HX0001 1 347 
 
 feuntfetatt feecfutec. 
 
 ON 
 
 CONVULSIVE SEIZURES. 
 
 Delivered before the Royal College of Physicians of London, 
 
 J. HUGHLINGS JACKSON, M.D., F.R.C.P., LL.D., F.K.S., 
 
 Physician to the London Hospital, and to the National Hospital for the 
 Paralysed and the Epileptic. 
 
 Eeprinted for the Author from the Bbitish Medical Journal, Vol. I., 1890. 
 
 PRINTED AT THE OFFICE OP 
 
 THE BRITISH MEDICAL ASSOCIATION, 429, STRAND W.C. 
 
vi 
 
OTs T CONVULSIVE SEIZURES. 
 
 Lectuee I. 
 Definition of Terms. — Classification of Convulsions. — The Three 
 Evolutionary Levels in the Nervous System. — Middle Level Fits. 
 " Epileptiform." — Highest Level Fits : " Genuine Epilepsy." — 
 Lower Level Fits: " Ponto-bulbar." — Varieties of Lowest Level 
 Fits. — Abnormal Affections of Consciousness in different hinds 
 of Fits. — The Discharging Lesion in Epileptic and Epileptiform 
 Fits. — The Lnterconnecting Fibres. — The Kinetic Route. — Re- 
 presentation of Movements. — The Right Motor Region. — The 
 Cerebellar System. 
 These are two pleasant preliminaries, the sole parts of my 
 address I can enter upon with a light heart. The first is most 
 earnestly to thank you, Mr. President, for the honour you con- 
 ferred on me in asking me to deliver the Lumleian Lectures. 
 There is one thing for which I cannot blame myself. I have, as 
 was my duty, taken all the pains I could over the task you were 
 so good as to assign to me. The second preliminary is to men- 
 tion my great obligations to Dr. Ferrier. There are very few men 
 of the day by whom both the art and science of medicine have 
 been so greatly helped. It is only since his remarkable researches 
 that medical men in this country have studied convulsions in a 
 thoroughly realistic way. Without further particular acknow- 
 ledgments I make the general one, that all over the field of neu- 
 rology I am profoundly indebted to Ferrier. 
 
 Convulsions and other paroxysms are owing to (1) sudden, (2) 
 excessive, and (3) temporary nervous discharges. 1 The term " ner- 
 vous discharge" (used before me by Spencer) has been much 
 objected to ; when I say that it is used synonymously with 
 " liberation of energy by nervous elements," it will mislead no one. 
 There are nervous discharges in all the operations of health. I 
 should use the term "explosive discharge" for the abnormal 
 liberation of energy in convulsions were it not that physiologists 
 speak of " explosive decomposition of the muscle's substance " 
 which gives rise to contraction of the muscle in health ; and thus 
 it may be that normal nervous discharges, those in the operations 
 of healthy people, are " explosive." So then 1 use the word " ex- 
 cessive" for the discharges which have the three characters men- 
 tioned, the words " sudden " and " temporary," or the word " par- 
 oxysmal," being understood ; when dealing with convulsions, it 
 will not be always necessary to add the term "excessive." I 
 
 1 A term introduced by Dr. Ed-ward Liveing in Lis masterly work On Megrim 
 if " nerve storm." This term has met with much favour, and the conception 
 it stands for has been of great value in elucidating some very complex pro- 
 blems in neurology. 
 
2 
 
 Btaall, however, occasionally use " explosive " for states of cells of a 
 discharging lesion, qualifying it by the word " highly," and some- 
 times the term " high instability." I do not speak of "disorderly 
 discharges," for if in some ways the expression be correct, it hides 
 from us the fact that the most brutal-looking convulsion is only 
 the sign of a departure by a vast excess and by a caricature from 
 normal nervous discharges. 
 
 I have always assumed, and shall continue to suppose, that con- 
 vulsion results from excessive discharges of nerve cells, meaning, 
 of course, liberation of energy during rapid decomposition (kata- 
 bolism) of some matter io, or of part of, those cells. 1 shall fre- 
 quently speak of cells concerned with excessive (primary) dis- 
 charges as constituting a " discharging lesion," and sometimes of 
 them as making up a "physiological fulminate," or occasionally, 
 using Horsley's term, of their being together an " epileptogenous 
 focus." Some material of the cells which make up the discharg- 
 ing le3ion has, by morbid nutrition, become of very high tension 
 and of most unstable equilibrium (briefly of high instability), and 
 occasionally discharges excessively. I do not assert that exces- 
 sive (primary) discharges producing convulsions always depend 
 on a persistent state of high instability of cells ; to give but one 
 example to the contrary, excessive discharges beginning in a 
 healthy rabbit's respiratory centres are induced by rapidly bleed- 
 ing the animal to death, or by quickly asphyxiating it. 
 
 The discharging lesion, though I speak of it as persistent, mean- 
 ing that it is of the same locality throughout each case, yet varies 
 in its condition. 2 The discharges are occasional. After their ex- 
 cessive discharge the cells are no doubt far below the degree of 
 stability (properly comparatively slight instability) of normal 
 cells ; they will reattain a highly abnormal degree of instability 
 — again become highly explosive — by further morbid nutrition. 
 These qualifying remarks should be borne in mind, and especially 
 when toe discharging lesion is spoken of as a fulminate — it is occa- 
 sionally fulminant. 
 
 I make three classes or kinds of convulsions. Convulsions, or I 
 will say, fits, differ in kind, according as centres discharged differ 
 in rank ; or, speaking more definitely, as the centres first engaged 
 in paroxysms make up different evolutionary levels of the central 
 nervous system. I have several times suggested that there are 
 three levels of the cerebral (central) nervous system; each is 
 sensori-motor, and each represents impressions and movements of 
 all parts of the body. I speak briefly of what I suppose to be the 
 hierarchy of centres of the nervous system as a basis for the classi- 
 fication of fits. 
 
