatum, rather than to any other part of the brain, as 
 the part affected.' 
 
 Dr. Broadbent, theorising on perfectly independent 
 data, would limit the portion of the nerve-centre 
 affected to the sensory-motor ganglia ; and he believes 
 that the symptoms point to the seat of the mischief, 
 not to its nature ; and that besides embolism, heemor- 
 rhage, softening, irritation, and other causes, may figure 
 among the causes of chorea. He instances local innu- 
 trition, reflex action from peripheral irritation, and 
 direct action upon the sensory-motor ganglia from 
 shock.
 
 336 CHOREA. 
 
 His views that embolism is not the only lesion of 
 the corpora striata in chorea are supported by a case 
 reported by Dr. Foot at the Pathological Society of 
 Dublin. He exhibited the viscera of a man, aged 68, 
 affected with unilateral chorea, who had died of capil- 
 lary bronchitis. On the surface, and towards the ante- 
 rior end of the corpus striatum of the side opposite to 
 that which had been affected, were two shallow depres- 
 sions, underneath which were two deliberately encysted 
 depots of white diffluent brain substance, showing 
 granular corpuscles with molecules and fatty debris. 
 Eunning transversely across the deepest part of the inte- 
 rior of the optic thalamus of the same side was a deeply 
 discoloured track, orange-red at the end approaching the 
 lateral ventricle, plum-red at the opposite end where 
 it approached the quadrigeminal bodies. Both basal 
 and cortical arteries were almost without exception 
 atheromatous. The spinal cord presented no anomaly ; 
 the cerebellum was soft and greasy ; the kidneys were 
 small, granular, and cystic ; their cortex was reduced 
 in thickness, their arteries were atheromatous. The 
 left ventricle of the heart was one inch thick at apex 
 and midpoint, seven lines at base ; the larger curtain 
 of the mitral valve was atheromatous, in fact, showing 
 mitral valvulitis from the increased strain of an enlarged 
 ventricle. The aorta presented all the various degrees 
 of the atheromatous process. 
 
 There can be no doubt of two facts in the patho- 
 logical anatomy of chorea : one, that embohsm of some 
 branches of the middle cerebral artery is a frequent 
 lesion in this disease ; and the other, that it is not the 
 only lesion.
 
 CHOREA. 837 
 
 Dr. West states very forcibly tlie theoretical objec- 
 tions to the embolic theory. 
 
 1 . ' The occasional occurrence of chorea from mere 
 imitation, so that we have sometimes been compelled 
 to change the position of patients in the Children's 
 Hospital, from observing the involuntary mimicry by 
 one child of the movements of another. 
 
 2. The extreme rarity of a sudden attack of chorea, 
 the great slowness with which it almost invariably 
 comes on. 
 
 3. The very small number of instances in which 
 chorea continues limited to one side, and the compara- 
 tively short time within which hemicliorea ahnost 
 always becomes bilateral. 
 
 4. The almost invariable recovery of complete 
 power over all the limbs in cases of chorea, and this 
 even in instances where the paralytic character of the 
 symptoms has most predominated ; so that I have only 
 two or three times in my life met with cases in which 
 permanent loss of power over a limb could be reason- 
 ably referred to antecedent chorea. 
 
 5. The fact that, as a general rule, and one with 
 very few exceptions, the second attack of chorea is 
 slighter than the first, and the third than the second ; 
 a result wholly unintelligible, if organic mischief were 
 the ordinary cause of the attack.' 
 
 I should myself be inclined to agree with Dr. 
 Broadbent that embolism, though perhaps the chief, is 
 far from being the only lesion ; and with Dr. Hughliiigs 
 Jackson, that not the corpora striata only, but also the 
 region of brain supplied by the middle cerebral artery 
 
 z
 
 338 CHOREA. 
 
 may be the seat of lesion. And without entering 
 upon any controversy as to what kinds of lesion are 
 capable of inducing the phenomena, it is sufficiently 
 comprehensive to state that any lesion that interferes 
 with the nutrition of this region of the brain may 
 cause choraic jactitation, if only the interference with 
 nutrition is not of sufficient extent to cause paralysis. 
 It is only in this way we can account for the causation 
 of chorea by shock and mental excitement of any 
 kind ; the direct mental influence producing arterial 
 spasm, not only partial in degree, but specially limited 
 in area. It is only on the ground of interference 
 with nutrition that we can explain agaiii the instances 
 of chorea without embolism occurring in patients the 
 subjects of chlorosis or of pregnancy. Indeed, chorea 
 occurring during, and in consequence of, pregnancy 
 has been considered by some observers to depend on 
 the chlorosis, so frequently a concomitant or a conse- 
 quence of the pregnant condition, though it might also 
 be explained by reflex irritation on the middle cerebral 
 arteries originating from the uterus itself. Even in 
 rheumatism, where no cardiac vegetations exist, the 
 choraic symptoms may be set up by the blood being 
 rendered imperfect for nutritive purposes. Dr. Ogle 
 at least considers the disease to be induced in some 
 cases by the anaemia consequent on rheumatism. Still, 
 in this instance we are unable to exclude the possibility 
 of embolism, even where no vegetations have existed 
 in the heart, as Dr. Bastian has found embolisms in 
 chorea composed of agglomerations of white blood 
 corpuscles.
 
 CHOREA. 339 
 
 And, once more, the success ot certain remedies 
 points to the same thing. We have to encom\age col- 
 lateral circulation in cases of embohsm, and better 
 nutrition in those cases in which no definite lesion 
 exists. The mineral tonics seem in many cases to 
 shorten the attack, and sometimes they do so with 
 such rapidity that it is impossible to believe that there 
 has been time for collateral circulation to be set up. 
 The advantage, the necessity, even, of good food in 
 the treatment of such cases, demonstrates the same 
 thing, viz., that we have to do with an instability of a 
 region of the brain due to imperfect nutrition ; that 
 this imperfection of nutrition may depend solely on a 
 poor and innutritions blood ; but that in many cases 
 we have to do with some coarsish lesion of the cor- 
 pora striata and the cortical structure of the cerebral 
 convolutions, such as haemorrhage, softening, tumour, 
 and especially embolism, inducing a species of dis- 
 charge. 
 
 A very uncommon case of congenital chorea has 
 been published by me, and is evidently not an instance 
 of embohsm : — 
 
 Henry S., aged 13. His mother was frightened at 
 the end of the second month of pregnancy, by squeezing 
 a kitten to death accidentally in moving a barrel, and 
 witnessing its death agony. The child was born about 
 six weeks before the full time. He has had chorea 
 from his birth, and has always been as bad as at 
 present. Lately has learnt to sa}^ a few words. Until 
 recently could not speak at all, but could hum tunes in 
 an indistinct way, and make various noises. Cannot 
 
 z2
 
 340 cnoEEA. 
 
 stand or liold anything firmly. His education has 
 been entirely neglected, but he is very sharp and ver}'- 
 merry. Can crawl in two ways, and at a great pace, 
 and for this purpose combines his muscular movements 
 pretty well. Is almost always in motion, except when 
 asleep, and then is quite still. Had fits when three 
 years old, and not since. No rheumatism or heart 
 disease ; and there is none in his flimily. 
 
 He was put on arsenic. After a few weeks he began 
 to say more words, and Vv^as much less restless. Walks 
 rather better, but cannot stand without support. The 
 nurse took great pains with him, and after two months 
 he was able to walk with the help of one hand, and to 
 stand without assistance. He learnt to say a good 
 many words, and proved exceedingly intelligent. Most 
 of his movements showed great deficiency of coordi- 
 nating power, but he combined movements for the 
 pur])ose of scuttling along the iloor in a wonderful 
 manner, one leg being stretched out in front and the 
 otiier behind, whilst he paddled along wdtli one hand 
 at- great speed. Playing at nine-pins brought him on 
 considerably, and so did the association with and 
 imitation of two non-choraic boys in the ward. 
 
 The following quotation from Professor Fenier's 
 first paper bears upon the causation of chorea : — 
 
 ' The movements wliich are seen in chorea bear an 
 intimate relation to those of epilepsy, and indicate the 
 same centric causation. They are not mere spasms 
 and cramps, but an aimless profusion of movements of 
 considerable com})lexity, nuich nearer the purposive 
 movements of huallh. They are not so much inco-
 
 CHOREA. 311 
 
 hereiiCGs of muscles as incoherences of movements of 
 muscles. There is some method in their madness. 
 Again, they are successions of movements ; moreover, 
 they are successions of different movements. I regard 
 the above experiments, in tliis case also, as an experi- 
 mental demonstration of the accuracy of the views 
 of Dr. Ilughlings Jackson, who places the proximate 
 cause of these movements in an unstable condition of 
 the grey matter of the cerebral convolutions.' 
 
 One point remains to be touched upon, viz., the 
 connection of chorea with abnormal mental pheno- 
 mena. This fact is easily recognised in very acute 
 cases, and, in less degree, can be verilied even in 
 ordinary cases of subacute form. 
 
 I once admitted into the Bristol Infirmary a girl 
 who had been epileptic for some years. It was about 
 the time of the Ulster revivals, and this girl had been 
 much worked upon by some injudicious ministrations 
 of a young curate. She became rather suddenly 
 choraic in an extreme degree, and at the same time 
 possessed with strange delusions. The devil w^as always 
 present with her, and she bit me one night severely, 
 under the impression that I was myself his Satanic 
 majesty. The treatment that cured the chorea ciQ'ed 
 the delusions. 
 
 Again, in five cases of chorea recorded by Dr. 
 Ilandfield Jones, the following points among others 
 were illustrated : (1) the tendency of chorea proper, 
 motor-centre disorder, to be attended witli an analo- 
 gous state of the emotional or of the intellectual 
 centres ; and (2) its liability to occur in a modilled
 
 342 CHOREA. 
 
 form, and to be complicated with quasi-epileptic 
 attacks. 
 
 We can easily realise that any lesion that blocks 
 important portions of the middle cerebral artery may 
 gradually induce softening, if collateral circulation is 
 not sufficiently set up, even if no rupture of the artery 
 takes place, and that abnormal mental phenomena 
 may be the result of this lesion. But such a lesion as 
 softening requkes some time for its development, and 
 it is not capable of explaining the delusion, the deli- 
 rium, or the hebetude so often met with in these 
 patients coincidently with the appearance of the jac- 
 titation. It is, however, quite easy to believe that 
 the same anasmia, the same want of nutrition, that 
 induces the peculiar motor phenomena of chorea by 
 its action on a special motor centre, may coincidently 
 induce the mental phenomena by extension to the 
 portions of the brain concerned in intellectual function. 
 
 And still more easy it is to understand the co- 
 existence of both series of phenomena, now that we 
 know by experiment that irritation of portions of the 
 cortex of the cerebral hemispheres — and these, too, 
 regions hitherto believed to be concerned solely in 
 intellectual work — will produce movements in certain 
 portions of the body. The mental, in fact, own in 
 most cases the same causative lesions as the motor 
 phenomena. 
 
 Consult, for Epilepsy — 
 
 Russel Reynolds on ' Epilepsy.' 
 Iladclifle on 'Epilepsy.' 
 Sieveking on * Epilepsy.'
 
 CHOREA. 343 
 
 Jaccoud, ' Path, interne.' 
 
 Itomberg, ' Dis. of Nervous System.' 
 
 Wilks, ' Path. Anatomy.' 
 
 Trousseau, ' Clin. Lect.' 
 
 Bright's ' 3Ied. Rep.' 
 
 ' London Hosp. Rep.,' vol. i. Dr. Ilughliugs Jackson. 
 
 ' "West Riding Asylum Rep.,' vol. ii. 304. Dr. Thompson. 
 
 Ibid., vol. iii. 04. Dr. Ferrier. 
 
 Ibid., vol. iii. 32G. Dr. Ilughlings Jackson. 
 
 'Journal of Mental Science,' April 1873. Dr. Crichton Browne. 
 
 Consult, for Chorea — 
 
 Dr. West on ' Diseases of Infancy and Childhood.' 
 
 Todd, * Clinical Lectures.' 
 
 Reynolds, ' Syst. of Med.' Dr. Radcliffe. 
 
 Jaccoud, ' Path, interne.' 
 
 Romberg, * Dis. of Nervous System.' 
 
 Hammond^ ' Dis. of Nervous System.' 
 
 "Wilks, 'Path. Anatomy.' 
 
 Bright's ' Med. Rep.' 
 
 * Med.-Chir. Review,' Ixxxii. Dr. Ogle. 
 
 'London Hosp. Rep.,' vol. i. Dr. Ilughlings Jackson. 
 
 * Ilemichorea.' Pamphlet. Dr. Hughlings Jackson. 
 ' Med. Record,' i. 263. Dr. Foot. 
 
 < New Syd. Soc. Yearbook,' 1867. Roger. 
 Ibid., 1871. Murchison and Handfield Jones. 
 
 * West Riding Asylum Rep.,' vol. iii. Dr. Ferrier.
 
 344 
 
 LECTURE XII. 
 
 TETANUS. 
 
