RCMlb 
 
 338 
 
 College of ^dpsicians anb g>urBeon« 
 l-ibrarp 
 
 HENRY KFMI lUiN, 
 Medical Booltseller & Publisher 
 263 High Hoi born London W.C. I . \i 
 
PAEALYSIS 
 
 rEOM 
 
 PBBIPHEEAL NEUEITIS, 
 
ON SOME FORMS 
 
 OF 
 
 PARALYSIS 
 
 FEOM 
 
 PEEIPHEEAL NEUEITIS; 
 
 OF GOUTY. ALCOHOLIC, DIPHTHERITIC, ANI) 
 OTHER ORIGIN. 
 
 THE HABVEIAN LECTURES FOB 1885. 
 
 BY 
 
 THOMAS BUZZARD, M.D.Lond. 
 
 FBLLOW OF THK ROYAL COLLEGE OF PHYSICIANS IN LONDON; FELLOW OF KING's COLLKGK 
 
 LONDOS; PHYSICIAN TO THE NATIONAL HOSPITAL FOB THE 
 
 PARALYSED AND EPILEPTIC. 
 
 LONDON 
 J. & A. CHURCHILL 
 
 11, NEW BUELINGTON STKEET 
 
 1886 
 
Si ■ VaJ 
 
PEEFACE 
 
 A CONSIDERABLE amount of material which 
 was unavoidably omitted (from considerations 
 of time and space) in the Lectures as they 
 were delivered at the Harveian Society of 
 London, and afterwards published in the 
 ' Lancet,' has been added to the text of the 
 work as it now appears. 
 
 June, 1886. 
 
Digitized by the Internet Archive 
 
 in 2010 with funding from 
 
 Open Knowledge Commons 
 
 http://www.archive.org/details/onsomeformsofparOObuzz 
 
CONTENTS. 
 
 LECTUEE I. 
 
 PAGES 
 
 Introduction — Liability of symptoms due to lesion of peripheral 
 nerves to be referred to central disease — Localised forms of 
 neuritis — Multiple neuritis — Causes of paralysis — Anatomical 
 considerations — Waller's degeneration — Electrical reactions 
 in lesions of nerves — Variation of symptoms in neuritis — 
 Favorable prognosis — The term " neuritis " used provision- 
 ally in certain cases — Case of typical neuritis — Cases sugges- 
 tive of neuritis from gout — Multiple neuritis described by 
 Graves — Multiple neuritis from various causes : alcoholism, 
 diphtheria, syphilis^ kakke or beriberi . . 1 — 40 
 
 LECTURE IL 
 
 Multiple neuritis — Two cases with syphilitic history — Grainger 
 Stewart's cases — Morbid anatomy — Symptoms of multiple 
 neuritis — Comparison with Kakke — Alcoholic paralysis — 
 Examples — Ataxic symptoms — Pains and hypersesthesia — 
 Degenerative changes in peripheral nerves the immediate 
 cause of paralysis — Lancereaux's investigations — Pains may 
 be absent — State of the knee-phenomenon — Nystagmus — Dr. 
 Churton's case — The peripheral neuro-tabes of Dejerine pro- 
 bably of alcoholic origin — In alcohoHc paralysis lower 
 extremities most but not exclusively affected — The symptom 
 " dropped feet" should always suggest inquiry as to habits 
 
viii CONTENTS. 
 
 PAGES 
 
 of intemperance— So " wrist-drop " suggests inquiry into 
 possible exposure to lead— Not in alcoholic paralysis alone is 
 found tendency to preponderating affection of the lower 
 extremities — Seen in multiple neuritis from other causes — 
 Also in Kakke — A paraplegic form of neuritis from unknown 
 cause — Examples .... 41 — 100 
 
 LECTURE III. 
 
 Peripheral neuritis in enteric fever — After dengue — Two cases of 
 peripheral neuritis after malarious fever — Alcoholic history 
 in each — Doubtful etiology — Phases of alcoholic paralysis — 
 Diphtheritic paralysis — Resemblance of symptoms to those of 
 multiple neuritis — Tenderness of nerves and muscles — Ab- 
 sence of knee-phenomenon — Varying condition of electric 
 excitability in diphtheritic paralysis — The ataxy after diph- 
 theria liable to be mistaken for tabes — Morbid anatomy — 
 Diphtheritic paralysis probably very often dependent upon 
 peripheral neuritis — Comparison between symptoms of alco- 
 holic and diphtheritic paralysis — Diagnosis of multiple 
 neuritis — Prognosis — Treatment . . . 101 — 142 
 
ON SOME FOEMS OF PAEALYSIS 
 
 FEOai 
 
 PBEIPHBEAL NEUEITIS 
 
 OF GOUTY, ALCOHOLIC, DIPHTHEEITIC, AND 
 OTHEE OEIGIN. 
 
 LECTURE I. 
 
 Introduction — Lial)ility of symptoms due to lesion of 
 peripheral nerves to be referred to central disease — 
 Localised forms of neuritis — Multiple neuritis — 
 Causes of paralysis — Anatomical considerations — 
 Waller's degeneration — Electrical reactions in lesions 
 of neryes — Variation of symptoms in neuritis — 
 Favorable prognosis — The term "neuritis" used pro- 
 visionally in certain cases — Case of typical neuritis — 
 Cases suggestive of neuritis from gout — Multiple 
 neuritis described by G-raves — Multiple neuritis from 
 various causes : alcoholism, diphtheria, syphiUs, kakke 
 or beriberi. 
 
 Me. President and Gentlemen, — Wlien jour 
 Council honoured me with a request to dehver 
 the Harveian Lectures this year, mj first care 
 was to see whether there was anything in the 
 Bye-laws of the Society to aid me in the difficult 
 task of selecting a subject upon which to address 
 
 1 
 
2 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 you. The only direction that I found was that 
 the lectures should be upon some subject of 
 practical interest in medicine, surgery, or mid- 
 wifery. In the choice which I have made, with 
 whatever amount of success it may prove to be 
 carried out, at least I can lay claim to the selec- 
 tion of a subject the practical interest of which 
 it would be difficult to surpass. The present 
 generation has seen remarkable advances in 
 our knowledge of diseases of the nervous sys- 
 tem. A flood of light has been thrown upon 
 the physiological anatomy and the pathology of 
 the brain and spinal cord, and it is perhaps to 
 some extent in consequence of this comparative 
 concentration upon the central nervous system 
 that the part played by the peripheral nerves in 
 the production of symptoms of disease has not 
 until recently received the amount of attention 
 which it undoubtedly deserves. 
 
 The improvement in our knowledge is largely 
 due to the development of microscopical exami- 
 nation. Science is indebted to the late Lockhart 
 Clarke for the origination of processes of 
 hardening and staining nerve tissue which have 
 now acquired great perfection. How much 
 of our acquaintance with diseases of the brain 
 and spinal cord we owe to the microscope 
 aided by methods of this kind is well known Jj 
 
RESEMBLANCE TO CENTRAL DISEASE. 3 
 
 all. Within the last few years these methods, 
 improved by experience, have been applied to the 
 examination of peripheral nerve- fibres with the 
 result of disclosing a large amount of previously 
 unsuspected change in the essential elements of 
 the nerve-fibre itself. 
 
 It will be my aim in these lectures to sbow 
 that many forms of paralysis which would at 
 first sight point to organic disease of the central 
 nervous system are in all probability dependent 
 essentially upon changes in the periphery of the 
 cerebro-spinal nerves. The subject is a long 
 one, and the time at my disposal is short. It 
 will be necessary, therefore, to deal with the 
 topic in a somewhat general manner, avoiding, 
 where possible, any wearisome minuteness of 
 detail, and passing over such branches of it 
 as may fairly be considered common know- 
 ledge at the present day. Even with these 
 limitations I shall have to ask your forbearance 
 for many a cautious expression and not a few 
 acknowledgments of ignorance. There are 
 indeed necessarily many great gaps in our 
 knowledge of the subject, and numerous points 
 on which it seems difficult to reconcile appar- 
 ently conflicting circumstances, for it is com- 
 paratively young, though growing vigorously 
 from day to day. 
 
4 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 The plan wlaicli I propose to adopt is first to 
 narrate a case wliicli maj be taken as a typical 
 example of a localised peripheral neuritis ; then 
 to show, by reference to clinical cases, the pro- 
 bability that neuritis may occur in forms not 
 easily recognisable, owing to the absence of one 
 or more of the characteristic symptoms. The 
 possibility of its frequent occurrence in the 
 gouty diathesis will be considered, and examples 
 furnished. In these circumstances it is in one 
 limb or portion of the body that the manifesta- 
 tion usually takes place, and the idea of a stroke 
 of hemiplegia is readily suggested. Passing 
 from the localised form of paralysis, we shall 
 next consider cases of multiple neuritis — cases 
 in which there is a tendency to rapid and almost 
 universal paralysis. It is in these that the 
 imitation of central nervous disease is apt to be 
 the strongest. We cannot in every case of this 
 disease feel at all certain as to what is the cause 
 of the changes in the peripheral nerves upon 
 which the symptoms depend. But there is in- 
 creasing evidence to show that many are due to 
 some toxic influence introduced from without. 
 Amongst influences of this kind are to be men- 
 tioned alcohol, lead, diphtheria, syphilis, and 
 something which gives rise to the endemic dis- 
 ease of Japan and the shores of Eastern Asia, 
 
WHAT IS PARALYSIS? 5 
 
 called Beriberi or Kakke. Paralysis, as my 
 master, tke late Dr. Todd, used to teach, is not 
 a disease of itself, but a symptom — an effect 
 due to a cause, wliicli cause itself is not always 
 the essential disease. The paralysis in the 
 cases under consideration is immediately due to 
 the change in the nerve-fibre, but this in its 
 turn depends upon a cause which is sometimes, 
 but not always, recognisable. The diagnosis of 
 this class of cases will next claim our attention, 
 and especially the mode by which they may best 
 be differentiated from diseases of the spinal cord. 
 The prognosis and treatment of the disease will 
 suitably conclude our observations. 
 
 A few preliminary remarks may not be out 
 of place. 
 
 Although it is desirable that we should under- 
 stand what we mean when speaking of paralysis 
 it is not necessary to attempt a strict definition 
 of the term. We know that in health the mus- 
 cles contract in obedience to impulses conveyed 
 to them from the cerebro-spinal centre. When 
 we speak of paralysis we mean that this process 
 fails to be efficiently performed. The imperfec- 
 tion may be extremely slight or the function 
 may be completely suspended, but in any case 
 the resulting condition is one of paralysis. 
 
 The cause of failure may lie in the centre 
 
6 PARALYSIS FEOM PEEIPHERAL NEURITIS. 
 
 itself, or in the peripheral nerves by which the 
 so-called " motor impulses " should be carried 
 to the muscles. 
 
 On the sensory side again we see analogous 
 deviations from normal functioning. In a state 
 of health afferent impulses from a sentient sur- 
 face are propagated along certain fibres in the 
 peripheral nerves up to cells in the central ner- 
 vous system, giving rise in them to changes 
 which are represented in consciousness as sen- 
 sations. Lesion of the peripheral nerve-fibres, 
 equally with lesion of the central nerve-cells, 
 will interfere more or less completely with the 
 normal function, and loss or some disorder of 
 sensation will be the result. 
 
 On the present occasion it will be understood 
 that I shall confine myself to some of those 
 forms of paralysis which are essentially depen- 
 dent upon lesion of the peripheral nerve-fibres, 
 and in considering these such as are the result 
 of traumatic agency will be excluded. 
 
 It will be sufficient to remind you, in a very 
 few words, of the anatomical constitution and 
 arrangement of the peripheral nerves. The 
 cerebro- spinal nerves are individually connected 
 by one or more roots with the brain or spinal 
 cord. Each spinal nerve arises by two roots, 
 an anterior, which contains the motor fibres of 
 
ANATOMY OF NERVES. 7 
 
 the nerve, and a posterior, whicli contains the 
 sensory fibres. On the latter root is a ganglion, 
 and immediately beyond this the two roots unite 
 into a single nerve-trunk, which quits the spinal 
 canal by the intervertebral foramen. The nerve 
 thus formed is spoken of as a ''mixed" nerve, 
 i. e. it is endowed with both motor and sensory 
 functions. Outside the canal it divides into 
 two branches, both containing motor and sen- 
 sory fibres, which are distributed to the anterior 
 and posterior parts of the body ; the anterior, 
 which is the larger, supplying the limbs and the 
 front of the body generally. 
 
 The trunk of a spinal nerve is composed of 
 nerve- fibres, side by side, in form of a bundle, 
 the fibres being individually separated by con- 
 nective tissue, and the bundle itself provided 
 with a special sheath of the same. This sheath 
 is lamellated, and contains lymph-channels. 
 The bundles of nerve-fibres thus constituted 
 are connected and held together in their turn 
 (so as to form a trunk) by connective tissue, in 
 which are contained lymphatics, blood-vessels, 
 and fat- cells. The individual nerve-fibre 
 (bundles of which go to make up a nerve-trunk) 
 consists of a primitive sheath or membranous 
 tube, containing the white substance of Schwann. 
 This probably serves to insulate the essential 
 
8 PAEALTSIS EROM PEEIPHERAL NEURITIS. 
 
 constituent of tlie nerve, the axis-cylinder wliicli 
 occupies, as tlie term given to it implies, the 
 centre of the tube. 
 
 The important observation made by Waller 
 is requisite to be borne in mind in connection 
 with our subject. It will be remembered that 
 this distinguished physiologist found that when 
 the anterior root of a mixed nerve is divided 
 the nerve-fibres thus separated from the spinal 
 cord degenerate to their remotest periphery in 
 the course of a few weeks. If, however, the 
 posterior root be cut through between the cord 
 and the ganglion upon the root it is now not 
 the periphery but the portion of the nerve 
 attached to the cord which degenerates. The 
 ganglionic cells of the anterior horns appear 
 therefore to act as trophic centres for the motor 
 fibres, whilst the spinal ganglia would seem to 
 serve the same office for the sensory fibres. 
 Waller formulated the general law that nerve- 
 fibres degenerate when separated from their 
 trophic centres. The term Wallerian degene- 
 ration is commonly applied to the changes 
 taking place in nerve-fibres in these circum- 
 stances. 
 
 A very brief reference is necessary to the 
 chang^es of reaction to electrical currents which 
 occur in a muscle when the nerve distributed 
 
ELECTRICAL EEACTION IN MUSCLES. 9 
 
 to it is from some cause more or less completely 
 disabled in its power of conduction. 
 
 In mild cases no change is to be noted. The 
 muscle reacts to induced currents of the same 
 strength as those which bring about contrac- 
 tion in a similarly placed muscle supplied by 
 a healthy nerve. 
 
 In more severe cases, as shown by Erb, 
 whilst the muscle continues to respond to in- 
 duced currents its excitability to a slowly inter- 
 rupted galvanic current may be increased 
 beyond what is natural in health. 
 
 Where the condition is one of still greater 
 severity, the muscle, after showing for a few 
 hours or days increased excitability to electric 
 currents, rather rapidly loses its power of 
 response to induced currents, so that in the 
 course of two or three weeks no contraction is 
 elicited by the application of the strongest 
 currents. At the same time slow interruptions 
 of a galvanic current of a strength quite insuffi- 
 cient to visibly affect healthy muscle determine 
 very definite contractions. These contrac- 
 tions differ from those of healthy muscular 
 tissue in being slower and, so to speak, of a 
 more lazy character. It is now found too that 
 the contraction consequent upon closure of the 
 galvanic circuit with the positive pole upon 
 
10 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 the muscle takes place wlien a mucli more 
 feeble current is employed than that which is 
 required to bring this about in health. In a 
 normal state, as is well known, the contraction 
 most easily and earliest brought about is that 
 produced when the galvanic circuit is closed 
 with the negative pole upon the muscle. Now, 
 however, the condition is reversed, and it is 
 when the circuit is closed with the positive pole 
 on the muscle that we get the earliest result, i.e. 
 we obtain a contraction with the least number 
 of cells. In the course of several months a 
 gradual recovery of power over the affected 
 muscles may be expected to take place when 
 the lesion does not cause permanent change. 
 It often happens that the voluntary power 
 of contracting the muscles is regained before 
 they will respond to the induced current but 
 after they have ceased to be abnormally ex- 
 cited by galvanism. When this occurs it is 
 probably only a question of time as to when 
 faradism will be again able to exert its ordinary 
 exciting influence. 
 
 These are the main features of the " reaction 
 of degeneration," a term introduced by Erb, 
 to which the symbol RD has been conveniently 
 applied in this country. This symbol will some- 
 times be employed in these lectures to avoid 
 
, ELEOTEIOAL EEACTION IN NERVES. 11 
 
 the wearisome repetition either of the long 
 phrase, or of the description of the condition 
 to which it has been apphed. 
 
 I have purposely referred first of all to the 
 changes of reaction in the mnscles, because it 
 is these which immediately strike the eye when 
 we proceed in the ordinary way to examine a 
 patient with electrical currents. With more 
 propriety, perhaps, from a physiological and 
 pathological point of view I should have first 
 referred to the changes to be noted in the nerve- 
 trunks on their way to furnish the intramus- 
 cular fibres. These, however, are more difficult 
 to test. As a rule, their reaction is the same as 
 that of the muscles to which they are supplied, 
 except in the partial form of RD, when the 
 response to currents remains normal in the 
 nerve whilst qualitative and quantitative changes 
 are manifest in the muscle. But the electrical 
 reactions of nerves are from various causes 
 subject to apparent anomalies which we cannot 
 as yet account for, and which interfere with the 
 exactness of the information to be derived from 
 their behaviour. We may, however, recognise 
 changes in the irritability of a nerve to electric 
 currents, whether in the direction of plus or 
 minus, and these will at least indicate that 
 the nerve is the seat of some lesion or organic 
 
12 PARALYSIS FEOM PERIPHERAL NEURITIS. 
 
 change — some alteration probably in its nutri- 
 tion. But neither the nature nor degree of the 
 lesion is always to be inferred from the changes 
 of excitabiHty to electric currents displayed by 
 the trunk of a nerve. 
 
 In general terms it may be said, as it is well 
 put by Ross, '* The state of the nutrition of a 
 nerve has great effect upon its irritabihty. If 
 the nutrition is wholly arrested the irritability 
 disappears. But a nerve whose nutrition is 
 merely defective discharges its energy more 
 readily than one whose nutrition is perfect." 
 
 Where the trophic influence of the spinal 
 cord is obstructed by such a lesion of the motor 
 nerve as brings about the reaction of degene- 
 ration^ it is usual to find that the muscles so 
 affected are apt to become rapidly atrophied. 
 This atrophy, like the reaction of degeneration, 
 is frequently but a temporary condition which 
 is quite capable of complete recovery. Where, 
 however, the nerve has undergone irreparably 
 destructive changes, the atrophy of the muscle 
 to which it is supplied is permanent. 
 
 With this brief reference to certain points 
 which may usefully be borne in mind, I will 
 proceed to relate a case which has not long 
 since fallen under my observation, and will 
 serve as a convenient introduction to our sub- 
 
SYMPTOMS OF NEURITIS. 13 
 
 ject. It is a typical case of neuritis affecting 
 certain brandies of tlie bracliial plexus, and 
 occasioning local paralysis, exquisite pains, 
 hyperalgesia, muscular atropliy, abolished or 
 diminished electrical excitability, and trophic 
 changes in the skin. In this example the col- 
 lection of symptoms points conclusively to 
 lesion of peripheral nerves, and if neuritis were 
 characterised like this in all instances there 
 would be comparatively little difficulty in its 
 diagnosis. But it is an important fact that we 
 may have paralysis from neuritis — frequently 
 of a progressive and multiple form—in which 
 one or more of the symptoms that I have just 
 enumerated may be entirely wanting. The 
 absence or want of prominence of such sym- 
 ptoms tends very often to obscure the diagnosis 
 so much that the condition stands the chance 
 of being referred to central instead of peri* 
 pheral nerve changes. ISTow, this alone is an 
 important point, because without correctness in 
 diagnosis our modes of dealing with disease 
 must necessarily be more or less of a haphazard 
 character. But more than this — the forms of 
 disease to which I am going to draw your 
 attention, whilst often presenting the most 
 alarming features, may show themselves highly 
 responsive to treatment, and issue in recovery 
 
14 PARALYSIS FEOM PERIPHERAL NEURITIS. 
 
 to an extent whicli could hardly be expected 
 from the grave aspect often presented at the 
 outset of the attack. Unfortunately, a con- 
 siderable part of the field of disease dependent 
 upon lesion of the nervous system is occupied 
 by more or less intractable disorder. It is 
 therefore with peculiar interest and satisfaction 
 that I find myself able to discuss, in these 
 lectures, forms of disease in which a favorable 
 prognosis is very often indeed justified by the 
 result. 
 
 A word is necessary as to the employment of 
 the term " neuritis." It is common at the 
 present time to distinguish two forms of 
 neuritis : interstitial neuritis, in which the con- 
 nective tissue of the nerve is the primary seat 
 of inflammatory changes, the essential element 
 being secondarily affected; and parenchyma- 
 tous neuritis, in which there is destruction of 
 the essential element of the nerve-fibres, with 
 but little, or even, perhaps, no recognisable 
 alteration in the interstitial tissue. It is open 
 to discussion how far we are justified in apply- 
 ing a term which suggests inflammation to the 
 latter of these two processes. The change 
 which takes place in the nerve-fibre is of the 
 character of degenerative atrophy, and is com- 
 parable with that which occurs below the point 
 
USE OF THE TEEM NEUEITIS. 15 
 
 of section when a motor nerve is artificially 
 divided. These two forms of lesion, interstitial 
 and parenchymatous neuritis, call to mind the 
 changes which are observed to take place in 
 the nerve-fibres constituting the posterior 
 columns of the spinal cord in cases of so-called 
 sclerosis. In some of these it is manifest that 
 the investing tissue of the fibre has been pri- 
 marily affected, the essential nerve-elements 
 suffering secondarily; whilst in others, as is 
 commonly though not universally accepted, the 
 nervous elements are the first to undergo 
 change which spreads to the interstitial tissue. 
 Whether in the latter case there is justification 
 for the employment of a term implying inflam- 
 matory action is not quite certain. The ques- 
 tion, both as regards the changes in the nerve- 
 fibres which run in the spinal cord, and in 
 those which take their course in a nerve-trunk, 
 must be acknowledged to be still in an un- 
 settled state. In applying, therefore, the term 
 ''neuritis" to changes in the essential nerve- 
 elements of a fibre when these are to all 
 appearance primarily as well as when they are 
 secondarily produced, it will be understood 
 that I suspend my judgment as to the propriety 
 of the parenchymatous form being considered 
 as certainly of inflammatory character, and 
 
16 PAEALYSIS FROM PERIPHERAL NEURITIS. 
 
 make use of tlie expression as a convenient one 
 which has the advantage of being generally 
 recognised. The following example of neuritis 
 was in all probability of interstitial character : 
 
 A single woman, aged twenty-four, was sent to me from 
 the country on February 20tli, 1883, suffering from loss 
 of power in tlie right hand, with agonising pain. Her arm 
 was in a sling, the hand covered up with cotton wool, 
 and she jealously watched the limb to guard it from the 
 slightest accidental touch, so exquisite was the tenderness. 
 The right hand and forearm had a soddened, puffy, help- 
 less appearance, with swollen fingers and purplish dis- 
 colouration of the skin in patches, which here and there 
 looked glossy. Her immediate illness had commenced in 
 the preceding August (six months previously) with pain 
 and swelling in the middle finger, which gradually extended 
 to the others, and for some months past her hand had 
 been quite useless. The pain was so constant and severe 
 that she could scarcely ever get sleep at night. She looked 
 extremely ill. It seemed that her business was to help in 
 the household of her father. She had lost her mother 
 from cancer of the liver. There was no rheumatism in the 
 family, but she had been considered to be weak in the 
 chest. A brother was supposed to be consumptive, and a 
 sister had cough. She herself had suffered much from- 
 so-called " rheumatism " in the knee and left hand. 
 Nothing wrong was to be found on examining her chest, 
 and the ophthalmoscope showed no change in the fundus 
 oculi. There was not the least reason to suspect either 
 alcoholism or syphilis. Her temperature was 100° F. 
 On examination, it was seen that the power of extending 
 the wrist was moderately good, but flexion of it could not 
 
CASE OF NEURITIS. 17 
 
 be performed. There was slight power of flexing the last 
 joint of each finger, and an equally slight power of extend- 
 ing it, and this applied also to the last joint of the thumb. 
 There appeared to be no power in the intrinsic muscles of 
 the thumb and fingers. Examined electrically, the thenar 
 muscles did not respond to either form of electric excita- 
 tion ; but the muscles of the back and front of the forearm 
 were excitable by induced currents, though only when a 
 considerable strength was employed. A detailed examina- 
 tion was not possible, owing to the exquisite sensitiveness 
 of the limb. Warmth was felt as well by the right hand 
 as by the left, but cold was felt best on the left (unaffected) 
 hand. A hair drawn over the skin of the left hand was 
 felt better than on the right. The patient was forced to 
 keep the hmb covered up, as the air would start pain, and 
 conveyed a burning, smarting sensation. There was a 
 more or less constant feeling of numbness in the fingers. 
 