 (1) The lowest or first level is roughly and incompletely defined 
 as consisting of cord, medulla, and pons, 3 and more completely, 
 and yet still roughly, as being that sensori-motor division of the 
 central nervous system, to and from which pass nerves (all cranial 
 and all spinal nerves) for every part of the body. This level, speak- 
 ing of its motor elements, represents simplest movements of all 
 parts of the body by a series of lowest motor centres (lowest motor 
 centre being a proper name for a centre of the lowest level) from 
 those in the aqueduct of Sylvius for simplest movements of the 
 
 8 The rapid reader must not take " persistent discharging lesion " to be " per- 
 sistently discharging lesion." 
 a I have spoken briefly on what I believe to be the importance of reckoning 
 the cord, medulla, and pons, or, rather, certain elements of these morpho- 
 logical divisions, as one, the lowest level— I believe it is the "spinal system" 
 of Marshall Hall— (Journal, July 14th, 1888). I do not pretend to be able to 
 define the upper limit of this le\ el. 
 
ocular muscles to those of the sacral cord for simplest movements 
 of the muscles of the perineum. This universally representing 
 level is cerebro-cerebellar ; it is at once the lowest level of the 
 cerebral system and of the cerebellar system. For the present I 
 ignore the higher levels of the cerebellar system, and go on to 
 epeak of two higher levels of the cerebral system. These levels 
 are, as the lowest level is, sensori-motor, but I find it possible to 
 illustrate by motor centres only, not, however, believing that these 
 so-called " motor centres " are purely motor. (2) The middle or 
 second level (its motor province) of the cerebral system is com- 
 posed of centres of the Rolandic region (so-called "motor region" 
 of the cerebral cortex), and, possibly, of the ganglia of the corpus 
 striatum also. It represents complex movements of all parts of 
 the body from eyes to perineum (re-represents). (3). The highest 
 or third level (its motor province) of the cerebral system is made 
 up of centres of the prsefrontal lobes (highest motor centres, 
 motor division of the " organ of mind "). It represents most com- 
 plex movements of all parts of the body from eyes to perineum 
 (re-re-represents). The highest centres (sensory and motor divi- 
 sions of the highest level) — the " organ of mind,'' or anatomical 
 substrata of consciousness — are the acme of the evolution ; they 
 have the same kind of constitution as lower centres ; they are sen- 
 sori-motor as certainly as the lumbar enlargement is. (Of course 
 each level is bilateral). 
 
 That the lowest level is a very distinct division of the central 
 nervous system will, I think, be granted. The separation of the 
 frontal lobe into middle motor centres (" motor region"), making 
 up the motor province of the middle level, and highest motor 
 centres (prsefrontal lobe) making up the motor province of the 
 highest level, is, of course, hypothetical; there is no obvious 
 morphological separation. I do not suppose that the evolutionary 
 distinction is so abrupt or so decided as that between the middle 
 and lowest levels. I will mention some differences in the two 
 regions of the frontal lobes, (a) It seems certain that the middle 
 motor centres (" motor region ") are those cerebral centres directly 
 connected with the lowest motor centres, as the facts of " Wal- 
 lerian wasting " show; there is, however, possibly some "wasting" 
 of fibres from the prsefrontal lobes as low as the pons. This 
 wasting has been differently interpreted, (b) The middle motor 
 centres contain most large cells, (c) The middle motor centres 
 are experimentally " excitable," and the prsefrontal lobes are not. 
 This is a very important difference ; it may be taken to mean 
 that the preefrontal lobes are not, as I s appose, motor. The 
 distinction currently made is vastly greater than the one I have 
 submitted. Believing that the whole central nervous system 
 (the organ of mind included — the mind, of course, not included) 
 is a sensori-motor mechanism of three levels, the distinction I 
 make is not of kind but merely of degree — it is that the pre- 
 frontal lobe is only greatly more complex, etc., than the " motor 
 region.' Bat, according to the received doctrine, whilst the latter 
 alone is motor, the former differs from it in two ways; the pree- 
 frontal lobe has no motor constitution, and is part of the " intel- 
 lectual centres." Distinguishing the psychical from the physical, 
 I would say that psychical states are not functions of any centre, 
 but are simply concomitant with functioning of the most com- 
 plex, etc., sensori-motor nervous arrangements — those of the 
 highest level (" organ of mind ") of which, level the preefrontal 
 lobe is the motor division. 
 
 There are, I submit, three kinds of fits corresponding to the 
 three evolutionary levels. It is convenient to speak of the three 
 
kinds in an order different from that used in stating the levels, 
 (2) I mention epileptiform seizures first because their localisation 
 is not doubtful. (They were first described by Bravais in 1824.) 
 They are "middle level fits" — that is, they are produced by 
 excessive discharges beginning in parts of the middle level (motor 
 province) of the cerebral system (" motor region "). My hypo- 
 thesis is that (3) fits of epilepsy proper (" genuine epilepsy " of 
 some nosologists) are " highest level fits," and that many of them, 
 not all, are produced by excessive discharges beginning in parts 
 of the praefrontal lobes, highest level (motor province) of the 
 cerebral system. Although the prsefrontal lobes are not experi- 
 mentally excitable, I suppose it will not be denied that their cells 
 katabolise and liberate energy in their normal activities, and it is 
 not unreasonable to suppose that cells of parts of them may, by 
 pathological changes, become highly explosive, so that they occa- 
 sionally discharge excessively. So that, if the prsefrontal lobes 
 are divisions of the " intellectual centres," as no doubt they are, 
 and not, as I think, motor too, excessive discharge beginning in 
 parts of them may produce epileptic fits. 
 
 Of course, this is speculative. I am not aware that anyone pre- 
 tends to know the seat or the pathology of cases of " genuine epi- 
 lepsy." I do not use the term " cortical epilepsy," because both 
 epileptic and epileptiform seizures are, to my thinking, cortical 
 fits. (The difference in meaning assigned to the two terms epi- 
 leptic and epileptiform must never be lost sight of.) (1) I think 
 that there are " lowest level fits." These are tits produced by ex- 
 cessive discharges beginning in parts of the lowest level, a level 
 which is common to the cerebral and the cerebellar systems. I 
 suppose that most of them are owing to excessive discharges 
 beginning in centres of the bulbar and pontal regions of the level, 
 hence I sometimes use the term " ponto-bulbar fits." With regard 
 to epileptiform and epileptic fits, I deal almost exclusively 
 with cases of patients subject to fits — with, so to speak, " chronic 
 cases." 
 
 I have so far spoken only of three Kinds of fits. No doubt there 
 are Varieties of each kind. Whilst toe kind answers to the level, 
 the variety of each kind answers to the particular part of the 
 level in which the excessive discharge begins. It is certain that 
 there are varieties of (2) epileptiform seizures ; each is marked by 
 a particular place of onset of the convulsion. There must be at 
 least as many varieties of (3) epilepsy proper as there are different 
 " warnings " of the paroxysms. Presumably there are varieties of 
 (1) ponto-bulbar fits. 
 
 Then, of course, there are Degrees of each variety dependent 
 directly on degree of the primary discharge, and indirectly on that 
 of the secondary discharges. (2) For example, there are degrees 
 of that variety of epileptiform seizures marked by the first spasm 
 being of the thumb. There are many ranges of it, from convulsion 
 almost limited to a thumb, thence onward to universal convul- 
 sion. (3) Everybody recognises that epileptic attacks occur in 
 two vastly different degrees, les petits maux and les grand maux, 
 aid there are sub-degrees of each of these degrees. (1) Thpre are 
 degrees of convulsion in lowest level fits produced by Brown- 
 S6quard's method in guinea-pigs. There are, no doubt, degrees of 
 respiratory fits produced in certain lower animals by rapid bleed- 
 ing, by ligature of the great arteries of the neck, and by sudden 
 stoppage of respiration. 
 