 A KECE^'T writer has said, with reference to the patho- 
 logical anatomy of tetanus, that the lesions have 
 nothing that marks them as exclusively peculiar to the 
 disease ; whilst the instantaneous development of the 
 tetanic phenomena and the possibility of the recovery 
 scarcely allow ns to assign a primary character to these 
 lesions. There are, it is true, some secondary alterations, 
 as Eokitansky and Demne have proved ; one of the 
 facts recorded by this latter observer proves this view 
 very satisfactorily, for the lesion was followed up from 
 the centripetal nerves to the posterior columns ; it 
 consisted in proliferation of the neuroglia amounting to 
 sclerosis, and was distributed sometimes uniformly 
 over a certain extent, sometimes in spots irregularly 
 disseminated. To these alterations, which have been 
 thoroughly recognised both in themselves and in their 
 relation with tetanus ever since the works of Eoki- 
 tansky, Demne, and Wagner, it may be well to add 
 the granular degeneration of the cells of the cord, 
 discovered more recently by Lockhart Clarke. Accord- 
 ing to him this latter lesion is constant, although this is 
 a point that further observation ought to clear up ;
 
 » 
 
 TETANUS. 345 
 
 but the alterations of the neuroglia may be wholly 
 absent, as Leyden's fiicts prove. The older authors liave 
 indicated a great number of other disorders of the 
 nervous centres, but these are accidental and accessory 
 lesions, without any certain relations with tetanus. A 
 single exception may be made for an alteration which 
 is not more constant than those above-mentioned, but 
 we can have no doubt it bears some relation to the 
 disease, viz., inflammation of the neurilemma mentioned 
 by Lepelletier and Froricp, and traced by them from 
 the nerves near the wound to the cord. 
 
 In a majority of cases in which the spinal cord has 
 been examined, both the cord itself and its membranes 
 have been found healthy ; in others there has been 
 found a collection of fat between the membranes and 
 the cord from the lower part of the cervical to the 
 middle of the dorsal region ; in one there was a small 
 softened patch in the cord just above the cauda equina ; 
 in another there was an effusion of blood outside the 
 dura mater about the 7th or 8th dorsal vertebra, and a 
 softenino; of cord in the dorsal region ; in this case there 
 had been a blow on the back. In the case of Cook, 
 poisoned by Palmer with strychnia, the prisoner in 
 great measure grounded his defence on the presence of 
 a few granules on the cord, the result, probably, of 
 slight antecedent meningitis. Effusions of serum into 
 the spinal membranes and even ha3morrhages are not 
 very uncommon in tetanus, and are results and not 
 causes of the phenomena. I shall refer directly to 
 lesions found by Lockhart Clarke, Dickenson, Allbutt, 
 and others, in s])eaking of the microscopical appear-
 
 346 TETANUS. 
 
 ances of my own cases. Tlie nerve in the wound in 
 traumatic tetanus has been found diseased. Mr. Erichsen 
 says that the twig in the wound is generally diseased. In 
 thirteen cases recorded by Mr. Poland in Guy's Hospital 
 reports the nerve twig was found inflamed in five and 
 bulbous in one. Trousseau also gives some instances. 
 In those cases, moreover, where the disease has been 
 arrested by releasing a nerve-fibre which had been 
 included in a ligature, or by excising the injured part, 
 and thus isolating the termination of the nerve, we must 
 receive some morbid condition of the nerve itself in the 
 wound as an explanation of the exciting cause of the 
 disease. Against the universality of this view, however, 
 tlie nerve is often found inflamed and otherwise diseased 
 without the occurrence of tetanus ; and again, in a 
 large majority of cases of traumatic tetanus we can 
 recognise no morbid condition of the nerve. 
 
 If, therefore, we are compelled to exclude the con- 
 dition of the nerve as causing the tonic spasm, we must 
 look to portions of the cerebro-spinal system or to the 
 blood. The vaso-motor system is necessarily excluded, 
 because the lesions found in the ganglia are met with 
 only exceptionally, although, probably, the sensitive- 
 ness of these nerves to reflex impressions is one of the 
 primary phenomena in the attack. WJiat, then, causes 
 this kind of spasm ? 
 
 Dr. Eoemer, referring to certain experiments of 
 Dr. Weir Mitchell on the cerebro-spinal fluid, and its 
 agency in producing convulsions under pressure, says : 
 'On injecting half an ounce of water (66° Fahr.) into 
 the spinal canal of a rabbit, convulsions ensued, and 
 shortly afterwards death. By this injection tlie blood
 
 TETANUS. o47 
 
 was displaced in the spiual vessels, and caused bleeding 
 from the exposed veins of the cord and head. A larger 
 amount of water under 100° Fahr. was borne in the 
 second experiment, and spasms followed instantly upon 
 the introduction of water at 32° Fahr. Every variety 
 of convulsive action was thus effected. Subsequent 
 experiments jiroved that the local and external appli- 
 cation of extreme cold upon the spine brought 
 about similar results. The agent usually employed was 
 rhigolene. It results from these experiments that at 
 or about the 14th vertebra from above downwards we 
 cease to notice backward spasm and stupor, and see 
 only signs of weakness or of tetanic rigidity in the legs. 
 A jet of rhigolene thrown upon the spine of a frog 
 occasions spasmodic movements of the legs, and at 
 intervals violent tetanic contractions. The pigeon, 
 under the application of cold to the side, may be 
 handled or laid on its back and side, while at 
 any moment a loud sound or a sudden motion will 
 break the spell, and it will abruptly run backwards 
 several feet. The following symptoms of partial 
 tetanus (emprosthotonos and opisthotonos) should be 
 marked. In the spasm from chilled spine or cerebellum 
 the head is carried at ease durino; the interval between 
 the fits, but at the moment of attack the bill strikes 
 the floor quickl}^, first on one side and then on the other, 
 the head being drawn violently forward. Even in 
 the most terrible of the somersaults caused by 
 cold, the head was drawn forward, and the backward 
 turn was produced by the action of the muscles of 
 the legs and wings, rather than by those of tlie back, 
 neck, and spine. Very little of the convulsive acts is
 
 348 TETAXUS. 
 
 due to tlie direct effect of cold, much more to the 
 intense and overpowering congestion, wliich in time 
 wears off. The added proof hes in the fact that local 
 irritants, which congest more slowly, occasion in the 
 spine the same phenomena after the lapse of a longer 
 interval. Intense cold to freezing and the injection of 
 water produced consequently similar effects, that is, any 
 displacing agency upon the spinal fluid gives tonic 
 spasm. Direct injury to the cerebellum and spinal 
 cord conditions similar results. Fodere, Majendie, 
 Flourens, Purkinje, and Krauss have observed tonic 
 spasm and oi)isthotonic movements in mammals and 
 birds after the loss of the cerebellum. Mitchell also 
 has verified these experiments. 
 
 Besides this. Professor Ferrier has shown that power- 
 ful irritation of one corpus striatum causes rigid pleuros- 
 thotonos, the flexors predominating over the extensors ; 
 wliilst the optic lobes, or corpora quadrigemina, besides 
 being concerned with vision and the movements of the 
 iris, are centres for the extensor muscles of the head, 
 trunk, and leg, and irritation of these centres causes 
 rigid opisthotonos and trismus. Again, it seems proved 
 that sudden arterial contraction in the spinal cord, the 
 medulla oblongata, and probably in the meso-cephale, 
 induces tonic spasm, of which tetanic spasm is so far a 
 mere variety that in it one set of muscles overcomes 
 the resistance of their opponents ; the flexors, for 
 instance, being more strongly affected than tlie 
 extensors. 
 
 As in epilepsy, this impressibility of the vaso-motor 
 nerves that rule tlie calibre of the arteries must be 
 ]:)roduced in some way. Is it due to a lesion of a seg-
 
 TETANUiS. 349 
 
 meiit of the cord with wliich the vaso-motor nerves are 
 associated, or to some alteration in the blood itself? 
 The condition of the nerve in the wound, if it were 
 true that the nerve was often found diseased, would be 
 necessarily unequal to the production of the tetanic 
 state, unless the spinal cord or its extensions in the 
 brain, the vaso-motor nerves themselves or their ganglia, 
 were already abnormally impressible. The nerve in 
 the wound may be the channel by which the excitation 
 is carried to the cord, the state of the nerve may even 
 be the exciting cause of the spasm, but there is some- 
 tliing over and above this without which the exciting 
 cause would fail to produce the tetanic phenomena. 
 Besides, tetanus is not only traumatic, but idiopathic, 
 set up by a variety of causes, cold, damp, bad ventila- 
 tion (especially in the case of infants), sudden changes 
 of temperature, &c. Here the state of the eisodic 
 nerves shows no abnormality. 
 
 We begin, then, with the lesions of the cord itself. 
 Now" that minute investigation is more frequently made 
 at autopsies on patients who have died of this disease, 
 it is more common to fuid some lesion or other of the 
 cord and its membranes. 
 
 We have to consider : (1) What these lesions of the 
 cord are. (2) Are they the cause of the phenomena, 
 or their effect ? (3) Are they met with in the cord 
 under circumstances wholly unconnected with tetanus ? 
 
 Itomberg tells us that we may fmd congestion, in- 
 flammation, exudation, softening, induration, but tliat 
 the appearances are very inconsistent ; and Dr. Wilks, 
 that the aHectiou of the nervous system is able to kill
 
 350 TETANUS. 
 
 without leaving any traces behind, and thus, in general 
 terms, the body is healthy. In a case of idiopathic 
 tetanus, however, Eomberg found that the density of 
 the medulla oblongata presented a marked contrast to 
 the great softening of the cervical portion of the cord, 
 which exuded from its membranes on slight pressure. 
 The dorsal portion was firm ; the lumbar portion, again, 
 almost liquid. 
 
 Sandras and Bourguignon say that one meets with 
 some lesions of the spinal membranes, or a little more 
 liquid than usual in the meninges, or injection and 
 even softening of the anterior columns of the cord. 
 But the former lesions, such as cartilaginous plates, 
 thickening, &c., belong to organic affections generally 
 much older than the commencement of the tetanus. 
 On the one hand, the increase of the fluid is not always 
 there, and, on the other hand, it is met with in a 
 number of diseases which have nothing in common 
 with tetanus ; and, lastly, it may reasonably be asked 
 if this lesion is not the effect of the malady rather 
 than the cause. 
 
 May we not say the same of ha^morrhagic injection 
 of the grey and white substance of the cord, and of 
 softening of the anterior columns? Doubtless, when 
 in the bodies of persons who have died of tetanus we 
 meet with a decided hemorrhagic injection of the 
 white or grey substance of the brain or cord, we are 
 justified in saying that we have got one notion more on 
 the anatomy of the disease. ' Mais cette notion est-elle 
 applicable a la cause ou a FefTet ? Que deviendraient 
 les cas dans lesquels on ne trouve rien do semblable ? '
 
 TETANUS. 351 
 
 For it is certain that these lesions, sometimes remarked, 
 are not invariably found ; many authors do not speak 
 of them as being constant. And these observers go on 
 to say that in death from strychnia the amount of tlie 
 cerebro-spinal fluid and the redness of tlie grey sub- 
 stance are not constant appearances, and when they 
 are met with they seem to be in direct ratio with the 
 gradual approach of the fatal event. "^It is clear,' says 
 Dr. Handfield Jones, ' that in all cases a certain 
 predisposition of the cord must exist before the spas- 
 modic symptoms declare themselves.' As Dr. Watson 
 says, the real mystery lies in this predisposition. 
 
 The first and most important observations made in 
 England, microscopically, on the spinal cord in tetanus 
 were by Lockhart Clarke. In 1865 he contributed 
 six cases to the Medical Chirurgical Society, in all 
 which areas of disintegration were found in the spinal 
 cord. The first case was reported at some length, and 
 the lesion was found more or less from the origin of 
 the second cervical nerves to the lumbar enlargement. 
 At the second cervical nerves, streaks and irregular 
 areas of disintegration were observed in different parts 
 of the grey substance, and particularly around the 
 central canal, on the right side of which was a space of 
 considerable size, containing a finely granular fluid, 
 with the debris of blood-vessels and nerves. Tlie 
 posterior and lateral white columns, especially along the 
 edges of the various fissures which transmit blood- 
 vessels, were damaged in a similar way ; and in some 
 sections the deeper portions of the posterior columns 
 which rest on the transverse commissure were softened
 
 852 TETAXUS. 
 
 to a considerable degree. This disintegration was still 
 more marked in the cervical enlargement, chiefly behind 
 and at the sides of the canal. The posterior commissure 
 was wholly and the anterior partially destroyed by a 
 fluid, transparent, and granular area. Throughout the' 
 cervical enlargement similar lesions were discovered, 
 varying from a state of softening to a state of complete 
 solution, and diminishing at intervals or almost disap- 
 pearing, to return shortly in the same form. At the 
 upper part of the dorsal region the shape of the cord 
 was much altered, and extensive lesions of the same 
 kind were everywhere seen. In both lateral halves of 
 the grey substance, the left lateral column, the right 
 antero-lateral column, the superficial portion of the 
 anterior columns, and in the posterior columns similar 
 appearances were found. Below this point there was 
 less disease as far as the fourth dorsal vertebra. Here, 
 in addition to the areas of disintegration, large extra- 
 vasations of blood were found along the whole lateral 
 part of the grey substance, on both sides in some 
 sections, on one side only in others ; whilst the lumbar 
 regions manifested the same lesions as the cervical. In 
 the second case, which was one of idiopathic tetanus, 
 areas of disintegration and exudation were discovered 
 in different parts of the cord, but chiefly in the central 
 grey substance. In the other cases similar conditions 
 were found, but not always over the same extent of 
 surface. 
 