 It was very difficult to obtain a clear history of the 
 commencement of her illness. Her mother, it seemed, 
 had died in March, and patient had nursed her night and 
 day for a year, never having a really good night's rest. 
 She fell ill herself after her mother's death, but at first 
 there was nothing wrong with the hands. But about 
 three or four weeks afterwards there came a patch of 
 inflammation on the middle finger of the left hand which 
 broke after being poulticed, and healed up. It had never 
 kept her awake. Soon after this she had an inflamed 
 throat, with fever and a swelling under the jaw which 
 did not discharge. She was confined to her bed during 
 fourteen days. In August, the middle finger of the right 
 hand began to get red, and the inflammation spread in turn 
 to the index, ring, and little finger, thence to the thumb 
 and hand, and then to the wrist of this side. At the 
 same time pain began to be felt on movement, with ten- 
 
 2 
 
18 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 derness of skin, whicli liad increased and continued ever 
 since. She had been especially getting worse since 
 Christmas. 
 
 I will not weary you by any detailed account of her 
 progress. 
 
 By way of treatment, the limb was supported by a 
 splint, ice and small flying blisters being applied ; nourish- 
 ing diet was ordered, and opium administered internally. 
 The symptoms, however, continued without any material 
 change, except that in June, after placing her arm in hot 
 water, it became " spotted " all over, as she described it 
 (for I did not see this), and blisters formed over her 
 fingers. The blisters, apparently of the nature of pem- 
 phigus, discharged, and became covered with crusts, which 
 remained when 1 saw her in July. I lost account of her 
 after this, but have since learned the sequel, which is sad. 
 She continued to suffer as described during the winter of 
 1883-84, and in the early spring of 1884 was attacked 
 with acute melancholia with strong suicidal intent, and 
 was confined for six months in an asylum. As described 
 by the superintendent of the asylum, "her arm at the 
 time of admission was somewhat smaller than the other, 
 with diminished mobility and considerable pain. There 
 was some discolouration of the skin." The arm was sup- 
 ported for a time, and by the end of April it appeared, to 
 have recovered its size, and she could use it a little. The 
 pain was not constant, but warmth caused a "burning 
 feeling," and cold " painful rheumatic sensations." By 
 September she could use the right hand as well as 
 the left. Morphia was administered to her in the 
 asylum until her melancholic symptoms were consider- 
 ably improved. In October she was discharged, re- 
 covered both in her mind and also in her arm, which 
 she used freely and without pain. The only complaint 
 
RESEMBLANCE TO TRAUMATIC LESION. 19 
 
 when last I heard of her was that in cold weather the 
 arm ached. 
 
 This case was one o£ a rare and important 
 character, for, without any history of violence, 
 the symptoms bore a close resemblance to those 
 so graphically described by Weir Mitchell as 
 the result of gunshot injury to nerves. It was 
 marked by paralj^-sis, loss of or diminished 
 electrical reaction of muscles, agonising pains 
 of lancinating character, constant burning sen- 
 sation, exquisite hyperaesthesia of the skin and 
 probably also of the muscles, but it was not 
 possible to separate absolutely the two condi- 
 tions. Besides these symptoms, pointing to 
 lesion of motor and sensory fibres, there were 
 others which appeared to indicate that the 
 vaso-motor fibres were also involved. These 
 were the sodden, oedematous look of the limb, 
 the patches of glossy skin (a symptom first 
 described by Paget), the purple discolouration, 
 and the bullous eruption which left behind it 
 adherent crusts. 
 
 It will have been noted that the lesion of the 
 right arm had been preceded by some kind of 
 local inflammatory condition of the middle finger 
 of the left hand, which had been followed by in- 
 flamed throat and swelling under the jaw. The 
 tendency to symmetrical affection of the opposite 
 
2Q PAEALTSIS FROM PERIPHERAL NEURITIS. 
 
 side in cases of neuritis has been referred to by 
 Weir Mitchell and others, but whether we are 
 to see in the symptoms described any connec- 
 tion of this kind, I am quite unprepared to 
 say. 
 
 The case was clearly one of neuritis, the 
 essential cause of which was, however, not 
 evident. In process of time all the formidable 
 symptoms subsided and the patient recovered. 
 There must therefore have been regeneration 
 of nerve-fibres. Whilst there was paralysis of 
 the muscles of the forearm as well as of the 
 hand, it is to be noted that those of the latter 
 were much more severely affected than the 
 former. There was no power of voluntarily 
 moving the thumb, except at its last joint, and 
 the thenar and interosseous muscles showed no 
 response to either form of electric excitation. 
 The power of moving the long muscles on the 
 back and front of the forearm was not alto- 
 gether lost, and they proved to be excitable by 
 induced currents, though of a much greater 
 strength than is needed by healthy muscles. 
 The effect of the lesion then became more and 
 more severe as the ^Deriphery was approached. 
 I would draw especial attention to this point, 
 because, as we shall see, it plays an important 
 part in the diagnosis of other forms of paralysis 
 
VARIOUS SYMPTOMS MAY BE ABSENT. 21 
 
 wliicli are not so palpably dependent upon 
 lesion of tlie trunks of nerves. 
 
 The trophic disorder of the skin which here 
 occurred in so marked a form is by no means 
 always present in cases of undoubted neuritis. 
 And just as this may be absent, so other of the 
 symptoms may be wanting. We are not yet in 
 a position to explain this important fact, but 
 there would seem to be no doubt that some- 
 times the motor, at other times the sensory, 
 and perhaps, on the whole, least commonly the 
 vaso-motor fibres, bear the brunt of the attack, 
 with a corresponding contrast in the symptoms. 
 To gain a true idea of the frequency of neuritis 
 it is necessary to remember this fact ; we shall 
 otherwise be liable to overlook the true charac- 
 ter of affections because they do not display 
 all the characters of a typical neuritis. 
 
 Where we are concerned with purely motor 
 nerves we can readily understand that neuritis 
 may occur without giving rise to pain. There 
 can be but little or no doubt that the facial para- 
 lysis of peripheral origin which is so common is 
 due to neuritis of some part of the portio dura. 
 The affection is not accompanied by pain, 
 unless, as I have known sometimes happen, the 
 draught of cold air which occasions the neuritis 
 of the seventh nerve sets up at the same time 
 
22 PARALYSIS FROM PEEIPHEEAL NEURITIS. 
 
 a corresponding change in the fifth. In other 
 purely motor nerves, again, such as the third 
 and sixth, neuritis causes no pain. It may be 
 added that the same immunity is seen when a 
 nerve of special sense — as the optic — is simi- 
 larly affected. But even in mixed nerves I 
 feel sure that neuritis may occur without 
 causing pain, and I shall have occasion pre- 
 sently to refer to cases which illustrate this 
 point. It has an important bearing upon the 
 question of multiple neuritis, which will be 
 considered later on in these lectures. 
 
 It is impossible to aflBrm positively that we 
 have to do with neuritis, unless, as in the case 
 just read, the aggregation of symptoms leaves 
 us in no doubt. But we are bound to remem- 
 ber that the degree of lesion must be a varying 
 quantity, and that the same symptoms are not 
 to be expected in mild as in severe cases. This 
 may well be illustrated by the example of 
 facial paralysis of perijDheral origiuj in severe 
 cases of which we find typical reaction of 
 degeneration besides some atrophy of the mus- 
 cles, whilst in mild instances the electrical 
 reaction is unchanged and the muscles do not 
 waste. There can be no reasonable doubt that 
 we are concerned in each case with a lesion of 
 similar character but of different severity. 
 
CASE EESEMBLING HEMIPLEGIA. 23 
 
 The following are illustrations of the resem- 
 blance which neuritis may cause to the sym- 
 ptoms of central disease : 
 
 A female patient, aged fifty-six, was said to have been 
 suddenly seized one day with loss of power and numbness 
 in the left arm. When she was first seen by her medical 
 attendant these symptoms had passed of£ to some extent, 
 but she was cold and agitated, with an irregular pulse. 
 There was no paralysis in the face, and the speech was not 
 affected. She walked upstairs with some assistance and 
 remained in bed for about ten days, her symptoms during 
 that time being occasionally severe headache, with loss of 
 appetite and nausea, and on several nights delirious 
 wandering. The urine, which was scanty and of high 
 specific gravity, was loaded with lithates, and contained no 
 albumen. The result of examination of her organs was 
 negative. The left arm was often complained of as weak, 
 heavy, and numb. On inquiry, it appeared that her illness 
 had not really been quite so sudden in its onset as had 
 been thought, but that the loss of power and numbness had 
 been preceded by a great deal of pain in the left arm and 
 shoulder. She now gradually improved, though unequal to 
 the slightest strain or fatigue, and began to get out in the 
 garden. A month after her first attack, whilst out walk- 
 ing, she experienced a sudden loss of power in both legs, 
 which passed off in an hour or so. This did not seem to 
 throw her back very much, but she had several slight 
 threatenings of a return in the following month, now in one 
 limb, now in another. About five weeks after the second 
 attack, whilst a mile from home, she had a severe attack 
 affecting both legs, and had to be brought back in a cab. 
 This gave her a considerable shock, but the paralysis 
 proved to be as transient as before, and a week afterwards, 
 
24 PARALYSIS FEOM PERIPHERAL NEURITIS. 
 
 when I saw her for the first time, she was free from any 
 loss of power or abnormal sensation. Examination failed 
 to discover any disease of the nervous centres, or of other 
 viscera. Since that time I understand she has again had 
 a relapse. 
 
 This patient had led rather an anxious and 
 chequered Hfe, and the habit of her household 
 was to take stimulants freely. The apparently 
 sudden loss of power in one arm, coupled with 
 numbness of the skin, in a woman fifty-six years 
 of age, is of course highly suggestive of an 
 attack of hemiplegia from some central lesion. 
 But it is to be remarked that the paralysis here 
 had really followed great antecedent pain in 
 the arm and shoulder, an association which is 
 practically conclusiye of the peripheral nature 
 of the lesion. The attacks which followed, 
 first in one limb and then in another, clearly 
 point in the same direction. I have no doubt 
 that we have here to deal with neuritis dependent 
 upon either the toxic effect of alcohol or of 
 gouty origin. 
 
 Cases of this description are not uncommon, 
 and frequently give rise to a great deal of anxiety. 
 A gouty patient who is past middle age is prone, 
 as we well know, to disease of the blood-vessels 
 and kidneys. An attack of numbness and 
 paralysis in a limb, in these circumstances, is 
 
NEURITIS IN THE GOUTY. 25 
 
 naturally liable to be referred without hesitation 
 to a central lesion : haemorrhage or thrombosis. 
 That this supposition is far more often than not 
 correct is certainly the case, but every now and 
 then we meet with examples like the one 
 described, which show the necessity of bearing 
 in mind the possibility of a peripheral cause in 
 such an attack. The question of the possibility 
 of gout causing neuritis was referred to by Mr. 
 Hutchinson in the Bowman Lecture at the 
 Ophthalmological Society last year. He ad- 
 duced some instances which appeared to point 
 to neuritis of the optic nerve originating in 
 gout, as well as others suggesting the occur- 
 rence of neuritis in other parts of the nervous 
 system from a similar cause. I have very little 
 doubt that neuritis is not seldom due to the 
 presence of gout ; the difficulty of proof is of 
 course extremely great. I cannot lay claim to 
 adduce anything which is absolutely positive 
 upon this point, but some clinical observations, 
 and especially certain electrical examinations 
 which I have made, appear to lend considerable 
 strength to this view. 
 
 An old friend of mine, a member of our profession, sent 
 for me a few months since in a state of alarm, having woke 
 up in the morning with numbness in the arms, which was 
 at first slight and affected the side on which he was lying, 
 
26 PAEALTSIS FROM PEKIPHERAL NEURITIS. 
 
 the left mucli more than the right. In the course of a few 
 hours it had grown rapidly worse, and was accompanied by 
 pain in the shoulders. There was considerable loss of 
 power in the arms. I found that he had had a character- 
 istic attack of gout in the ball of one big toe some six years 
 previously, and more than once had suffered badly from 
 lumbago. He had been liable to pains in the shoulders 
 for many years, and on several occasions had been troubled 
 with sciatica. I was able to reassure him unreservedly, 
 and treatment, directed entirely to his gouty habit, brought 
 about immediate improvement and complete recovery in no 
 great time. 
 
 It is not certain tliat we are justified in 
 applying the term '* neuritis " to such cases as 
 this, with the small amount of evidence of the 
 pathological condition which is usually to be 
 obtained. The contrast as regards the number 
 and severity of the symptoms with such a case 
 as that of the young woman which I first 
 described is very striking ; but it appears to 
 me that we have only to imagine a hke affection 
 of the nerves, though comparatively of very 
 shght kind, to explain the symptoms of nerve 
 lesion observed in gouty patients. Not only 
 are both the motor and sensory fibres often 
 involved in these circumstances, but it fre- 
 quently happens that there are signs of the 
 vaso-motor fibres being likewise affected, caus- 
 ing coldness of the extremities and discoloura- 
 tion of the skin. I lately saw a case in 
 
ELECTEICAL SIGNS. 27 
 
 wliicli, along with pains wliicli were almost 
 universal and there was strong evidence to 
 show were dependent upon a gouty habit, there 
 was an extraordinary amoant of oedema of the 
 lower extremities. This extended half-way up 
 each leg. As there was nothing in the state 
 of the heart, kidneys, or liver to explain the 
 dropsical condition, it seems quite possible that 
 the cause of it as well as of the pains may lie 
 in neuritis, which involves both sensory and 
 vaso-motor fibres. 
 
 Electrical examination will often give a good 
 deal of support to the view that these are cases 
 of slight neuritis : 
 
 A lady, aged fifty-two, complained that lier left liand 
 would close during the night, and that she could not get it 
 open again without dreadful pain at the wrist and up the 
 fingers. It would be found icy cold. Some time previ- 
 ously, her left arm, and to a less extent the right arm and 
 the toes of either foot, would " go to sleep." On examina- 
 tion she complained of pain, pricking, and tingling in the 
 thumb and first three fingers, as well as slight numbness 
 and coldness in the toes. Occasionally there would be a 
 dart of pain down the arm and finger. She was a healthy- 
 looking woman, who presented no signs of degenerative 
 changes. Her tongue was clean. She had usually enjoyed 
 good health, except from what she called rheumatism and 
 occasional attacks of indigestion. In these there would be 
 acid risings with bilious vomiting and palpitation of the 
 heart. She was troubled also sometimes with flushes of 
 heat, and according to her account her stomach was easily 
 
28 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 put out. Her urine was deseribed as being tbick. Exami- 
 nation witb induced electrical currents sbowed tbat the 
 intrinsic muscles of the left thumb were less excitable 
 than those of the right, and, to a marked degree, less 
 excitable than the corresponding muscles of a bealthy sub- 
 ject. Inquiry into the history elicited tbat tbe patient's 
 father had suffered badly from gout, and that she herself 
 drank a great deal of sherry and occasionally also whisky. 
 
 A tradesman, aged forty- seven, complained that the 
 thumb and first two fingers of the left hand had lost grasp- 
 ing power. The skin covering them was more sensitive 
 than on the right side. He could not flex the phalanges 
 of the thumb, but could adduct the member ; nor could he 
 flex any of the phalanges of the index and middle fingers 
 except the first. His forearm had become thinner ; at its 
 upper part it measured 8| in. as against 9| in., the measure- 
 ment of the right forearm at the same point. The patient 
 had suffered for upwards of three weeks. There had been 
 no pain in the arm, but a numbness and dead feeling over 
 the inside half of it. The fingers, however, were always in 
 a state of painful "pins and needles," a feeling, as the 
 patient himself described it, " exactly like that which 
 occurs after pulling ice about for some time, and then 
 putting the hands near the fire." At the parts of the hand 
 and arm affected by this active numbness there was 
 exaggeration of all forms of sensibility — that of touch, 
 pressure, heat and cold, and j)ain. I found the faradic 
 reaction of the intrinsic muscles of the thumb defective. 
 
 With the galvanic current a rheophore over the musculo- 
 spiral nerve a little above the elbow showed that the 
 closure contraction with the anode was equal to that with 
 the kathode, and that there was an opening contraction 
 with the kathode equal to that with the anode. These 
 
NEUEITIS IN THE GOUTY. 29 
 
 serial changes apparently pointed to lesion of the nerve. 
 No note was made of the reaction of the median nerve. 
 The nerves implicated in this case were the branches of the 
 median supplied to the palm and first three fingers, as well 
 as those to the opponens, abductor, and flexor brevis 
 pollicis : also the cutaneous branches of the radial distri- 
 buted to the dorsal surface of the thumb and two outer 
 fingers ; and, in addition, the internal cutaneous from the 
 trunk of the musculo- spiral. Passive extension of the fore- 
 arm (the hand being in a position of semi- pronation) 
 was strongly resisted by the supinator longus, which was 
 brought out in bold relief by the procedure, and was 
 evidently uninjured. 
 
 My notes are, unfortunately, deficient in 
 details regarding the habits of this patient, but 
 I think I am right in saying that they were 
 conducive to gout. There was no history of 
 exposure to cold or pressure. The symptoms 
 are clearly referable to neuritis, which had gone 
 so far as to produce some muscular atrophy, 
 as well as changes of electrical reaction. The 
 case is especially interesting from the absence 
 of pain. In this respect it is comparable with 
 cases of paralysis of the musculo-spiral nerve 
 from cold, first prominently described by 
 Duchenne (de Boulogne), who refers the cause 
 to congestive hypereemia of irritative character. 
 
 A big, healthy-looking man, forty years of age, suffered 
 from numbness in the index finger of the left hand, followed 
 by a pricking or " pins and needles " sensation, and aching 
 
80 PAEALYSIS FROM PERIPHERAL NEURITIS. 
 
 pain in the arm, so tliat he was unable to lie on the left 
 shoulder at night. There were also, besides this, occasional 
 bursts of darting pain in the arm. His grasp had lost 
 power. Examination with the voltaic current showed 
 increase of excitability in the musculo-spiral nerve of the 
 left side ; the interruption of a current from two niilli- 
 amperes (rheophore on the nerve in the arm above elbow) 
 caused a very painful feeling of an electrical shock to be 
 experienced down to the forefinger on the left side. A cur- 
 rent of five milliamperes was required to produce the same 
 effect on the right side. There were no serial changes. 
 (KSZ >ASZ.) 
 
 In cases of this kind you will often find a 
 point on tlie shoulder where pressure gives 
 exquisite pain. It lies just inside the inner and 
 upper angle of the scapula, and the pain caused 
 by the pressure there seems to travel down to 
 the hand. Apparently there is neuritis of the 
 posterior branch of a spinal nerve, the anterior 
 branch of which enters into the formation of 
 the brachial plexus. 
 
 A female patient, aged fifty-eight, for two years had 
 suffered from pain in the right thumb of a violent throb- 
 bing and darting character. It would recur daily and last 
 for a longer or shorter time. After a little while it shot 
 up the radial border of the forearm into the shoulder-joint, 
 collar-bone, and sternum, and later still she got pain in the 
 right eye. There was a certain periodicity in the pain ; she 
 would wake with it ; after breakfast there would be some 
 relief, and in the forenoon, although not free from suffer- 
 ing, it would be tolerable. But about 10.30 every night 
 
NEURITIS IN THE GOUTY. 31 
 
 the pain would strike the thumb and forearm, and give her 
 insupportable suffering till midnight — the attack being 
 accompanied by great flatulence. The arm was said to 
 have lost power. 
 
 On electrical examination it was found that at the right 
 median nerve, above the wrist, the excitabihty to the 
 induced current was increased, whilst with the galvanic 
 current the contraction on opening circuit with the posi- 
 tive pole occurred sooner than the contraction on closure 
 with the negative pole. (A Z > K S Z.) 
 
 This patient drank large quantities of beer besides sherry 
 in the morning and passed much uric acid. 
 
 Under treatment there was great reduction of the undue 
 excitability of the nerve, but no marked diminution of the 
 pain. How far the restricted dietary ordered was followed 
 I have no means of knowing. 
 
 A man, aged forty- seven, on going to bed one night, felt 
 his right arm become quite numb. He had not been 
 asleep. Next morning he found that he could not throw 
 his coat on as usual. There was no pain. Next day, when 
 I first saw him, there was a feeling of "pins and needles" in 
 the arm, and this, with the powerlessness which still con- 
 tinued, alarmed him very much. On examination it was 
 found that the deltoid muscle was paralysed ; he was quite 
 unable to raise the elbow outwards and upwards. When 
 the forearm was extended it could not be passively flexed 
 showing integrity of the triceps. But when the forearm 
 was flexed on the arm I could forcibly extend it, whether 
 the forearm were in a supine position or semi-pronated 
 showing weakness of biceps, brachialis anticus and supi- 
 nator longus. In the right deltoid the reaction to the 
 induced current was slightly reduced, whilst that to slow 
 interruptions of the galvanic current was greatly increased 
 
32 PAEALTSIS FROM PERIPHE'RAL NEURITIS. 
 
 contractions occurring to a strength of 1*7 m.a. by the gal- 
 vanometer (RD). Five days later it needed a strength of 
 2*7 m.a. to bring about contractions in the deltoid, and by 
 this time the other muscles appeared to act normally. In 
 another fortnight he used the right deltoid freely, and the 
 muscle acted to a normal strength of induced current. 
 This patient had suffered from sciatica, lumbago, and 
 neuralgic symptoms in various parts at different times, and 
 had, I think, lived freely. But I have not details sufficient 
 to say with any degree of certainty that his affection was 
 of gouty origin. 
 
 In testing electrically for variations of ex- 
 citability in tlie nerve-trunks and muscles, it is 
 important to remember that the resistance 
 offered by the skin and subjacent tissues may 
 sometimes vary in the two sides of the body, 
 although in my experience great care in thor- 
 oughly wetting both the skin and the rheophores 
 in hot water, as well as attention to the position 
 of the latter, minimises this objection. Dr. de 
 Watteville has insisted strongly on the neces- 
 sity of employing a galvanometer in order to 
 check the results obtained by the application 
 of currents, and his recommendation should 
 certainly be followed. It is necessary to bear 
 in mind that, although in cases of local para- 
 lysis with more or less sensory disturbance, 
 striking alterations in the electrical excitability 
 of nerves and muscles may be met with, these 
 
NEURITIS IN THE GOUTY. 33 
 
 are by no means always present. Nor, as I 
 Lave said, are the changes when present so 
 constant in character that we can draw any 
 exact inference from them in the present state 
 of our knowledge, except that there is probably 
 some tissue change in the substance of the 
 nerve-trunk. 
 
 A working man, sixty-nine years of age, applied at the 
 hospital on account of shooting pain, aching, and numbness 
 in the left forearm and hand. He described a kind of 
 tingling from the shoulder to the fingers. After a time, 
 under treatment, he lost the painful sensations, but the 
 hand felt as if asleep, heavy, and big, and the grasp was 
 much weaker than that of the right. Common sensibility 
 was not much affected, but be could not feel a pin to pick 
 it up so well as with the other hand. Cold felt colder, 
 and heat hotter, to the left hand than the right. Although 
 he had never suffered from gout and had not noticed gravel 
 in the urine, the treatment was directed towards the pos- 
 sibility of this disorder. In the course of his attendance 
 he had an unmistakeable attack of acute gout in one of 
 his big toes. About a month afterwards, in July last, he 
 reported his hand and arm much improved, though still 
 to a certain extent numb. In the ulnar and musculo- 
 spiral nerves electrical examination gave K S Z > A S Z. 
 Towards the end of October, having meanwhile been almost 
 free from discomfort, he again attended with a return of 
 the old symptoms. The thumb and first three fingers 
 were described as feeling quite dead, and the grasp of the 
 hand was very weak. Examination of the median nerve 
 at the bend of the elbow with a galvanic current was now 
 made. The resistance of the tissues over the nerve in 
 
 3 
 
34 PAEALYSIS FEOM PEEIPHERAL NEUEITIS. 
 
 each arm was ascertained, by using tlie galvanometer, to 
 be equal on the two sides. In the right (unaffected) arm 
 K S Z was produced by a current measuring ten milli- 
 amperes ; in the left only seven and a half milliamperes 
 were required for the production of this contraction. In 
 the right arm the closure of a current from twenty cells 
 gave A S 0, whilst on the left A S Z was produced with a 
 current from sixteen cells. 
 
 From the character of the symptoms, coupled 
 with this evidence of heightened excitabihty, 
 there can be no doubt of the occurrence of 
 neuritis in this case, and I beheve it to be 
 dependent on a gouty condition of the patient's 
 blood. In his occupation, which consists in 
 handling and putting in paper metal goods which 
 have been recently soldered, he has been exposed 
 for forty years to a certain small amount of the 
 influence of lead, which would predispose him 
 to gout, an acute attack of which occurred, as I 
 have said, whilst he was under observation. 
 The disorder of sensibility, by which alongside 
 of some ansesthesia for common sensation there 
 was hypergesthesia for temperature, is curious, 
 but by no means uncommon. I have referrecj 
 to it on more than one occasion as occurrino^ in 
 rheumatic neuritis, and have also observed it 
 in hemiplegia with sensory disturbance. It was 
 marked in a case of multiple neuritis, which I 
 shall have to speak about hereafter. 
 