 To repeat, " fit " is a term U9ed to include convulsive paroxysms 
 of all kinds dependent on excessive discharges beginning in any 
 part of any one of the three levels, the epileptic and epileptiform 
 
beginning in one half * of a level. There are three kinds of fits, 
 (1) ponto- bulbar, (2) epileptiform, and (3) epileptic. There are, 
 the supposition is, varieties of each kind, and degrees of each 
 variety of each kind. 
 
 I have used the wide term " fit " advisedly because my method 
 is not merely an empirical or clinical one. It is not only an en- 
 de .vour to find out whether a convulsive paroxysm a patient has 
 is like or unlike that of the type " genuine epilepsy " of nosolo- 
 gists or any other type, but is also an endeavour to discover how 
 it shows a particular departure from normal states of his nervous 
 gystem. 
 
 Is there any difficulty in recognising the difference in the two 
 mental attitudes, or, as I shall now say, the distinctness of the 
 two view-points ? From the empirical or clinical view-point we 
 look to see how this or that fit approaches this or that nosological 
 type. From the scientific view-point we look to see how these or 
 those paroxysmal manifestations are produced, asking ourselves, 
 " What is the level and what is the particular part of it in which 
 the excessipe discharge producing this or that set of manifesta- 
 tions begins ?" or, regarding all kinds of fits, the more general 
 question, " What different effects can an excessive discharge ' get 
 out of the different levels?" 5 The use of the general term " tit," 
 compels careful segregation of kinds and analysis of individual 
 cases. In this frame of mind we note the manifestations whether 
 they have "the characters of an ordinary epileptic fit" or not. 
 Whilst for purely scientific purposes I care very little for an 
 answer to the question, " Do excessive discharges beginning in 
 ponto-bulbar centres produce paroxysms resembling those of the 
 epilepsy of nosologists ?" I care very much for one to the ques- 
 tion, " What effects do excessive discharges beginning in ponto- 
 bulbar centres produce?" This question is, as yet, only to be re- 
 plied to by experimenters who artificially produce fits in lower 
 animals. 1 should be very much astonished if ii turns out that 
 excessive discharges beginning in any centres of the lowest level 
 do produce convulsions having the same characters as those pro- 
 duced by such discharges beginning in centres of the higher levels. 
 It would be marvellous if excessive discharges beginning in 
 centres lowest in rank produced fits like those (epileptiform 
 beizures) which are produced by excessive discharges beginning in 
 parts of the more evolved centres, the middle motor cerebral 
 centres (" motor region") 6 . 
 
 * It is convenient to use the word "half" (lateral) for nervous system and 
 " side " for body. 
 
 5 I formerly used the term epilepsy generically for all excessive discharges of 
 the cortex aud their consequences. At that time I did not think there were 
 any fits in depending on excessive discharges beginning in any part of 
 the ponto-bulbar centres. Using then the term epilepsy generically, I sub- 
 mitted that any part of the cerebral cortex might become highly over-unstable 
 and discharge excessively. So that under the term epilepsy 7 used generically 
 there were epilepsy proper, epileptiform seizures, and migraine (the last men- 
 tioned being then spoken of as a sensory epilepsy), and, indeed, any paroxysmal 
 symptoms attributable to sudden excessive discharges of any part of thecortex. 
 I now use the term epilepsy for that neurosis, which is olten called '• genuine " 
 or "ordinary" epilepsy, aad for that only. Of course in all quotations I pre- 
 serve the term epilepsy when used regarding any class of fits. 
 
 6 Long ago (A't. And. Med. Grid Trans., vol. iii, 1370,) I had the'same mental 
 attitude. After speaking of observations of the local onset and march of spasm 
 in cases of fits from cerebral tumour, at a time when the cortical " motor region " 
 had not been defined, I wrote : " We do not care to say that a tumour of the 
 brain (or minute changes near it) had ' caused epilepsy,' but that changes in a 
 particular region of the nervous system — say in the region of the middle cere- 
 bral artery — led to convulsions in which the spasm began in the right hand, 
 epiead to the arm, attacked next the face, then the leg, etc." 
 
6 
 
 As I shall not have time to deal with lowest level fits, I will 
 here mention what I think are some fits of this kind, not classify- 
 ing them, but making a rough arrangement into three groups : 
 1. Respiratory fits (respiratorily beginning from primary dis- 
 charge of the main (medulla) respiratory centre. 7 1 think that 
 fits of laryngismus stridulus come in this category, but Semon 
 tbinks they are cortical seizures.** Respiratory fits are easily in- 
 duced in animals, and are described in all works on physiology 
 when asphyxia is considered. JELussmaul-Tenner fits are respira- 
 tory fits. 9 It is said that convulsions occur in newborn animals 
 after division of the cord below the medulla when they are 
 asphyxiated; if so, these are certainly lowest level fits if not 
 respiratory; it is possible that they are owing to discharge of 
 subordinate (spinal) respiratory centres. 2. lits produced 
 by convulsant poisons (fits from nitrous oxide and curara 
 are respiratory fits). Pits are experimentally produced in 
 animals by absinthe and camphor. According to Magnan, 
 convulsions are produced in animals by absinthe when 
 the cerebrum has been removed. Many years ago Dr. George 
 Johnson showed that convulsions occur in man from poisoning by 
 camphor. Possibly some fits in renal disease (some so-called 
 ursemic fits), and, it may be, fits occasionally part of a constitu- 
 tional disturbance after urethral lesions, are ponto-bulbar fits 
 from home-made poisons, as those just mentioned are supposed to 
 be from foreign poisons. 3. A condition for fits consequent on 
 certain injuries of the cord or sciatic nerve in guinea-pigs (Brown- 
 S^quard). These are so well known that mere mention will 
 suffice. There are often fits attending the onset of infantile para- 
 lysis ; these are very difficult of explanation. I submit the hypo- 
 thesis that they are lowest level fits produced by action on the 
 ponto-bulbar centres of ptomaines, the result of disintegration of 
 nervous matter of anterior horns ; if so, they come in Group 1. 
 