 Dickenson describes somewhat similar lesions in a 
 case of traumatic tetanus, attacking the central grey 
 matter specnally. The cord seemed to the naked eye
 
 TETANUS. 353 
 
 the seat of three swelhngs. On the right side of the 
 cervical enlargement was an oval swelling about the 
 size and shape of a split bean, which lay between the 
 roots of the nerves. A more extensive change of the 
 same kind was found opposite the first lumbar vertebra; 
 and about half-way between this tumefaction and the 
 lower end of the cord was a smaller circumscribed 
 prominence of the same nature, which lay likewise on 
 the posterior aspect of the cord. There was great 
 injection of the spinal diu*a mater and pia mater. In 
 this case the blood-vessels appeared to be, if not the 
 first, at least an early seat of change. Distended witli 
 blood, not only to the uttermost of their natural 
 capacity, but dilated to many times their proper width, 
 and crammed with blood corpuscles so as to look like 
 solid cylinders, their condition gave evidence of an 
 altogether abnormal relation between the pressure of 
 the blood and tlie resistance of the walls. Either 
 blood had been propelled into them with supernatural 
 force, or, what is more hkely, the tension of their coats 
 had been lessened by a change in their innervation. 
 
 The overcharge of the vessels led to the escape of 
 their contents. In some places blood corjDuscles were 
 extended. More often only the fluid portions of the 
 blood traversed the walls, to appear as the translucent 
 structureless material which played so prominent a 
 part in the destruction of the cord. That this trans- 
 lucent material was an exudation from the vessels, and 
 not a product of disintegration of tissue, is evident 
 from the following facts. It constantly lay in contact 
 with the vessels and often surrounded them. It held 
 
 A A
 
 354 TETANUS. 
 
 the most changeable relations to the nervous matter, 
 lying in the grey matter, in the white, abundantly 
 in the fissures, and occasionally outside the cord 
 altogether. It was the source of increase of bulk, of 
 laceration, and of displacement, such as to suggest that 
 it was an addition to the structure, and had been 
 forcibly driven into it. At the same time a certain 
 amount of disintegration of the nervous elements had 
 taken place where the exudation came in contact with 
 them ; and this tendency to disintegration in the 
 nervous matter may have been enhanced by the 
 unnatural state of the blood-vessels, and the consequent 
 imperfect nutrition of the cord. The distension and 
 repletion of the blood-vessels throughout the cord 
 involved both arteries and veins, and, in a less degree, 
 the capillaries. 
 
 Dr. Chfford Allbutt has pubhshed notes of four 
 cases of tetanus, witli an examination of the spinal 
 cord in each. The lesions were diminution of con- 
 sistence of various degrees and situations in the cord, 
 hsemorrhage in two of them, visible to the naked eye. 
 On microscopical examination, there was great dis- 
 tension of the blood-vessels in both white and grey 
 matter, with occasional exudation and disintegration of 
 tissue around them ; isolated patches of disintegration 
 of various shapes and sizes in both grey and white 
 matter; and in the grey mattei: numerous vacuities, 
 having on trapsverse section circular or oval outlines, 
 and resulting from disintegration of the nerve-fibres. 
 
 In my own cases, in which minute examination was 
 made, the appearances varied very much.
 
 I
 
 E,L,Fox,M. D. 
 
 Plate 17 
 
 C. BerjeaTi.Lith 
 
 Banks & Co., 
 
 TETANUS 
 (new matter on dura mater.
 
 E,L,Fox,M, D 
 
 C Berjeau.Lith. 
 
 T E T A I^I U S 
 (colloid d e ge t^ a rat I n )
 
 TETANUS. 355 
 
 In case 1, the only abnormality to be remarked was 
 dilatation and distension of the vessels of the spinal pia 
 mater. The cord itself was healthy. 
 
 Case 2, Plate 17. Man, aged 36. Brain quite 
 healthy, except that the central white matter round 
 the ventricles and the crura cerebri were rather soft. 
 Spinal cord universally soft in its whole extent and 
 thickness. About the 6th or 7th cervical vertebra this 
 softening of the whole thickness of the cord amounted 
 to a diffluent condition ; and the cord here under tlie 
 microscope seemed composed of broken-down nerve- 
 fibres; nerve-ganglia, and oil. At this point also the dura 
 mater was rather adherent to the bodies of the vertebrce, 
 and beneath it was poured out some new material. 
 
 Case 3. Boy, aged 15. The spinal cord and 
 membranes were healthy down to a spot corresponding to 
 the lOth or 1 1th dorsal vertebra. Here there was a small 
 quantity of blood effused outside the spinal dura mater ; 
 a httle gummy-looking fluid existed beneath the arach- 
 noid. The spinal cord at one spot here was much 
 softened, almost diffluent, and was ruptured on the very 
 gentlest traction. This condition existed through its 
 whole thickness for about half an inch at this spot. 
 There were many amyloid bodies in the grey substance 
 and some thickenino; of the vessels. 
 
 Case 4, Plate 18. Boy, aged 9. A good deal of 
 blood existed in the external veins of the cerebral 
 hemispheres. Brain healthy, cerebellum a little soft, 
 as was also the posterior portion of the medulla 
 oblongata. The posterior columns of the spinal cord 
 throughout their whole length were extremely softened,
 
 356 TETANUS. 
 
 almost resembling cream. This was especially apparent 
 immediately below the medulla oblongata, and about 
 the middle of the dorsal region of the cord. This 
 softening was entirely limited to the posterior columns, 
 except at the very top of the cord, where for about an 
 inch the whole cord seemed almost equally soft. In 
 all other parts the rest of the thickness of the cord was 
 firm and healthy. The softened portion was very 
 white, not reddened at any spot ; and was composed of 
 an immense number of globular bodies, somewhat 
 irregular in size and shape, ' colloid degeneration of the 
 neurogha nuclei,' and no trace of the structure of the 
 cord remained. 
 
 Case 5, Plate 19. This plate was from a case of 
 tetanus of which I have not the history. It is very 
 little magnified, but shows very well the white spots of 
 colloid degeneration, the dark dots of amyloid bodies, 
 and thickening of vessels. The portion of cord repre- 
 sented is that between the posterior horns of the grey 
 matter. 
 
 Here then are a considerable number of instances 
 in which the spinal cord has been examined micro- 
 scopically and lesions found ; lesions, it is true, varying 
 in nature, but having pretty much the same significance. 
 It is tolerably certain that these lesions do not exist in 
 cases of recovery ; or, if they do, they must be of 
 extremely small extent. We may be sure that haemor- 
 rhage has not taken place if a tetanic patient recovers 
 without any trace of paralysis being left. Grave 
 degenerations of the cells of the neuroglia, amyloid, or 
 colloid, would be conditions wholly irrecoverable, as
 
 E L.Fox,M. I) 
 
 Plate 19 
 
 fijeau.Lith. Banks 3c Co.. EdmT 
 
 T E T A N U s 
 
 C.^LIOIL AND AMYLCID DEGENERATION. THICKENED VESSELS^)
 
 I 
 
 I 
 
 TETANUS. 357 
 
 far as we know. Again, when the exudation, either by 
 pressure or by some solvent action, lias caused grave 
 and extensive disintegration of portions of the spinal 
 cord, it is highly improbable that recovery can take 
 jilace. As, however, a certain number do get well, 
 especially of idiopathic tetanus, we may be sure that 
 these severe lesions do not obtain in all cases. The 
 distension of the vessels and a certain amount of 
 exudation can be got rid of, and the cord become 
 almost, if not completely, the same as before. 
 
 Lockhart Clarke asks ' Are the structural lesions or 
 the disintegrations of tissue the effects of the functional 
 excitement of the cord manifested in the tetanic spasms?' 
 That they are not the effects of this excitement would 
 appear, he thinks, from the following facts : ' That they 
 more frequently occur in the central parts of the grey 
 substance around the canal, where the nerve-cells 
 are scanty ; that the nerve-cells of the anterior grey 
 substance, which give origin to the motor nerve-roots, 
 remain apparently unimpaired ; that the structural 
 changes commence frequently in company with exuda- 
 tions around or in the vicinity of blood-vessels which 
 are themselves commonly found dilated and frequently 
 in a state of disintegration ; and lastly, that they are 
 exactly similar in kind to the lesions and disintegrations 
 which I find in various cases of ordinary paralysis, in 
 which there is little or no spasmodic movement. It 
 appears, therefore, that they result from a morbid state 
 of the blood-vessels, and not from excessive functional 
 activity of the cord.' 
 
 Still, though the whole of the lesions may not be
 
 358 TETANUS. 
 
 the effects of the spasms, some may be. The disten- 
 sion of the vessels is not unhke what is often seen in 
 the medulla oblongata in epilepsy, the dilatation having 
 occurred in consequence of the primary arterial con- 
 traction. It is not impossible that the exudation may 
 have been the consequence of this same over- distension, 
 the congested vessels relieving themselves under con- 
 siderable pressure. Much of the disintegration may be 
 due to the mechanical pressure of this very exudation, 
 whilst some of it may own as its cause the impaired 
 nutrition consequent on the frequently repeated con- 
 traction of the arteries. The amyloid and colloid 
 degeneration of the neuroglia cells are met with under 
 circumstances both of impaired nutrition and of slow 
 inflammatory action. 
 
 The third question, as to whether the same lesion 
 may be found under circumstances wholly uncon- 
 nected with tetanus, has been practically answered 
 already. There is no one lesion of those above-men- 
 tioned that may not be found in cases of ordinary para- 
 lysis, in progressive muscular atrophy, in locomotor 
 ataxy, &c ; only in these latter diseases the lesion is 
 more or less strictly confined to a particular district of 
 the spinal cord. In such diseases there is nothing 
 analogous to tetanic spasm. 
 
 Thus far we find the pathological anatomy of tetanus 
 in this position: 1. Lesions of the peripheral end of 
 the nerve in a certain proportion of cases of traumatic 
 tetanus; such lesion being absent in many cases, and 
 of course not present in instances of idiopathic tetanus. 
 2. There are many and various lesions of the spinal
 
 I 
 
 TETANUS. " 359 
 
 cord frequently met with, involving both grey and 
 white matter, but especially the commissures of the 
 cord and the immediate neighbourhood of the blood- 
 vessels ; not only, however, may tetanus exist without 
 any of these spinal cord lesions, but the abnormalities 
 of the cord may be present without tetanus. These 
 lesions may, in fact, be effects of the tetanic spasm, or 
 of the arterial contraction which is one of the first phe- 
 nomena of the attack ; but they jdo not enter into the 
 causation of the tetanus further than in this limited 
 way, that any malnutrition of the cord may render it 
 abnormally impressible. 
 
 What then is the cause of the tetanic phenomena? 
 
 No doubt sudden variation in temperature, bad 
 ventilation, cold and damp, may all be predisposing 
 causes. But how.? Is there one cause for traumatic 
 and another for idiopathic tetanus ; or is the chief dif- 
 ference this, that the primary lesion is external in the 
 one case and internal in the other ? 
 
 Lockhart^ Clarke attempts to answer the question 
 thus : ' Since lesions of the cord in cases of paralysis, in 
 which there is commonly no spasm, are similar to those 
 of tetanus, it follows that the latter disease, in regard to 
 its morbid anatomy, differs from»the former only in 
 being associated with a morbid condition or injury of 
 some of the peripheral nerves. It would therefore 
 appear that this condition or injury of the peripheral 
 nerves is the determining cause of the phenomena, and 
 that the spasms of tetanus depend on the conjoint 
 operation of two separate causes. First, that they 
 depend on an abnormally excitable state of the grey
 
 360 * TETANUS. 
 
 nerve-tissue of the cord, induced by the hypersemia and 
 morbid state of its blood-vessels, with the exudations 
 and disintegrations resulting therefrom. This state of 
 the cord may be either an extension of a similar state 
 along the injured nerves from the periphery, or may 
 result from reflex action on its blood-vessels excited 
 by those nerves. Secondly, that the spasms depend 
 upon the persistent irritation of the peripheral nerves, 
 by which the exalted excitabihty of the cord is aroused ; 
 and thus the cause, which at first induced in the cord 
 its morbid susceptibility to reflex action, is the same 
 which is subsequently the source of that irritation by 
 which the reflex action is excited ; whilst in idiopathic 
 tetanus arising from exposure to cold and damp it is 
 probable that the morbid condition of the blood-vessels 
 of the cord results from change in the state of the peri- 
 pheral nerves, which may act through reflex actions or 
 otherwise.' 
 