NEUEITIS IN THE GOUTY. 35 
 
 "No change whatever may be found in the 
 
 electrical reactions : 
 
 A man, aged fifty, whose father had suffered from gout, 
 and who had himself had three attacks of typical gout, 
 complained of loss of power in the left arm. There was 
 pain in the shoulder and down the left arm, with a slight 
 tendency to puffy swelling of the limb, tingling in the 
 fingers, and later a httle herpes in the forearm. The 
 electrical reaction in the nerves appeared unaltered. 
 
 I believe that the cases which have thus been 
 briefly alluded to are examples of slight neuritis. 
 In almost every instance they occurred in 
 persons with known gouty antecedents. When 
 we remember the tendency that gout has to 
 cause local inflammation, it seems reasonable to 
 suppose that local irritation from the presence 
 of urate of soda might cause inflammatory 
 action in the trunks of the nerves. One can 
 readily understand, indeed, that when urate of 
 soda is present in the blood it may be liable to 
 find its way into the lymph-spaces which are in 
 immediate connection with the bundles of nerve- 
 fibres, and there set up inflammation. The 
 difficulty is to say why this does not always 
 happen, not to explain its occasional occurrence. 
 ISTor is it easy to give a reason for its limita- 
 tion in such circumstances to one small part of 
 the frame. 
 
 I am not alone in feeling this difficulty. In 
 
36 PARALYSIS FEOM PERIPHERAL NEURITIS. 
 
 his recent work on gout, Dr. E,oose remarks : 
 '' Sciatica and facial neuralgia sometimes alter- 
 nate with articular gout. We may assume that 
 the pain is due to hypersemia and oedema of the 
 neurilemma, but why only certain branches of 
 a nerve should be affected as a result of the 
 constitutional disorder is a question which can- 
 not be solved."* 
 
 It is not without express reason that I have 
 brought before you such strongly contrasted 
 cases as one of typical neuritis and others which 
 are largely dependent upon concomitant circum- 
 stances for evidence that they probably belong 
 to the same class, though of a very different 
 degree of intensity. When we come to the 
 variety of neuritis which shows itself in multiple 
 form, engaging often the peripheral parts of all 
 the limbs as well as sometimes various cranial 
 nerves and nerves of the trunk, we shall find 
 that the symptoms often appear to diverge so 
 widely from those of typical neuritis as to throw 
 some doubt upon their relation to that disease. 
 The various examples to which I have referred 
 may prove not unimportant steps towards a 
 recognition of the obscure forms which the sym- 
 ptoms of neuritis may assume. 
 
 * ' Gout and its Eelations to Diseases of tlie Liver and 
 Kidneys,' by Eobson Eoose, M.D., 1885. 
 
PERIPHERAL OR CENTRAL DISEASE. 37 
 
 It is not my intention to dwell upon tlie 
 various forms of localised paralysis, wliicli are 
 well recognised, thanks especially to tlie graphic 
 teaching of Duchenne. One of the objects, in 
 the brief reference which has been made to 
 certain examples, has been to call attention to 
 conditions which may easily give rise to suspicion 
 of central disease, as indeed had occurred in 
 more than one of those which I have related. 
 This is a point which has been somewhat lost 
 sight of in recent times, although Grraves, in 
 his great work on Clinical Medicine, directed 
 especial attention to it. Another reason for 
 occupying time with these narratives has been 
 with the view of showing that in cases of 
 paralysis, in which the lesion certainly occupies 
 the peripheral nerves, we may find a singular 
 diversity of symptoms. As will have been 
 remarked, pain is sometimes present, and some- 
 times absent, numbness may be slightly or 
 strongly pronounced, muscular atrophy, which 
 is sometimes conspicuous, may be entirely 
 wanting, whilst the results of electrical exami- 
 nation may vary to a remarkable extent. We 
 shall find that the same variety is apt to mark 
 cases in which not one nerve-trunk or plexus 
 alone is the seat of lesion, but where there is a 
 more or less universal affection of the peripheral 
 
38 PABALTSIS FEOM PERIPHERAL NEURITIS. 
 
 nerves. The name of progressive multiple 
 neuritis has been given by Leyden to this dis- 
 ease, which, although long since observed, has 
 only been clearly differentiated and referred to 
 its pathological source during the last few years. 
 
 It did not escape the attention of Graves, 
 and his reference to the disorder is so graphic 
 and to the purpose that I make no excuse for 
 quoting it : 
 
 *' One of the most remarkable examples of 
 disease of the nervous system commencing in the 
 extremities, and having no connection with 
 lesions of the brain or spinal marrow, was the 
 curious * epidemic de Paris,' which occurred in 
 the spring of 1828. Chomel has described this 
 epidemic in the ninth number of the ' Journal 
 Hebdomadaire,' and having witnessed it myself 
 in the months of July and August of the same 
 year I can bear testimony to the ability and 
 accuracy of his description. It began (frequently 
 in persons of good constitution) with sensations 
 of pricking and severe pain in the integuments 
 of the hands and feet, accompanied by so acute 
 a degree of sensibility that the patients could 
 not bear these parts to be touched by the bed- 
 clothes. After some time, a few days, or even 
 a few hours, a diminution or even abolition of 
 sensation took place in the affected members ; 
 
GRAVES ON MULTIPLE NEURITIS. 39 
 
 they became incapable of distinguisliing the 
 shape, texture, or temperature of bodies, the 
 power of motion declined, and finally they were 
 observed to become altogether paralytic. The 
 injury v^as not confined to the hands and feet 
 alone, but advancing with progressive pace, ex- 
 tended over the whole of both extremities. 
 Persons lay in bed powerless and helpless, and 
 continued in this state for weeks and even 
 
 months. 
 
 ^ ^ ^ ^ 
 
 '*At last, at some period of the disease, 
 motion and sensation gradually returned, and a 
 recovery generally took place, although in some 
 instances the paralysis was very capricious, 
 vanishing and again reappearing. 
 
 " The French pathologists, you may be sure, 
 searched anxiously in the nervous centres for 
 the cause of this strange disorder, but could find 
 none; there was no evident lesion, functional 
 or organic, discoverable in the brain, cerebellum, 
 or spinal marrow." 
 
 This account, which was published by Graves 
 forty years ago, has been strangely overlooked 
 by most of us. 
 
 There is now ample evidence that a more or 
 less widely spread paralysis may depend upon a 
 degeneration of the nerve-fibres themselves, 
 
40 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 most pronounced towards the periphery and in- 
 dependent of any recognisable change in the 
 nerve-centres or roots. Such cases may occur 
 in connection with chronic alcohohsm, diphtheria, 
 enteric fever, syphihs, tuberculosis, and appa- 
 rently the widespread disease of Japan, called 
 Kakke or Beriberi, is an endemic form of the 
 same affection. There is some reason, too, to 
 think that exposure to cold, which is a frequent 
 antecedent, may be a factor in the production 
 of the disease. Occasionally also cases occur 
 in which no etiological cause whatever can be 
 traced. In this class of neuritis we have not to 
 deal with gross changes in the nerve-trunk. 
 The alterations are in great measure confined 
 to the nerve-fibre itself, and are usually only 
 recognisable under the microscope. 
 
 I propose in the next lecture to give an illus- 
 trative sketch of the symptoms and course of 
 multiple degenerative neuritis, and discuss after- 
 wards some of the modifications which are apt 
 to occur in one or other form of the disease. 
 
MULTIPLE NEURITIS. 41 
 
 LECTURE II. 
 
 Multiple neuritis — Two cases with syphilitic history — 
 G-rainger Stewart's cases — Morbid anatomy — Sym- 
 ptoms of multiple neuritis — Comparison with Kakke 
 — Alcoholic paralysis — Examples — Ataxic symptoms 
 — Pains and hypersesthesia— Degenerative changes in 
 peripheral nerves the immediate cause of paralysis — 
 Lancereaux's investigations — Pains may be absent — 
 State of the knee-phenomenon — Nystagmus — Dr. 
 Churton's case — The peripheral neuro-tabes of Deje- 
 rine probably of alcoholic origin — In alcoholic paralysis 
 lower extremities most but not exclusively affected — 
 The symptom " dropped feet " should always suggest 
 inquiry as to habits of intemperance — So '* wrist- 
 drop " suggests inquiry into possible exposure to lead 
 — Not in alcoholic paralysis alone is found tendency 
 to preponderating affection of the lower extremities — 
 Seen in multiple neuritis from other causes — Also in 
 Kakke — A paraplegic form of neuritis from unknown 
 cause — Examples. 
 
 In 1874 I brouglit before the Clinical Society 
 a case which I have since had reason to think 
 must have belonged to the class of multiple 
 neuritis. I recognised at the time that the 
 symptoms must, from their anatomical distribu- 
 
42 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 tion, depend upon altered conduction in nerve- 
 fibres, and not upon central changes, but was 
 disposed to refer these alterations of conduc- 
 tivity to pressure upon the roots of nerves by 
 inflammatory changes in the membranes. At 
 that time the idea that paralysis of a more or 
 less universal kind could depend upon lesion 
 of the periphery of the nerve-trunks, the central 
 portions being undamaged, was not entertained. 
 The case is so important that I think it well 
 to give a brief account of it, as well as of 
 another, manifestly of similar character, which 
 came before me in 1879. Dr. Ross, in referring 
 to these cases in the second edition of his 
 admirable work on the ' Diseases of the Nervous 
 System,' has also expressed the opinion that 
 they were examples of progressive multiple 
 neuritis. I have described them* under the 
 head of *' rapid and almost universal paralysis," 
 remarking that " it was convenient to use some 
 suc^ general title for the designation of certain 
 cases which are of extreme interest and import- 
 ance, but the true pathology of which we have 
 yet to learn." Since the first example, which 
 was published in the ' Transactions of the 
 Clinical Society ' in 1874, I have met with 
 
 * ' Clinical Lectures on Diseases of the Nervous System,' 
 p. 301. 
 
CASE OF MULTIPLE NEURITIS. 43 
 
 several, some of wliich are referred to in my 
 book. The cases that I am about to quote in 
 brief abstract are the most typical that I have 
 seen, and the most useful, therefore, for illus- 
 trating the subject. 
 
 W. H — , a working man, aged forty-four, of previous 
 good health, was brought to me at the hospital in January, 
 1873, in the following condition. He had double facial 
 paralysis, total absence of power of voluntary contraction 
 in the muscles of either leg, the grasp of both hands 
 almost entirely lost, and partial paralysis of respiration and 
 deglutition. There was incomplete paralysis of the right 
 external rectus muscle and of the soft palate, especially 
 on the left side. There was but little movement of the 
 diaphragm, and the intercostal muscles were likewise 
 acting so imperfectly that the patient could not lie down 
 in bed. His sterno-mastoid and trapezii muscles acted 
 freely. Cutaneous anaesthesia was more or less general 
 throughout the trunk, extremities, and face — the tips of 
 the fingers being especially numbed. The plantar reflex 
 was absent in each foot. There was slight power of 
 voluntarily contracting the muscles on the front of each 
 thigh, but he was unable to contract in the least those on 
 the front of either leg below the knee. A sense of numb- 
 ness and weight was complained of in each leg, and occa- 
 sionally a "throbbing ran down the left thigh and calf." 
 For the first two or three weeks also he had suffered from 
 "pins and needles" in his legs. But at no time appa- 
 rently had there been any actual pains in his extremities 
 or involuntary muscular contraction. The power of the 
 sphincter ani was normal, that of the bladder impaired to 
 a slight extent. The muscles about the mouth showed 
 
44 PARALYSIS FEOM PERIPHERAL NEURITIS. 
 
 the reaction of degeneration. In those of the arms the 
 reaction to faradism was greatly diminished, whilst in 
 those of the legs, below the knees, it was quite absent ; in 
 the left thigh it was greatly diminished. (The right 
 lower extremity was lame and wasted from an old attack 
 of infantile paralysis.) But in no part of the upper or 
 lower extremities was there increased action to slow inter- 
 missions of the galvanic current. In the face, however, 
 this was marked. The facial muscles reacted to inter- 
 ruptions of a current from six cells (Stohrer). His attack 
 had commenced one month previously with numbness in 
 the finger-ends, followed on the same day by weakness in 
 the legs, which increased next day and was then accom- 
 panied by numbness about the calves, thighs, and but- 
 tocks. The weakness increased day by day, and a week 
 after the beginning of his illness he had the sensation of 
 a tight band round his abdomen. A few days later he 
 could use neither arms nor legs. The difficulty of swal- 
 lowing was not observed till a fortnight after the onset. 
 There had been no fever. There was nothing abnormal 
 in the mental condition, nor in the heart, lungs, and 
 kidneys. The patient was at once admitted and placed 
 on a water-bed. For twenty-four hours his condition was 
 one of imminent danger from the state of respiration. As 
 there was a syphilitic history, he was treated with iodide 
 of potassium, and later with mercury. He soon began to 
 improve, and in six months was able to resume his 
 employment. A few months later I showed him at the 
 Clinical Society, entirely recovered. 
 
 On April 14th, 1879, T. O— , aged forty-four, was 
 admitted into hospital with paralysis of all four extremi- 
 ties and both sides of the face, together with inability to 
 swallow solids. The respiration was mainly upper tho- 
 
CASE OF MULTIPLE NEXTEITIS. 45 
 
 racic, and there was some loss of control over the bladder 
 and sphincter ani. His grasp was feeble ; he was unable 
 to stand ; as he lay in bed he could move one foot across 
 the other, but could not lift either more than three or four 
 inches off the bed. There was great muscular flacciditj. 
 He did not know where his legs were. The knee pheno- 
 menon was absent on each side. Over the right side of 
 the face there was complete loss of sensibility to tonch 
 and pain, with apparently increased (but at all events 
 well-retained) sensibility to heat and cold. The anaes- 
 thesia was likewise observed, though to a less extent, over 
 the left side of the face, and also, though here again in a 
 less complete degree, on his forehead (Fig. 1). He com- 
 plained of great pain in the right half of the forehead, 
 spreading towards the vertex. Below the middle of the 
 
 Fig. 1. 
 
 forearm on each side there was almost entire loss of sensi- 
 bility to touch and pain, whilst heat and cold were well 
 recognised. Where the alteration in sensibihty began 
 
46 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 there was what the patient described as a "band-like 
 feeling around the arm." In the tips of his fingers there 
 was a constant tingling sensation, and anything which he 
 touched with them felt hot (Fig. 2) . In his lower extre- 
 
 FiG. 2. 
 
 mities sensibility was also greatly modified. Below the 
 middle of the thigh on each side neither a touch nor the 
 prick of a pin could be recognised. Over the whole of 
 both feet, as well as half»way up the legs, and on the pos- 
 terior surface of the rest of each lower extremity, sensi- 
 bility to heat and cold appeared intensified. Over the 
 whole of the trunk, and in the extremities down to the 
 boundaries described, cutaneous sensibility was normal. 
 He had frequent pains like knife -stabs in the lower extre- 
 mities, and the legs would twitch when they occurred. 
 At other times the pains were of a dull heavy character 
 
CASE OF MULTIPLE NEURITIS. 47 
 
 (Fig. 3).* In this case facial paralysis on the left side 
 seems to have been the first symptom, which was observed 
 by his friends a month before admission. The patient 
 
 Fig. 3. 
 
 knew nothing of this, and felt quite well till a fortnight 
 before I saw him. He then noticed "pins and needles" 
 in his hands and feet. Three days later he had diplopia, 
 and his legs became weak. In five more days he could not 
 
 * The illustrations are from diagrams made at the time 
 by Mr. A. E. Broster, then resident medical ofiicer, and 
 exhibited at the Clinical Society, before which the patient 
 appeared when recovered. 
 
48 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 walk, and tliere was difficulty in swallowing. In another 
 three days he could not dress himself. On admission, and 
 for a few days afterwards, reaction to induced currents 
 was almost entirely absent in the muscles of the face, and 
 also in the thenar eminence and interossei of each hand ; 
 it was lessened, though not to the same extent, in the 
 muscles of the front and back of the forearms. There was 
 very slight reaction to induced currents in all the muscles 
 of the lower extremities. Under active mercurial treat- 
 ment the patient entirely recovered in about six months. 
 On August 10th the knee-phenomenon was found to have 
 returned in the right leg, and three days later in the left. 
 This patient was likewise shown at the Clinical Society.* 
 
 There is no doubt tliat the patient, W. H — , 
 was a temperate man. As regards T. — , lie 
 is described in my notes as having " lived fast 
 and drunk fairly," whatever that may mean. 
 Both had had syphilis, and recovery in each case 
 was absolutely complete under specific treat- 
 ment. Diphtheria could be entirely excluded. 
 I would draw attention to the fact that in the 
 first case the patient suffered from girdle pain, 
 a symptom which is usually considered as point- 
 ing distinctly to disease of the spinal cord or 
 its membranes. In the second case, again, 
 what was equivalent to girdle pain was felt in 
 the two forearms, at the point where the anaes- 
 thesia ceased. It is a curious circumstance, 
 
 * * Transactions of the Clinical Society,' voL xiii. 
 
GEAINGEK STEWART's CASES. 49 
 
 and well illustrates the difficulty there is in 
 quitting well-worn grooves of opinion, that, 
 although I recognised that the lesion must be 
 one of nerves, I failed to see in the diagrams 
 of the an93sthesia powerful evidence that the 
 affection must involve the periphery of the 
 nerves, and not their roots, nor did any member 
 present at the meeting at which they were shown 
 suggest such an explanation. 
 
 In March, 1881, Dr. Grainger Stewart 
 brought before the Medico- Chirurgical Society 
 of Edinburgh three cases of paralysis of the 
 hands and feet from disease of the nerves.* 
 
 The first was tliat of a clerk, aged fiftj-two, wlio got 
 bruised and shaken from a fall, and on the following day 
 liad some " rheumatic " pains which came and went during 
 the succeeding week. A fortnight later there was tingling 
 and num.bness in the hands and feet, with stiffness in the 
 joints of the hands, and difficulty in grasping and walking, 
 swelhng of the feet and hands, with severe cutting pains 
 in them. All these symptoms gradually increased until 
 admission. When examined his temperature was under 
 100°. There was severe cutting pain of an intermittent 
 character in the hands and feet, increased on pressure, 
 especially of palmar or plantar surfaces, and aggravated by 
 movements of the body. With the pain there was numb- 
 
 * The account which follows has been much abbre- 
 viated from the report in the ' Edin. Med. Journal,' April, 
 1881. 
 
 4 
 
50 PAEALYSIS FEOM PERIPHEEAL NEUEITIS. 
 
 ness, but the tingling was gone. Sensibility to touch was 
 much lessened in both hands, slightly in the forearms and 
 was normal above the elbows. It was also greatly dimi- 
 nished and delayed in both feet, and, to a less extent, i,n 
 the legs. Sensibility to heat and tickling were cor- 
 respondingly affected. The perception of painful impres- 
 sions was delayed, but felt acutely, a distinct interval 
 elapsing between pinching the hand and its perception, but 
 a slight pinch was felt to be very painful, and the pain 
 persisted longer than normal and set up considerable reflex 
 movements. The muscular sense in the hands and feet 
 was much diminished. 
 
 Voluntary motion was greatly impaired in the hands 
 and feet, all the groups of muscles being weakened, but 
 those of the fingers and toes completely paralysed. There 
 was diminution of electric excitability in proportion to the 
 degree of paralysis. 
 
 There was glossiness of the skin over the backs of the 
 fingers and some appearance as of bruises over the toes, 
 but no oedema. The muscles were diminished in volume. 
 There was acute pain in passive movements of the hands 
 and wrists. The case was treated at first by ergot and 
 then by the induced current. A degree of improvement 
 soon manifested itself, and by the end of September the 
 patient could walk about, and the muscles of the extremi- 
 ties were recovering their volume. 
 
 In another case the patient's illness began with chilliness, 
 numbness, and weakness in both legs ; next day, " pins and 
 needles " and increasing weakness. Some days after the 
 feet and hands became similarly affected. Pain, though 
 not of severe character, was felt in the small of the back, 
 but no mention is made of pains in the hands and feet, as 
 in the last case. Sensibility to touch was distinctly 
 impaired in the parts which suffered from coldness, formi- 
 
GEAINGEE STEWAEt's CASES. 51 
 
 cation, and numbness, i. e, in tlie feet and tips of tlie 
 fingers. 
 
 Voluntary motion was lost in tlie toes, very imperfect at 
 the ankles, normal at the knees and hips. The hands, 
 especially the right, were much weakened, and the move- 
 ments of the wrists, fingers, and thumbs, although feeble, 
 were not lost. The patient could neither walk nor stand 
 unsupported. At one time it was necessary to draw off 
 the urine by catheter. The patellar tendon-reflex was 
 absent on each side. 
 
 After four months this patient was likewise recovering. 
 
 The third patient was thirty- one years old. In him a 
 weakness of the legs appears to have been the first symptom 
 noted, which was followed by " prickling " in the legs, 
 which increased, and in a short time was accompanied by 
 a similar feeling in the fingers and hands also, with loss of 
 power and stiffness. 
 
 This man likewise had pain of a tingling character in 
 both legs from the knee to the dorsum of the foot, but 
 no girdle pain or formication. Sensibility to touch was 
 diminished in the legs below the knees and in the hands. 
 There was delay also in the transmission of impressions. 
 Patellar tendon-reflex was absent. Voluntary motion was 
 greatly impaired in the legs and hands. Electric excita- 
 bility was much diminished in the legs and forearms, 
 especially in the extensor muscles. Any attempt to use 
 the muscles caused great pain. 
 
 The cerebral and mental functions of this patient were 
 somewhat impaired. He was drowsy and his memory was 
 imperfect. He was improving when an attack of croupous 
 pneumonia carried him off. No mention is made of his 
 habits. Was it not an example of alcoholic neuritis ? 
 
 In this case microscopical examination showed very 
 notable changes in the median, ulnar, and tibial nerves. 
 
52 PARALYSIS FROM PERIPHEEAL NEURITIS. 
 
 The axis-cylinders had undergone degeneration. On the 
 other hand, two cords of the brachial plexas which were 
 examined showed no evidence of such changes as were 
 found lower down in the nerves of the limb. Most of the 
 bundles of nerve-fibres appeared normal. There were no 
 such alterations of the axis-cylinder as were found in the 
 nei'ves of the forearm. Certain changes were found in the 
 cord, but these apparently were of a secondary character. 
 They occupied the columns of GoU, and the most superficial 
 and posterior part of the lateral columns, and this only in 
 the cervical region and to a less extent in the lumbar 
 enlargement. Neither the grey matter nor the nerve- 
 roots were involved. 
 
 " In the nerves," Dr. Stewart remarks, '' the 
 lesion was extremely distinct. It involved a 
 large proportion of the nerve-fibres of the 
 affected portions of nerves, and consisted in a 
 breaking up of the axis- cylinder. To the naked 
 eye the nerve appeared quite normal, the affected 
 parts of the median and radial being undistin- 
 guishable from the unaffected parts further up." 
 
 Leyden describes an acute or subacute inflammatory 
 process as aff'ecting the nerve-trunks, especially the radial 
 and peroneal, in a case of this description. The nerves 
 appeared in some cases swollen, reddened, and hypersemic, 
 but sometimes also unaltered to the eye. The nerves 
 themselves presented signs of sclerotic atrophy. The 
 sheaths were thickened, the primitive nerve bundles con- 
 tained exceptionally few medullated fibres, most of them 
 atrophic and composed of thickened axis-cylinders. About 
 
MORBID ANATOMI OF MULTIPLE NEURITIS. 53 
 
 tbe blood-vessels in the fatty tissue between the nerre 
 bundles, and also in these themselves, there lay numerous 
 heaps of yellow granular pigment ; evidence of a previously 
 existing bloody infiltration. 
 
 This degeneration of nerves extended downwards into 
 the smallest twigs of muscular nerves. The muscles them- 
 selves showed a moderate degree of myositic atrophy. 
 Upwards this disease ceased about the middle of the upper 
 arm. The anterior roots were quite intact ; the cords also 
 intact, and the great ganglion cells well preserved. 'No 
 disease was to be found in the nerves of the lower ex- 
 tremities. 
 
 The symptoms had been fever, sharp pains, involving 
 the upper and lower extremities. Pains extended from 
 the elbow and knee-joints to the fingers and toes, either 
 spontaneously or as a result of pressure. 
 
 There was loss of power below the knees and in the 
 forearms, with considerable atrophy of muscle in the fore- 
 arms, especially in the extensors, but trifling in the leg and 
 foot. In the lower extremities, the affection after some 
 months was completely recovered from. But it lasted in 
 the upper ; the atrophy increased and the difficulty of using 
 the limbs became greater. The muscles showed reaction 
 of degeneration. 
 
 The patient died with disease of the kidneys one year 
 after the commencement of the illness. 
 
 In another case the nerves showed fatty degeneration 
 and atrophy. A great part of the fibres had their medul- 
 lary sheath entirely lost, and the nerve was changed into 
 band-like axis- cylinders which showed varicose swellings in 
 different parts. 
 