 In all severe lowest level fits it is supposed that the primary 
 discharge of ponto-bulbar centres not only induces discharge of 
 other lowest motor centres, but also that by intermediation of 
 sensory (" ascending ") fibres it discharges centres of higher levels. 
 (I never thought of implication of higher centres in these or any 
 other fits by intermediation of sensory nerves until after con- 
 sideration of the researches of Victor Horsley and Binswanger). 10 
 
 It is necessary now to speak of abnormal affections of con- 
 sciousness with regard to kinds of fits. I presume that there is 
 loss of it in severe fits of all kinds. Consciousness is not a func- 
 tion of the highest cerebral centres ; it is simply concomitant 
 
 i Brain, April, 1886. 
 
 8 See an able paper by Dr. Gay in Brain, January, 1890, for much valuable 
 information on laryngismus stridulus, and for arguments against the view I 
 take of the causation of the paroxysms. 
 
 9 The fits produced in lower animals by rapid bleeding, by ligaturing the 
 great arteries of the neck, and by asphyxia, are alike respiratory lits ; they all 
 depend on stimulation of the respiratory centres by lack of oxygen. Asphyxia 
 experimentally produced in animals does not produce cerebral convulsions, but, 
 on the contrary, renders the cortex inexcitable, whilst at the same time it in- 
 creases the excitability of the ponto-bulbar centres. Again, as Franck says 
 (Fonctionn Motrices du Cerveau, pp. 86, 87), "l'anemie soit totale, eoitpartielle de 
 l'encephale, n'est nullement la cause des convulsions epileptiformes." Arrest of 
 the heart by excitation of the vagus stoos these fits. 
 
 10 Horsley (Lancet, December 25th, 1886, abstract of Brown Lectures) believes 
 that " all the convulsive, tonic, and clonic phenomena may originate from the 
 ordinary bulbospinal centres such as exist for carrying out normal mechan- 
 isms. Tonic or clonic spasm, then, may be produced by any motor centre, but 
 the combination and sequence of tonic-clonic could originate only from the 
 cerebral motor cortex." This is important with regard to the question of ponto- 
 bulbar fits. 
 
with their functioning. There is no physiology of the mind any 
 more than there is psychology of the nervous system. On the 
 basis of mere concomitance, mental symptoms (synonymously ab- 
 normal states of consciousness) are, strictly speaking, only signs 
 to physicians of what is not going on or of what is going on 
 wrongly in part of a patient's material organisation. Thus cessa- 
 tion of consciousness at, or close upon, the onset of an epileptic 
 fit is of value to physicians as a sign that the correlative physical 
 process, the excessive discharge, begins in some part of the "organ 
 of mind," or equivalently, highest centres of the cerebral system ; 
 the physical process in these and all other kinds of fits is our 
 proper concern as medical men. Consciousness is lost late in epi- 
 leptiform seizures, and in those of but little range there may not 
 be even defect of consciousness ; this agrees with the empirical 
 evidence that the excessive discharge begins in lower (middle 
 motor) centres; probably excessive discharges are induced (up- 
 wards) in the highest sensori-motor centres by intermediation of 
 sensory fibres when consciousness begins to cease in an epilep- 
 tiform seizure. Availing ourselves of abnormal affections of con- 
 sciousness as signs of states of the central nervous system, we 
 next, so to speak, put them on one side in order to study the pro- 
 cess in fits in a purely materialistic manner. 
 
 We must bear in mind that not only is consciousness absent in 
 negative functional states of the highest centres, but also that it 
 ceases during the diametrically opposite functional state, excessive 
 discharge beginning in those centres ; there is loss of consciousness 
 not only during, but also for some time after, a severe epileptic fit ; 
 in post-epileptic states there is temporary exhaustion of elements 
 of the highest centres, and, corresponding to that exhaustion, there 
 is absence of consciousness. There are, however, degrees of nega- 
 tive affection of consciousness. There are degrees from that slight 
 defect in some fits of epilepsy (les petits maux) to seemingly entire 
 loss of it in severe epileptic paroxysms ; and there are degrees from 
 that existing with trivial confusion of thought after a very slight 
 epileptic fit to seemingly loss of all consciousness in deep coma 
 after a very severe one. I now return to the physical process 
 of fits. 
 
 It will be observed that I have spoken of the excessive discharge 
 productive of fits beginning in this or that level ; further, of its 
 beginning in some part of a level. In recapitulation, the primary 
 discharge in all kinds of fits is of some part of but one of the levels. 
 And now I add that in epileptic and epileptiform seizures, of which 
 alone I speak in the remainder of this lecture, the excessive dis- 
 charge begins in some part of one half (lateral) of a level ; thus, so 
 to say, in these two kinds of fits the discharging lesion is " doubly 
 local." If the discharging lesion be, as I suppose, of but a few cells, 
 very little of a convulsion is directly due to it. Most of the con- 
 vulsion is produced by intermediation of fibres between the cells 
 of the discharging lesion and other cells of its own level and of 
 other levels; there are induced, consecutive discharges of normal 
 stable cells. Hence the interconnecting fibres of each level and 
 the fibres connecting the several levels with one another, and the 
 fibres connecting the lowest level with all parts of the body 
 (lowest level of the whole organism), have to be considered. (I am 
 straining the meaning of the word fibre, making it stand for any 
 kind of nervous pathway ensuring physiological union, definite or 
 indefinite.) Consideration of these connections is essential for 
 clear ideas of the full process in fits, the only visible part of which 
 is convulsion ; it is especially important with regard to the way by 
 which in epileptiform seizures a very local (a " doubly local") dia- 
 
charging lesion causes wide- spreading and even universalisation of 
 convulsion. Again, the study of the interconnections of the levels 
 is a necessary preliminary to the comparison and contrast of the 
 effects of " discharging lesions" and of " destructive lesions," an 
 essential thing in the scientific investigation of diseases of the 
 nervous system, as I urged in my Gulstonian Lectures (1869). I 
 speak only of connections of motor centres of the levels. 
 
 Each level heing bilateral is a twin series (right and left) of 
 centres. There are connections (commissures) between "identical" 
 centres and between " non-identical " centres of its two halves — 
 presumably between centres of the two halves as they correspond 
 for co-operation of the parts of the body they represent in joint 
 operations by the two sides of the body. There are also connec- 
 tions between the centres making up the lateral half of each 
 level. The fibres of the two connections spoken of are Intrinsic 
 fibres of levels. I speak next of Extrinsic fibres— that is, of those 
 interconnecting levels. Considering for a moment all the levels, 
 the motor path, 11 or, as I shall say, kinetic route, extends from 
 the highest motor centres to the muscles, which in a certain 
 regard, being dischargeable, are centres too. This route (strictly 
 the three series of motor centres are parts of the kinetic route) is 
 in three segments : from highest to middle centres, first segment ; 
 from middle to lowest, second segment ; and from lowest to 
 muscles, third segment. I can, however, consider in detail only 
 the second segment of the kinetic route, that connecting the 
 middle and lowest levels. I shall, for convenience, speak of the 
 motor centres of the right half of the middle level. There are 
 three sets of motor fibres, kinetic lines of the second segment, 
 uniting all right middle motor centres to all lowest motor centres 
 — at least to all motor centres of the left half of the lowest level, 
 if not, as I imagine, to those of the right also. 
 