 The objections to this view are: 1. That there is 
 often no morbid condition of the nerve at all, or at 
 least no other abnormality than is constantly seen after 
 operation without tetanus ; 2. That it is improbable 
 that hypereemia of the cord can be induced by an 
 extension of a similar state along the injm^ed nerve 
 from the periphery, whilst reflex action from the 
 injured nerve would induce contraction of arteries 
 rather than hyperiemia ; 3. It affords no explanation 
 for those cases in which no spinal cord lesion exists. 
 
 I believe that in tetanus we must look for the con- 
 nective lesion in the chemistry of the blood. In 
 strychnia-poisoning, a disease so closely analogous to
 
 TETANUS. 361 
 
 tetanus, the presence of strychnia in the blood, or 
 rather the effect that strychnia has on tlie physiolo- 
 gical conditions of the blood, has been demonstrated as 
 the cause of the spasmodic phenomena. Dr. Harley 
 has shown that blood mingled with a solution of 
 strychnia is incapable of absorbing oxygen in the usual 
 proportion. 
 
 With symptoms almost precisely similar, it is diffi- 
 cult to believe that tetanus is a functional disease, 
 acknowledging as its cause no necessary organic change 
 and no abnormality in the blood. And as death may 
 occur from strychnia, independently of asphyxia, or 
 inanition, or exhaustion, by destroying the chemical 
 power of the blood for assimilating oxygen, and thus 
 rendering muscular respiration impossible, so cases do 
 occur in traumatic tetanus where death ensues while 
 the patient is taking plenty of nourishment and stimu- 
 lants, where there is no bar to the pulmonary circulation, 
 and with too little spasm to cause exhaustion, and the 
 patient sinks as surely from a poisoned condition of 
 blood, a blood unfit for the purposes of life, as in those 
 cases of cholera well-nigh instantaneously fatal which 
 occur occasionally in the course of an epidemic. The 
 abnormal blood may or may not lead to the various 
 lesions of the cord which have been already mentioned. 
 It must, however, from the first, modify decidedly the 
 nutrition of the cord. If this nutrition is not modified 
 to too great an extent, and especially if the organic 
 lesions dependent on such modifications of nutrition 
 are not developed, the patient recovers, if the blood is 
 gradually restored to its power of taking up oxygen.
 
 362 TETANUS. 
 
 It is very suggestive, especially when we consider 
 the distended condition of the vessels in fatal cases, 
 that the remedies most useful in tetanus are those 
 which partially paralyse the vaso- motor nerves and 
 thereby distend the vessels. I feel sure that prolonged 
 contraction of the arteries is the phenomenon to be 
 most dreaded, and that the hypercemia found after 
 death is really the reaction from this previous state of 
 contraction. 
 
 The abnormal blood imperfectly nourishes the cord ; 
 an imperfectly nourished cord is ipso facto an excitable, 
 an impressible cord ; this impressibility renders arterial 
 spasm abnormally facile, whether the exciting cause is 
 the circulation in the cord of more of the morbid 
 blood, or reflected irritation from a diseased nerve at 
 the periphery, or reflex irritation from any other 
 cause and from any other point in the body ; and if 
 this arterial contraction goes on for any protracted 
 period, or is frequently repeated, we may find various 
 lesions due to imperfect blood-supply in addition to 
 those due to diminished nutrition from the original 
 nature of the blood, whilst as a sequence of the 
 spasmodic arterial contractions we get hypersemia and 
 perhaps exudation ; and lastly, the pressure of the 
 exudation, or some peculiarity in its nature, may lead 
 to further disintegration of the nervous centre. 
 
 It is right to say a few words on tetany or 
 tetanilla, as both in its symptoms and its pathology it 
 seems somewhat connected w^ith tetanus. It is 
 characterised by intermittent paroxysms of tonic 
 spasms affecting the upper and lower limbs, and in
 
 TETANY. 3G3 
 
 severe cases nearly all the muscles of the body. Thespasin 
 is ushered in by a sensation of tingling, followed by a 
 feeling of hesitation in movement, and is attended often 
 by considerable pain, and by no loss of consciousness. 
 
 Trousseau thinks it can be diagnosed by the ap- 
 pearance of the hand during a paroxysm ; the thumb 
 is forcibly and violently adducted, the fingers are 
 pressed together closely, and semiflexed over the 
 thumb in consequence of the liexion of the meta- 
 carpo-phalangeal articulation, and the palm of the 
 hand being made hollow by the approximation of its 
 outer and inner margins, the hand assumes a conical 
 shape, or rather the shape which the accoucheur gives 
 to it when introducing it into the vagina. 
 
 It is dia^rnosed from tetanus, in that in tetanus the 
 muscles of the ja^vs are first affected, then of the face, 
 and then the trunk, whilst the spasm only by degrees 
 extends to the extremities ; but in tetany the contrac- 
 tions run an opposite course, and it rarely happens 
 that the muscles of the extremities and those of the 
 rest of the body are affected at the same time. 
 
 The disease is seldom fatal, and pathological 
 anatomy has done very little in clearing up the nature 
 of the complaint ; but, as Trousseau says, ' from a mere 
 review of the symptoms it is impossible to admit that 
 such mobile and transitory phenomena can be due to 
 the existence of serious organic lesions,' He considers 
 it to be due to rheumatism. 
 
 Uydrophobia. — So little has been known hitherto 
 of the pathological anatomy of this disease, that many
 
 3G4 HYDROPHOBIA. 
 
 writers avoid all mention of it in their works, and 
 others are content to dismiss it in a few words. 
 
 Morgagui, Mead, and Van Swieten affirm that 
 there is nothing abnormal in patients who have died of 
 this malady. Others only make the remark that there 
 are some traces of asphyxia, some engorgement of the 
 lungs, a venosity of the blood, and sometimes an 
 effusion of serum in the ventricles and in the meninges 
 of the brain and cord, a condition that might well be 
 due to the asphyxia. Trousseau says that the patho- 
 logical changes found after death are only those 
 dependent on the asphyxia which occurs in the last 
 stage. 
 
 Hyperemia of all the parenchymatous organs is 
 met with as a consequence of the final convulsion. 
 
 The spleen is sometimes found abnormally en- 
 larged. 
 
 Eudnew holds that hydrophobia, like almost all 
 other infectious diseases, is connected with a profound 
 disturbance of all the important organs. In all his 
 cases the kidneys manifested a highly developed 
 parenchymatous inflammation, the peculiarity of which 
 was that both cortical and pyramidal portions were 
 alike affected, presenting all the conditions necessary 
 for the production of uraemia. He thinks it ex- 
 tremely probable that the latter may be the cause of 
 many of the symptoms. A second peculiarity was the 
 degenerative character of the nephritis ; in the most 
 advanced and fatal stage of the disease the urinary 
 tubules were completely bare of epithelium, and filled 
 with a granular fatty degenerated material.
 
 HYDROPHOBIA. 3G5 
 
 In Dr. Wilks' fatal cases the body was livid, par- 
 ticularly the face, which looked like strangulation. The 
 blood was of a dark colour and quite fluid, both in the 
 vessels and in the heart ; the lungs were much congested, 
 and the posterior parts of a very dark colour and soft ; 
 the bronchial tubes also conoested and of a dark colour. 
 The kidneys, liver, &c., all congested ; and the brain 
 and spinal cord showed no other appearance than con- 
 gestion, due to the mode of death. The larynx was 
 healthy, but the pharynx presented a very unusual con- 
 dition, being dilated, as if violent muscular contraction 
 had occurred in it ; the mucous membrane was swollen ; 
 the glands were enlarged and covered with thick 
 secretion, as were all the glands at the back of the 
 tongue. 
 
 In the beginning of this century a Russian physician, 
 Dr. Marochetti, in a memoir on hydrophobia, and Dr. 
 Xanthos of Siphnos, in a letter to Hufeland, called atten- 
 tion to the presence, on the under surface of the tongue, 
 near the frsenum, of pustules or vesicles of a special 
 character during the stasfe of the incubation of rabies. 
 These had long been known in Greece under the name 
 of ' lyssi.' The presence of these pustules had long 
 been known also traditionally in Eussia and in Greece. 
 These physicians believed that, if these vesicles or pus- 
 tules were laid open in time and cauterised, all manifesta- 
 tions of rabies were prevented. These lyssi, however, 
 have not been found in all cases. 
 
 Cases of hydrophobia are happily not very common, 
 and in many instances observers have been content with 
 recording naked-eye appearances. To Dr. Clifford
 
 363 HYDROniOBIA. 
 
 Allbiitt, however, the profession are indebted for careful 
 observation of two cases. In one only the medulla 
 oblongata, the pons, and the spinal cord were examined ; 
 in the other the whole of the cerebro- spinal centres. 
 Throughout all these centres the same morbid conditions 
 were observed. There was visible great vascular con- 
 gestion, with transudation into the surrounding tissues. 
 In the cerebral convolutions, the meso-cephale, the pons, 
 medulla, and spinal cord, the vessels were seen in 
 various degrees of distension ; in many places their walls 
 were obviously thickened, and here and there in them 
 were patches of incipient nuclear proliferation. On 
 removing the parts there was found in many places a 
 diminished consistence, and this was well marked in the 
 medulla. 
 
 This seemed to be due to serous infiltration with 
 soddening, and was seen in the convolutions, in a few 
 parts of the central ganglia, in the medulla in both 
 cases, and here and there in the cord. In both cases, 
 too, there seemed to have been a transudation of some- 
 thinix more than serum. In some sections laro^e hsemor- 
 rhages were visible ; in some few other places minute 
 hoamorrhage had occurred, and in many spots there was 
 a refracting material outside the vessels, which probably 
 was of the nature of a coagulated fibrinous exudation. 
 Finally, there were found in the encephalon, occasionally, 
 in both spinal cords more frequently, and in both me- 
 dullas abundantly, little gaps caused by the disappear- 
 ance of nerve-strands, which had passed through the 
 granular disintegration of Clarke. These phenomena, 
 together with the enlarged spleen found in both cases,
 
 HYDROPHOBIA. 367 
 
 point to the action of an animal poison acting primarily 
 on the cerebro-spinal nervous system. The order of 
 the severity in the various parts seemed to be — first and 
 worst, the medulla ; secondly, the cord ; thirdly, the 
 cerebral convolutions ; and fourthly, the central ganglia 
 of the encephalon. 
 
 These lesions would be of still higher importance if 
 they occurred in all cases ; but Dr. Elder has recorded 
 three cases of hydrophobia in which no lesion was found 
 in the cerebro-spinal nervous system, and in one of these 
 the cerebellum, the medulla oblongata, and part of the 
 cerebrum had been microscopically examined by Lock- 
 hart Clarke himself, who reported that they were free 
 from all lesion, except congestion. 
 
 Abercromby mentions that in hydrophobia inflam- 
 mation of the cord had once been remarked. 
 
 Besides, then, the morbid phenomena due to the 
 mode of death, such as engorgement of the lungs and 
 other viscera, congestion of brain and spinal cord, &c., 
 there have been at present recognised a peculiar 
 development of the glands of the fauces, vesicles, or 
 pustules under the tongue, and these especially during 
 the period of incubation of the disease, a special degene- 
 rative nephritis, an enlargement of the spleen, and 
 granular disintegration of the convolutions, the medulla 
 oblongata, and the spinal cord ; but at present we cannot 
 say that there is any definite lesion peculiar to the disease, 
 and certain to be found post mortem. 
 
 Consult, for Tetanus — 
 
 Jaccoud, ' Path. Interne.' 
 
 Eeyuolds, ' System of Medicine.'
 
 368 HYDROPHOBIA. 
 
 Wilks, ' PatL. Anatomy.' 
 
 Rokitansky, 'Path. Anatomy.' 
 
 Romberg, ' Dis. of Nervous System.' 
 
 Trousseau, ' Clinical Lectures.' 
 
 Sandras & Bourguignon, * Maladies Nerveuses.' 
 
 Handfield Jones, ' Functional Dis. of Nervous System.' 
 
 Briglit's ' Med. Reports.' 
 
 ' New Syd. Soc. Yearbook,' 1871-72. Dr. Allbutt. 
 
 ' Med.-Chir. Review,' 84, 86. Dr. Ogle. 
 
 * Guy's Hosp. Rep.,' xv. Mr. Poland. 
 
 * Med.-Chir. Trans.,' 51. Dr. Dickenson. 
 
 * Med.-Chir. Trans.,' 48. Lockhart Clarke. 
 ' Med. Record,' 1, 533. Roemer. 
 
 Consult, for Hydrophobia — 
 Wilks, ' Path. Anatomy.' 
 Trousseau, ' Clin. Lectures.' 
 'New Syd. Soc. Yearbook,' 1871-72. Rudnew. 
 ' Brit. Med. Jour.,' vol. ii. 1871. Dr. Elder. 
 « Med. Record,' 1, 22. Dr. Allbutt. 
 'Med.-Chir. Review,' July, 1874.
 
 369 
 
 LECTURE XIIL 
 
 LESIONS OP THE SPINAL CORD IN SMALL-POX. 
 