 It will not be necessary for me to multiply 
 illustrative cases of the kind, but I may say 
 
54 PAEALYSIS FROM PERIPHEEAL NEUEITIS. 
 
 that many sucli liave lately been recorded both 
 in Germany and France. The two cases of my 
 own show a considerably greater diffusion of 
 the lesion than was observed in those reported 
 by Dr. Grainger Stewart, but in other respects 
 they are strictly comparable, and there can be 
 no doubt that a lesion of peripheral nerves 
 similar to that which the fatal termination in one 
 of Dr. Stewart's cases enabled him to disclose 
 was also the cause of the symptoms in my 
 patients, who perfectly recovered. The double 
 facial paralysis in my cases, whilst apparently 
 complicating the diagnosis, really aids it. The 
 facial muscles showed well-marked '' reaction 
 of degeneration," evidencing lesion either of 
 the facial nucleus or of the trunk of the portio 
 dura. The simultaneousness of the paralytic 
 phenomena in other parts of the body make it 
 evident that they all (facial included) depended 
 on strictly similar lesions. Therefore, had 
 lesion of the facial nucleus been in question, 
 the motor symptoms in the extremities would 
 have been due to lesion of the ganglion cells in 
 the anterior horns of the cord, homologous with 
 the facial nucleus in the bulb. But the sensory 
 symptoms were as strongly marked as the motor, 
 and lesion of the anterior ganglion cells could 
 not explain these. We are obliged, therefore. 
 
SUGGESTIONS AS TO PATHOLOGY. 55 
 
 to seek the cause in the nerve-trunks ; and the 
 strict hmitation of the ansesthesia, as shown in 
 the diagrams, coupled with the corresponding- 
 situation of the most marked paralysis, is con- 
 clusive evidence that the lesion was in the 
 periphery of the nerves. 
 
 The fact that in many examples of multiple 
 neuritis the spinal cord and the roots of nerves 
 are perfectly free from pathological change, 
 which is confined to a greater or less extent of 
 the periphery of the nerves, is very startling and 
 dijQScult of explanation. One cannot help feel- 
 ing that notwithstanding the absence of observ- 
 able lesion there must be some change in the 
 central nervous system to influence a coincident 
 afiection of the periphery of so many nerves. 
 An ingenious suggestion has been made by De 
 Watteville in reference to certain cases of lead 
 paralysis where this limitation of morbid change 
 to the peripheral nerves sometimes occurs. He 
 inquires whether, in these circumstances, there 
 is not a functional lesion of the cord which 
 interferes with the trophic influence which 
 ought normally to be exerted by it upon the 
 motor nerve-fibres, and consequent degenera- 
 tion. More recently Erb has suggested the 
 same explanation for the paradoxical condition 
 obtaining in cases of multiple neuritis generally. 
 
66 PAEALYSIS FEOM PEEIPHERAL NEUEITIS. 
 
 But one would not expect, if this were the case, 
 that the lesion of nerves would continue as it 
 sometimes does after long illness strictly con- 
 fined to the periphery. Were the functional 
 activity of the cord to be long suspended the 
 atrophy might well be looked for throughout 
 the length of the motor fibres. For my part I 
 should rather seek to explain the fact by the 
 hypothesis that a toxic influence of some kind 
 is exerted upon vaso-motor centres in the bulb 
 and cord. The effect of this would be to give 
 rise to some alteration in the calibre of minute 
 arteries — those in which the muscular element 
 is relatively most developed. These belong to 
 the periphery of the arterial system, and in 
 general terms correspond with the periphery of 
 the distribution of nerves. It is conceivable, 
 therefore, that the supply of blood to the 
 periphery of nerves might in 'this way be 
 diminished by an irritative influence exerted 
 upon vaso-motor centres in the bulb and cord. 
 Notable diminution of blood supply sulQ&ciently 
 long continued would occasion degeneration of 
 the essential element of nerve-fibre. I merely 
 throw this out as a suggestion. It is impossible 
 to discuss the point just now with advantage. 
 
SYMPTOMS OF MULTIPLE NEUEITIS. 57 
 
 Symptoms of Multiple Neuritis. 
 
 In cases of acute or subacute multiple neu- 
 ritis, it very commonly happens that the first 
 symptom noted by the patient is a feeling of 
 '' pins and needles " or numbness in the feet, 
 and about the same time, or a little later, in the 
 finger ends. In others there is less acuteness 
 in the attack, and vague pains of a " rheu- 
 matic " character have been complained of 
 before the occurrence of numbness. Fever is 
 not usually a marked symptom, but occasionally 
 there is considerable elevation of temperature. 
 It is difficult to speak very definitely on this 
 point, because from the insidious mode of 
 onset which often characterises even the acute 
 cases, the patient is not usually examined with 
 the thermometer until some days after the 
 commencement of his illness. More often than 
 not the patient in the early stage of the dis- 
 order tries to go about his usual avocations, 
 but finds day by day an increasing difficulty in 
 doing so. The numbness and deadness which 
 had commenced in his feet and fingers gradu- 
 ally spread up the extremity, his legs appear 
 to grow heavy so that he cannot move them 
 quickly, his arms become more and more 
 
58 PAEALYSIS FEOM PERIPHERAL NEURITIS. 
 
 powerless, and in a few days he cannot stand 
 or help himself in any way. The disease tends 
 to affect both sides of the body symmetrically, 
 though sometimes there are considerable differ- 
 ences in the severity of the symptoms as 
 displayed on either side. In severe cases, we 
 find not only the muscles of the extremities, 
 but also those of the trunk, becoming more or 
 less powerless ; there may be facial paralysis, 
 and some ' of the muscles of the eye may 
 become involved ; swallowing and respiration 
 may also become affected ; and death may occur, 
 with signs of the vagus becoming implicated. 
 
 But it much more commonly happens that at 
 a certain point, which differs remarkably in 
 various cases, the climax of the attack is 
 reached, and then each day brings with it signs 
 of amelioration, until in many cases absolute 
 recovery takes place. But here, again, it is 
 difficult to give a general sketch which shall be 
 consistent with the many varieties which occur. 
 The amelioration in some instances may take 
 place with such quickness as to make it appear 
 doubtful whether any serious organic lesion 
 could have been present. In others, the 
 amount of improvement which each day brings 
 is so slight that the prognosis remains for a 
 long time doubtful. Or there may be condi- 
 
SYMPTOMS OF MULTIPLE NEUEITIS. 69 
 
 tions between these two extremes. In that 
 stage of the disease in which the patient is able 
 to walk abont, the gait is apt to be ataxic. 
 The duration of the illness may be from a few 
 weeks to many months, or even, if the sequelae 
 be reckoned, some years. During the entire 
 illness there is in the large majority of cases 
 great flaccidity of the paralysed muscular 
 system. There is no doubt that this is the 
 rule. But I have seen several exceptions, and 
 to these I shall have to refer more particularly 
 later on. In many cases there is distinct mus- 
 cular atrophy. This is especially marked in 
 the muscles of the leg below the knee, and in 
 those of the hand and forearm. As the patient 
 lies in bed, even from a very early stage it is 
 characteristic of this disease that the feet are 
 *' dropped," so to speak, the power of dorsal 
 flexion of the foot being the first to disappear. 
 And so also with the upper extremities. The 
 wrists are ''dropped" exactly as is seen in 
 cases of lead palsy. The flaccidity of the mus- 
 cular tissue, its tendency to atrophy, and its 
 behaviour to electric stimuli, likewise cause a 
 strong resemblance to this well-known form of 
 toxic paralysis — a resemblance due to the cir- 
 cumstance that a similar condition of the peri- 
 pheral nerves may be due to the influence of 
 
60 PAEALYSIS FEOM PERIPHERAL NEURITIS. 
 
 lead. When the facial muscles are paralysed, 
 the cheeks fall in bags, the food collects in 
 them, and there is absolute want of power of 
 expression. The soft palate, when it is in- 
 volved, hangs loose, and is unable to be lifted, 
 so that fluids regurgitate through the nostrils, 
 and the voice has a nasal character. In very 
 slight cases the electrical excitability of the 
 muscles may be unchanged; and in severe 
 examples, if the muscles about the body be 
 severally tested, you will find a great variety 
 in their response. In some, faradic excitability 
 will be slightly, in others greatly, lessened. 
 Along with great lowering of faradic excita- 
 bility in the first of my cases there was no 
 increase of excitability by the galvanic current. 
 Lowenfeld, on the other hand, has observed 
 isolated lowering of galvanic excitability, the 
 response to induced currents remaining normal- 
 In others, again, "reaction of degeneration " 
 will be distinctly marked. This is especially 
 likely to be the case as regards the intrinsic 
 muscles of the hands, and the anterior muscles 
 of the leg below the knee. The patellar tendon 
 reflex is almost always lost. It is usual to find 
 the cutaneous reflexes of the sole, abdomen, and 
 cremaster more or less weakened, or altogether 
 absent. As a general rule the functions of the 
 
SYMPTOMS OF MULTIPLE NEURITIS. 61 
 
 bladder and rectum are not disordered, but in 
 severe cases there is a loss of control over the 
 sphincter ani, and if the patient is not quick 
 to answer to the call of his bladder the urine 
 runs from him. Or there may be some delay 
 in passing urine when the desire to do so is 
 present. 
 
 It has been suggested by Ley den that in the 
 exceptional cases in which bedsores and paralysis 
 of the sphincters occur we have to deal with 
 an affection which is not limited to the periphe- 
 ral nerves, but extends also to the spinal cord. 
 Occasionally more or less oedema of the extremi- 
 ties is to be observed, and trophic changes in 
 the skin have been noted, especially a glossiness 
 like that described by Paget as the result of 
 injuries to the trunks of nerves. 
 
 On the sensory side we may expect to find 
 pains which are often of lightning character, 
 coming and going in sudden darts like stabs of 
 a knife, and recalling those which are charac- 
 teristic of tabes dorsalis. Or they may be de- 
 scribed as " gnawing" or " burning" or " like 
 molten lead in the veins." They are usually 
 more pronounced in the lower than in the upper 
 extremities. It is commonly found that great 
 tenderness of the muscles is complained of when 
 these are grasped by the hand. The patient 
 
62 PAEALYSIS FEOM PEEIPHERAL NEUEITIS. 
 
 himself will sometimes describe a sensation of 
 aching in the muscles, and very commonly, 
 indeed, a feeling of ''numbness," ''deadness," 
 or " pins and needles," which are referred espe- 
 cially to the hands and feet. 
 
 Leyden calls attention to the fact that sensa- 
 tions of " pins and needles " or " deadness " are 
 apt to be produced by pressure on the nerye- 
 trunks, and remarks upon the interesting bear- 
 ing of this circumstance upon the pathology of 
 the affection. Remarkable differences may be 
 found as regards the affection of various modes 
 of sensibility of the skin. There may be, as we 
 have seen, in the lower half of the forearm and 
 hand, entire loss of sensibihty to touch and 
 pain, whilst heat and cold continue to be well 
 recognised, or even exaggerated in intensity. 
 Or we may find exquisite hypersesthesia, so that 
 not only is a touch unbearable, but even a 
 current of air excites the greatest torture. In 
 other cases there is only a " muffling" of common 
 sensation, and in some no disorder of sensibility 
 is to be noted. There is almost always a 
 striking absence of tendency to bedsores. The 
 mental faculties may be expected to remain 
 entirely free from disorder. It will happen, 
 however, in those cases which are connected 
 with alcoholism that intercurrent affections of 
 
SYMPTOMS OF MULTIPLE NEUEITIS. 63 
 
 the brain or its membranes may produce their 
 peculiar effects. These comphcations are not 
 unlikely, unless remembered and allowed for, to 
 cause some obscurity in the diagnosis. 
 
 I have said that many of these cases recover 
 perfectly. On the other hand, the process of 
 recovery may remain permanently incomplete 
 owing to irreparable atrophy of muscular tissue 
 having taken place. It is in cases marked by a 
 great amount of muscular atrophy that we are 
 apt to meet with apparent exceptions to the rule 
 that the paralysis is of a flaccid character. 
 From the circumstance that all the nerve-fibres 
 supplied to a limb are not affected with, equal 
 severity, the amount of atrophy in different sets 
 of muscles will necessarily differ. Some will 
 lose but little tissue or none at all ; others, their 
 antagonists, may be profoundly affected. 
 Duchenne has shown how, as a consequence of 
 loss of power in a certain muscle, the limb, 
 obeying the tonic power of its antagonists, whose 
 exaggerated movement is no longer held in 
 check, is ultimately dragged in the direction of 
 these latter. Hence occur faulty positions and 
 deformities. The contractures are rigid and not 
 to be overcome by passive movement. So 
 you will often see the foot stiffly pointed from 
 unopposed contracture of the sural muscles due 
 
64 PARALYSIS PROM PERIPHERAL NEURITIS. 
 
 to atrophy of tliose lying on the front of the 
 leg, and analogous rigid malpositions in the 
 upper extremities. 
 
 Attention has been called to the strong 
 resemblance to multiple neuritis in its clinical 
 features which is borne by the disease called 
 Kakke or Beriberi. 
 
 Hirsch * reports that after prodromal malaise 
 there is a gradually increasing paralysis of the 
 lower limbs which extends also to the upper 
 extremities, and the patient is more or less 
 completely disabled by loss of power. On the 
 sensory side there are at first paraBsthetic sym- 
 ptoms, tickling, creeping feeling, or " pins and 
 needles " and burning sensation, particularly in 
 the feet and legs, muscular tenderness (especially 
 in the muscles of the calf). Later on, the sensory 
 disorder takes the form of anaesthesia, and is 
 especially distinguished by loss of the sense of 
 pressure, and of heat and cold. These sym- 
 ptoms, like those on the motor side, are noted 
 earliest and most uniformly in the lower limbs, 
 extending afterwards in a smaller proportion 
 of cases to the upper extremities. There are 
 also disorders of the blood-making organs and 
 circulation. The patients wear an anaemic 
 
 * 'Handbook of Geographical and Historical Patho- 
 logy,' New Sydenham Society, ii, p. 571. 
 
SYMPTOMS OF BEEIBEEI. 65 
 
 look and complain of palpitation and dyspnoea. 
 There are cardiac murmurs with increase of 
 the area of cardiac dulness (from dropsy of the 
 pericardium or dilatation of the heart) ; the 
 pulse is small and very compressible. The 
 urine is always diminished but never contains 
 albumen. Such are the symptoms which cha- 
 racterize what is called the paralytic or dry 
 form of Beriberi, but in another class more or 
 less dropsy is added to them. The oedema 
 usually shows itself first in the ankles and legs, 
 extending gradually until it at length becomes 
 general anasarca; then follow dropsical effu- 
 Bions into the serous cavities, always into the 
 pericardium, more occasionally into the pleura 
 or peritoneum, and rarely into the cerebral 
 and spinal arachnoid. It would appear that 
 whilst that form which is characterized by the 
 presence of dropsy is rapidly fatal, the other, 
 called the " atrophic " form, but rarely causes 
 death. 
 
 Dr. Theobald Palm,* who was for ten years 
 resident in Japan, says, " I soon became aware 
 of a large number of patients who came to me 
 with symptoms of defective innervation of the 
 legs. They complained of numbness in the 
 
 * Kakke, ' Edin. Clinical and Pathological Journal,' 
 September, 1884. 
 
 5 
 
66 PARALYSIS FEOM PEETPHERAL NEURITIS. 
 
 lower extremities, wliiclitliey generally described 
 as a feeling as if a piece of thin tissue paper 
 were spread over the skin; of slight loss of 
 power, showing itself by inability to walk any 
 distance without inordinate fatigue, a tendency 
 to stumble and for the knees to give way. 
 They experienced a difficulty, especially in 
 going upstairs, and sometimes in holding the 
 thong of the wooden clog usually worn by the 
 Japanese, which passes between the great toe 
 and the next. Some patients dropped the point 
 of the foot in walking, showing a paralysis or 
 paresis of the flexors of the foot and extensors 
 of the toes. When the foot was planted evenly 
 on the floor they had little or no power to raise 
 the toes from the ground, or if they could raise 
 the toes little force was required to press them 
 down. They had also a trace of oedema over 
 the tibiae or about the ankles. In many cases 
 there was tenderness of the muscles of the calf, 
 which were in some instances hard and swollen, 
 in other cases abnormally flabby and apparently 
 partially atrophied. In almost all of these 
 patients there was an absence or marked dimi- 
 nution of tendon reflex at the knee. Beyond 
 the above symptoms they seemed to be in 
 average good health. Some of them com- 
 plained of vague dull pains in the legs." 
 
SYMPTOMS OF BEEIBEEI. 67 
 
 Scheube* mentions that in the upper ex- 
 tremities, as well as in the lower, it is the ex- 
 tensor muscles which are most affected. The 
 feet are "dropped" by their weight, and it is 
 only rarely that a position of varo-equinus is 
 caused by contraction of the unopposed sural, 
 muscles. He notes the decrease or loss of 
 faradic excitability and disorders of sensibility 
 closely resembling those I have described, and 
 remarks that it is especially the tactile sensibility 
 and the muscular sense which are affected. In 
 advanced cases there is pain on pressing masses 
 of muscle. In about a third of the patients 
 whom he examined the knee-jerk was absent. 
 Frequently it disappeared several days before 
 the apparent onset of the disease, and did not 
 return till some months after recovery from all 
 other symptoms. He did not note any laryn- 
 geal symptoms, but is disposed to refer the 
 quickening of the pulse and the vomiting which 
 may be frequent towards the end to neuritis of 
 the pneumogastric. Recovery occurs in the 
 majority of cases, but in a certain number this 
 is not complete. 
 
 Dr. Harada reports details of autopsy in two 
 cases of Kakke in its subacute form. Amongst 
 other points he noted degenerative changes in 
 
 * ' Die Japanisclie Kakke (Beriberi),' Leipsig 1882. 
 
68 PARALYSIS FEOM PERIPHERAL NEURITIS. 
 
 the muscles. Tlie nerves of tlie lower extremi- 
 ties showed overgrowth of connective tissue in 
 the epi- and endo-neurium. The vessels of the 
 nerve-trunks were thick-walled, with narrowing 
 of the lumen, or hypergemic with widening. 
 The nerve-fibres were very irregular, being either 
 sodden and often granulated, or atrophic ; the 
 axis-cylinder was often very thin. The changes 
 were very considerable in the peripheral part 
 of the tibial and peroneal nerves, less in the 
 sciatic and crural ; they were also distinct in 
 the renal nerve and vagus. The brain was 
 normal. The substance of the spinal cord was 
 indistinctly seen under the microscope, owing 
 to the presence of fibrinous exudation. Some 
 of the ganglion cells in the anterior horns were 
 atrophic, round or irregular in form, granular, 
 often without nucleus, the processes sometimes 
 strikingly thin. Some of the vessels showed 
 thickening of the intima with round cells. 
 
 So close is the resemblance between this 
 endemic disease and the " spontaneous " form 
 of multiple neuritis met with in Europe, that 
 E-. H. Pierson, of Dresden, is inclined to con- 
 sider the latter as sporadic cases of the Oriental 
 disease. Whilst on this point I would remind 
 you that in anassthetic leprosy we have a train 
 of symptoms pointing to lesion of peripheral 
 
ANESTHETIC LEPEOST. 69 
 
 nerves, loss of power, muscular atrophy, tropliic 
 changes in tlie skin and deep tissues, with 
 cutaneous ansesthesia. In ten such cases Van- 
 dyke Carter found the brain, spinal cord, and 
 roots of the nerves healthy, whilst the nerve- 
 trunks were swollen, dull red, or grey, or semi- 
 translucent, rounded, and firm. According to 
 Virchow^ the morbid process begins with a 
 peri-neuritis causing proliferation of cells and 
 consequent atrophy of the essential nerve- 
 elements by pressure. In a patient affected 
 with anaesthetic leprosy, whose case I brought 
 before the Chnical Society in 1870, and who 
 died an accidental death, the nerve-trunks of 
 the affected limbs were found swollen, and 
 microscopic examination disclosed great over- 
 growth of cells in the connective tissue, with 
 atrophy of nerve-fibres. I may remark here, 
 by the way, that I long ago suggested to the 
 late Dr. Anstie that the scattered cases of 
 localised muscular atrophy met with in this 
 country might possibly be the lineal descend- 
 ants of the leprosy which once abounded in 
 Grreat Britain. But I must not be tempted to 
 travel further in a by-way full of attraction for 
 the exercise of the scientific imagination. 
 
 Let us pass on now to another form of pro- 
 gressive multiple neuritis — that which is apt 
 
70 PAEALTSIS FROM PEEIPHERAL NEURITIS. 
 
 to take place in alcoliolic patients. The earliest 
 reference to this disease that I have met with 
 occurs in a short essay, ' History of Some of 
 the Effects of Hard Drinking,' by the well- 
 known Dr. Lettsom, which was published in 
 1789.* In describing the symptoms which 
 are liable to arise from an acquired habit of 
 spirit drinking he writes, '' The lower extremi- 
 ties grow more and more emaciated, the legs 
 become as smooth as polished ivory, and the 
 soles of the feet even glassy and shining, and 
 at the same time so tender that the weight of 
 the finger excites shrieks and moaning. 
 The legs and the whole lower extremities lose 
 all power of action ; wherever they are placed 
 there they remain till moved again by the 
 attendant ; the arms and hands acquire the 
 same palsied state, and the patients are ren- 
 dered incapable of feeding themselves. 
 They talk freely in the intervals of mitigation, 
 but of things that do not exist ; they describe 
 the presence of their friends as if they saw 
 realities, and reason tolerably clear upon false 
 premises." 
 
 Some thirty years later Dr. James Jackson, 
 
 * I am indebted to mj friend Dr. Thomas Morton, 
 late President of the Harveian Society, for the opportunity 
 of consulting this work. 
 
ALCOHOLIC PARALYSIS. 71 
 
 of Boston, published an account of tlie dis- 
 order,* and Magnus Hiiss, of Stockholm, drew 
 attention to it in 1852. Since then important 
 contributions to our knowledge of the subject 
 have been made by Lancereaux and Leudet in 
 France, and by Reginald Thompson, Handfield 
 Jones, and Wilks in England. But little has 
 appeared on the subject in England since Dr. 
 Wilks' communication to the ^Lancet' in 1872, 
 except a paper at the Royal Medical and 
 Chirurgical Society by Dr. Broadbent in the 
 course of last year, and more recently valuable 
 contributions from Dr. Dreschfeld and Dr. 
 Hadden. My personal observation of the 
 disease dates from a case which I attended in 
 1870 in consultation. 
 
 The patient was a lady wlio had for years been addicted 
 to great alcoholic excesses, consuming large quantities of 
 brandy. When called to her she was in bed suffering 
 from considerable loss of power in the npper and lower 
 extremities. The hands were dropped at the wrists, and 
 she could not extend them. The feet, too, were likewise 
 in a dropped condition, and there was no power of dorsal 
 flexion. There was much mental disturbance, and such 
 loss of memory that the patient could give no intelligible 
 account of the duration of her illness. She could move 
 her arms and raise the knees, though with diflSculty. The 
 
 * Quoted by Dr. Dreschfeld, ' Brain,' part 32. 
 
72 PAEALTSIS FROM PERIPHEEAL NEURITIS. 
 
 functions of tlie bladder and rectum were not interfered 
 with. Her naked feet projected from the foot of the bed- 
 clothes, and she would not allow anything to be laid 
 upon them, so exquisite was the tenderness of the skin. 
 Her constant complaint was of the agonising pains in the 
 legs, " as though the veins were filled with molten lead,'* 
 and she appealed piteouslj to those around her for relief 
 from this suffering. She was placed in charge of two 
 nurses, who gave her no more than the very small amount 
 of stimulant which was allowed, and under careful feeding 
 and treatment her pains got rapidly less. There was much 
 muscular atrophy of the hands and forearms and the ante- 
 rior tibial muscles, with what is now known as "reaction 
 of degeneration." Her hands assumed the typical form of 
 the " main en griff e of Duchenne." In the course of a 
 little more than a year she had recovered so far as to be 
 able to go about by herself, and the movements of the 
 hands also were practically restored. The first use which 
 she made of her liberty was to visit a succession of taverns, 
 and inaugurate a debauch, which terminated her existence 
 in the course of a week or two. 
 
 This case made a great impression upon me, 
 for it was at that time a novel experience. 
 Since then I have seen many examples of vary- 
 ing gravity and with certain differences in the 
 symptoms. 
 
 The following are short notes of a case which 
 I saw in consultation in September, 1875 : 
 
 A female patient, aged thirty -five, lay in bed with her 
 knees up, and said she could not straighten her legs, but 
 being partially assisted and by great effort she contrived to 
 
ALCOHOLIC PAEALTSIS. 73 
 
 get lier legs down nearly to extension, complaining, how- 
 ever, of the pain thereby caused in her hamstrings, which 
 were very taut. 
 
 There was partial anaesthesia of the feet and legs np to 
 the knees. Tickling the sole was felt as touch, not as 
 tickling. Her hands, too, were similarly numbed, the 
 fingers looked white, puffy, soddened, and there was 
 tremulousness of the tendons. 
 