 First Set of Fibres of the Second Segment. — Those which have 
 been traced (on the Wallerian method by Charcot and others) 
 from the right "motor region" along the right corona radiata, 
 right internal capsule, through the right crus cerebri, right halves 
 of pons and medulla into the (left) lateral column of the cord as 
 low, Sherrington has found in one case, as the origin of the coc- 
 cygeal nerve roots. These fibres are (and so are the second and 
 third sets) extrinsic of the levels ; they belong to neither level, 
 and yet they belong to both in the sense of interconnecting the 
 two. 
 
 Second Set of fibres.— Those of the direct pyramidal tract. 
 They have been said to be traceable no lower than the mid-dorsal 
 region. Tooth has traced them by the Wallerian method in one 
 case as low at least as the second lumbar ; these are fibres of the 
 inner part of the right anterior (Turck's) column. 
 
 Third Set of Fibres, comparatively recently (1884) discovered by 
 Pitres, and seen by Schafer, Sherrington, Hadden, Tooth, France, 
 and others. 12 These fibres have been traced, on the Wallerian 
 
 11 Dr. Gowers (Dis. of Nervous System, vol. i, p. 116) gives a diagram of the 
 "motor path." He makes two segments, " cerebro-spinal " and ' spino- 
 muscular." The kinetic route is a modification of his scheme. 
 
 i 2 Mr. E. P. France (Phil. Trans.. B. 48, 1889) has not found after lesions of 
 the marginal convolution in monkeys (made in some very important researches 
 by Schafer, Horsley, and Sanger-Brown, Phil. Trans., B., 1888), nor in any 
 other case in these animals degeneration of the direct pyramidal tract ; but in 
 all cases in which the degeneration in the crossed pyramidal tract was well 
 marked he found degeneration much less in amount, but in the same position, 
 in the other half of the cord (side of lesion). Horsley and Schafer have, so to 
 Bay, completed the " motorrogion " by their discovery of trunk centres in the 
 marginal convolution. 
 
method, into the right lateral column. 13 The degeneration in the 
 (right) lateral column in cases of (left) hemiplegia is recognised 
 by Charcot. So we see that the interconnection of the middle and 
 lo vest motor centrt-s is very complex. 
 
 S.»me years ago 14 I inferred from the then known connections 
 of the right corpus striatum (internal capsule) with both halves of 
 the cord (by the first and second set of fibres) that both sides of 
 the body are represented in the right half of the brain (I still say 
 "r gat " for convenience), but the degenerated fibres being of dif- 
 ferent columns (the left lateral and the right anterior), that the 
 lettani right sides of the body were differently represented in 
 the right half of the brain. (Tuis, I have since stated, seems to 
 me to be but an expansion and modification of the principle of 
 Broa'ibent's well-known hypothesis as to the double representa- 
 tion of the bilaterally acting muscles ) I should have thought 
 the discovery of the third set of fibres rendered my hypothesis 
 more tenable. But there are serious difficulties. The second set 
 of fibres (those found in the right anterior column) are supposed 
 by some great neurologists to cross to the left half of the cord. 15 
 The same has been said of the third set of fibres found in the right 
 lateral column. S > tnat it may be that all three sets of fibres pass 
 from the right middle to the left lowest motor centres. It is, 
 however, not really known where the second and third sets of 
 fibres end. No wasted fibres are found in the anterior commis- 
 sures. H-nce, I provisionally keep to the hypothesis mentioned, 
 and now say regarding it that the three sets of fibres may show 
 that the rigrit middle motor centres are connected with lowest 
 motor centres of the left and right halves of the lowest level, and 
 thus that the right middle motor centres represent, by inter- 
 mediation of the twin lowest motor centres, movements of muscles 
 of both sides of the body. The expression " movements of mus- 
 cles" introduces a matter which mast be considered before I can 
 illustrate the hypothesis. 
 
 Having considered the whole central nervous system with the 
 rest of the body represented by it to be a sensori motor mechan- 
 ism, I now wish to urge that the motor centres of every level re- 
 present movements of muscles, not muscles in their individual 
 character. The same muscles that is, all the muscles, are repre- 
 sented in Simplest, in Complex, and in Most Complex movements by 
 respectively the lowest, middle, and highest motor (better "move- 
 ment") centres. If so, it is possible, as I believe happens in hemi- 
 plegia, to lose one series of movements of muscles, and to retain 
 another series of movements of the very sime muscles. Thus, to 
 take a case of left hemiplegia in which the right middle motor 
 centres, if not destroyed, are cut off from lowest motor centres (to 
 neglect the second and third sets of fibres), the condition is not 
 properly described as " loss of power of the muscles" of the left 
 arm and leg, but as loss of complex movements of the muscles of 
 
 13 They were called by Sherrington " re-crossed fibres ;" tut he now thinks 
 (Journal- of Pnysiology, January, 1890 i that this mme is unsuitable. Sherring- 
 ton, in a case "f small and superficial lesion of one- half of the brain at the lower 
 end of the fissure of Rolando has traced degenerated fibres into both halves o£ 
 the pons and medulla. 
 
 i* Wed Times and Gnz , October 23rd, 1869. In the abstract of one of my Gul- 
 stoniau Lectures (1869), after reference to Broadbent's hypothesis, there ap- 
 pears : "Taking one tide of the brain, the right, the lecturer thinks the 
 muscles acting unilaterally, I'Oth of the lefr, an<i of the right side of the body, 
 are represented in the right side of the brain, but that the muscles of the left 
 side of the body are especially represented there. 1st. More in q"antity, for they 
 are more affected when the hemisphere discharges. 2ndly. First in time (in- 
 stability), for they are affected before those of the right, tide." 
 
 H Gowera, Diseases of Nervous System, vol. i, p. 114. 
 