 Some few cases have been observed and the cords 
 examined by Westphal, Lockhart Clarke, and others, 
 where, in the course of an attack of variola, certain 
 paralytic phenomena had manifested themselves. In 
 Westphal's first case the patient felt in the third day of 
 discrete small-pox some weakness of the legs. Complete 
 paralysis supervened, so that he only retained some 
 slight power of moving his great toes ; reflex move- 
 ments were abolished ; sensibility unimpaired ; there 
 was paralysis of bladder and a slough over the 
 sacrum ; faradic irritability of the muscles was 
 retained. In the second case motor paralysis of the 
 left leg, with a sensation of numbness in it, was 
 experienced on the eleventh day of the disease. The 
 day afterwards the right leg became paralysed, with 
 incontinence of fa3ces and a peculiar sensation as if 
 the abdomen were dead. The patient died of cystitis 
 and slough over the sacrum. At the necropsy the grey 
 substance of the spinal cord was found congested, but 
 there was no alteration in either the white columns 
 or in the nerve-roots. In one of the sciatic nerves 
 a slight infiltration of blood was noticed between 
 
 B B
 
 370 LESIONS OF THE SPINAL CORD IN SMALL-POX. 
 
 its bundles. On making thin sections of the cord, 
 after it had been treated with bichromate of potash, 
 patches variously altered in colour were found to be 
 irregularly scattered through the grey and white sub- 
 stance. Areas of softening, about the size of a pin's 
 head, were seen in the grey substance at the superior 
 thoracic region. In all those places where the colour 
 of the tissue was modified there was an abundance of 
 fatty granulations. Westphal proposes to name this 
 condition ' Disseminated Myelitis.' Vulpian gives a 
 very interesting case in which life was preserved and 
 partial recovery had taken place from a state of partial 
 paralysis of the upper extremities supervening on small- 
 pox. Vulpian thinks that in each case during the 
 development of small-pox there was an inflammatory 
 irritation of the spinal cord in the region corresponding 
 to the roots of the nerves which supplied the muscles 
 and skin of the shoulders. The inflammation probably 
 attacked different elements of the grey substance, and 
 amongst others the nerve-cells of the anterior horns. 
 Then the nerve-fibres of the anterior roots, at least 
 those in connection with the altered cells, underwent 
 granular degeneration, which takes place when the 
 normal influence which these cells have on the nerve- 
 fibres ceases. The muscles supphed by these nerve- 
 fibres became atrophied, and their contractibility was 
 so weakened that it became no longer excitable through 
 the skin by the induced current. This is the necessary 
 result of the lesion which is supposed to have existed 
 here. There was therefore, probably, in this case a 
 group of lesions connected with each other, which
 
 LESIONS OF THE SPINAL CORD IN SM.\LL-POX. o71 
 
 remind us of the group that exists in the atrophic 
 paralysis of infancy. M. Vulpian says that in several 
 cases of small-pox in which there was severe rachi- 
 algia he has not found after death any change what- 
 ever in the grey or the white substance of the cord. 
 
 Lockhart Clarke, who reports these observations of 
 Westphal and Vulpian, published a case of extreme 
 muscular atrophy of the arms and shoulders consequent 
 on inoculation with the virus of small-pox, with 
 extensive disease of the cervical portion of the spinal 
 cord. 
 
 We give this case in Lockhart Clarke's own words. 
 The man, aged 32, had been inoculated when about a 
 year old. Before tliis operation he was a fine healthy 
 child. He suffered much after the inoculation, and 
 gave evidence of severe indisposition ; and when the 
 eruption was fully developed, the left arm was observed 
 to droop and become powerless. Soon afterwards the 
 right arm followed the same course. From this period 
 the muscles of the arms and shoulders ceased to be 
 developed, and at the same time the heart's action 
 became irregular and disturbed, and continued so ever 
 after. When he was examined, a few months before 
 his death, the muscles of the shoulders and arms had 
 almost entirely disappeared. The muscles of the fore- 
 arm were apparently unaffected. The muscles of the 
 ball of each thumb were almost altogether gone, while 
 those of the lingers were well developed. The 
 muscles of the dorsum of each scapula were nearly 
 gone ; all those of the lower extremities were well 
 developed. On examination of the cervical enlargement 
 
 B B 2
 
 872 LESIONS OF THE SPINAL CORD IN SMALL-POX. 
 
 of the spinal cord after d^ ath, I found extensive lesions 
 and displacements of the grey substance. On the right 
 side the posterior horn was drawn backward with a 
 long streak towards the softened surface of the cor- 
 responding white column. The cervix cornu on each 
 side was more or less damaged in different sections 
 by a streak of disintegration, and in the anterior grey 
 substance there was an extensive area of softening and 
 disintegration. On the right side the lesions in the central 
 part of the anterior grey substance were less conspicuous, 
 but there was a dilated blood-vessel with its branches 
 bordered by a thin layer of exudation, and by the sur- 
 rounding tissues in a state of disintegration. Besides 
 other changes in different parts of the cervical region, a 
 great number of the nerve-cells were found to be in 
 different states of atrophy and disintegration. In many 
 instances, the large cells of the anterior cornu were 
 reduced to at least one-eighth or one-tenth of their 
 ordinary size, and some even to mere granular points ; 
 while in other instances, although not much reduced in 
 size, they had lost their sharpness of outline, and con- 
 sisted of an uneven aggregation of granules. 
 
 LESIONS OP THE NERVOUS SYSTEM IN DIABETES. 
 
 It is probable that the lesions of the nervous system 
 in diabetes are of a twofold nature — the one primary and 
 causative, the other secondary and dependent on the 
 altered nutrition induced either by the presence of an 
 abnormal amount of sugar in the blood, or of the 
 negative loss to the blood in this disease. 
 
 I
 
 LESIONS OF THE NERVOUS SYSTEM L\ DIABETES. 373 
 
 The first series of lesions can be produced artifi- 
 cially. If the floor of the fourth ventricle is punctured 
 in a very limited space, the production of sugar is 
 increased, and the animal becomes diabetic. This spot 
 is comprised between the origin of the vagi and the 
 auditory nerves. Bernard found that the channel of 
 communication between this portion of the nervous 
 centre and the liver was not by the pneumogastric 
 nerves. It was proved by his experiments that the 
 superior parts of the spinal cord could be alone con- 
 cerned ; for on going beyond the first dorsal vertebra 
 he failed to produce the phenomenon. The excitement 
 is therefore transmitted by the spinal cord as far as the 
 top of the first pair of spinal nerves, and from this 
 point it follows the only path leading to the liver, the 
 large and small splanchnic branches of the sympathetic. 
 
 Certain pathological alterations of the nervous 
 system, of which I will speak immediately, have had 
 the same result. A Rouen physician, M. Leudet, has 
 ascertained that diabetes and glycosuria are produced 
 in certain affections of the encephalon. Glycosuria has 
 been known to be the consequence of a fall on the 
 head. Anotlier process is the administration of some 
 poisonous substance ; as woorara, for example. The 
 poisoned animal becomes diabetic. Morphia in large 
 doses will produce the same effect. 
 
 In all these cases, if the viscera of the animal be 
 examined, it is seen that the circulation is considerably 
 increased there. Bernard's expression is — ' The hepatic 
 cells, foci of glycogenic matter, find themselves sur- 
 rounded by a kind of sanguineous network. The
 
 374 LESIONS OF THE NEEVOUS SYSTEM IN DIABETES. 
 
 circulation becoming more active in this network, the 
 contact of the sanguineous fluid with tlie cellular 
 fluids is better assured, the action on the glycojzenic 
 matter is more energetic, the transformation becomes 
 more abundant, and the sugar produced is immediately 
 carried away. The increase in the rapidity of the 
 circulation of the liver increases the glyca3mia.' This is 
 the theory of the operation. Still, this increase in the 
 circulation of the liver is not the result of paralysis of 
 the vaso-motor nerves. The floor of the fourth ventricle 
 is certainly one of the most clearly defined of the 
 vaso-motor centres, and diabetes, caused by woorara or 
 by morphia, is produced not by any direct influence of 
 these poisons on the vessels of the liver, but through 
 the medium of the nervous system, precisely as in 
 artificial diabetes from puncture of the floor of the 
 fourth ventricle. Thus, if it were by means of vaso- 
 motor paralysis, the functional trouble would persist as 
 long as the lesion ; whereas it is not so. The diabetes 
 is essentially temporary. It is by nervous excitation 
 which is temporary. The instantaneous action of the 
 fourth ventricle and the resultant irritation are the 
 causes of the circulatory superactivity and of the 
 diabetes. The effect persists as long as the irritation. 
 Bernard believes that the phenomenon may be referred 
 to the momentary excitement of the medulla oblongata 
 produced by the puncture. The first action, too, of 
 woorara and morphia on the nerves is an irritation of 
 their peripheral or central extremities. The effect of 
 various pathological lesions is similar. A lesion of 
 the medulla oblongata or of the upper part of the
 
 LESIONS OF THE NERVOUS SYSTEM IN DIABETES. 375 
 
 spinal cord sufficient to cause irritation and excitation, 
 and not paralysis, will be likely to produce diabetes. 
 Cyon and Aladoff corroborate Eckhard's statement — 
 that diabetes occurs in dogs an hour after the section of 
 the inferior cervical or upper dorsal ganglia. 
 
 What, then, are tlie pathological conditions that 
 have this direct influence on the causation of diabetes ? 
 Congestion of the floor of the fourth ventricle near the 
 calamus scriptorius, blows on the occiput, falls on the 
 head, fracture of the cranium, or traumatic injuries of 
 the brain, apoplexy, with intracranial effusion, intra- 
 cranial tumours, are some of the most important. 
 Dr. Eoberts observes that it is probable that in all 
 the traumatic cases the injury implicated some part of 
 the nervous system. Luys describes a case of a 
 diabetic in whom lesion of the anterior wall of the 
 fourth ventricle was found ; and in connection with 
 this point an observation of Dr. Eichardson is inte- 
 resting. He found the symptoms of a diabetic painter 
 much increased whenever he, as a house painter, had 
 to look constantly upwards, with the head thrown 
 back, as in painting a ceiling. Several cases, too, have 
 been recorded where diabetes has co-existed with the 
 presence of tender spots in the back of the neck, and 
 the diabetes has vanished with the tenderness on the 
 appUcation of blisters, cupping, or setons to the neck. 
 
 Dr. Ogle mentions that intermittent diabetes has 
 been said to have followed traumatic and other varieties 
 of lesion of the brain, and other parts of the nervous 
 system, including non-traumatic extravasation of blood, 
 a calcareous growth projecting from the basilar groove
 
 3/u LESIONS OF THE NERVOUS SYSTEM IN DIABETES. 
 
 of the occipital bone, pressing on the pons, as also certain 
 general commotions of the nervous system, mental and 
 emotional excitement, even old age, disturbance of the 
 functions of the liver and lungs, inhalation of chloroform, 
 affections of the skin and superficial parts, such as boils 
 and carbuncle, and certain unwonted states of the blood, 
 temporary fever, attacks of a convulsive character, such 
 as eclampsia, hysteria, the use of certain articles of 
 food or of medicine. 
 
 Dompeling has translated from the Dutch a case of 
 diabetes, caused by a tumour (sarcoma fasciculatum) of 
 the size of a nut in the right half of the medulla oblon- 
 gata, producing partial atrophy of the right vagus and 
 spinal accessory nerves, partial paralysis of the internal 
 muscles of the right eye, and persistent diabetes, with 
 death occurring in six years. A very interesting case 
 in which diabetes mellitus supervened upon a severe 
 injury to the heart, in an infant of eight months, is 
 recorded by Dr. Eossbach, of Herbsleben, in the ' Ber- 
 liner Klinische Wochenschrift ' for June 1874. The child 
 fell from the nurse's arms ; a convulsion immediately 
 came on, followed by unconsciousness, vomiting, and 
 other symptoms of shock ; depression of the fontanelles, 
 and dilatation of the pupils. No fracture of the skull 
 could be discerned. Eeaction began on the third day, 
 and in a few days the child had almost recovered. 
 Four weeks after the child was found emaciated and 
 ravenous, and the urine, which was passed in large 
 quantities, found to contain sugar. 
 
 Much more minute investigations have, however, 
 been undertaken in England on this question.
 
 LESIOXS OF THE NERVOUS SYSTEM IN DIABETES. 377 
 
 Dr. Dickenson brought a series of cases before the 
 Medico Chirurgical Society, and showed tliat pecuHar 
 morbid changes were constantly found in tlie cerebro- 
 spinal system. 
 