 She herself dated her illness from a miscarriasre two 
 years previously, after which she began to feel curious 
 sensations in the feet as though walking on sponges, with 
 occasional pricking, tingling, and pins and needles. These 
 feelings continued and were later accompanied by pain of 
 a very excruciating character, which began in the toes, 
 especially the big toe, and ran up the foot and leg to the 
 knee, She described the toes as " drawing up " and the 
 pain " as though the skin were being dragged off her flesh 
 with a knife." A fortnight before I saw her she had 
 walked about fifty yards supported on either side. She 
 had been obliged to look continually at her feet or would 
 have fallen. 
 
 There was no spinal tenderness on touch or percussion, 
 nor marked stiffness of the spinal column on rising or 
 reclining in bed. She suffered from insomnia, " seeing 
 things about the room," and there had long been retching 
 in the morning. She had no albumen in the urine. Her 
 habits had long been very intemperate. 
 
 The necessity of looking at her feet in walk- 
 ing described by this patient recalls a similar 
 symptom so common in patients snflPering from 
 tabes dorsalis, and is evidence of ataxy. It is 
 a symptom which has caused not a few cases 
 
74 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 of alcoholic paralysis to be mistaken for loco- 
 motor ataxy. 
 
 In tlie case of a gentleman, aged f orty-tliree, whom I saw 
 in 1876, there was j^aralysis of the bladder as well as of 
 the lower limbs. He had been drinking spirits very hard 
 indeed for three or four years, and previously to that had 
 always lived freely. He was paraplegic and complained of 
 horrible pains, " like something sharp thrust into his legs 
 and making him twinge again." The legs did not jerk 
 nor did he complain of cramp. There was no pain in the 
 spine or tenderness on pressure upon it. His conjunctivae 
 were yellow, his hands tremulous. There was no altera- 
 tion in the fundus oculi. The urine was albuminous. 
 It appeared that seven or eight years previously he had 
 suffered from a similar attack, from which he had com- 
 pletely recovered. 
 
 By my direction, the patient (whom I only saw on one 
 occasion) was kept without alcohol, and for a week he 
 appeared, it was said, to be doing well. His pains became 
 much less and he slept, but I learned in the sequel that 
 he contrived to get drink again and shortly afterwards 
 died. 
 
 In 1882 I saw in consultation a lady, of about thirty- 
 five years of age, who had gradually lost power in the 
 lower extremities during the preceding six months. The 
 muscles of her legs were excessively wasted and powerless ; 
 the feet were dropped and dorsal flexion of the foot was 
 impossible. The knee-jerk was absent on each side. 
 Examination with the induced current showed entire loss 
 of faradic contractility. There was also atrophy of the 
 interossei of the hands. She complained of pains like 
 
ALCOHOLIC PAEALYSIS. 75 
 
 " molten lead " in the feet. In this case there was a 
 history of confirmed alcoholism. Abstinence was enforced, 
 and under appropriate treatment the patient, as I learned 
 some months afterwards, quite recovered. 
 
 Some years ago a female patient of middle age came 
 under my observation. She had suffered much from 
 neuralgia in the head, which had been relieved by stimu- 
 lants. In the preceding summer she had been subjected 
 to great moral and physical strain, and after a few weeks 
 it was noticed that her feet began to swell and she became 
 very weak. (There was no cardiac or renal disease.) 
 Severe vomitiug and diarrhoea began, which brought her 
 down very low. Then loss of memory came on and 
 delirium — or rather a vacuity of mind and alteration of 
 manner. About this time she began to suffer from severe 
 paroxysms of pain in her joints and limbs. Menstruation 
 ceased for four months. Some of her joints became con- 
 tracted, but the general health improved under treatment, 
 and when I saw her the wasted and contracted state of the 
 limbs was the chief ailment to be observed. I found the 
 little finger of one hand contracted to a right angle, the 
 ring finger also, though less contracted, and there was a 
 thickening to be noted about the tendons in the palm of 
 the hand. The extensor communis digitorum responded 
 to the induced current. She could lift the right knee 
 fairly well, but could not straighten the leg owing to con- 
 traction of the hamstrings. There was a good deal of 
 wasting of the quadriceps extensor muscle. The vastus 
 internus muscle was only excitable by a strong induced 
 current. The foot was in a position of equino-varus. The 
 muscles in front of the tibia were wasted, the tibialis 
 anticus and extensor longus responding to a faradic cur- 
 rent which did not excite the peroneus longus. On the 
 
76 PAEALISIS FEOM PERIPHEEAL NEURITIS. 
 
 left side tliere was a similar state of things but not to the 
 same extent. 
 
 Under massage, faradisation, manipulation, 
 and division of some tendons, this patient 
 recovered to a remarkable extent, being able in 
 tbe course of three years to walk with very 
 little aid. 
 
 Pains and extreme sensitiveness to touch are, 
 as I have said, of extremely frequent occurrence 
 in alcoholic paralysis. It is interesting to note 
 that when recovery takes place and a second 
 attack occurs later on, the symptoms in this 
 respect may vary in the same individual. 
 
 A few years ago I saw a lady, aged thirty-seven, who 
 was unable to stand, and complained of dull aching pains 
 in her legs, which had been going on for three or four 
 weeks. For four months she had been feehng weak, and 
 six weeks before I saw her she rather suddenly lost power 
 in her legs. As she lay in bed she could draw up her 
 knees, but was quite unable to flex either foot. The 
 anterior tibial muscles on the right side had entirely, and 
 those on the left side almost entirely, lost their faradaic 
 excitability. There was no hyperalgesia to touch. 
 
 On inquiry it appeared that two years previously she 
 had slowly lost power in the legs *' after a chill." Next 
 day there were pains all over her, and on the follow- 
 ing day she was unable to walk without help. She was 
 then laid up with almost complete loss of power in the 
 lower extremities. She su:ffered from excruciating pains 
 in the legs from the foot to the knee. She also felt 
 
ALCOHOLIC PARALYSIS. 77 
 
 miirLbness over tlie lower part of the trunk and down each, 
 thigh. Her hands at the same time were so weak that she 
 could not hold things. She had slowly recovered after 
 about twelve months. The character of the pains in this 
 second attack she described as differing entirely from what 
 she had suffered in the previous illness. They appeared 
 then to have been of exceedingly acute character. 
 
 It may be worth mentioning in reference to 
 this patient (whom I saw on one occasion only, 
 she having been brought up to town for the 
 purpose) that when the diagnosis was commu- 
 nicated to her husband he at first denied the 
 possibility of its being correct, but on persisting 
 in my opinion I obtained a history of an 
 extremely large consumption of brandy, and an 
 acknowledgment of the correctness of the view 
 which had been taken. 
 
 One very important feature of this subject 
 is that we may see a remarkable difference of 
 severity in these cases, so that it is difficult at 
 first sight to understand that they can possibly 
 be examples of one and the same disorder. 
 Dr. Broadbent, in his recent paper, brought 
 forward several examples of a form of alco- 
 holic spinal paralysis which he described as 
 characterised essentially by insidious onset, 
 progressive weakness, especially of the exten- 
 sors on the forearms, giving rise to double 
 
78 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 ■wrist-drop, inability to stand, loss of knee-jerk, 
 and retention of plantar reflex. The sensa- 
 tion was said to be unimpaired, except that in 
 every case there was tenderness on firm pres- 
 sure, and in one lancinating pains. There was 
 oedema of the lower extremities. The sym- 
 ptoms gradually grew more intense, and death 
 took place by asphyxia inconsequence of para- 
 lysis of the diaphragm and intercostal muscles. 
 In the case in which a necropsy took place no 
 change could be detected in the spinal cord, 
 the only organ which was allowed to be exam- 
 ined. I think the inference to be drawn from 
 the clinical characters of these cases and the 
 negative results of examination of the cord is 
 that they were examples of multiple neuritis. 
 
 Dr. Wilks, Dr. Barlow, and myself, who took 
 part in the discussion on Dr. Broadbent's paper, 
 spoke of recovery as very common.* I remarked, 
 too, that in more than one case that I had seen 
 there was a history of a previous attack, from 
 which under abstinence the patient had recov- 
 ered, only to become again affected as the old 
 habit was resamed. In an interesting work, 
 ' Etude sur les Paralysies Alcooliques,' recently 
 
 * Vide 'Proceedings of tlie Eoyal Medical and Chi- 
 rargical Society of London,' February 12th, 1884, voL i, 
 No. 5. 
 
ALCOHOLIC PAEALTSIS. 79 
 
 publislied in France hj Dr. Oettinger, tlie author 
 speaks of the prognosis as ''most grave," and 
 does Dot conceal his surprise at the recorded 
 experience of some Enghsh physicians who 
 speak of patients recovering after abstinence 
 from alcohol, to relapse when they again returned 
 to it. This difference of experience would 
 imply that a number of cases pass unrecognised, 
 being referred to some other cause than alcohol ; 
 and this, it seems to me, may be quite as true 
 probably in reference to the very severe as well 
 as to the slight examples. An observer, whose 
 experience of the disease had been derived from 
 a certain number of fatal cases, might easily 
 overlook the true origin of comparatively slight 
 examples which came before him. On the 
 other hand, one who had got to associate 
 alcoholic paralysis with cases which uniformly 
 recovered might not unnaturally sometimes fail 
 to ascribe a rapidly fatal case of paralysis to its 
 real source. 
 
 In writing some years ago upon the subject 
 of lead palsy, I remarked that '' the history of 
 exposure to lead has often to be sought out by 
 pertinacious inquiry after the diagnosis has 
 been formed through other sources." And 
 this, which is true of lead, is at least equally the 
 case in regard to alcoholic paralysis, for here 
 
80 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 the patient will often not only fail to give the 
 clue to the cause of his disorder but delibe- 
 rately, and sometimes with extreme dexterity, 
 put his medical attendant off the scent. 
 
 The art with which a secret drinker, espe- 
 cially if a female, will conceal her vice is well 
 known. Where there is an absolute conceal- 
 ment of all traces of alcohol and a dexterous 
 suggestion on the part of the patient of other 
 possible causes of the illness, it is not surprising 
 that the medical attendant is sometimes deceived. 
 This must evidently be especially liable to occur 
 in hospital practice on account of the difficulty 
 of obtaining accurate information as regards 
 the habits of the patient. 
 
 There is now enough of evidence from histo- 
 logical examination to show that in alcoholic 
 paralysis of the kind which I have described 
 the essential lesion consists in parenchymatous 
 neuritis of the peripheral nerves. It is evident 
 that, as a result of chronic alcoholism, more or 
 less extensive lesions may be expected to be 
 found in various parts of the body, especially 
 in the liver and intra-cranial membranes. But 
 there can be little doubt that the degenerative 
 changes in the peripheral nerves are the imme- 
 diate cause of the paralytic symptoms. 
 
 In a series of examples published by Lance- 
 
ALCOHOLIC PARALYSIS. 81 
 
 reaux in 1882, a careful examination of tlie 
 fatal cases showed tlie spinal cord entirely free 
 from pathological change. The roots of the 
 spinal nerves also were apparently quite healthy, 
 even under careful microscopical examination. 
 The periphery of certain trunks, however, the 
 posterior tibial and radial, presented the cha- 
 racteristic appearances of degenerative neuritis. 
 Confirmatory evidence from other observers 
 abounds as to the immunity of the cord and 
 roots of nerves. With some reservation as to 
 the nature of the neuritis, whether it is purely 
 parenchymatous or of interstitial origin, they 
 are evidently cases which come into the category 
 of multiple neuritis. 
 
 I have already sketched before you the sym- 
 ptoms and course of multiple neuritis. These 
 need not therefore be recapitulated, but it may 
 be useful to refer to some of the clinical features 
 of the alcoholic form of the disease as I have 
 observed it. In the nature of things, more 
 or less intellectual disturbance is present. The 
 memory is especially weakened ; the patients 
 '*talk freely," as Dr, Lettsom writes in the 
 pamphlet before alluded to, " but of things that 
 do not exisb; they describe the presence of 
 their friends as if they saw realities." A 
 journalist told me of the articles he had just 
 
 6 
 
82 PAEALTSIS FROM PEEirHERAL NEURITIS. 
 
 written and sent off to certain newspapers with 
 an air of such, vraisemhlance, that it was diffi- 
 cult to credit the fact that he had not lifted a 
 pen for three months. It may be found on 
 inquiry that the patient suffers from nervous 
 symptoms suggestive of incipient delirium 
 tremens. I have remarked that pains and 
 hyperalgesia have been, as a rule, extraor- 
 dinarily pronounced. So, also, the degree 
 of muscular atrophy seems to me to be fre- 
 quently greater in this than in other forms 
 of multiple neuritis. It is remarkable to see 
 the extent to which in many cases the muscles 
 of the legs and forearms are wasted. The 
 muscular tissue seems to have almost entirely 
 disappeared. This is especially to be seen in 
 the extensor group, so that the feet, as the 
 patient lies, drop helplessly forward. As has 
 been already pointed out when dealing gene- 
 rally with the symptoms of multiple neuritis, 
 the varying degree of muscular atrophy in a 
 limb may easily give rise to contracture of 
 rigid character. You may thus at one stage of 
 the disease find a patient lying in bed with 
 powerless, wasted, and flaccid limbs — the feet 
 and hands, as mentioned, helplessly dropped; 
 and in another stage find the same patient with 
 the tendo-Achillis rigid, the foot unable to be 
 
ALCOHOLIC PAEALTSIS. 83 
 
 brouglit into dorsal flexion by strong passive 
 movements, the hamstring muscles contracted, 
 whilst the hands show the claw-like character 
 described by Duchenne. 
 
 The pains and inordinate sensibility of the 
 skin may, I believe, be altogether absent in 
 alcoholic paralysis, as happens likewise in some 
 cases of multiple neuritis of non-alcoholic origin. 
 The following case, which recovered in the 
 hospital, was a striking example of this : 
 
 A single woman, aged thirty-one, was admitted into 
 hospital with loss of power in all four limbs, but especially 
 in the legs and feet. She could not stand even with help, 
 the legs doubling up under her when the attempt was 
 made. Lying in bed she could straighten her legs and flex 
 the knees. She could also move the feet a very little, but 
 the toes not at all. 
 
 As regards the upper extremities the loss of power in 
 the hands was very great in proportion to the strength of 
 the arms — indeed, the arms did not seem at all affected, as 
 tested by exertion against resistance. The grasp of the 
 right hand was 10° of the left 0. The sensibility of the 
 legs below the knees and the feet was impaired, and also 
 that of the hands. The plantar reflex was obtained with 
 difficulty; there was no knee jerk on either side. 
 
 The patient was a very fat woman with sallow com- 
 plexion and unhealthy aspect. Her feet and the lower 
 part of the legs were oedematous, pitting on pressure, and 
 so were the hands and forearms, though to a less extent. 
 
 The heart was free from any signs of disease ; there 
 was no albumen in the urine, nor was there any ascites. 
 
84 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 Owing to her obesity the size of the liver could not ^he 
 made out. Her account of her illness was that six months 
 previously she had noticed gradual loss of power in her 
 legs, and after six weeks was obliged to leave off her work, 
 which was of a mechanical nature. The history she gave 
 was indefinite, but apparently she had suffered from " pins 
 and needles " in the feet and legs, and no complaint was 
 made of pains. She had not had any pain in the back, 
 The swelling of the legs had occurred for some time, but 
 had increased during the month previous to her coming 
 under observation. The hands and forearms had only 
 shown swelling for about a week ; the want of power in 
 them had been of about one month's duration. There was 
 no difficulty in regard to the bowels, but she had latterly 
 been obliged to be quick in obeying the call to urinate. 
 
 This patient began to improve shortly after her admission, 
 and in a month could take about a dozen steps with slight 
 assistance. The grasp of the left hand then marked 8°, 
 that of the right only 10°, as on admission. She could 
 move the toes a little and the sensibility of the lower 
 limbs had returned except over the oedematous feet. 
 
 After another month she could walk the length of the 
 room alone, although in an ataxic fashion. The knee-jerk 
 was still absent. 
 
 After a few months she entirely recovered and returned 
 to her employment. 
 
 Whilst in hospital she lay in bed for the first month, 
 and later on some electrical treatment was employed. 
 Iodide of potassium was given. 
 
 She had never had rheumatic fever, but a year pre- 
 viously appeared to have suffered from pains about some 
 of her joints. It is right to say that no reliable in- 
 formation could be obtained as to her habits. From her 
 general appearance, however, the fact that she had long 
 
ALCOHOLIC PAEALYSIS. 85 
 
 been affected with morning retching and sickness, with 
 aversion from food, and that immediately previous to the 
 commencement of the paralytic symptoms she had suffered 
 from jaundice, it was judged probable that there had been 
 an excess in alcohol. Whilst in hospital she had no oppor- 
 tunity of continuing the indulgence, and, as I have said, 
 her improvement was rapid and recovery complete. 
 
 This patient showed in a marked degree the 
 characteristic excess of paralytic symptoms in 
 the feet and hands as well as the vaso-motor 
 paralysis causing oedema. 
 
 The case was one, there can be little doubt, 
 of multiple neuritis, which was of alcoholic 
 origin. 
 
 The absence of knee-phenomenon is so common 
 in these cases that we may almost confidently 
 expect to find this symptom. It will now and 
 then happen, lioweyer, that we may find the 
 knee-reflex not only present but somewhat 
 exaggerated. I do not see how to explain this 
 as a result of neuritis, and as, I believe, it is 
 only in alcoholic examples that the anomaly is 
 observed, it may be due to interference with 
 the inhibitory influence of the cortex cerebri 
 caused by the action of alcohol. 
 
 In the early stage of a case related by Dr. 
 Oettinger, a highly characteristic one of this 
 class, the knee-phenomenon is described as 
 " notably exaggerated," and it is remarked that 
 
86 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 tickling the soles of tlie feet gives rise to '' very 
 extensive reflexes." In the sequel of that case 
 the knee-phenomenon disappeared. 
 
 A case which has lately been under observa- 
 tion in hospital is an example in point. It 
 presents too, some interesting features, which 
 induce me to bring it before you in some 
 detail. The patient, previous to admission, 
 had been under the care of my colleague, Dr. 
 Ormerod, who had diagnosed the case as one 
 of alcoholic paralysis. 
 
 A working man, aged thirtj-eiglit, experienced a feeling 
 of stiffness in both legs, especially in tlie calves, with 
 aching in the spine and shooting pains in his limbs. 
 When these symptoms had lasted about two months he 
 felt both his hands become weak and numb, and, according 
 to his own description, '* as though they did not belong to 
 him." If he rubbed them together they would tingle. 
 He was admitted into hospital seven months from the 
 commencement of his illness. At that time he could not 
 walk except with great difficulty and with a very peculiar 
 gait. The legs were widely separated, the body thrown 
 forward, and the ground was only touched with the ante- 
 rior part of the foot, the heels never coming down. He 
 could not stand still in this " equine " position, but was 
 obliged to hurry forward. When his eyes were closed he 
 was very insecure. 
 
 The tendo-Achillis on each side, and especially on the 
 left, was tense. When lying down he could perform all 
 movements with his legs, but the power of dorsal flexing 
 and inverting the right foot was most imperfect, whilst 
 
ALCOHOLIC PARALYSIS. 87 
 
 on tlie left side these movements could scarcely be per- 
 formed at all. 
 
 Examination witli electric currents in February showed 
 loss of faradic excitability in the muscles of both legs 
 below the knee, and in the vasti of the left thigh. There 
 was slight reaction to strong induced currents in the vasti 
 of the right thigh. 
 
 The knee-phenomenon was well marked on both sides, 
 especially on the left. Plantar reflex was well marked 
 and produced more vivid reflex movements in the opposite 
 leg than in the one touched. This was especially to be 
 remarked of the left leg when the sole of the right foot 
 was tickled. The abdominal and epigastric reflexes were 
 well marked, especially on the left side. Tactile and 
 painful sensibility were not apparently affected, but he 
 complained of numbness in the feet and hands. The 
 sciatic nerves and the anterior tibial nerves in their lower 
 third were tender on pressure. Many points of tenderness 
 were to be found over the spinal column, especially about 
 the lower dorsal region. 
 
 The arms looked thin and wasted but presented no 
 marked loss of reaction to electric currents. The grasp 
 of each hand was very weak, the dynamometer giving 40° 
 for the right, 45° for the left. 
 
 Patient had a half -jaundiced appearance ; his liver was 
 large ; there was no albumen in his urine. For many 
 months he had suffered from diarrhoea, morning sickness, 
 and loss of appetite. He had been in the habit of drink- 
 ing a great deal of beer since he was twelve years of 
 age. On an average he had taken ten pints of beer daily, 
 and sometimes whisky as well. He had twice suffered 
 from delirium tremens. 
 
 This patient was treated by confinement to his bed for 
 some months, total abstinence from alcoholic liquors, and 
 
88 PARALYSIS FROM PERIPHEEAL NEURITIS. 
 
 the constant current was applied to his legs. In May 
 a very distinct improvement had taken place. He could 
 walk without hurrying, and the tendo-Achillis was much 
 less tense, the sole of the foot being now able to be placed 
 on the ground. At the end of May the tibialis anticus 
 muscle on each side reacted fairly to induced currents, 
 the extensor longus digitorum acted slightly to very strong 
 currents, the peroneus longus and the vasti showed 
 normal reaction to induced currents. In June he could 
 dorsal- flex and invert either foot. A few weeks later he 
 was discharged quite recovered, his gait having ceased to 
 present any peculiarity. 
 
 The absence of tlie knee-phenomenon which 
 is so generally observed in all forms of multiple 
 neuritis, coupled with the lightning pains so 
 often experienced by the patient, may be 
 strongly suggestive of tabes dorsalis. This 
 resemblance is sometimes increased by the 
 occurrence of a notable amount of ataxy. In 
 the case of ray patient, T. — , there were 
 sharp pains, sudden, and of momentary duration, 
 like a knife stab in the right thigh and knee, 
 his gait was ataxic, and he said the ground did 
 not feel natural to him. His legs seemed to 
 spring under him. The knee-phenomenon was 
 absent. At a certain stage of his illness the 
 superficial resemblance to a case of tabes was 
 very striking. A notable point of distinc- 
 tion was to be found in the behaviour of the 
 
ALCOHOLIC PAEALTSIS. 89 
 
 muscles to electrical currents. It is well 
 known that in tabes there is essentially no 
 change from the normal condition in this 
 respect. In certain cases no doubt the anterior 
 grey matter of the cord may become invaded 
 and cause muscular wasting with loss of fara- 
 dic excitability in limited parts, but this is 
 quite, as it were, an accidental complication, 
 and is not an essential part of the disease. 
 Now, in my case of multiple neuritis there was 
 very slight reaction to strong induced currents 
 in all the muscles of the lower extremities, 
 and almost total absence in the interrossei and 
 thenar muscles of the right hand. This of 
 itself, to say nothing of other differences, was 
 sufficient to distinguish the case from one of 
 tabes. 
 
 Dr. Hadden has drawn attention to the occa- 
 sional occurrence of nystagmus in these cases. 
 The observation is an important one, as the 
 ataxy gives sometimes a prima facie resem- 
 blance to disseminated sclerosis, which the pre- 
 sence of nystagmus would be liable to support. 
 
 A case was lately published by Dr. Churton, 
 of Leeds, which has an interesting bearing on 
 this subject. It was one in which ataxy and 
 other nervous disorders occurred in a syphi- 
 litic patient. 
 
90 PAEALYSIS FROM PEEIPHERAL NEURITIS. 
 
 The patient was a groom, twentj-four years of age, 
 accustomed to drink rather heavily of beer and spirits. 
 When admitted into hospital he was unable to wait, and 
 could stand with great difficulty even when supported on 
 each side, anxiously looking down all the time at his legs, 
 and so tending to fall forwards, being unable to balance 
 his trunk upon his lower limbs. He bad also lost power 
 of co-ordinate movements in his upper limbs, could not cut 
 up his food nor even pick up a match without great 
 trouble, nor tell by the sense of touch what the match 
 was. His grasp was not very feeble ; he complained of 
 numbness and pins and needles in his fingers. His replies 
 to questions were hazy, and he seemed dazed. There was 
 no tenderness nor swelling of bones or joints and no spe- 
 cial wasting of muscles. The plantar and patellar reflexes 
 were absent ; the cremasteric and abdominal present ; the 
 pupils, optic discs and retinae were normal. He had had 
 a chancre sixteen weeks before admission, followed by 
 sore-throat and rash. Five or six weeks before admission 
 the toes of his right foot began to be numb and tingling, 
 he staggered in walking, and the numbness spread up the 
 leg, Then the left foot and leg became affected and he 
 could not stand with the eyes shut or in the dark. At 
 this time he was still drinking rather freely. About a 
 month later he was quite unable to walk, and a few days 
 after that his hands became numb and weak. 
 
 He was submitted to a vigorous mercurial treatment, 
 and recovered so rapidly that he was discharged from 
 hospital on January 21st, having been there a little more 
 than a month. A month later, it is noted, the reflexes 
 were normal. 
 