10 
 
 those limbs. The simplest movements of the very same muscles 
 remain represented by the left lowest motor centres. The muscles 
 certainly are unaffected, and when rigidity comes on the simplest 
 movements of them are developed by over-activity of their lowest 
 motor centres. To repeat, there are, in cases of hemiplegia with 
 rigidity, the double opposites, loss of complex movements and over- 
 development of simplest movements of the very same muscles. The 
 fixed rigid state of the left arm and leg, which clinically we speak 
 of as a symptom, as if it were something sui generis, is only the alge- 
 braical sum of the co-operating and antagonising " pulls" of the 
 simplest movements of the muscles of these limbs. If the hemi- 
 plegia be very slight, we may say that the muscles of the Jeft arm 
 and leg " are only a little weak," but the strict description is that 
 there is then loss of but a very few complex movements of all the 
 muscles of these limbs, with persistence of the rest of the complex 
 and of all of the simplest movements of those same muscles. Simi- 
 larly, convulsion is not to be looked on as convulsion of muscles ; 
 in an epileptiform seizure the convulsion is a contention of com- 
 plex, and also of simplest, movements. In this contention the in- 
 dividuality of each movement is lost. I will consider a more com- 
 plex case, that of a man imperfectly hemiplegic permanently, and 
 yet subject to occasional epileptiform convulsion of the region 
 paralysed ; the paralysis is loss of but some of the complex move- 
 ments of all the muscles of the arm and leg, and there is persist- 
 ence of the whole of the simplest movements of all those muscles ; 
 when the fit comes there is a temporary contention of the remain- 
 ing complex movements and of the simplest movements of all 
 those muscles. 16 
 
 The distinction between muscles and movements of muscles is 
 exceedingly important all over the field of neurology; I think the 
 current doctrine of " abrupt" localisation would not be so much in 
 favour if it were made. The occurrence of convulsion of a mus- 
 cular region which is already imperfectly and yet permanently 
 paralysed, is unintelligible without that distinction. And without 
 it we shall not understand how it can happen that there is loss of 
 some movements of a muscular region without obvious disability 
 in that region. This bears closely on the realistic study of the 
 physical conditions in aphasia and insanity. We are concerned with 
 both these morbid affections in this inquiry. The anatomical loss 
 in cases of aphasia is of certain complex movements of the tongue, 
 palate, etc. ; there is a paralysis in that sense. In cases of in- 
 sanity (post-epileptic states, for example) there is, I submit, corre- 
 sponding to the negative element of the psychical symptomato- 
 logy, paralysis in the sense of loss of some of the most complex 
 combinations of impressions or of most complex movements, or of 
 both ; for one example of those most comphx, etc., movements of 
 the hands, which are represented in the anatomical substrata of 
 tactual ideas. In brief, a negative lesion of any part of the 
 nervous system (" organ of mind" included) cauees, and always 
 causes, paralysis in the sense spoken of, sensory or motor, or both, 
 and causes nothing whatever else. 
 
 It may seem absurd to say that when there is no obvious dis- 
 ability in a muscular region, there may be loss of some move- 
 
 1B The distinction between movements and convulsion is of extreme import- 
 ance, and is not silwiys made. In some slight epilep'ic fits there are mixed up, 
 so to say, with convulsion movements properly so called, as those of chtwing, 
 spitting, clutching the throat, etc. It is very necessary not to mistake writhing 
 movements of the arms with suspended respiration for convulsion of those 
 limbs. I regret that time will not allow me to consider this part of my subject, 
 for the question raised bears closely on the interpretation of post-epileptic 
 mania, and thus indirectly on the study of insanity in general. 
 
II 
 
 ments of that region. This is, however, what I do affirm confi- 
 dently. We shall be particularly concerned with this dictum 
 when dealing with post-epileptiform aphasia. An eminent physi- 
 cian, referring to a previous statement 1 made 17 of the dictum, 
 described my aim as being to prove two things — that a 
 motor centre does and also that it does not represent 
 movements. I never consciously attempted that very mar- 
 vellous feat. Then, as now, I am content with the sup- 
 position that the non-disability of a muscular region when some 
 movements of it are lost by destruction of part of a centre is ac- 
 counted for by that muscular region being represented by other 
 movements in other parts of the centre or in other centres. On 
 this supposition of Compensation, we can explain recovery from 
 hemiplegia (without relying altogether on the hypotheses of sub- 
 sidence of "shock" or diminished pressure) dependent on very 
 small destructive lesions ; there is recovery when a few movements 
 are permanently lost. That the seeming paradox holds for some 
 cases is undeniable, as the experiments cf Semon and Horsley on 
 the cortical representation of toe vocal cords show. These experi- 
 ments give a crucial verification of Broadbent's well-known hypo- 
 thesis for one case. ^Moreover, France 1S has found degenera- 
 tion in the lateral column of the cord after lesions of the 
 gyrus fornicatus in monkeys. This shows, by the way, that that 
 gyrus, although no doubt (Horsley and Scbafer) mainly sensory, 
 is not purely sensory. Although in the monkeys mutilated as 
 mentioned, there is no discoverable disability in any muscular re- 
 gion, I submit that the degeneration France describes is proof of 
 loss of some movements, skeletal or visceral, or possibly of nega- 
 tive movements (inhibitory). It would be remarkable if there 
 were any con-picuous disability, considering the enormous com- 
 pensation given by the intact "motor region." I can now return 
 to the question of representation of both sides of the body in each 
 half of the brain. 
 
 I suppose that the right "motor region" represents complex 
 movements of muscles of both sides of the body (1) as they serve in 
 bilateral actions, (2) as they serve in alternate actions (or, I should 
 say, with preponderance of activity on one side), and (3) as they 
 serve in unilateral actions. But I suppose, too, that those move- 
 ments which are " bilateral " are represented most nearly equally 
 in right and left halves ; that those which are " alternate " are re- 
 presented less equally in the two halves (those of the left side 
 more in the right hall), and that those which are " unilateral " are 
 represented most unequally in the two halves (those of the left 
 side most in the right halt). We must bear in mind that move- 
 ments are spoken of, for the so-called alternate muscles may serve 
 in bilateral movements ; they may serve with a great degree of 
 preponderance on one side approaching unilateral movement ; and 
 the most unilateral muscles may serve in bilateral movements. 
 
 It may, however, be asked, Where is the paralysis corresponding 
 to abrogation of the second and third sets of fibres from the right 
 *' motor region ? " The existence of some weakness of the right 
 side (the so-called non-paralysed side) has been urged by Brown- 
 Sequard, Pitres, Friedlander, and Gowers ; but when in the diffi- 
 cult circumstances attending investigation of the state of the 
 right side no disability is demonstrable, there may yet be loss of 
 some few movements of the muscles of that side. The loss of 
 these few movements is masked by the compensation given by the 
 
 " JotrajjAi, May 10th, 1873. 
 W Phil. Tram., B. 41, 1889. 
 
12 
 
 left half of the brain, which represents most numerous movements 
 of the right side. If we take the case of excessive discharge be- 
 ginning in some part of the right middle motor centres, we find 
 that, in severe epileptiform fits, both sides of the body are con- 
 vulsed. In this case compensation is "inverted," that is to say, 
 centres which would compensate a loss are compelled to co-ope- 
 rate in an excess. The comparison and contrast of hemiplegia 
 and an epileptiform seizure are, however, by no means simple, as 
 we shall see when the process of universalisation of an epilepti- 
 form convulsion is considered. 
 