 In all, the alterations were of the same nature and 
 in similar situations. The earliest alteration recoarnised 
 
 o 
 
 consisted in a dilatation of the blood-vessels, particularly 
 of the arteries, with accumulation and frequent extrava- 
 sation of their contents. The next was a degeneration 
 of the nervous matter at certain points outside the 
 swollen vessels, probably caused by the intrusion into 
 it of blood corpuscles. The degenerative process occa- 
 sioned destruction and excavation of the tiseue round 
 the vessel. Cavities were thus produced, often large 
 enough to be striking objects, even without the micro- 
 scope ; cavities which contained blood-vessels, extra 
 vasated blood, grains of pigment, and the products of 
 nervous decay. Finally, the contents appeared to have 
 become absorbed, so that simple vacuities were left. 
 The perivascular sheath was variously stretched and 
 altered in character, and became loaded with pigment ; 
 but it seemed that these alterations were consequent 
 upon the dilatation of the vessel, extravasation of blood, 
 and excavation of nervous matter. As to their situa- 
 tions, the chansres occurred in constant association with 
 arteries. They were found in every part of the spinal 
 cord and encephalon, attaining their greatest develop- 
 ment in the medulla oblongata and pons Varolii. The 
 excavations were generally the most marked where the 
 blood-vessels piercing the brain were the largest and 
 most numerous. They were frequently in connection
 
 378 LESIONS OF THE NERVOUS SYSTEM IN DIABETES. 
 
 with folds of the pia mater. The regions affected with 
 the greatest frequency were the olivary bodies, the 
 vicinity of the median plane of the medulla, the grey 
 matter of the floor of the fourth ventricle, a fissure just 
 internal to the origin of the facial nerve which lodges a 
 process of the pia mater, and a depression similarly 
 occupied, which penetrates from between the anterior 
 crura towards the centre of the pons Varolii. The optic 
 thalami and corpora striata were involved, though to a 
 comparatively slight extent. The septum of the ven- 
 tricles and the white matter of the convolutions dis- 
 played the alterations in a remarkable manner. The 
 changes especially affected the white matter, though 
 the grey matter at the floor of the fourth ventricle and 
 of the spinal cord are exceptions to this statement. 
 
 In the cord the most conspicuous change was the 
 enlargement of the central canal, probably connected 
 with the degeneration of tissue, of which many evidences 
 were found there and elsewhere. The nerve- cells of 
 the brain and cord were generally perfect. Such parts 
 of the sympathetic system as were examined, namely, 
 the upper cervical and semi-lunar ganglia, were appa- 
 rently natural. 
 
 Dr. Dickenson thinks that the nervous chanjxes are 
 not the result of the state of the blood, because, though 
 the arteries are diseased, the veins and capillaries 
 are not ; and because, although the blood traverses 
 the whole body, no analogous failure in nutrition is 
 produced in any other organ ; and he believes the 
 nervous changes are primary, first, because the changes 
 in the brain are in their nature and situation such as
 
 LESIONS OF THE NERVOUS SYSTEM IN DIABETES. 379 
 
 physiology has shown to be capable of producing that 
 symptom ; secondly, because alterations similar in kind, 
 though difTering in distribution, occur as belonging 
 exclusivel}^ to the nervous system, quite independently 
 of diabetes. 
 
 In a sixth case ])r. Dickenson found similar lesions 
 in the cord, in one olivary body, and in the corpora 
 striata, but in addition to these there was an ovoid 
 channel in the white matter of the cerebellum partly 
 filled with the globular debris of nerve-structure. 
 
 In a seventh case, where the patient died at a very 
 early period of diabetes, there were similar lesions in 
 the medulla oblongata, and punctiform haemorrhages of 
 the pons, whilst in the white matter of the cerebellum, 
 and especially in the central part of the corpus 
 dentatum, large vessels packed with corpuscles lay in 
 eroded channels. 
 
 Dr. John Ogle gives some cases of great interest 
 with reference to the connection of diabetes and 
 abnormalities of the nervous system. 
 
 In his first case the diabetes of old standing dis- 
 appeared coincidently with the appearance of some 
 paralytic symptoms, which increased and persisted up 
 to the death of the patient. The scalp and the bones 
 of the skull presented nothing unusual. The dura 
 mater was considerably adherent to the skull generally, 
 but was itself healthy. There was much dark staining 
 of the cerebral membranes along the track of the 
 blood-vessels. The surface of the brain presented no 
 unnatural appearances ; but on section it proved to 
 be what is termed a wet brain. The anterior portion
 
 380 LESIONS OF THE NERVOUS SYSTEM IN DIABETES. 
 
 of the middle lobe of the brain, on the right side, was 
 to a very great extent exceedingly softened, but not in 
 any degree reddened or otherwise discoloured. On 
 examining the arteries at the base of the brain, the 
 middle cerebral one on the right side and in the 
 neighbourhood of the softened portion of brain was 
 found to be plugged up with a mass of firmish fibrine. 
 The coats of the vessel did not appear to be affected. 
 Other parts of this hemisphere of the brain were 
 natural. The corresponding portion of the middle lobe 
 of the left side of the brain was also, but to a very 
 slight degree, softened, and the middle cerebral artery 
 occupied by a small plug. Dr. Ogle thinks that the 
 nerve lesion was secondary in point of time to this 
 diabetes. It is doubtful if this was so. More probably 
 the lesion of the nerve-centre at an early period only 
 gave rise to excitation, and diabetes was induced; when 
 it advanced so far as to cause paralysis, excitation 
 ceased and the diabetic symptoms vanished. Many 
 diabetic patients die paralytic or comatose. In 15 
 fatal cases recorded in the St. George's Hospital Eeports 
 there was no account of any nerve lesion except in the 
 last case, where Lockhart Clarke examined the medulla. 
 It is worthy of remark that this was the only one of 
 the 15 in which a microscopical examination was made. 
 To the naked eye the whole of the medulla appeared 
 perfectly healthy ; but on examining these sections 
 under the microscope, it was evident that the fourth 
 ventricle, from thj point of the calamus scriptorius 
 upwards for about a quarter of an inch, was the seat of 
 finely granular deposit, extending through the epithe-
 
 LESIONS OF THE NERVOUS SYSTEM IN DIABETES. 381 
 
 liiim for some distance down the raphe, in which, as 
 well as in the substance of the medulla on each side of 
 it, numerous corpora amylacea were interspersed. In no 
 other part of the medulla, nor in the third ventricle, 
 could he perceive any abnormal appearance. The 
 central part of the pons seemed rather more vascular 
 than usual ; but this might be accidental. It is more 
 than probable that some lesions would have been found 
 in other cases had they been sought for. There are at 
 least two varieties of diabetes, one so far remittent 
 that the sugar disappears from tlie urine when all 
 saccharine and amylaceous articles of food are removed ; 
 whilst in the other the sugar remains under any diet. 
 It is probable that in the former the irritation is of a 
 temporary nature — in the latter the lesions which we 
 have been describing are present. 
 
 Consult — 
 
 Wilks, ' Path. Anatomy.' 
 
 ' Med.-Chir. Trans.,' 53, Dr. Dickenson. 
 
 ' Med. Times and Gazette,' March 8, 18G2. Dr. Richardson. 
 
 'Med. Times and Gazette.' June 20, 1874. 
 
 ' Med. Record,' 1, 692. Dr. Claude Bernard. 
 
 ' St. George Hosp. Rep.,' vol. i. Dr. Ogle ; and notes of cases by 
 
 Pavy, Noble, Tardieu, Luys, Roberts, Griesinger, Richardson, 
 
 Kunkler, Buttura, Abeille, and Goolden.
 
 382 
 
 LECTUEE XIV. 
 
 OPHTHALMOSCOPY IN DISEASES OF THE NERVOUS 
 SYSTEM. 
 
 Lesions of the retina and optic nerve are not only 
 important as accounting for amblyopia and amaurosis, 
 but as evidences of various abnormalities in the brain 
 or membranes. 
 
 Speaking roughly, we meet with four chief lesions 
 of the retina — choked discs (called by Dr. Allbutt 
 isch^emia papillas), heemorrhage, optic neuritis, and 
 atrophy. 
 
 I need not say that it is impossible to learn much 
 of the ophthalmoscope in a lecture. It is only by very 
 constant use of the instrument that any adequate 
 knowledge can be arrived at. Still it may be possible 
 to point out to you some of the lesions observed, and 
 to tell you of the morbid circumstances, other than 
 retinal, under which these lesions have been found. 
 
 Observations have been made on the retina in the 
 course of the following diseases or abnormal states : — 
 Meningitis, encephalitis, cerebral softening, cerebral 
 hasmorrhage, phlebitis of sinuses, chronic hydrocephalus, 
 cerebral tumour in various situations within the cranium, 
 cerebral sclerosis, compression of brain and fracture of
 
 OPHTHALMOSCOPY IN DISEASES OF NERVOUS SYSTEM. 383 
 
 skull, acute insanity, dementia, idiocy, general jmralysis, 
 epilepsy, chorea, chronic myelitis, various injuries to 
 the spine and cord, locomotor ataxy, syphilis, leukccmia, 
 albuminuria, diabetes, delirium in acute diseases, toxaamia 
 from various causes, paralysis of the third pair, embolism 
 of the central artery of the retina, and diphtheria. 
 It will be convenient to take the most im})ortant of 
 these in order. 
 
 First, then, meningitis. By the mirror alone it is 
 generally impossible to decide whether we have to deal 
 with tuberculous meningitis or not. In a few very 
 rare cases tubercle has been found in the retina, and 
 has even been observed during hfe by the aid of the 
 mirror. But it is wise to realise what an instrument 
 like this will not do, as well as what it will do. It 
 does not save, it is not meant to save, the practitioner 
 from taking all the symptoms and history of the patient 
 into careful consideration. It will help in two ways ; 
 it will show conditions of meningitis of which the 
 symptoms are so slight that the disease is not easily 
 recognised by them ; and it will teach the positions of 
 the meningitis. It will tell us very little of meningitis 
 of the convexity, very little of meningitis at the most 
 posterior portion of the base, but it is a delicate test 
 for meningitis of the base affecting the anterior portions 
 of the brain, and persisting for a certain time. 
 
 In acute idiopathic meningitis, in tuberculous and in 
 rheumatismal meningitis, the disturbance of the cerebral 
 circulation is almost identical, and therefore very 
 similar vascular lesions are produced mechanically at 
 the fundus of the eye ; but we may remember that
 
 384 OPHTHALMOSCOPY IN DISEASES OF 
 
 meningitis of the anterior portion of the base is much 
 more hkely to be of the tuberculous form than any 
 other. The cerebral hypersemia, the effusion into the 
 ventricles, the engorgement and thrombosis of the 
 meningeal veins, the repletion of the cerebral sinuses, 
 especially the cavernous, obstruct the venous circulation 
 of the eye in meningitis of the base, may retain the 
 blood in the veins of the retina, and so produce intra- 
 ocular lesions, which are known by the name of choked 
 discs or ischsemia papillse. Besides this, the inflamma- 
 tion seems often to creep down the optic nerves, 
 causing optic neuritis, and this lesion is very often 
 associated with ischsemia papillae. 
 
 Further, also, the sheath of the nerve may be 
 implicated in the inflammatory changes, and perineuritis 
 be the result. 
 
 Ischemia papillas then is due to mechanical causes : 
 
 1. Pressure on the cavernous sinus chiefly, causing 
 a diminution or an arrest of the flow of venous blood, 
 and so a great congestion of the optic nerve and escape 
 of the vascular contents, either serum only, or small 
 ecchymoses as well. 
 
 2. This condition is partly caused, and always 
 intensified, by partial strangulation of vessels by the 
 sclerotic ring, a necessary result of the anatomical 
 distribution of the parts. 
 
 ' In ischsemia papilkc (quoting Dr. AUbutt) the 
 trunk of the nerve is unchanged, and all the morbid 
 signs are confined to its intra-ocular termination. 
 This part is greatly swollen, and it generally rises 
 steeply on one side, and sinks gradually to the level on
 
 Till': NERVOUS SYSTEM. 385 
 
 tlie other. There is some swehinGf also of the fibres 
 tliemselves, so that they lose their transparenc}'. Tlie 
 colour of the papilla3 is often a mixture of dirty grey 
 and red, due to" the mingling of passive effusions with 
 distended capillaries and 1 Hemorrhages, l)ut in other 
 cases there is not nuich extravasation of blood, and the 
 protruded disc looks bright or almost transparent.' 
 The veins of the retina are enlarged and generally very 
 tortuous. 
 
 Von Griife's account of this lesion in the first case 
 he observed was that tlie optic papilla Avas considerably 
 and irregularly swollen in such a manner tJiat it rose 
 abruptl}'' on one side, and on the otlier sloped down 
 almost imperceptibly to its ordinary level. The normal 
 trans})arency of its tissue had disappeared, giving place 
 to a greyish tint, with a very strong sliade of red ; the 
 adjacent portions of the retina exhibited exactly tlie 
 same change, so tliat the choroidal margin of the 
 papilla was hidden from view. The retinal opacity 
 was uniform, presenting, nevertheless, with the erect 
 image a slightly striated aspec^t, which followed the 
 course of the optic nerve fibres. The retinal veins 
 were larger than normal, extremely tortuous, very 
 dark-coloured in parts, and issued in a very irregular 
 manner . from the opaque tissue ; the arteries were 
 relatively diminished in size. The opacity of the 
 retina progressively decreased from the border of the 
 papilla. 
 