 Dr. Cliurton remarks that altliougli the 
 prominent features of this case were those of 
 
ALCOHOLIC PAEALTSIS. 91 
 
 locomotor ataxy or posterior sclerosis it cannot 
 be taken as a simple case of that disease. I 
 shonld myself feel disposed to think that this 
 case was one of multiple neuritis. Where the 
 history points both to syphilis and alcoholism, 
 it is difficult to allot the part played by each in 
 the production of the disease in this instance, 
 but it is probable that alcohol was largely con- 
 cerned. The absence and return of patellar 
 tendon reflex is of constant occurrence in cases 
 of multiple neuritis. I have never seen it 
 restored (after being lost) in a case of well- 
 marked posterior sclerosis. The mental obfus- 
 cation which is described has no association 
 with that disease, whilst it might be expected 
 in a case of multiple neuritis from alcohol. 
 The absence of plantar reflex also, so far as it 
 goes, favours the view that this was the nature 
 of the case. 
 
 Dejerine, in France, has drawn attention to 
 cases in which pains, inco-ordination, absence 
 of knee-phenomenon, and anaesthesia have pro- 
 duced a striking resemblance to tabes, and in 
 which after death no lesion of the cord was 
 found, but there were degenerative changes in 
 the peripheral nerves. He has suggested for 
 these the title of " neuro-tabes peripherique/' 
 Facts of this kind have to be borne in mind ere 
 
92 PARALYSIS mOM PERTPHEEAL NEURITIS. 
 
 we conclude of a case marked by ttie character- 
 istic symptoms described tliat it is one of scle- 
 rosis of the posterior columns. In Dejerine's 
 cases I cannot lielp thinking that alcohol was 
 the important etiological factor. 
 
 Considering that the toxic influence of alcohol 
 must be brought about through the medium of 
 the circulation, it is not surprising that the 
 upper as well as the lower extremities should 
 be affected in cases of alcoholic paralysis. 
 Indeed, it might be anticipated that the effects 
 would display themselves equally upon all the 
 voluntary muscles of the body. But this is not 
 the case. It is upon the lower extremities that 
 the brunt of the mischief falls. They usually 
 suffer the most, and may possibly, perhaps, be 
 occasionally alone affected. But I am disposed 
 to think that their immunity is not nearly so 
 great as has been supposed, and that careful 
 observation would show that in cases where 
 the patient only complains of loss of power in 
 his legs, the arms are also, though to a less 
 extent, likewise affected. The patient's atten- 
 tion is apt to be so engrossed by the prepon- 
 derating disorder in his lower extremities that 
 he takes little or no notice of the weakness in 
 his hands. An observation which I made many 
 years ago in a case of lead-poisoning very much 
 
DEOPPED FEET IN ALCOHOLIC PARALYSIS. 93 
 
 struck me. Althougli the patient only com- 
 plained of one arm and one leg (which were 
 manifestly paralysed), and asserted that there 
 was nothing wrong with the other extremities, 
 I found in the muscles of the latter a very 
 well-marked decrease of faradic excitability. 
 I have also many times noticed a similar con- 
 dition in cases of infantile paralysis. 
 
 In general terms, it may be said that just as 
 in a case of lead paralysis we expect to find 
 wrist-drop so in a case of alcoholic paralysis we 
 look for dropped feet. I would go further 
 even, and say that if we meet with a case of 
 dropped feet — a paraplegic condition affecting 
 with marked preponderance the anterior tibial 
 group of muscles — we should be on the alert to 
 inquire respecting the possibility of alcohol 
 being a cause. Let me not be misunderstood. 
 The existence of foot-drop is not alone a proof 
 of habits of excess, but the symptom is so ex- 
 tremely frequent in cases of alcoholic paralysis 
 that we should be wanting in our duty if we 
 failed to bear this in mind, and direct investiga- 
 tion accordingly. This is of course a delicate 
 matter, and on more than one occasion I have 
 observed a look of somewhat indignant surprise 
 on the face of the medical attendant of whom 
 the inquiry has been made. But we have no 
 
94 PAEALTSIS FEOM PERIPHEEAL NEUEITIS. 
 
 more right to omit the inquiry than we should 
 have to avoid examining into the possibility of 
 lead poisoning when a case of dropped wrist 
 comes under our observation. It is especially 
 when we find not only the extensors of the 
 feet but those of the hands paralysed, and also 
 when there are some sensory disturbances as 
 well as motor, that we shall do well to bear in 
 mind the possibility of alcohol being at least 
 a factor. Where careful observation shows 
 that the lower extremities are alone involved, 
 the upper extremities being quite normal as 
 regards strength, sensibihty, and electrical 
 reaction, it will usually, I think, be found 
 that the influence of alcohol may be put out 
 of the question. It is evident that there is 
 little likelihood of the effects of alcohol being 
 limited to certain extremities ; but, as I have 
 said, it is very common for the legs to show 
 the disorder before the arms — and supposing 
 that abstinence begins to be practised at this 
 point of time it is perhaps conceivable that the 
 latter might escape. But this is probably very 
 uncommon. 
 
 I am notable to explain the greater tendency 
 of the lower extremities to sufl'er in this affec- 
 tion. It is an interesting circumstance that 
 a similar proclivity for the lower extremities to 
 
PARAPLEGIC POEM OP NEURITIS. 95 
 
 be most affected (sometimes indeed exclusively 
 so) is shown, as I have before remarked, in the 
 case of the endemic disorder. Beriberi. But it is 
 not only in connection with alcohol and Beriberi 
 that this preponderance is observed. Several 
 cases have fallen under my observation marked 
 by characteristic symptoms of peripheral neuritis 
 which have been entirely confined to the lower 
 extremities. 
 
 The following is a striking example : 
 
 A gentleman, aged forty-nine, consulted me on account 
 of numbness of the feet, a difficulty in standing with his 
 eyes shut, and a feeling as though he were walking on 
 bladders. His gait was not ataxic. He had been invalided 
 from abroad on account, as he told me, of incipient loco- 
 motor ataxy. His pupils were small ; the knee-jerks were 
 not elicited by blows with the percussion hammer. The 
 jprimd facie resemblance to tabes was, I need scarcely say, 
 very strong. Further examination showed the follow- 
 ing : 1st. The patellar tendon-reflex was brought out in 
 perfectly normal fashion when the side of the hand was 
 used for striking the ligamentum patellae. 2ndly. The 
 pupils, though small, contracted to Hght. 3rdly. The 
 power of dorsal-flexing the feet was much impaired. 4thly. 
 There was marked anaesthesia in the lower half of each 
 leg. The wire-brush, vdth the strongest induced currents 
 applied over the parts shaded in the diagram, Fig. 4, was 
 scarcely felt at all in the feet, but gradually evoked sensation 
 as the leg was ascended, and above the line of shading the 
 pain of application became intolerable. About the upper 
 part of the anaesthetic districts an ordinary touch with the 
 
96 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 finger-point was described as feeling like " tlie pricking of 
 an electric battery." The patient complained of a con- 
 
 FiG. 4. 
 
 stant acting and numbed sensation in the soles of his 
 feet, which was not increased by walking. The sensation 
 was like that of the feet being very cold indeed in the 
 boots on a cold day. Electrical testing showed on each 
 side considerable loss of faradic excitability in the ex- 
 tensor longus digitorum and tibialis anticus, the peroneus 
 longus being apparently normal. The response to inter- 
 rupted galvanism was not increased. 5thly. The patient 
 had never had any sudden shooting pains, but there had 
 been for some time a dull heavy pain in the soles of the 
 feet, along the shin-bone, and the back of the leg. This 
 
NEURITIC PAEAPLEGIA. 97 
 
 was constant. It was diflScnlt to obtain a very distinct 
 account of the mode in which the symptoms had com- 
 menced. So far as I conld judge there had been extremely 
 painful swelling of the right foot six years before, which 
 liad confined him to his bed for two months, and termi- 
 nated in an abscess at the root of the little toe. Two years 
 later he appears to have had a collection of matter in the 
 left foot which discharged near the little toe. Since that 
 time he had a sensation of numbness in the sole of th.e 
 left foot, and for the past nine months the numbness had 
 become acute in both feet. There was no history of 
 syphilis nor of gout, and I do not think there had 
 been alcoholic excess suflB.cient to explain the symptoms. 
 Under the employment of faradic currents with a wire 
 brush a great improvement took place in the sensibility of 
 the skin of the feet. Unfortunately at this point I lost 
 sight of th.e patient. 
 
 In this case there would seem to have been 
 chronic neuritis affecting the terminal branches 
 of the popliteal nerves, with the exception of 
 the supply to the peroneus longus and brevis. 
 The cause of the neuritis, however, is by no 
 means clear. 
 
 Another patient was a man of middle age who con- 
 sidered himself to be gouty. When I saw Mm he had 
 paralysis of the anterior tibial group of muscles in both 
 legs, the feet being dropped in consequence. He was 
 covered from head to foot with copper-coloured papulo- 
 squamous eruption, which had appeared about five months 
 previously. It was whilst under mercurial treatment for 
 tbe eruption of the skin that he suddenly one night lost 
 the use of the left foot, and this was followed by a corre- 
 
 7 
 
98 PARALYSIS FEOM PERIPHERAL NEURITIS. 
 
 sponding failure of power, but not to the same extent, in 
 the right foot. 
 
 On electrical examination I found in the left leg no 
 reaction to either current in the anterior tibial muscles, 
 and so much cutaneous anaesthesia in the lower half of 
 this leg that the strongest faradi^m was not felt. In the 
 right leer there was also some anaesthesia in the same 
 situation. The extensor of the toes required very strong 
 induced currents to cause contraction ; the tibialis anticus 
 was less abnormal. 
 
 A fortnight later there was slight negative pole closure 
 contraction with the strongest galvanic current in the 
 tibialis anticus of the left side. 
 
 A couple of months later I failed to get any contraction 
 to either current in the muscles of the left leg in front of 
 the tibia on the left side. The patient described a numbed, 
 dead feeling in the feet. He could not tell what he was 
 walking upon. Both ankles swelled at night. I found 
 on two or three occasions that the left extensor carpi 
 radialis muscle was a good deal less excitable to faradism 
 than the right. He was treated with iodide of potassium. 
 I lost sight of this patient, but a few months later learned 
 that he had quite recovered. 
 
 The following case appears to me one closely 
 resembling those described as dependent upon 
 alcoholism, but this cause can be absolutely 
 excluded. I am unable to suggest a cause 
 for the chronic neuritis which evidently exists. 
 
 A female, aged sixty-three, of active and temperate 
 habits, had enjoyed good health till 1880, when she com- 
 plained of general weakness. In 1881 numbness was 
 noticed in the feet and legs, and she began to be readily 
 
NEURITIO PAEAPLEGTA. 99 
 
 fatigued in walking. Tliese symptoms increased slowly 
 but steadily during tlie next twenty-four montlis until 
 walking for more than a few steps became impossible. 
 There was distinct loss of power in the muscles lying on 
 the left tibia, the foot being dropped. Little or no pain 
 was felt at any time except when the affected parts were 
 handled or pressed. The following parts were acutely 
 sensitive, even to gentle pressure : dorsal and inner surface 
 of the feet, the front and sides of the legs and of the 
 thighs, the lumbar and sacral regions of the trunk ; to a 
 less extent the soles of the feet, the middle of the back, 
 buttocks, and flanks. This sensitiveness was most marked 
 on the left side, especially in the lower part of the left leg 
 and foot. There was considerable oedema of the legs from 
 the knees downwards, none elsewhere. There was no 
 albuminuria or cardiac mischief. 
 
 With the exception of occasional attacks of something 
 described as resembling petit mal, the patient's general 
 health has remained good, notwithstanding that she has 
 been obliged to give up all exercise, and is confined to her 
 couch. 
 
 Such was her history given me when I saw her about a 
 year and a half ago. I found the power of flexing thighs 
 on trunk and legs on thighs unimpaired. She could 
 dorsal-flex the right foot fauiy well, but the left very im- 
 perfectly, and there was marked "dropping" of the left foot. 
 Heat and cold produced normal impressions. The sensi- 
 tiveness to touch and handling I have described above. 
 The plantar reflex was absent on the left side. The knee- 
 jerks were fairly marked in each leg. There were no lan- 
 cinating pains, and no marked atrophy except perhaps iu 
 front of the left leg, but this is obscured by oedema. The 
 toe-nails were darkened in colour and some were roughened, 
 especially those of the great and second toe of the left 
 
100 PARALYSIS FEOM PERIPHERAL NEURITIS. 
 
 foot. I thought the response to induced currents lowered 
 in the left leg and fairly good in the right one, but the 
 cedeniatous condition interfered with exact observation. 
 
 At the present time, I am informed by her medical 
 attendant, the legs are as morbidly sensitive as ever, the 
 right being equally so with the left, but the oedema is less, 
 especially in the left leg. There is no loss of muscular 
 power in any fresh place, and a distinct gain in the left 
 anterior tibial region, as manifested by greatly improved 
 power of dorsal-flexing the ankle-joint, and a little more 
 power of extending the toes. This improvement has coin- 
 cided with the application of the constant current. 
 
AFTER ENTEMO FEVER. 101 
 
 LECTURE III. 
 
 Periplieral neuritis in enteric fever — After dengue — Two 
 cases of peripheral neuritis after malarious fever — 
 Alcoholic history in each — Donbtful etiology — Phases 
 of alcoholic paralysis — Diphtheritic paralysis — E,e- 
 semblance of symptoms to those of multiple neuritis 
 — Tenderness of nerves and muscles — Absence of knee 
 phenomenon — Varying condition of electric excita- 
 bility in diphtheritic paralysis — The ataxy after 
 diphtheria liable to be mistaken for tabes — Morbid 
 anatomy — Diphtheritic paralysis probably very often 
 dependent upon perijoheral neuritis — Comparison 
 between symptoms of alcoholic and diphtheritic para- 
 lysis — Diagnosis of multiple neuritis. — Prognosis — 
 Treatment. 
 
 It is necessary to bear in mind tliat periplieral 
 neuritis occasionally occurs in the sequel of 
 some febrile affections. Besides diphtheria, of 
 which I shall have to say more presently, other 
 specific febrile disorders are apt to be followed 
 by paralysis, which is sometimes more or less 
 general and at other times strictly localised. 
 Dr. Ross has collected a number of published 
 examples in which there has been localised 
 
102 PARALYSIS FEOM PERIPHERAL NEURITIS. 
 
 paralysis of peripheral origin in the sequel 
 chiefly of enteric and relapsing fevers. I was 
 consulted a few months ago by a gentleman 
 who was suffering from paralysis of the serratus 
 magnus of the right side, which had occurred 
 whilst he was convalescing from an attack of 
 enteric fever, acquired during a tour in Italy. 
 
 It often happens that owing to the prostra- 
 tion and unconsciousness of the patient, the 
 characteristic symptoms of neuritis are obscured 
 and a localised paralysis is alone noted, the im- 
 mediate cause of which there is no evidence to 
 explain. But in other cases, violent pains and 
 other disturbances of sensibility accompanying 
 paralysis, with muscular atrophy, and partial or 
 complete removal of faradic excitability, point 
 conclusively to a peripheral neuritis as the 
 pathological condition.* 
 
 I have lately seen an ofl&cer of the army, 
 formerly on service in the tropics, who has had 
 for the last year and a half paralysis of the 
 flexors of his left foot. There is atrophy and 
 loss of electrical excitability in the tibialis anti- 
 cus and extensor longus digitorum muscles 
 
 * Since this lecture was delivered an important contri- 
 bution to our knowledge of this subject has been published 
 by Pitres and Yaillard in the ' Eevue de Medecine,' 
 December, 1885. 
 
CASES WITH HISTORY OF MALAEIA. 103 
 
 coupled with some ansesthesia of the corre- 
 sponding surface. He has never suffered from 
 syphilis, and the only antecedent of importance 
 is a severe attack of dengue. This occurred, 
 it is true, more than two years before he began 
 to get pain in the left knee, by which the 
 paralysis was ushered in, but meantime he had 
 suffered now and then from an attack of rigor 
 like the recurrence of ague. 
 
 The possibility of paralysis from peripheral 
 neuritis occurring in the sequel of specific febrile 
 affections may give rise to a curious difficulty 
 of diagnosis. 
 
 A few years ago a gentleman brought me a letter from 
 Ms medical attendant abroad, from whicb I will quote : 
 
 " The patient, after a severe attack of pernicious 
 malarious fever, became paralysed in both legs. When he 
 came under my notice he was unable to move his legs or 
 raise himself in bed. The sensibility was quite normal. 
 The electric contractility of the muscles of the legs was 
 much diminished, the liver and spleen were normal, the 
 urine contained an unusual amount of phosphates. The 
 memory was very weak. Under the treatment the patient 
 improved rapidly so that he can now walk without anv 
 help, can ride, and shows a great facility of remembering 
 facts and dates. The motion of the ankle remains still 
 injured. With his eyes closed patient can neither stand 
 nor walk. The treatment consisted in the application of 
 weak currents along the spine and local faradisation of 
 the muscles of the leg twice a day, tonics, nitrate of 
 silver, strychnine. 
 
104 PARALYSIS PROM PERIPHERAL NEURITIS. 
 
 '* I advised Mr. — to visit a liydropatliic establisliment, 
 to undergo there a cure and continue, if necessary, tlie 
 faradisation. As lie is very fond of liquors, and as tliese 
 had always a very injurious influence upon his memory 
 and the steadiness of his walking, I only allowed him two 
 pint bottles of beer and a few small wine-glasses of 
 Madeira a day. At night he received a small quantity of 
 whisky with water. The disease has surely been caused 
 by the fever, serous exudation being the secondary cause 
 of the paralysis." 
 
 When I saw this patient he had quite recovered, 
 and the diagnosis is necessarily therefore un- 
 certain. How far the attack of pernicious 
 malarious fever was concerned in the produc- 
 tion of the nerve changes, it is impossible to say, 
 but the symptoms are quite consistent with 
 those of the multiple neuritis which is connected 
 with chronic alcoholism. 
 
 A few years ago (the date is purposely omitted) I saw 
 a female patient, aged thirty-three, who came to me with 
 the following written account from her medical attendant 
 in the tropics. After stating that during her residence 
 in the country she had had several attacks of tropical 
 dysentery and had been the subject of some obscure biliary 
 affection at the close of which he saw her, he went on to 
 say, " The symptoms called ' biliousness ' had then dis- 
 appeared and had given place to debility, anaesthesia, and 
 an incipient paralytic condition of the upper and lower 
 limbs, in many respects resembling locomotor ataxy. 
 There was also and had been for two months cessation of 
 the menstrual flux. In addition there was marked loss of 
 
ALCOHOLIC PAEALYSIS. 105 
 
 memory, and more tlian once I observed lier conversation 
 incoherent. Under phosphorus, strychnine, iron, gal- 
 vanism, friction, this condition of incipient paralysis slowly 
 departed, and, with the exception of reduced strength and 
 impaired memory, she was nearly well till the end of 
 February, 18 — . At that time the menses had again 
 ceased, irritability of stomach, flying pains and numbness 
 of limbs, with utter inability to walk had again returned. 
 Though she could move her limbs when lying in bed, and 
 though sensation was but little at fault, she could neither 
 stand on her legs nor walk a step. She complained 
 bitterly of pain and tingling and numbness in both arms 
 and hands, and the co-ordinate power of the small muscles 
 of thumb and fingers was greatly impaired, the left more 
 than the right." She was treated with counter-irritation 
 over the spine, iodide of iron, later by galvanism and 
 phosphide of zinc with strychnia. " She was allowed a 
 very nutritious diet of milk, beef tea, bread, eggs, but no 
 alcoholic stimulant. After three or four weeks she had 
 im.proved, and a little later the menses reappeared." The 
 opinion expressed by the medical attendant was that her 
 disease was due to anxiety from severe bereavement, 
 coupled with residence in a malarious tropical country. 
 
 This patient arrived in England, and came to me two 
 and a half months from the beginning of the relapse de- 
 scribed. Her complexion was sallow and conjunctivae 
 yellow. She had recovered ]5ower to a great extent. On 
 starting for England she had been unable to dress herself. 
 Now she could do anything with her hands, but delicate 
 movements, as in buttoning things, were not well per- 
 formed. She could walk a moderate distance. The knee 
 reflex was absent on each side. Electrical examination 
 showed a great reduction in excitability of the muscles 
 in front of each leg. This lowering of excitability 
 
106 PARALYSIS EROM PERIPHERAL NEURITIS. 
 
 obtained botli in regard to tlie galvanic as to the induced 
 current. 
 
 This ladj came from a country where 
 malarious fever was rife, but I could get no evi- 
 dence of any characteristic intermittent sym- 
 ptoms. Nor did I learn anything with regard to 
 the patient's habits. The case was evidently one 
 of multiple neuritis, and from the symptoms de- 
 scribed, so characteristic of peripheral changes, 
 besides the occasional incoherence and loss of 
 memory, pointing to intracranial lesion, it seems 
 probable that alcoholic excess had been at least 
 an important factor in the case. 
 
 One occasionally meets with alcoholic cases 
 in which there is paralysis to a considerable 
 extent which has escaped the notice of the 
 patient's friends. The patient (usually a female) 
 lies in bed in such a muddled condition of mind 
 that she does nothing for herself, and takes 
 sustenance at the hands of others. When 
 moved from side to side in bed, or when her 
 limbs are touched, she cries out with pain. It 
 is not at all uncommon to find this condition 
 referred to rheumatism or gout. In some cases, 
 as an explanation of the mental condition, one 
 is told that the rheumatism or the gout has 
 '' flown to the brain." Although evidently 
 there is a great probability of persons who 
 
OASES WITH HISTORY OF MALARIA. 107 
 
 indulge to excess in alcohol being affected with 
 gout, yet I am disposed to think that much 
 more often this condition is due to peripheral 
 neuritis from alcohol. The persons who suffer 
 in this way do not drink wine or beer — the 
 liquors which tend so much to induce gout — 
 but brandy or gin. In such cases as I have 
 described there will often be an amount of 
 muscular wastiog of the extremities, not to be 
 explained by mere emaciation. If examination 
 be made, it will very likely be found that the 
 knee-jerks are absent, and the faradic excita- 
 bility in the muscles greatly reduced or lost. 
 
 In a case whicli I saw in consultation some time ago 
 there was intense pain of a neuralgic character in both 
 lower extremities, with dropping of the feet and absence of 
 knee-jerk. A curious question arose in reference to dia- 
 gnosis. The patient had been operated upon for a carci- 
 nomatous tumour (unconnected with the spine) a year or 
 more previously. The symptoms pointed to secondary 
 growth in the lower part of the spinal column, causing 
 neuritis in some portions of the cauda equina. But there 
 was also a distinct history of long-continued and great 
 alcoholic excess. Examination showed that whilst faradic 
 excitability of the muscles of the lower extremities was 
 greatly reduced, that of the muscles of the arms was quite 
 normal. This being the case, I came to the conclusion that 
 the paraplegic symptoms were due to malignant disease. 
 It was unlikely that such severe symptoms of neuritis 
 would have been exclusively confined to the legs had 
 
108 PAEALTSTS FEOM PERIPHERAL NEURITIS. 
 
 alcohol been the cause. At least one would have expected 
 to find some change in the electrical reactions of the upper 
 extremities. The opinion given was in accordance with 
 this observation, and was, I believe, justified by the 
 sequel. 
 
 Amongst tlie toxic influences apparently 
 liable to give rise to multiple neuritis, besides 
 alcohol, syphilis, and the essential cause of 
 Beriberi, whatever that may be, I have men- 
 tioned lead and diphtheria. There are circum- 
 stances connected with the question of the 
 pathology of lead-poisoning which appear to 
 place it on a somewhat different footing from 
 the other varieties described ; and this, together 
 with the narrow limits of my space, renders 
 its discussion on the present occasion imprac- 
 ticable. I will therefore conclude this part of 
 my subject by a few remarks upon diphtheritic 
 paralysis. The symptoms of diphtheritic para- 
 lysis are so well known that I need not trouble 
 you with any systematic account of them. My 
 intention is to refer chiefly to those clinical 
 features which show that the disease ought 
 probably to find a place alongside of the other 
 forms of paralysis essentially dependent upon 
 peripheral neuritis which we have been con- 
 sidering. 
 
 Last year I unfortunately had the opportunity 
 
DIPHTHERITIC PAEALTSIS. 109 
 
 o£ observing very constantly a case of diph- 
 theria which was followed by paralysis. 
 
 The patient was a boj nine years of age, who was 
 severely attacked with diphtheria on December 16th. The 
 temperature, which was nearly 105° F. during the first 
 twenty-four hours, then declined to a little over 100°, run- 
 ning up to 102° on the sixth day coincidently with the 
 appearance of albuminuria. On the thirteenth day the 
 throat had recovered, the albuminuria continuing till the 
 twentieth day. 
 
 On the thirteenth day the patient spontaneously com- 
 plained of much tenderness on the inside and bact of each 
 thigh and on the fifteenth day pressure over the sciatic, 
 posterior, tibial, and median nerves was decidedly painful. 
 Throughout his limbs handling and gently squeezing the 
 muscles appeared to cause considerable discomfort. The 
 knee-jerks at this time were quite normal. 
 
 About the twenty-third day he began to complain of 
 difficulty in reading, and in a few days he could not read 
 at all. Mr. Macnamara, who kindly examined him, found 
 almost absolute inability to accommodate. On the ninety- 
 ninth day Mr. Carter found that the left eye had recovered 
 its accommodation, that of the right still remaining para- 
 lysed. This also recovered later. 
 