 Although when speaking of the hierarchy of nervous centres I 
 excluded from consideration the higher divisions of the cere- 
 bellar system, it is necessary to say something of them. There 
 are in some cases of tumour of the median lobe of the cerebellum, 
 seizures very like, if not quite like, those of ordinary surgical 
 tetanus. I have suggested that the convulsion of surgical tetanus 
 is owing to cerebellar discharges; but no doubt the poison caus- 
 ing that morbid affection affects lowest centres too. It his been 
 suggested that the tetanus-like seizures in the cases of cerebellar 
 tumour mentioned, are owing to pressure upon, or to changes in- 
 duced in, the corpora quadrigemina or medulla oblongata, or both. 
 But surgical tetanus is, at all events, in order of development of 
 spasm over its regional distribution the "complementary inverse" 
 of epileptiform seizures. And when we consider nervous diseases, 
 each as a fliw in a whole nervous system, the study of "corres- 
 ponding opposites" is most important. There is a more direct 
 reason for t iking note of the cerebellum in the present inquiry. 
 What the structures are connecting the cerebellum with the 
 lowest motor centres I know not. If there be a connection — if 
 the lowest level is at once the lowest level of the cerebral and of 
 the cerebellar system — we may expect the higher levels of the 
 cerebellar system to be concerned in post-epileptiform states; the 
 question is important, especially with regard to increased tendon 
 reactions in post-epileptiform paralyses. I have suggested 19 
 that the cerebellum is concerned wth the rigidity and exngge- 
 rated tendon reactions of (lefr) hemiplegia 20 when that parahsis 
 is the result of a destructive lesion of the (right) internal capsule, 
 that there is not only exaltation of function of the e f r ) l'west 
 motor centres from loss of control, but also that the cerebellar in- 
 flux upon them is no longer antagonised. This hypothesis has 
 been objected to on the ground that in transverse lesions of the 
 upper dorsal or cervical cord (the cerebellum being thus exclnd-d) 
 there is nevertheless rigidity of the legs with exaggerated knee- 
 jerk and foot clonus. I was obliged to admit that the cerebellum 
 is not necessary for the production of the exaggerated jerk and 
 rigidity. 21 But Charlton Bastian, 22 who has advanced proof where 
 I only speculated, has found that, in man, on complete transverse 
 lesion of the regions of the cord mentioned, the mu*cles of the 
 legs are flabby and the knee-jerks absent: what is very striking, 
 he finds that the condition of rigidity of the legs and exaggerated 
 knee-jerk in cases of incomplete transverse lesions changes to one 
 of na^cidity with no tendon reactions when that lesion becomes 
 completely transverse. If Bastian be correct, as I think he is, 
 the hypothesis of cerebellar influx, on which we are in funda- 
 mental agreement, is supported. 
 
 l 9 M».dical Examiner, April 5th, 1877, and March 29th, 1878. 
 
 20 Not rarely both knee- jerks are exasperated ; this perhaps helps to show that 
 
 the third set of fibres ends in the right low-pst motor centres. 
 
 21 Medical Times and Gazette, February 12th. 1881. 
 
 12 Quaiu's Dictionary of Medicine, p. 1481. 
 
IS 
 
 Lecture II. 
 
 Epileptiform (Middle Level) Fits. — Varieties. — Diluted Convul- 
 sions. — Crude Sensations. — Locality and Order of Convulsive 
 Movements. — Degrees and Range* of Fits. — Hyper- and Hypo- 
 physiological States. — A Discharging Lesion. — the '"Buttoning 
 Centre" — Physiological Fulminate — The March of the Convul- 
 sion. — Compound Order. — Cells of a Discharging Lesion Quasi- 
 parasitical. — Nutrition of Cells. — Summary. 
 
 I take for most particular consideration the second kind of fits, 
 epileptiform seizures (middle level fits) ; they were first described 
 by Bravais in 1824. There are many reasons why we should study 
 them first. (1) Their investigation is comparatively easy. We 
 can, if present at a paroxysm, ascertain the place of onset and 
 trace the March of the convulsion; and if we witness no attacks, 
 since consciousness is not lost or is lost lafe in the seizures, the 
 patient can tell us the place of onset and much more abuut his 
 fits. (2) They have permanent paralytic coun r erparts in mono- 
 plegia* and hemiplegias from destructive lesions of the "motor 
 region." (3) There is after them, at least in many cases, tempo- 
 rary paralysis of the parts first and most convulsed. (4) There 
 is not rarely permanent paralysis of the parts which are occa- 
 sionally convulsed, this showing — a very important thing with 
 regard to doctrines of localisation — that in the same case there 
 is coexistence of a destructive lesion and a discharging ltsion of 
 difft rent elements of the same centre. (5) Because there is after 
 some seizures temporary defect of speech ("partial aphasia'). 
 (6) Because, if we can rind the condition of centres answering to 
 paralysis and aphasia after these seizures, we shall be greatly 
 helped in our investigation of the state of the highest centres in 
 insanities after epileptic fits. (7) Because epileptiform seizures 
 often depend on gross organic disease, such as tumour (syphilitic 
 or non-syphilidc) ; hence, we may at post-mortem examinations 
 obtain proof or disproof of any notions on localisation and gross 
 pithology we had from a study of the patient's symptomatology 
 during his life. (8) It is in epileptiform seizures that operations 
 have been done by Macewen, Godlee, Horsley, Barker, and 
 others. Hence, very precise study of fits of this kind is neces- 
 sary. In this regard, as well as in many others, the minute 
 investigations of the "motor region" by Beevor and Horaley are 
 of great value. 
 
 It would be very unmethodical to begin the scientific study of 
 the more complex (epileptic) kind of fits before the study of the 
 epileptiform kind. 
 
 There are Varieties of epileptiform seizures. The convulsion 
 begins in some part of one side of the body. Varieties are dis- 
 tinguished by the particular pluce of onset ("signal symptom" of 
 Seguin) of the convulsion. The fit may begin in some part of 
 either right or left side of the body ; I call that on which it does 
 begiu the " first side," and the corresponding (opposite) half of the 
 brain in which the discharge begins the " first half." If the fit begins 
 on the left side, that is the first side, and the right half of the 
 brain is the first half; suppose that the convulsion becomes uni- 
 versal, then the right side of the body is the second side, and the 
 left half of the brain (if it discharges after the right) is the second 
 
14 
 
 half. Whether the onset be right or left sided is a very important 
 matter, because there is often defect of speech after right-side- 
 beginning tits ; moreover, on account of the " speech centre," oper- 
 ations on the left half of the brain are more serious than opera- 
 tions on the right. 
 