 Of course any pressure in the same situation may 
 lead to this condition of choked discs, and existing by 
 itself it is nuich more commonly found as the I'csult 
 
 c c
 
 386 OPHTHALMOSCOPY IX DISEASES OP 
 
 of cerebral tumour than of meningitis. Here at once 
 is seen the necessity of taking all the symptoms of a 
 case into consideration. But it may exist as the main 
 optic phenomenon even in meningitis. Commonly, 
 however, we find associated with it true optic neuritis, 
 in which the inflammation has crept down the nerve 
 from the base of the brain ; it is often called ' neuritis 
 descendens.' In this form the disc is also swollen, but 
 not to the same extent, and it does not rise abruptly 
 on one side ; it is of a greyer colour, at the most of a 
 reddish tinge ; but it never presents the intense red of 
 the other form. Moreover, the morbid process, which, 
 as a rule, seems to develop more gradually, extends 
 to a much greater distance beyond the disc, and attacks 
 all the layers of the retina, where it may manifest its 
 presence by white patches, not to speak of numerous 
 hasmorrhages. 
 
 No doubt Dr. AUbutt is right in saying that the 
 optic neuritis may not be seen by tlie mirror in all 
 cases of tuberculous meningitis, because the neuritis 
 may not have had time to reach the discs ; but that it 
 is most common in those meningeal inflammations 
 which, like the syphilitic, have the favourable conditions 
 of contiguity, duration, and activity. 
 
 An interesting illustration of this point is seen in 
 a case reported in Medical Times and Gazette, June 17, 
 1874. 
 
 The case was one of tuberculous meningitis, running 
 a rapid course of only seven days after the first well- 
 marked symptoms. 
 
 In this case there was an entire absence of affection
 
 THE NERVOUS SYSTE]\r 387 
 
 of tlie eye as seen with the ophthahnoscopc. I have 
 myself, on several occasions, realised the same thing 
 in early stages of tuberculous meningitis. 
 
 In those cases in which there has been much pro- 
 liferation of the interstitial connective tissue of the 
 nerve there results atrophy of the nerve from the 
 compression of the nerve-fibrcs by the connective tissue. 
 The appearance of the disc iu this condition will vary 
 according to the stage of the disease and the amount 
 of the compression. Atrophy, however, is a change 
 that demands time, and is therefore a phenomenon 
 seen in chronic meningitis rather than in acute. 
 
 Although there is no certain ride on tlie subject, 
 yet in many cases the vascular lesions at the fundus of 
 the eye are more marked in the eye that corresponds 
 to the cerebral hemisphere where the inflammation is 
 most intense and the obstruction to the circulation 
 most considerable. 
 
 It is thought by Bouchut and others that children 
 may get well of acute meningitis, and that in them 
 there are often persistent disturbances of vision, dej^end- 
 ing on the alteration of the media and the memJDranes 
 of the eye, consequent on the vascular lesions occasioned 
 by inflammation of the meninges. It is more than 
 probable that many children recover from meningitis 
 when the inflammation is very subacute, even from 
 meningitis of a tuberculous form. Such cases, however, 
 never, I believe, present decidedly acute symptoms. 
 Drs. Allbutt and Crichton Browne have recognised in 
 many non-congenital idiots optic changes which are 
 precisely those that are found in persons wlio have 
 
 c c 2
 
 388 OPHTHALMOSCOPY IX DISEASES OF 
 
 had meningitis. In fact, it is partly from ophtlialmo- 
 scopic observations that the diagnosis of the occasional 
 causation of idiocy by meningitis has been made. 
 
 In the chronic meningitis, so often met with in 
 drunkards, the convexity of the brain is usually attacked, 
 and no retinal changes are met with. 
 
 In syphilitic meningitis of the base we may meet 
 also with what is called primary atrophy, in which the 
 distal parts of the nerve have been separated from the 
 central, and we find dwindling of the vessels, and either 
 a diminution of the disc and a tendency to cupping, 
 or a very white disc in which little is found but con- 
 nective tissue. 
 
 Encephalitis. — Partial encephalitis is never suffici- 
 ently extensive or intense to act mechanically on tlie 
 circulation at the fundus of the eye ; and it is by 
 destroying the cerebral pulp at the origin of the sensors 
 and motor nerves of tlie eye that it causes different 
 alterations of vision. 
 
 It stands to reason, therefore, that we find atrophy 
 as the lesion at the fundus of the eye, atrophy i'rom 
 separation of tlie distnl from the central end of the 
 nerve. There is rarely torsion or dilatation of the veins 
 of tlic retina, never haemorrhage of the retina, almost 
 always amaurosis from atrophy. I need not say that 
 this lesion will only be met with when disorganising 
 encephalitis attacks the corpora quadrigemina. 
 
 Bouchut says that inllanuuation of tlie optic nerve 
 or the neurilemma may be propngated to the brain in 
 an ascending course, and is often the cause of a clu'onic 
 partial encephalitis, occupying tlie corpora striata, the 
 optic thalami, and the coi'pora geniculata.
 
 THE XERYOUS SYSTEM. 389 
 
 It is probable that in general encephalitis there is 
 great suffusion of the retina, such as has been seen in 
 the eyes of patients immediately after a paroxysm of 
 mania. Facts, however, are Avanting in support of this 
 statement. 
 
 Cerebral Softenimj. — Softening of the brain seldom, 
 if ever, by itself causes any alteration that can be 
 detected by the mirror. It cannot induce any obstruc- 
 tion to the flow of blood from the retina, nor can it 
 cause neuritis. Softening, however, of the optic centres 
 will cause atrophy ; and cerebral softening itself often 
 depends upon disease of the cerebral vessels, disease 
 which, even if it does not aflect the vessels of the optic 
 centres, may attack the arteria centralis retina?, causing 
 first ana3mia and then atrophy of the disc. With the 
 exception, therefore, of the cases in which softening 
 attacks the optic centres, it is right to say that atrophy 
 of the disc coexistinij; with cerebral softeninii' owns no 
 connection furtlier tlu^n a similarity of cause in arterial 
 degeneration. 
 
 Cerebral IJcui)iorrha(je. — The condition of the retina 
 in cerebral heemorrhage is somewhat complicated, 
 because ha3morrhage of the brain so often depends upon 
 renal disease, and renal disease frequently })roduces 
 retinal changes, of which I sliall speak bv-and-by. 
 Apart, however, from these albuminuric alterations in 
 tiie eye, cerebral haemorrhage seldom leads to any 
 change in the fundus of the eye ; but optic neuritis is 
 occasionally a sequence of it. Bouchut thinks, liowever, 
 tliat large cerebral liiemorrluiges may cause optic 
 lesions by the obstruction they produce to the return
 
 390 OPHTHALMOSCOPY IN DISEASES OP 
 
 of venous blood from tlie eye, by compression, in the 
 same way as cerebral tumour ; such cases are rare. 
 If this compression from cerebral hemorrhage occurs, 
 we shall have choked discs. 
 
 I cannot agree with him when he says that in 
 cerebral liEemorrhage there is sometimes produced an 
 atrophy of the papilla, which is the ultimate consequence 
 of irritation of the optic nerve by the serous infiltration 
 of which it had been for a time the seat. Atrophy is 
 never produced by these means, even if serous in- 
 filtration is ever one element among many in its 
 causation. 
 
 It should be remembered in connection with this 
 subject that haamorrhage of the retina may be met 
 with independent of cerebral hasmorrhage and of 
 albuminuric retinitis ; that it may be due to backward 
 pressure upon the capillaries, or to rupture of a minute 
 aneurism either in cases in wliich there are many 
 aneurisms (microscopic) of the pia mater or of the 
 vessels of the cortex, or independently of aneurism 
 elsewhere. 
 
 Phlehiiisy or Thrombosis of Sinuses. — In this 
 morbid state we see very intensely the influence of 
 obstructed venous circulation. With phlebitis of the 
 sinuses of the dura mater, or indeed with the formation 
 of coagula in them from causes other than phlebitis, we 
 may have, according to the sinuses affected, interference 
 with, if not absolute obliteration of, the cavernous 
 sinus, liydrophthalmia, and congestion of the choroid, 
 dilatation, tortion, and thrombosis of tlie veins of the 
 retina, and choked discs.
 
 THE NERVOUS SYSTEM. 391 
 
 Chronic Hydrocephalus. — The changes in the fun- 
 dus of the eye in chronic hydrocephahis are twofokl ; 
 first, the choked discs, &c., mentioned as occurring from 
 obstructed sinuses, and in tliis case caused by the 
 pressure of tlie fkiid iu the distended ventricles on 
 tlie cavernous sinus, witli the additional strangulation 
 by the sclerotic ring of the already congested vessels, 
 with sometimes hcemorrhages and exudations consequent 
 on the congestion ; and secondly, the pressure of the 
 fluid on tlie optic chiasma may produce atrophy of the 
 optic nerve, and therefore of the optic disc. Under 
 such circumstances the pressure lias probably been from 
 the fluid accumulated in the third ventricle. 
 
 Cerebral Tumour. — Alterations in the retina of 
 very various kinds may depend on the presence of 
 cerebral tumour. No doubt the rule is that cerebral 
 tumour causes ischcemia papilla?.. But great variations 
 in the lesion occur according to the position of the 
 tumour, according as it has interfered directly with the 
 optic centres, according as there is any meningitis round 
 it, and according as it may or may not press on the 
 optic nerves and chiasma. 
 
 Taking then our three main varieties of lesion, we 
 fmd tumour causing choked disc by interfering with the 
 venous ebb from the eye ; optic neuritis only, if there 
 is meningitis associated with the tumour, and depending, 
 therefore, not on the tumour directly, but on the 
 meningitis ; atrophy, by pressure of tlie tumour on the 
 optic nerve, of the tumour or of the hydrocephalus 
 secondarily induced by it on the optic centres or tracts, 
 by softening around tumours, such softening imphcating
 
 392 OPHTHALMOSCOPY IN DISEASES OP 
 
 the optic centres, and lastly by the propagation of 
 sclerosis. 
 
 It is easy to understand that a tumour far back in 
 the encephalon, by interfering with the venous How 
 through the venae Galeni, may produce hydrocephalic 
 distension of the ventricles, the effect of which on the 
 circulation of the eye would be the same as that of 
 hydrocephalus produced by any other cause. 
 
 Dr. Allbutt has passed in review the effects of the 
 modes of action of tumours situated in various portions 
 of tlie brain. It is not possible in these few lines to do 
 adequate justice to the beauty and accuracy of his 
 observations and reasoning. Briefly, however, it may 
 be stated that tumours of all the lobes of the cerebral 
 hemispheres induce optic phenomena by their inter- 
 ference with the basilar portion of the brain, either by 
 direct pressure on the cavernous or petrosal sinuses or 
 on the optic nerves, tracts, or centres, or by leading to 
 softening of the same important parts, or by setting up 
 meningitis of the base, wl^ich will lead to neuritis 
 descendens, or by indirect pressure on the same part 
 induced by hydrocephalic distension of the ventricles, 
 from interference with the ebb of blood from the vena3 
 Galeni by a tumour obstructing these vessels in their 
 course. 
 
 There are no optic phenomena when tumour is 
 confined to the corpus callosum ; and these appearances 
 are often also absent in tumours of the optic thalami. 
 Here incidentally we have another proof in addition to 
 many afforded us by pathology that tlie optic thalami 
 have nothino; to do with sifdit. 
 
 Tumours of the crura cerebri ai'c so close to the
 
 THE NERVOUS SYSTEM. 393 
 
 great visual centres or tracts that it is prol>al)lc they 
 would cause atrophy by direct pressure. Facts, how- 
 ever, are wanting. The oculo-niotorius is almost in- 
 variably affected, and in some of the few cases on 
 record amblyopia or amaurosis has been observed. 
 
 Tumour of the cerebellum has no direct action on 
 the eye, but indirectly it may cause choked disc, or in 
 another way atrophy. ' Thus pressure on the occipital 
 bone, such as would be exercised by tumour, means 
 pressure upon the lateral sinuses, and pressure upon the 
 tentorium also means pressure upon the straight sinus, 
 upon tlie outlet of the veins of Galen, and upon the 
 Torcular Herophili itself. Slight enlargements, therefore, 
 of the cerebellum must very soon interfere seriously 
 Avith the reflux of venous blood. Again it is clear 
 that in enlargement of the cerebellum, especially of its 
 median and anterior parts, there must be a resolution 
 of the pressure in the direction of the meso-cephalon, 
 as tliis is the direction of the least resistance.' From 
 this cause the corpora quadrigemina may be very easily 
 disorganised, and atrophy of the optic nerve would be 
 the result. Or softening may proceed from the circum- 
 ference of the tumour along the processus ad testes to 
 the corpora quadrigemina, and the optic nerves will 
 waste, either as a consequence of the destruction of the 
 visual centres, or because they are themselves com- 
 pressed. 
 
 Tumours of the crura cerebelli cause distension of 
 ventricles by fluid, and thereby choked discs. 
 
 Tumours of the corpora quadrigemina lead to 
 amaurosis and progressive atrophy of tlie optic nerves. 
 Tumour of the pons may cause a twofold lesion ;
 
 394 OPHTHALMOSCOPY IN DISEASES OF 
 
 choked discs by the pressure of hydrocepliaUc fluid, 
 and atrophy from softening or destruction of the 
 corpora quadrigemina. 
 