 On the thirty-eighth day be complained of a peculiar 
 feeling at "the top of the throat," and some water which 
 he drank came for the first time through his nostrils. 
 He spoke with a nasal twang. He fidgeted much and 
 felt as if his legs would give way, and said he could not 
 stand still. At this time he never passed a day without 
 complaining of pain referred to the epigastric region. 
 The pupils were dilated. They responded to light. There 
 was no optic neuritis. 
 
110 PAEALTSIS PROM PEEIPHERAL NEUEITIS. 
 
 On tlie fortietli day, in going downstairs, he staggered a 
 good deal, and bad not complete control over Ms feet. 
 As lie himself expressed it, " he wanted to take one step, 
 but took two." The knee-jerks, which had been examined 
 daily from the time of subsidence of the throat symptoms, 
 were still quite normal. It was not until the ataxy of 
 gait had lasted nearly three weeks that the knee-jerk be- 
 came rather suddenly very feeble. Next day (the sixty- 
 first of his illness) the phenomenon was absent on the 
 right side and very small on the left, and on the following 
 day, the sixty-second of his illness, there was not a trace 
 of tendon reflex in either leg. Anticipating a little for 
 the sake of clearness, I may here say that the knee-jerks 
 returned about the first week in June — i. e. about the 
 170th day of his illness, They were absent, therefore, 
 about 108 days. I had examined him daily until April 
 21st, when the lad went into the country. He had 
 learned perfectly to test his knees for liimself, and 
 reported with much satisfaction the date of return of the 
 reflexes. 
 
 It was especially from about the end of January till the 
 end of March that the boy showed great awkwardness of 
 gait and clumsiness in the use of his hands. He could 
 only walk at a slow pace, and was very soon fatigued. 
 He would now and then, with boyish instinct, try to run, 
 but in this he quite failed. He could not perform the 
 movement. At times, in walking, he would suddenly 
 come to the ground, having tripped or in some way missed 
 his foothold. 
 
 In the beginning of April, whilst the knee-jerks were 
 still completely absent, he had so much improved in the 
 power of his limbs that he could walk, run, and join his 
 brothers in play, and this progressive improvement con- 
 tinued un inter ruj)tedly until his recovery. The nasal 
 
DIPHTHEEITIC PAEALYSIS. Ill 
 
 character of liis voice and the regurgitation of fluids, 
 wHcli bad commenced on tlie thirty- eiglith. day of his 
 illness, were at no time very strongly marked sjToijDtoms. 
 It was only occasionally that he had difficulty in swallow- 
 iog fluids, and these symptoms ceased to trouble him at 
 all after lasting about a month. At the time when the 
 voice first became nasal in character it was noted that in 
 speaking the lips were moved much more than was natural. 
 There was, indeed, an ataxic over-action of the muscles 
 about the mouth. A note to this effect was made on 
 January 24th. It is interesting that within a week a com- 
 plete change in this respect had taken place. On January 
 31st the muscles of the lips are described as "very in- 
 dolent." On February 4th, again, along with mention of 
 regurgitation of his coffee and the nasal tone of his voice, 
 it is remarked, " Very little movement about the muscles 
 of the mouth." 
 
 On the sensory side a prominent complaint was of pain 
 in the stomach, of which he had early spoken, and which 
 lasted longer than any other symptom. It occui-red 
 especially but not exclusively after eating, and was not 
 accompanied by vomiting. I frequently pressed upon the 
 nerve-trunks of his limbs in different situations, and satis- 
 fied myself that there was very distinct tenderness in the 
 trigeminal, musculo-spiral, median, ulnar, sciatic, and 
 popliteal nerves, as well as in the epigastric region. 
 
 JSTo change in the electrical reaction of his 
 muscles was at any time apparent. Although 
 in this instance, and several others that I have 
 observed, there has been no alteration in the 
 electrical reaction, this is by no means constantly 
 the case, and I have notes of several in which 
 
112 PAEAMSIS FEOM PERIPHERAL NEURITIS. 
 
 tlie excitability was distinctly lessened in some 
 muscle-groups of the extremities. 
 The following are examples : 
 
 A gentleman was affected with diphtlieria in July, 1872. 
 When he consulted me in October of the same year he was 
 suffering from general paresis. He walked with difficulty, 
 the feet being lifted laboriously, and his grasp was very 
 feeble. There was great weakness indeed of all the volun- 
 tary muscles. The pupils were dilated, and accommoda- 
 tion lost. 
 
 It seemed that three weeks after his convalescence from 
 diphtheria he began to find difficulty in swallowing, fluids 
 returning through his nostrils. Then he observed dulness 
 of sensibility in the arms and legs, and his articulation 
 became nasal, " like a Yankee," as he described it. 
 
 I found on examination that the degree of excitability 
 by the induced current differed very much in various sets 
 of muscles of his extremities. 
 
 A girl, aged eight, was seen by me on January 6th, 1876. 
 She had suffered from diphtheria in the preceding July — 
 an extremely bad attack, lasting five or six weeks, in which 
 she was not expected to survive. 
 
 A month or six weeks after convalescence she had 
 measles. Just before this fluids had begun to run from 
 her nostrils. She walked clumsily, and her fingers became 
 weak, so that she could not grasp. Her eyes looked 
 peculiar, and one was fixed so that she saw double. The 
 voice was nasal. ^ This was after the measles, about 
 October. I found the faradic excitability distinctly 
 lessened in some muscle-groups of the extremities. 
 
 The ataxy of gait to which allusion has been 
 
DIPHTHERITIC PARALYSIS. 113 
 
 made, and which is so frequently seen in the 
 sequel of diphtheria, is precisely of the kind 
 which occurs in multiple neuritis arising from 
 other influences, such as alcoholic, syphilitic, 
 and also in certain unclassed forms. It never, 
 so far as I have seen, acquires the pronounced 
 character of the ataxy which is so often asso- 
 ciated with sclerosis of the posterior columns 
 of the cord. We do not see in these cases the 
 wild flourishing about of the legs, with stamping 
 action, so characteristic of the latter disease. 
 The ataxy in multiple neuritis is probably due, 
 I think, not to any affection of the posterior 
 columns of the cord, but to the want of harmony 
 in the strength of various muscular contractions 
 owing to the varying amount of the lesion of 
 peripheral nerves. 
 
 I long ago drew attention to the chance of 
 diphtheritic paralysis being mistaken for tabes 
 dorsalis, of which several instances have come 
 before me. When the electrical reaction of the 
 muscles is unimpaired this is peculiarly liable 
 to occur. The condition of the pupils should 
 be a help towards differentiation. In tabes, as 
 was first pointed out by Argyll Robertson, the 
 pupils are very apt to lose their capacity for 
 contracting to light whilst retaining the power 
 of contraction during an effort at accommoda- 
 
 8 
 
114 PAEALYSIS FEOM PERIPHERAL NEURITIS. 
 
 tion. In cliplitlieritic paralysis, so far as I 
 have seen, the pupils retain the power of con- 
 tracting to hght. How they behave in an 
 effort at accommodation I cannot say, and 
 several ophthalmological friends to whom I 
 have applied have not been able to tell me, but 
 have kindly promised to observe the point. In 
 view of the peculiar affection of accommodation 
 in this disease, it would be interesting to know 
 whether there is normal contraction of the 
 pupil during convergence for accommodation. 
 The tenderness of the trunks of nerves which 
 was here conspicuous was long ago observed 
 by Dr. Greenhow. In a paper read before the 
 Clinical Society of London upon " Diphtheritic 
 Paralysis," in 1871, he suggested the existence 
 of neuritis, having been struck by the tender- 
 ness of the sciatic nerve in a case of this kind. 
 He referred to the fact that Mr. Hulke in one 
 example had discovered optic neuritis. In the 
 cases of multiple neuritis which I have seen, 
 including those of the alcoholic form, the optic 
 nerve has been unaffected ; but in one patient 
 who, I beheve, suffered from the non-alcoholic 
 form of the disease (though the diagnosis is not 
 absolutely sure) there was optic neuritis. It 
 occurred also in a case related by Striimpell. 
 Opportunities of examination after death in 
 
DIPHTHEEITIC PARALYSIS. 115 
 
 cases of diphtlieritic paralysis are comparatively 
 rare. The results in such cases as have been 
 recorded are at first sight conflicting. Changes 
 of an atrophic character in the ganglion cells 
 of the anterior horns of the spinal cord have 
 been described by Yulpian, Dejerine, Aber- 
 crombie, and others. The year before last Dr. 
 Percy Kidd brought before the Royal Medical 
 and Chirurgical Society facts in support of the 
 view that diphtheritic paralysis is founded on 
 a distinct anatomical lesion of the spinal cord. 
 Specimens from a fatal case showed alterations 
 in the shape of the large motor cells in the 
 anterior horns and changes in their cell proto- 
 plasm. The affected cells were as a rule more 
 or less globular in shape and devoid of pro- 
 cesses. In certain regions of the cord corre- 
 sponding to the distribution of the muscular 
 paralysis during life there was apparently a 
 numerical atrophy of motor cells. The changes 
 were purely parenchymatous. There was 
 no distinct affection of the neuroglia. I had 
 the opportunity of examining Dr. Kidd's speci- 
 mens, and so far as I am capable of judging, 
 convinced myself of the accuracy of his obser- 
 vations. In the case in question no examination 
 of the nerve-trunks had been possible. 
 
 On the other hand, many investigations 
 
116 PARALYSIS FEOM PERIPHERAL NEURITIS. 
 
 support tlie opinion tliat the cause of diplithe- 
 ritic paralysis lies in a lesion of the peripheral 
 nerves. Charcot, Yulpian, Lorain, Lepine, 
 Lionville, Leyden, and Meier have contributed 
 testimony in this direction. Changes also in 
 the vascular system and its contents have been 
 noted by Buhl, Oertel, Mendel, and others in 
 the form of hypersemia, capillary haemorrhage, 
 and thrombosis. 
 
 A recent and important contribution to our 
 knowledge of the subject has been made by 
 Mendel, who had the opportunity of examining 
 a case which terminated fatally only ten days 
 from the commencement of paralytic symptoms 
 appearing in the muscles of the eyes and of the 
 extremities. In the right orbit there had been 
 paralysis of the superior and inferior rectus 
 muscles, and paresis of the external rectus ; 
 in the left, paresis of all the muscles. Micro- 
 scopical examination showed the ganglion cells 
 of the deep origin of the oculo-motor nerves 
 unusually large, as if swollen. The most striking 
 changes, however, were found in both oculo- 
 motor nerve-trunks, in the right more than in 
 the left, and consisted in signs of interstitial and 
 parenchymatous neuritis in the form of multi- 
 plication of the nuclei of the neurilemma and 
 changes in the medullary sheaths. There were 
 
DIPHTHERITIC PARALYSIS. 117 
 
 besides small capillary lisemorrliages in parts of 
 the intracranial centres, one especially in the 
 course of the abducens nerve in the pons Varolii. 
 The alterations in the peripheral nerves were 
 evidently primary and independent of those in 
 the central organs. From the description it 
 would appear that the changes in the nerve- 
 fibres and neurilemma must certainly have pre- 
 ceded those in the nuclei of the oculo-motor 
 nerves. Mendel concludes, and I think with 
 justice, that the diphtheritic poison may attack 
 not only nerve-sheaths and neurilemma, but 
 also walls of blood-vessels, and that we have no 
 right to assert that affection of one or the other 
 of these tissues represents exclusively the patho- 
 logy of diphtheritic paralysis. 
 
 It must be remembered that the cases in 
 which disease of the spinal cord has been dis- 
 covered have been of necessity fatal cases ; and 
 the question is, What is the pathology of the 
 infinitely more numerous cases which not only 
 recover, but recover without leaving a trace of 
 any permanent change ? I do not think that, 
 with the clinical evidence before us, we are 
 justified in saying that diphtheritic paralysis in 
 its ordinary form, passing to complete recovery, 
 is dependent upon an affection of the spinal 
 cord. It is, in my opinion, more reasonable to 
 
118 PAEALYSIS FROM PERIPHERAL NEURITIS. 
 
 conclude tliat in this disease we have usually to 
 do with peripheral neuritis of very varying 
 severity which in the mildest cases is probably 
 represented by a mere transitory hypersemia 
 with effusion in the interstitial element. 
 
 Were such changes in the spinal cord as I 
 have referred to ordinarily present, the complete 
 recovery which is well known to be the rule 
 would be impossible. The alterations in the 
 number and structure of the ganglion cells 
 would certainly be attended, as they are in cases 
 of infantile paralysis, by more or less permanent 
 j)aralysis and atrophy in corresponding nerve- 
 districts. Nor should we find, as we do in 
 many instances, the electrical reaction of the 
 muscles remaining normal. Moreover, the sen- 
 sory disturbance which is so often present in 
 diphtheritic paralysis, cutaneous anaesthesia, 
 tenderness of muscle and nerve-trunks, and 
 darting pains, cannot possibly depend upon 
 lesion of the ganglion cells of the anterior horns 
 of the cord, whilst they point as strongly as 
 possible to affection of nerve-fibres. 
 
 Practically, one very seldom indeed meets 
 with examples of diphtheritic paralysis exhibit- 
 ing such a near approach to the symptoms of 
 typical interstitial neuritis as is so frequently 
 seen in alcoholic paralysis. No doubt now and 
 
DIPHTHEEITIO PARALYSIS. 119 
 
 then a case is seen in whicli severe shooting 
 pains are very prominent, another in which 
 there is extreme and widespread loss of muscu- 
 lar power, or it may be that loss of cutaneous 
 sensibility is strongly marked. So also here 
 and there we may find one in which there 
 remains a narrowly localised and permanent 
 muscular atrophy. 
 
 I saw not long since, in consultation with Drs. 
 Playfair and Semon, a case which illustrates 
 the more rare consequences of diphtheritic 
 paralysis. 
 
 The patient, a lady aged forty-two, was suffering from 
 difficulties of articulation and occasionally of deglutition. 
 She had heen attacked eleven months previously with a 
 diphtheritic sore-throat. Apparently she did not suffer 
 badly, but kept her bed for ten days, during which there 
 was at no time much fever. The sore-throat was followed 
 very soon by paralysis of the soft palate, slight pain and 
 unwieldiness of the tongue and weakness of the voice, and 
 paresis of the upper extremities. 
 
 When I saw her (nearly a year having elapsed) the 
 right half of the tongue was considerably atrophied, and 
 when protruded inclined much to the patient's right. It 
 quivered a good deal. The action of the lips was not 
 nearly so lively as it should be, the result being that the 
 lower half of the face was comparatively expressionless. 
 I was not sure, likewise, that there was not some slight 
 weakness of the right pterygoid muscle, for in opening her 
 m.outh and putting out the tongue, the jaw appeared to be 
 carried somewhat over to her right. Sensation was quite 
 
120 PAEALTSIS FEOM PEEIPHERAL NEURITIS. 
 
 normal. There was no tenderness on pressure over the 
 points of emergence of the fifth nerve. The soft palate 
 moved freely both on irritation and during phonation. 
 
 Dr. Semon reported that he found nothing wrong when 
 the larynx was examined by the laryngoscope, though the 
 character of the voice was rather peculiar and often 
 changed into falsetto. The sterno-mastoids appeared 
 equally strong and well developed. The patient com- 
 plained of diflBculty of articulation, especially in the use 
 of the latter. 
 
 The tendon-reflexes were considerably exaggerated. This 
 had not been the case, Dr. Semon said, two months pre- 
 viously, and he was disposed to refer the increase of reflex 
 activity to the large quantity of strychnia which the 
 patient had taken. 
 
 In this case the symptoms indicate lesion of 
 the following nerves, or of their deep origin : 
 the hypoglossal, facial, pterygoid branch of the 
 inferior maxillary. Dr. Semon suggests that 
 the curious character of the voice appears to 
 point to some minute lesion of the spinal acces- 
 sory. The limitation of the facial paresis to 
 the muscles about the mouth points rather to 
 lesion of a nerve than of its centre, and so does 
 the weakness (if such there were) of the right 
 pterygoid muscle, but it does not make this 
 certain. 
 
 If we take a very common type of alco- 
 holic paralysis and the most frequent form 
 of diphtheritic paralysis, the contrast appears 
 
DIPHTHERITIC PAEALYSIS. 121 
 
 to be strongly marked. In tlie former we have 
 notable paralysis of the extensor muscles of the 
 extremities, with cutaneous tenderness or anes- 
 thesia, pains of an agonising description, rapid 
 muscular atrophy, and complete loss of faradic 
 excitability. In the most common examples of 
 diphtheritic paralysis there is weakness and 
 ataxy rather than marked paralysis, a varying 
 amount of cutaneous anesthesia, pains either 
 absent or of trifling character, no muscular 
 atrophy, and electric reaction to induced 
 currents either normal or but slightly reduced. 
 But alongside of these strikingly contrasted 
 symptoms there are others which point more or 
 less strongly to a kindred origin. In each case, 
 for example, loss of patellar tendon-reflex is a 
 very constant symptom, and tenderness of the 
 muscles to palpation is likewise very generally 
 marked in both. If, again, we pass from the 
 strikingly contrasted forms to which I have just 
 referred, we shall find cases more and more 
 approaching a common character — cases of 
 alcoholic paralysis with ataxic symptoms pre- 
 dominant, with pains but slightly marked or 
 absent and only a moderate amount of anes- 
 thesia; or, it may be, cases of diphtheritic 
 paralysis without affection of accommodation 
 or of the palate, and with ataxy rather than 
 
122 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 paralysis. Moreover, in some rare cases of 
 diphtheritic paralysis there may be exceedingly 
 severe lancinating pains, great tenderness of 
 the muscular masses, "dropped" hands and 
 feet, followed by more or less general powerless- 
 ness of the upper and lower extremities, absent 
 tendon-reflex, without affection of accommoda- 
 tion or of the velum palati — a train of symptoms, 
 indeed, which is literally only distinguishable 
 from those of alcohohc paralysis by the absence 
 of any mental disorder. It is hardly possi- 
 ble to doubt, from the mode in which the 
 clinical characters of the two conditions thus 
 approach each other and sometimes meet, that 
 they depend essentially upon similar lesions 
 varying in severity in different instances. 
 
 Diagnosis. 
 
 From what has gone before it is evident that 
 we may have to do, as regards peripheral 
 neuritis, with either of several conditions : (1) 
 There may be paralysis in the district innerva- 
 ted by a single nerve ; (2) or in that supplied 
 by a plexus of mixed nerves ; (3) or the para- 
 lysis may be symmetrical and become more or 
 less universal. 
 
DIAGNOSIS. 123 
 
 In the first case, if it be one of severity and 
 the nerve concerned be a mixed one, there can- 
 not be mnch difl&culty in the diagnosis. There 
 will be loss of power in the muscles supplied by 
 a particular nerve, and in those only, with more 
 or less atrophy of their substance and loss of 
 electrical excitability, together with pain in the 
 nerve-trunk, and abnormal sensation of some 
 kind — numbness, formication, or anesthesia of 
 the skin in the district supplied by the nerve. 
 If pressure be made upon the nerve-trunk, it 
 may be found to be tender, and in certain cases 
 will be felt to be enlarged. A moderate pres- 
 sure is likely to give rise to a tingling sensation 
 referred to the periphery of the nerve distribu- 
 tion. If the nerve in question, instead of being 
 mixed, is purely motor in function, the evidence 
 afforded by alterations of sensibility is wanting^ 
 and it is then often very difficult, and may be 
 impossible, to decide whether the symptoms 
 observed, are due to changes in the trunk of the 
 nerve, or in the nucleus of its central origin. 
 A consideration of accompanying circumstances, 
 together with the history of the attack, can 
 alone afford help in deciding this point. 
 
 In the second case the association of sen- 
 sory disturbance with motor paralysis would 
 serve to distinguish lesion of a plexus from 
 
124 PARALYSIS FROM PERIPHERAL NEURITIS. 
 
 disease of the anterior grey matter of tlie 
 cord. 
 
 As regards the third category, it is necessary 
 to enter into more detail. The diagnosis of 
 multiple neuritis is of great importance, and 
 may present no small diflSculty. It is evident 
 that there are certain points in the symptom- 
 atology of this disease which enable us to 
 narrow the question of diagnosis, so far at 
 least as strongly-marked cases are concerned. 
 The alteration in the electrical reactions of the 
 muscles alone permits us to say at once that 
 the disease is not dependent upon an intracranial 
 lesion. We know that we have to do with 
 paralysis of either spinal or peripheral origin. 
 
 In its mode of onset and progressive cha- 
 racter there is a strojig prima facie resemblance 
 between multiple neuritis and what is called the 
 acute ascending paralysis of Landry. This dis- 
 ease (of which I know but little, save what I have 
 read), beginning usually like multiple neuritis 
 with numbness in the finger-ends and feet, is 
 characterised by motor paralysis, which com- 
 monly first affects the lower extremities, and 
 spreads upwards over the trunk and upper ex- 
 tremities. The circumstance that the distal 
 portions of the extremities are first involved 
 gives rise to a great resemblance to the aspect 
 
DIAGNOSIS. 125 
 
 of multiple neuritis. But in acute ascending 
 paralysis the general sensibility is said to be 
 scarcely, if at all, affected ; there is no notable 
 atrophy of the muscles, and no change in their 
 electrical reaction. 
 
 Weakness of the arms, with pain in one or 
 other of them, accompanied by loss of power in 
 the lower extremities, and anassthesia extending 
 to the upper ribs, may be caused by a tumour 
 pressing upon the cord in the lower cervical 
 region of the spinal cord. But in such a case 
 we should expect to find more or less paralysis 
 of the bladder, with a strong tendency to the 
 occurrence of bedsores. The reflexes, deep 
 and superficial, would be increased below the 
 waist — the electrical excitability of the muscles 
 of the lower extremities would be unchanged. 
 There would be notable tendency to spasmodic 
 contractions of the lower limbs. 
 
 The symptoms arising from Pott's disease of 
 the spinal column when the affected vertebraa 
 are in the cervical region are of course very 
 comparable with those resulting from tumour 
 in the same region. The symptoms of com- 
 pression-lesion just enumerated will be found, 
 and will alone suffice to distinguish from mul- 
 tiple neuritis, even without the evidence afforded 
 by the spinal deformity. 
 
126 PARALYSIS FEOM PEEIPHERAL NEURITIS. 
 
 Where there is paraplegia from acute soften- 
 ing of the cord, the symptoms are far more 
 rapid than is the case in multiple neuritis. The 
 bladder is apt to be paralysed quite early in the 
 case — sometimes, indeed, a failure to pass urine 
 is the first symptom. Disorder of the bladder 
 and rectum are ordinarily as conspicuous in 
 this disease as they are altogether absent or 
 trifling in multiple neuritis. There is also con- 
 stant tendency to destructive bedsores in the 
 sacral region and other parts, in striking con- 
 trast with the immunity from such lesions which 
 almost always obtains in multiple neuritis. 
 
 The diagnosis of multiple neuritis from spinal 
 lepto-meningitis is more complicated ; for in the 
 latter there are shooting pains in the course 
 of nerve-trunks, with more or less hypersesthesia 
 or anaesthesia in the districts of certain nerve&i 
 together with impairment of muscular power. 
 But in meningitis we should find superadded to 
 these symptoms deep-seated pain in the back, 
 materially increased by movement, especially by 
 turning from side to side in bed. There would 
 probably also be rigidity of the spine, as well as 
 muscular spasms in the limbs. None of these 
 symptoms form part of the symptomatology of 
 multiple neuritis. Perhaps the greatest diffi- 
 culty might be found in the differential dia- 
 
DIAQNOSIS. 127 
 
 gnosis from cervical pacliynieningitis with exten- 
 sion of meningitis of the soft membranes through 
 the length of the cord. In this condition there 
 might easily be a more or less complete loss of 
 power of grasp, coupled with darting or burning 
 pains in the nerve-trunks of the arms, exactly 
 resembling those which are apt to occur in the 
 course of multiple neuritis. Moreover, there 
 would be atrophy of certain of the muscles of 
 the hands and arms, with loss of electrical ex- 
 citability. It is not, indeed, surprising that 
 there should be this striking resemblance, 
 because when the cervical dura mater is thick- 
 ened by inflammation (which necessarily involves 
 also the soft membranes below it), the lesion 
 attacks likewise both anterior and posterior 
 roots of the nerves and sets up neuritis in them. 
 But besides the symptoms in the upper extremi- 
 ties, the pressure on the cord in the cervical 
 region would occasion loss of power in the 
 lower extremities, combined with more or less 
 sensory and trophic disturbance in them accord- 
 ing to the degree and extent of the inflammation 
 of the soft membranes. But in this condition, 
 again, we should expect to find stiflhess of the 
 neck, with a good deal of pain in the back, in- 
 creased by movement, and twitching in the 
 muscles of the extremities. Moreover, there 
 
128 PAEALYSIS FEOM PERIPHERAL NEURITIS. 
 
 would be a great preponderance of symptoms 
 referred to the upper extremities, whereas in 
 multiple neuritis it is usually the lower extremi- 
 ties which suffer most. 
 