 We have no examples of tumour of the medulla 
 oblongata, but Dr. Allbutt says : 'It is unlikely that 
 tumours of the bulb are attended with amaurosis, unless 
 they are complicated with sclerosis or meningitis, or 
 are large enough to involve the encephalic centres 
 above.' 
 
 Tumours of the anterior fossa cause amaurosis 
 pretty constantly ; they may act in three ways : either 
 by direct injury to the nerve, severing it from its 
 central attachments, and so causing atrophy ; or by re- 
 tarding the reflux of blood, and thus choking the discs ; 
 or by irritation of the connective elements of the 
 nerves, with consequent neuro-retinitis. 
 
 Tumours of the middle fossa may cause atroph)^ if 
 the nerve is compressed ; choked discs or neuro-retinitis 
 if meningitis is present. 
 
 Tumours of the posterior fossa may induce choked 
 discs indirectly by setting up liydrocephalic distension 
 of the ventricles, or by meningitis ; or they may by 
 means of the meningitis lead to optic neuritis. 
 
 Neither the aid of the mirror nor any physical sign 
 or symptom will inform us with moderate certainty of 
 the nature of the tumour. It can only be said that, 
 as a rule, aneurisms interfere less than other tumours 
 with the special senses, and that therefore intracranial 
 aneurism does not often cause any direct abnormality 
 in the fundus of the eye. No doubt this is due to the 
 less density of these tumours.
 
 THE NERVOUS SYSTEM. 395 
 
 More or less intense congestion of the retina, partial 
 or general oedema round the papilla, dilatation and 
 torsion of the veins of the retina, in a patient who has 
 lost consciousness after a wounding of the brain, in- 
 dicate a severe contusion or a considerable compression 
 of the brain. 
 
 There is no specific lesion diagnostic of fracture, 
 unless fracture of the base injure the optic nerve or 
 cause basilar meningitis, Eetinal hcemorrhage may be 
 met with after fracture. 
 
 Acute Insanity . — In acute delirium there is generally 
 congestion of the vessels only. As far as we may judge 
 from the inherent difficulties in making accurate ob- 
 servations in acute mania, or even in acute melancholia, 
 there is no very special lesion found in the retina. It 
 is certain that, even in cases in which there is evident 
 cerebral hyperemia, the circulation of the retina is fidl 
 in no proportionate degree. Bouchut says there are 
 no optic lesions peculiar to folic. Still some such 
 hypersemia has been found after the paroxysm of acute 
 insanity has passed over. Dr. JSFoyes found in acute 
 and subacute mania hypera3mia of nerve and retina in 
 fourteen out of twenty cases, and the eye norj^al in six. 
 
 Chronic Mania, however, is frequently connected, 
 as we- have seen, with absolute persistent lesion, and the 
 changes at the fundus of the eye bear a due relation to 
 the amount, the nature, and the position of these 
 changes. We may have choked discs from interference 
 with the nervous refiux, or neuritis from extension to 
 the optic nerve of basilar meningitis, or atro})liy as the 
 result of tliis latter condition, or as a consequence of
 
 396 OPHTHALMOSCOPY IX DISEASES OF 
 
 sclerosis of the nerve. Dr. Noyes found in tliree cases 
 out of six of chronic mania hypera^mia or signs of 
 inflammatory action. 
 
 In Dementia the appearances vary somewhat ac- 
 cording to tlie stage of the disease. In 12 out of 18 
 cases observed by Dr. Noyes there were found 
 hypera3mia and infiUration of the optic nerve and 
 retina, the vascularity affecting chiefly the venous and 
 capillary circulation. In late stages of the disease, 
 however, where amaurosis exists, it is due to atrophy 
 of the discs. 
 
 In General Paralysis of the insane a very similar 
 remark may be made. In early stages hypcriemia and 
 infiltration of the nerve and retina may be found. Dr. 
 Noyes says, the striation of the retina near tlie nerve is 
 often extremely pronounced, rendering occasionally the 
 edge of the nerve hazy and indistinct. But the specific 
 featiu^e of such cases later on is atrophy of the nerve, 
 beginning. Dr. AUbutt thinks, at the end of the first 
 stage or the commencement of the second, and pro- 
 ceeding to amaurosis. The proper nerve-structure 
 vanislies in consequence of pressure by a hyperplasia 
 of connective tissue. Dr. Aldridi2;e thinks this condition 
 is most complete in females, and is generally most 
 })ronounced in the left eye. 
 
 In Epilepsy the results recorded by various observers 
 do not completely agi-ee. Bouchut and Allbutt consider 
 that in the intervals between the fits there is no lesion, 
 and this would be in accordance witli my own ex- 
 perience. I understand Dr. Akhidge to say, however, 
 tliat in liis cases there have been geuerally found
 
 THE .XKRVOUS SYSTEM. 397 
 
 liyperasmia of retiim and o])tic disc witli tortuosity of 
 veins. He finds also durinui; the convulsive stao;e 
 injections of the optic discs, witli tlie arteries larger 
 than usual ; whilst Dr. AUbutt has seen at the same 
 period anosmia of the discs corresponding to what is 
 believed to be the state of arterial contraction and 
 consequent amemia within the brain, and hypera3mia 
 in a similar number of cases. Dr. Hu<j!;hlinf]fs Jackson 
 has several times found ana3mia of the discs in the 
 epileptic state. 
 
 All, however, agree that there is a congested appear- 
 ance of the discs when the fit is over, especially a 
 dilatation of the veins of the retina, which often will 
 persist for some days, and diminish only very gradually. 
 Coincident with this, and also continuing for a variable 
 period, is a general anajmia of the retina. Optic 
 neuritis, choked discs, and atrophy are rare in epilepsy, 
 but Bouchut asserts that there are often in epilepsy 
 atrophies of the choroid, inflammation of the retina, 
 with deposit of pigment, exudations on the retina, and 
 hasmorrhages of it, which evidently depend on this 
 disease. 
 
 In Chorea there is usually no change ; ])ut Dr. 
 Jackson speaks of the optic discs being badly margined, 
 w^ith large and wavy veins, and hyperemia of disc in 
 this disease. 
 
 Diseasefi of the Spinal Cord are sometimes accom- 
 panied by lesions of the optic nerve or retina. In 
 locomotor ataxy, for instance, these abnormalities are 
 found, and are variously explained by diflerent authors. 
 Bouchut states that in almost all ca^es of locomotor
 
 398 OPHTHALMOSCOPY IX DISEASES OF 
 
 ataxy there are produced disturbances of vision, cloudi- 
 ness, strabismus, diplopia, and amaurosis, which are in 
 relation with the lesions of the columns of the cord, 
 and reveal the existence of this alteration ; and he 
 believes the connection between the optic and motor 
 phenomena to be carried out by means of impairment 
 of the power of the sympathetic in the neck, so closely 
 associated with the columns of the cord. 
 
 This idea, however, has been quite disproved. The 
 connection between the optic and motor phenomena is 
 simply a similarity in the nature of the lesion ; the 
 appearance in the eye is atrophy of disc caused by 
 sclerosis of the nerve, just as the want of motor co- 
 ordination is caused by sclerosis of part of the cord, 
 mainly the posterior columns. There is no direct con- 
 nection. 
 
 In certain cases of injury of the spine, especially in 
 its upper portion, in meningitis of the spinal cord, in 
 chronic myelitis, always after the disease of the spine 
 or of the cord has persisted for some time, there may 
 be found hypersemia of the fundus of the eye, due in 
 all cases to the extension upwards along the base of the 
 brain of the inflammation of the meninfyes. 
 
 Chronic myelitis, if it ever does exist without 
 meningitis, would not cause this hypera3mic change. 
 Injury to spine, if only it existed pei' se, and did not 
 involve the spinal meninges, and by extension of 
 mischief upwards the cerebral meninges, would have 
 no elTect on the retina. These optic lesions are due 
 solely to the creeping upwards of a meningitis that was 
 originally spinal, but ends in behig cerebral.
 
 THE NERVOUS SYSTEM. 399 
 
 We have already mentioned that atrophy of tlie 
 nerve is sometimes found in syphilitic patients, and is a 
 sequence of slow creeping meningitis, a neuro-retinitis 
 being set up, and atrophy being a later result. A lesion 
 appearing early in the history of sy|)hilitic patients is 
 retinitis, in which we see hyperaemia of the retina, 
 effusion of serum into its nervous texture, with a grey 
 hazy look, especially, as Mr. Oglesby says, near the 
 macula lutea. In marked cases there may be great 
 tortuosity of the veins. 
 
 Leukcemia. — General pallor of tlie retina and 
 choroidal vessels and of the papilla is the characteristic 
 feature, according to Allbutt, of leukaemia. He speaks 
 also of a striated cloudiness of the retina in the neigh- 
 bourhood of the papilla and irregular spots near the 
 macula lutea, with a number of glistening white round 
 spots at the periphery. 
 
 In Albuminuria we find various lesions of the 
 fundus of the eye. These are much more usually met 
 with in the small granular kidney than in any other 
 form of renal disease, but they have been seen asso- 
 ciated with the large kidney of chronic tubal nephritis. 
 The lesions are twofold ; either a mere amaurosis, 
 existing with uraemia, and due most probably to ana3mia 
 of the cerebral vessels, and without retinal change, 
 except, maybe, some ansemia both of retina and disc ; 
 or the true albuminuric retinitis, which is never an 
 early symptom of the disease, and is evidenced at first 
 by infiltration of the diac, with great vascularity, and 
 later on by spots of degeneration, these being whitish 
 spots or masses, and extravasation of blood. Virchow
 
 400 OPIITHALMOSCOPY IN DISEASES OF 
 
 thinks these white spots are merely decolourised clots, 
 but it is probable that Dr. Allbutt is right in denying 
 this. The spots and hasmorrhages seem to have a 
 special proclivity for the surroundings of the disc and 
 the macula. 
 
 Liebreich's account of his beautiful plate of albumi- 
 nuric retinitis is that the greyish cloudiness of the 
 papilla and its immediate neighbourhood'is caused by 
 serous infiltration and augmentation of the cellular 
 tissue of the retina. The white opaque zone which 
 surrounds this portion of the fundus is produced by 
 the sclerosis of the nerve-fibres and fatty degeneration 
 of the cellidar tissue. The latter occurs isolated in the 
 very small round spots which are on the edge of the 
 white figure, and which assume a star-like arrangement 
 at the macula lutea, looking as if sprinkled upon the 
 fundus. The numerous hajmorrhag-ic extravasations 
 
 o 
 
 nearly all lie in the most internal layer of the retina ; 
 the striation of the spot is produced by the arrange- 
 ment of the blood corpuscles in rows between the 
 nerve-bundles ; and everywhere the direction of the 
 striae corresponds with the course of tlie nerve-fibres. 
 In other cases there were also round extravasations 
 situated in the deeper layers of the retina, and other 
 very extensive ones situated between the retina and 
 the choroid. The veins may be overfilled, the arteries 
 almost empty. 
 
 Bouchut says : ' A more or less extensive serous 
 infiltration of the papilla, linear hasmorrhages along 
 the vessels, spots of haemorrhage, or white fatty patches 
 on the retina, sometimes, in fine, a fixtty infiltration of
 
 THE NERVOUS SYSTEM. 401 
 
 the band of the optic nerves extending to tlie tubercula 
 quadrigemina, are tlie causes of the amaurosis, which 
 shows itself at the beginning and in the course of acute 
 and chronic albuminuria.' 
 
 In Diabetes atrophy of the discs may be met with ; 
 the serous infiltration of the papilla or of some points 
 of the retina, the small hajmorrhages, and white fatty 
 granulations of the retina occasionally found, are pro- 
 bably due to the coincidence of albuminuria with 
 diabetes. 
 
 In Embolism of the arteria centralis retincB there is 
 anEemia of the disc and diminution in size of all the 
 vessels, but very specially of the arterial branches, 
 which may be extremely small. 
 
 In convalescence from acute disease there may l^e 
 amaurosis, or at least some interference with perfect 
 vision, due either to auaBmia of the retina, consequent 
 on general anosmia, or to various lesions, Ischa3mia, or 
 optic neuritis, depending on a low form of meningitis 
 that has occurred in the previous disease, even if this 
 previous disease has not been accompanied by renal 
 changes sufficient to cause albuminuric retinitis. This 
 latter lesion is often doubtless the cause of amaurosis 
 occurring during convalescence from diphtheria. 
 
 Consult, for Ophthalmoscopy — 
 
 Liebreicli, ' AtLos of Ophthalmoscopy.' 
 
 CliHbrd Allbiitt on tlie ' Ophthalmoscope.' 
 
 Bouchut, ' Ophthalmoscopie.' 
 
 Giilezowski, 'Maladies des Yeiix.' 
 
 ' Ophthalmic Hosp. Rep.' 
 
 '.lournal of Mental Science,' April ^^7^^. Dr. Xoyes. 
 
 ' West Ridinp: Asylum T l^-^ ^.^f ^j sJ. & ii. Dr. Aldridge. 
 
 Dr. Fitzgerald (pair
 
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