 In meningitis it is the roots or central ends 
 of the nerves which are the subject of inflamma- 
 tory change. The symptoms resulting will 
 therefore be liable to appear equally developed 
 in the various districts of distribution of the 
 nerves, and will not be confined, as is so often 
 characteristic of multiple neuritis, to the distal 
 portions of these districts. The localisation of 
 pronounced paralysis and sensory disorder in 
 the periphery of the limbs points most strongly 
 to multiple neuritis, but in certain cases a more 
 or less extensive spread of the lesion upwards 
 towards the centre may easily mask the signifi- 
 cance of this sign. 
 
 HsBmorrhage into the substance of the cord 
 or outside the membranes will, if extensive 
 enough, occasion motor paralysis of limbs and 
 trunk, with complete loss of cutaneous sensi- 
 bility, muscular atrophy, as well as loss of 
 electric excitability. The suddenness of the 
 onset will alone suffice to distinguish such a 
 case from one of multiple neuritis, to say nothing 
 of the fact that paralysis of the bladder and 
 bowel, together with strong tendency towards 
 
DIAGNOSIS. 129 
 
 the occurrence of bedsores, would almost 
 necessarily form part of the symptoms. 
 
 I have already referred to the resemblance to 
 tabes dorsalis found at a certain stage of mul- 
 tiple neuritis. The patient is able to walk, but 
 it is with an ataxic gait ; the knee phenomenon 
 is absent, and he complains very likely of sharp 
 shooting pains. The alteration of electrical 
 reaction in the muscles of the affected limbs 
 will serve, when present, to distinguish the 
 condition. But at a certain stage of recovery 
 from multiple neuritis the muscles may be 
 found to respond normally to induced currents. 
 In these circumstances the difficulty of diagnosis 
 on the part of anyone who had not watched the 
 case in its antecedent stages would be very great. 
 A little time, however, would clear up the ob- 
 scurity, for the return of the knee-phenomenon 
 would show that the case was not one of tabes. 
 
 The subacute atrophic spinal paralysis de- 
 scribed by Duchenne is characterised by sym- 
 ptoms on the motor side closely resembling 
 those of multiple neuritis, but it differs from the 
 latter in presenting no affections of sensibility. 
 
 The differential diagnosis between multi2:)le 
 neuritis and acute anterior poliomyelitis may be 
 very easy indeed, or so difficult as to give rise 
 to considerable doubt. It appears to me that 
 
 9 
 
130 PAEALYSIS FROM PERIPHEEAL NEURITIS. 
 
 there are three principal points to be borne in 
 mind : (1) In acute anterior poliomyelitis, what 
 may be called the first stage — the stage of in- 
 creasing intensity of symptoms — is usually 
 much shorter than in progressive multiple 
 neuritis, the paralytic symptoms far more com- 
 plete, and the motor disturbance much more 
 marked than the sensory symptoms, where these 
 chance to be present. In multiple neuritis, on 
 the contrary, such forms of the latter as *' numb- 
 ness," '' deadness," and '' pins and needles " are 
 usually more prominent at first than the loss of 
 power. (2) In acute anterior poliomyelitis 
 groups of muscles functionally related are apt 
 to be struck simultaneously with complete loss 
 of power, whilst in progressive multiple neuritis 
 the groups of muscles invaded by the disease 
 are apt to be those in the district of distribution 
 of various nerve-trunks rather than of plexuses. 
 (3) In progressive multiple neuritis, severe 
 enough to cause marked paralysis, you may 
 expect to find distinct tenderness if you press 
 upon the trunks of nerves where these are 
 superficial. Sharp shooting pains in the course 
 of peripheral nerves, lasting several days, 
 furnish in an otherwise doubtful case conclu- 
 sive evidence in favour of progressive multiple 
 neuritis. This is the best diagnostic scheme 
 
DIAGNOSIS. 131 
 
 whicli I can suggest, but I acknowledge that in 
 certain cases it will not be sufficient for the 
 required distinction. For it may chance, in a 
 case of multiple neuritis, that the motor distur- 
 bance is exceptionally rapid, severe, and nnac- 
 companied by sensory disturbance. It may be 
 so extensive as to merge in one common power- 
 lessness all the muscles of a limb, whether 
 functionally or anatomically related. As regards 
 the tenderness on pressing the nerve-trunks, I 
 am not able to say whether this is constant in 
 cases marked by motor symptoms chiefly or 
 entirely, as well as in those characterised by 
 striking pain and hyperalgesia. It is in the 
 latter only that I have noted the symptom. 
 
 1^0 doubt, if we take the example of a purely 
 motor nerve — the portio dura, — in cases of 
 neuritis of its trunk causing facial palsy, there 
 is not any tenderness on pressure. But in a 
 spinal mixed nerve, a nerve containing sensory 
 as well as motor fibres, even when the symptoms 
 point only to lesion of the motor nerve- fibres, it 
 may well happen that there is over- excitability 
 of the sensory fibres. But, as I have said, 
 whether this is the case or not I do not know. 
 
 It may be asked whether, considering that in 
 each case the lesion of the peripheral nerves is 
 immediately the cause of the paralytic symptoms. 
 
132 PAEALTSTS FROM PERIPHERAL NEURITIS. 
 
 it is not over-refining to try to determine to 
 which category a particular example belongs. 
 The importance lies in the fact that the prog- 
 nosis is, on the whole, far more favorable in 
 a case of multiple neuritis than in one of 
 anterior poliomyelitis. The explanation of this 
 cannot be better put than it has been done by 
 Dr. Poore, who, in his selection from the works 
 of Duchenne, reminds us of the " probability 
 that the repair of motor cells once lost is im- 
 possible, whilst the repair of conducting fibres 
 emanating from healthy motor cells need never 
 be despaired of." 
 
 It will be remembered that typical cases of 
 infantile paralysis are characterised by sudden 
 onset, with or without fever, and paralysis, at 
 first complete and extensive, gradually diminish- 
 ing and becoming restricted to a greater or fess 
 number of muscles. It is characteristic that 
 after the first day or so any change which takes 
 place in the power of movement is a change for 
 the better. The limbs do not become more 
 paralysed ; on the contrary, after a few weeks, 
 or sometimes days, there is a gradual clearing 
 ofi" of the powerlessness as regards some of the 
 limbs, one or more remaining perhaps unim- 
 proved, or the paralysis may remain limited to 
 a few muscles in one limb. Many of the para- 
 
DIAGNOSIS. 133 
 
 Ijsed muscles lose their faradic excitability 
 entirely witHn a week and rapidly waste. But 
 although they fail to respond to the strongest 
 induced currents they react to slow interrup- 
 tions of the galvanic current. The nerves to 
 the muscles lose their excitability to both forms 
 of electrical excitation. Some of the muscles 
 whose faradic excitability has been lowered 
 but not lost, are not long in regaining the 
 power of contraction to voluntary impulses. 
 This rapid loss of faradic excitability is pecu- 
 liar to the disease. In no other form of more 
 or less generalised paralysis (which is not 
 accompanied by marked sensory disturbance) 
 do you find within a few days that the muscles 
 fail to contract to induced currents. In this 
 disease the pathological change is found to 
 affect the anterior horns of grey matter in the 
 spinal cord in which areas of softening are 
 found, with disappearance of numerous multi- 
 polar ganglion cells, those that remain being 
 degenerated and atrophied. The anterior roots 
 of the nerves are atrophied. The lesion of the 
 ganglionic cells has very much the same effect 
 upon the motor nerve-fibre that would be pro- 
 duced by section of the nerve. Structural 
 changes are produced throughout its ramifica- 
 tions. 
 
134 PARALYSIS mOM PERIPHEEAL NEURITIS. 
 
 Now, altliougli the pathological changes in 
 the anterior horn constitute the essential 
 lesion in infantile paralysis (anterior polio- 
 myelitis), yet it seems likely that at first the 
 disease process may include more or less of 
 the entire section of the spinal cord. In this 
 way it has been sought to explain the circum- 
 stance that although sensory disturbance forms 
 no part of the typical disease, and, indeed, is 
 conspicuous by its absence, yet in some cases 
 at the onset we find that sharp pains occur and 
 tenderness of the limbs to the touch is com- 
 plained of. It is the occasional occurrence of 
 these symptoms in cases of infantile paralysis 
 which renders it possible that cases of multiple 
 neuritis may be mistaken for examples of 
 anterior poliomyelitis. Some of us perhaps, 
 and in this I include myself, have been too much 
 inclined to mass under the name of anterior 
 poliomyelitis all cases of paralysis occurring in 
 children which have been characterised by 
 sudden onset with loss of faradic excitability 
 in the muscles, even when the amount of 
 sensory disturbance has been greater than 
 could be easily explained by diffusion of the 
 pathological area over more or less of the 
 whole section of the cord. 
 
 It is highly probable then that a certain 
 
PEOGXOSIS. 135 
 
 number of cases of so-called " infantile para- 
 lysis" are examples of multiple neuritis. I am 
 much disposed to think that in the cases of 
 *' infantile paralysis " which make unexpectedly 
 good recoveries after very long delay, the lesion 
 may have been in the nerve trunks, and not in 
 the anterior ganglia of the cord. 
 
 Peognosis. 
 
 A very few words are necessary in reference 
 to prognosis. In the early stage of multiple 
 neuritis of non-alcoholic form, when the disease 
 is spreading almost hourly so as to invade fresh 
 nerve districts, the prognosis is necessarily an 
 anxious one. The cardiac and respiratory 
 apparatus may easily become involved, and 
 death occur almost suddenly. But it is quite 
 remarkable, as was seen in the two cases of my 
 own which I have related, to what an extent 
 the respiratory apparatus may become affected 
 and recovery yet take place. When the disease 
 seems to be no longer making fresh inroads, 
 but, on the contrary, slight ameliorations begin 
 to appear, a highly favorable result may gene- 
 rally be looked for. It is not so easy to speak 
 as regards the alcoholic cases, as in them the 
 
136 PARALYSIS FEOM PERTPHEEAL NEURITIS. 
 
 brain also is always more or less involved in 
 the disorder. But, as I have already remarked, 
 my personal experience has decidedly disposed 
 me to give a very favorable prognosis even in 
 cases which are marked by extensive paralysis 
 and muscular atrophy. 
 
 In diphtheritic paralysis the prognosis is dis- 
 tinctly favorable. It is probably through inva- 
 sion of the pneumogastric that a fatal result 
 now and then occurs, and for that reason 
 serious modifications of the circulation, especi- 
 ally if accompanied by vomiting, should cause 
 anxiety and care. So long as the knee-reflex 
 is absent the patient should be looked upon as 
 still an invalid, and not allowed to be incautious. 
 This will obtain equally in other forms of 
 multiple neuritis. 
 
 Treatment. 
 
 There are various degrees of severity shown 
 by this disease, from a slight loss of power 
 scarcely noticed by the patient, to a rapidly 
 extending and complete paralysis, involving not 
 only the nerves of the extremities and trunk, 
 but also those belonging to the organs whose 
 functions are essential to life. 
 
TEEATMENT. 137 
 
 The treatment of localised neuritis occurring 
 in a person of gouty habit, and presumably 
 dependent upon that exciting cause, should be 
 in accordance with the customary methods 
 adopted for acute gout. After the acute sym- 
 ptoms have subsided, good is sometimes expe- 
 rienced from the application of small flying 
 blisters in the neighbourhood of the affected 
 nerves, and comfort may be derived from the 
 employment of the constant current. 
 
 In severe cases of progressive multiple neu- 
 ritis it is advisable to place the patient at once 
 upon a water-bed, although it will have been 
 noted that in this disease there is not seen the 
 same tendency to dangerous bedsores which is 
 observed in certain lesions of the spinal cord. 
 But I think that the water-bed supports the 
 weak patient better than an ordinary couch ; 
 and this becomes of importance when, as some- 
 times happens, life is carried on with difl&culty, 
 owing to the nerves presiding over respiration, 
 deglutition, and the heart's action becoming 
 involved in the progress of the disease. In 
 such cases as these the administration of food 
 in easily assimilable form and quantity, and at 
 very short intervals, is urgently required, and 
 stimulants are often needed. During the first 
 stage of the disease it will be advisable to 
 
138 PARALYSIS FEOM PEBIPHEEAL NEUEITIS. 
 
 administer iodide of sodium in all cases except 
 examples of diphtlieritic paralysis and those in 
 whicli a syphilitic taint can be safely put aside. 
 In the progress of the disease it may be found 
 necessary to give the salt in increasing doses. 
 In one of my cases the dose of iodide of 
 potassium was increased from ten to sixty 
 grains three times a day with evident advan- 
 tage, and to this mercurial treatment was 
 added. In a case of multiple neuritis with a 
 distinct syphilitic history, I should now begin 
 with mercurial inunctions, and also employ 
 iodide of sodium at the same time. In cases of 
 non-specific character, and especially where 
 there is reason to think that exposure to cold 
 and other causes of rheumatism have been 
 present, it will be well to employ the salicy- 
 late of sodium, which in the hands of Leyden 
 has apparently yielded favorable results. The 
 dose and mode of use is like that for acute 
 rheumatism. For the relief of pain a combina- 
 tion of morphia with Indian hemp and bella- 
 donna may be employed internally with advan- 
 tage, and lint steeped in chloroform may be 
 pressed for a minute or two on the seats of 
 greatest suffering if the state of the skin 
 admits of this. But very often, and especially 
 in alcoholic cases, there is an amount of exqui- 
 
TEEATMENT. 139 
 
 site liypergestliesia which renders it difficult to 
 apply any local remedy. In such instances the 
 best thing is to envelop the tender limb in 
 cotton-wool, and cover this lightly with oil-silk. 
 When multiple neuritis has arisen in connec- 
 tion with the abuse of spirits, I am accustomed, 
 as a general rule, to withhold alcohol in any 
 form, and to depend entirely upon frequent 
 administration of food for the support of the 
 patient. Nutrient enemata will sometimes be 
 required. In such cases as these it is remark- 
 able how rapidly the pains and hyperesthesia 
 which have been the cause of intense suffering 
 to the patient cease. 
 
 It is very difficult to say how long a patient 
 suffering from multiple neuritis should be kept 
 strictly and absolutely at rest. This should 
 certainly be done during the continuance of 
 pain or hypergesthesia, and in case there is any 
 important elevation of temperature. But when 
 it is evident that the process of regression or 
 repair has taken place to a considerable extent, 
 the patient should be allowed to get up and cau- 
 tiously try to move the muscles of the affected 
 limbs. By slow and careful steps the effort at 
 voluntary movement may be increased. At the 
 same time the galvanic current slowly inter- 
 rupted should be applied to the muscles. 
 
140 PARALYSIS FEOM PERIPHERAL NEURITIS. 
 
 The motive for the application of the galvanic 
 current may be thus explained. When you 
 apply the two rheophores of an induced current 
 machine to the skin covering a healthy muscle, 
 and thereby obtain a contraction of muscular 
 structure, that contraction is probably brought 
 about by the momentary currents stimulating 
 the intra-muscular nerve, and not by the action 
 of the currents directly on the muscular fibre ; 
 so that when the conductivity of the nerve- 
 fibres is lost by disease one result is that you 
 fail to produce contraction of the muscle by 
 applying the induced current to it. The essen- 
 tial element of the nerve-fibre has degenerated, 
 but the muscular fibre has not (at least this 
 obtains for a long time) suffered any important 
 change. It is still, therefore, capable of being 
 thrown into contraction by the making and 
 breaking of a galvanic current which acts 
 directly upon muscular tissue itself — not indi- 
 rectly, like the induced current, through the 
 medium of a nerve twig. Now it is probable 
 that muscular structure may retain its power 
 of contraction to this direct electrical stimulus 
 for a very long time after it has lost its physio- 
 logical connection with the anterior grey matter 
 of the spinal cord. I have seen the property 
 retained in these circumstances for several years 
 
TREATMENT. 141 
 
 — in one case thirteen years — but I have also 
 seen it lost altogether within a year. As the pro- 
 cess of regeneration of nerve-fibre may require 
 in severe cases a very long time for its comple- 
 tion, it is evidently important that the muscular 
 structure should not by the time the nerve has 
 recovered have itself undergone a degeneration 
 from which there would be no return, and 
 which would render it unable to respond by 
 contraction to impulses arriving through the 
 regenerated nerve. Physiologists have found 
 that if muscle which has lost its nervous ele- 
 ments be artificially stimulated now and then 
 to contraction, its irritability will continue. 
 When left to itself, however, the irritability is 
 apt to disappear and the muscular substance to 
 undergo degeneration. There is, therefore, a 
 good reason for the use of slow interruptions 
 of the constant current in these cases. 
 
 There are some grounds for believing also 
 that faradisation with the wire-brush upon the 
 dry skin may be employed with advantage. 
 As you are aware, this means was introduced 
 by Duchenne for the treatment of ansesthesia. 
 There can be no doubt of its service in anaes- 
 thesia, and by inference we may perhaps 
 reasonably conclude that it may help by its 
 action on the sensory fibres of the nerve 
 
142 PAEALYSIS FROM PERIPHEEAL NEURITIS. 
 
 towards the restoration of function in the lesion 
 of nerves under consideration. Massage is also 
 useful in this stage, and in this I would include 
 passive movements by the operator, as well as 
 active movements against resistance on the 
 part of the patient. In the contracted state of 
 limbs which occasionally results, the contrac- 
 ture being due to unbalanced muscular an- 
 tagonism, division of a tendon may sometimes 
 be adopted with advantage. Considerable 
 patience should be employed before proceeding 
 to this measure, as I have known contractures, 
 which were to all appearance hopelessly per- 
 manent, yield, without operation, to assiduous 
 massage combined with active and passive 
 movements. Along with the contracture of 
 the muscles, it will sometimes be found that 
 adhesions have taken place in some of the 
 joints, owing to disuse. These should be forci- 
 bly broken down. The aim generally should 
 be to disengage muscles from obstructions to 
 their movement, and to encourage their growth 
 and functional activity by various kinds of 
 physiological stimuli. 
 
INDEX 
 
 Alcoliolic paralysis, 70 — 93, 105, 106; compared witli dipt- 
 tteritic paralysis, 120; marked occurrence of pain in, 
 82 ; and of mnscnlar atrophy, 82 
 
 Ataxy in alcoliolic paralysis, 73, 121 ; in diphtheritic para- 
 lysis, 110, 112, 113, 121 
 
 Atrophy of muscle, 12, 28, 50, 53, 59, 63, 69, 72, 75, 82 
 
 B 
 
 Bedsores, 61, 62 
 
 Beriberi, 5, 64 ; Hirsch on, 64 ; Palm on, 65 ; Scheube on, 67 
 
 Harada on, 67 ; Pierson on, 68 
 Broadbent on alcoholic paralysis, 77 
 
 C 
 
 Central disease simulated by peripheral neuritis, 4, 23, 24 
 Cervical pachymeningitis, 127 
 Churton on a case of ataxy, 89, 90 
 Contracture, 63 ; treatment of, 142 
 
 D 
 
 Degeneration, reaction of, 9 
 
 Dejerine on peripheral neuro-tabes, 91 
 
 Dengue, peripheral neuritis after, 102 
 
144 INDEX. 
 
 Diagnosis, 122 — 135 
 
 Diphtheritic paralysis, 108 — 122 ; liable to h& mistaken for 
 tabes, 113 ; points of differential diagnosis, 113 ; morbid 
 anatomy of, 115, 116 ; pathology of, 117 ; muscular 
 atrophy in, 119; compared with alcoholic paralysis, 120, 
 121 ; electrical reaction in, 111 
 
 Dropping of the feet, 59 
 
 Duchenne's subacute spinal atrophic paralysis, 129 
 
 E 
 
 Electrical changes in muscle, 9, 10, 60 ; in nerves, 11, 12 
 Electrical testing, precautions necessary in, 32 
 Enteric fever, peripheral neuritis in, 101 
 Erb on multiple neuritis, 55 
 
 F 
 
 Facial paralysis, double, in multiple neuritis, 43 
 
 Faradism, therapeutical application of, 141 
 
 Foot-drop, 59; highly characteristic of alcoholic paralysis, 93 
 
 G 
 
 Galvanism, employment of, 140 
 Glossy skin, Paget on, 19, 61 
 Gouty, neuritis in the, 24 — 35 
 Graves, Dr., on multiple neuritis, 38, 39 
 Greenhow, Dr., on tenderness of nerve-trunks in diphtheritic 
 paralysis, 114 
 
 H 
 
 Hadden on alcoholic paralysis, 71, 89 
 
 Harada on Beriberi, 67 
 
 Hemiplegia simulated by neuritis, 24 
 
 Hirsch on Beriberi, 64 
 
 Hutchinson, Mr., on neuritis in the gouty, 25 
 
 Hypersesthesia, 16, 62 
 
INDEX. 145 
 
 Imitation of central disease by neuritis, 4, 23, 24 
 Interstitial neuritis, 14, 15 
 Irritability of nerve-fibre, 12 
 
 K 
 
 Kakke, 5, 64, see Beriberi 
 
 Kidd, Dr. Percy, on diphtheritic paralysis, 115 
 
 Knee-phenomenon, state of, in multiple neuritis, 60, 85, 86, 87 
 
 Lancereaux on alcoholic paralysis, 81 
 
 Landry's paralysis and multiple neuritis, 124 
 
 Leprosy, 69 
 
 Lep to- meningitis, 126 
 
 Lettsom on alcoholic paralysis, 70 
 
 Leyden on multiple neuritis, 52 
 
 Localised forms of neuritis, 16 — 35 
 
 Lower extremities especially affected, 92 
 
 M 
 
 Malarious fever, peripheral neuritis after, 103 
 
 Massage, 142 
 
 Mendel on diphtheritic paralysis, 116 
 
 Mental faculties, 62, 81 
 
 Motor nerves, neuritis of, 21, 22 
 
 Multiple neuritis, 38 ; Graves on, 38, 39 ; author's cases of, 
 with syphilitic history, 43 ; author's hypothesis as to 
 causation, 56 ; symptoms, 57 ; diagnosis, 122 ; prognosis, 
 135 ; treatment, 137 
 
 Muscle, atrophy of, 12 ; electrical changes in, 9, 10 
 
 Muscles, tenderness of, 61 
 
 10 
 
146 INDEX. 
 
 N 
 
 Nerves, peripheral, anatomy of, 6, 7 ; electrical changes in, 
 
 11, 12 
 
 Neuritic paraplegia, 96, 97, 98, 99 
 
 Neuritis, typical case of, 16; symptoms of, 13, 19 ; some sym- 
 ptoms may be absent, 13, 21 ; favorable prognosis in, 13 ; 
 two forms of, 14 ; interstitial, 14, 15 ; parenchymatous, 
 14, 15 ; the term used provisionally, 15 ; in the gouty, 24 
 
 Neuro-tabes, 91 
 
 Numbness, 57 
 
 Nystagmus, 81 
 
 O 
 
 (Edema, 27, 61 
 
 Oettinger on alcohol paralysis, 79 
 
 Optic neuritis, 25, 114 
 
 Pain sometimes absent in neuritis, 21 ; exquisite character of, 
 
 16 ; treatment of, 138 
 Palm on Beriberi, 65 
 Paralysis, Dr. Todd on, 5 ; what is meant by, 5 ; seats of 
 
 lesion causing, 6 
 Paraplegic form of neuritis, 95 — 99 
 Pemphigus, 18 
 
 Peripheral liable to be mistaken for central disease, 3, 4 
 Pierson on Beriberi, 68 
 
 Playfair, Dr., case of diphtheritic paralysis, 119 
 Poliomyelitis and multiple neuritis, 129 — 135 
 Pott's disease, 125 
 Prognosis, 135 ; favorable in neuritis, 13 
 
 R 
 
 Reaction of degeneration, 10 
 
 Roose, Dr., on gouty aflfections of nerves, 36 
 
 Ross on irritability of nerves, 12 
 
INDEX. 147 
 
 S 
 
 Sclieube on Beriberi, 67 
 
 Semon, Dr., on a case of diphtheritic paralysis, 119 
 
 Sensory symptoms in multiple neuritis, 61 
 
 Skin, trophic changes in, 18, 19 
 
 Softening of spinal cord, 126 
 
 Spinal cord, tumour of, 125 ; softening of, 126 ; haemorrhage 
 
 into, 128 
 Stewart, Dr. Grainger, on multiple neuritis, 49 
 Syphilitic antecedents in multiple neuritis, 43 ; treatment of, 
 
 138 
 
 T 
 
 Tabes dorsalis, 88, 113 ; differentiated from multiple neuritis, 
 
 113, 129 
 Tenderness of nerves and muscles, 109, 111, 114, 118, 121 
 Tingling of skin, 86 
 Tumour of cord, 125 
 Treatment, 137 
 Trophic changes in skin, 18, 19 
 
 U 
 
 Use of galvanism in multiple neuritis, 140 
 
 W 
 
 Wallerian degeneration, 8 
 
 Watteville, Dr. de, on electrical resistance of the skin, 32 ; on 
 
 lead paralysis, 55 
 Wilks on alcoholic paralysis, 78 
 
 PRINTED BY J. E. ADLABD, BAETHOLOMEW CLOSE. 
 
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