 The three commonest Varieties of epileptiform seizures are — (1) 
 Pits starting in the hand (most often in the thumb or index finger 
 or in both). (2) Fits starting in one aide of the face (most often 
 near f ,he mouth) or in the tongue, or in both these parts. (3) Fits 
 starting in the foot (nearly always in the great toe). (Of course 
 one always means convulsive development of movements of 
 muscles belonging to the several parts mentioned.) 
 
 Of necessity the three Varieties depend on the fact that the 
 local discharging lesion is of cells of different parts of the "motor 
 region" — of hand, face, and foot centre respectively. The starting 
 point is almost invariably the same in each patient, hut not 
 always. A patient whose fits commonly begin in the hand may 
 sometimes have the face of the same side slightly and solely 
 affected; or a patient may tell us that his fits "fly about" — that 
 is, leaving the face for the hand, or vice versa. 
 
 We sometimes meet with paroxysms of one-sided tremor — what 
 looks superficially like tremor, really a ''diluted convulsion" — 
 dependent, 1 think, on discharges beginning in motor elements of 
 the so-called sensory centres behind the motor region. 23 1 do not 
 call these epileptiform seizures. 
 
 Often enough there is "tingling" or some other crude sensation 
 in the place of onset before convulsion starts; this is part of the 
 proof that the so-called motor region, although mainly motor, 24 is 
 not purely motor. Sometimes there is at or near to the onset of an 
 otherwise ordinary epileptiform seizure excessive development of 
 colour, or of sound ; these also are Crude Sensations. Epilepti- 
 form seizures with crude sensations deserve very careful attention, 
 but time will not allow me to consider these complications. 25 
 
 It is worth mentioning that some patients have a feeling as if a 
 part were convulsed when it does not really move; one of my 
 patients subject to veritable convulsions beginning in his left 
 thumb had sometimes what he called " convulsions not to be seen" 
 of that part. Another patient bad the feeliDg of convulsion of 
 one side of his face, but looking in a glass he saw that it did not 
 move. He died of brain tumour (necropsy), but its exact position 
 I did not learn. A patient who has fits starting in the hand will 
 say tt at he feels " it " in the face, when, however, the face does 
 not move ; this " it " may be owing to very slight discharges 
 of sensory or motor elements, or of both. 28 
 
 23 I have never believed that any part of the cortex is purely motor or purely 
 sensory. It the elaborate visual projections in some cases of migraine occur 
 during discharge beginning in a " sensory centre," then the elements of that 
 so-called sensory centre are only chiefly sensory ; the fortification outline and 
 the vibrations of parts of the migrainous visual spectre imply discharge of 
 motor elements as certainly as the colours imply discharge of sensory 
 elements. 
 
 24 See remarks (Lecture I) on France's Researches on Degeneration of Fibres of the 
 Lateral Column of the Cord, consequent on Lesions of the Gyrus Fonucatus. 
 
 25 Of course crude sensations (psychical) and convulsion (physical) are in no 
 way comparable : the comparisons and contrasts are of excessi/e discharges of 
 sensory elements during which crude sensations arise, with such discharges of 
 motor elemeuts./'rowi which convulsion arises. 
 
 26 When a healthy person thinks of doing something (" has an idea of a move- 
 ment ";, I consider that what occurs physically is slight discharge not only of 
 sensory but also ot motor nervous arrangements of his highest centres ; there is 
 "nascent movement" — slight discharge of the very same motor nervous ar- 
 rangements of the highest centres which, if more strongly discharged, would, 
 by intermediation of middle and lowest motor centres, produce the actual 
 movement. It is probable that a similar explanation (the middle motor centre* 
 
IS 
 
 Epileptiform fits begin in the Animal parts of the body, and 
 commonly in those of them which are the most animal. Thus the 
 majority begin in the arm, and nearly all these in the most animal 
 part of that most animal part, the hand, and most of them in the 
 thumb or index finger or both — the most animal parts of the 
 ■whole organism. Perhaps the term animal is awkward in this 
 connection ; it is convenient in contrast to organic. We can, how- 
 ever, use other terms, and say that epileptiform seizures most 
 often begin in those parts which, speaking popularly, have the 
 most " voluntary " uses ; in those parts which have great inde- 
 pendence of movement; in those parts which have the greater 
 number of different and more special (definite) movements, at the 
 greater number of different intervals. The foot in man has, how- 
 ever, few different movements ; the hallux in him is much less 
 specialised than in the monkey. It is, then, a very striking thing 
 tuat epileptiform seizures beginning in the leg almost invariably 
 start by spasm of the great toe, in the most, and yet but little, 
 differentiated part of the whole lower limb. 
 
 It may be objected to the principle stated that, to take an ex- 
 ample, convulsion in an epileptiform seizure may begin in the 
 shoulder, the least "voluntary " part of the arm, and spread down 
 thelimb 27 I have considered this objection in the Journal of August 
 17th, 1889. We have, as I continually insist, in strictness to speak 
 not of representation of parts of the body (muscular regions), but 
 of representation of movements. Movement of any part of the 
 body done with intention is a "voluntary" movement. Evident- 
 ly when a card-sharper shrugs his shoulder as a sign to a con- 
 federate to play a trump, that is his then most voluntary move- 
 ment. In so far as any part of the body has a movement inde- 
 pendent of the rest, in so far that movement has, I suggest, a 
 degree of localness of representation in the middle and highest 
 motor centres. Horsley and Beevor assign a point of the "motor 
 region" for the primary movement of each segment of the upper 
 limb. It may, however, be taken that epileptiform seizures most 
 often begin in the most " voluntary " parts, and that admitting 
 many varieties the three commonest are selected for comment. 
 
 Epileptiform seizures illustrate Dissolution — dissolution in pro- 
 cess of being effected — in which the order is from "voluntary" 
 towards automatic. In normal development of movements the 
 order is the opposite — is that of Evolution ; it is from automatic to 
 " voluntary." 2 * 
 
 The " motor region " (motor province of the middle level) pre- 
 sumably represents at least motorily the whole of the body, de- 
 monstrably nearly all parts organic as well as animal. Hence, a3 
 the discharging lesion may theoretically be of any part of the 
 " motor region," it is a legitimate hypothesis that there are fits 
 starring by excessive discharges of cells of nervous arrangements 
 of the "motor region" which especially represent parts in the 
 organic field, and that some fits called epileptic are such seizures. 
 I do not hold that hypothesis. There are parts — for example, the 
 vocal cords — which we may speak of as organico-animal. 
 
 being here primarily concerned) applies to the " ideas of convulsion " spoken of 
 in the text. No doubt if a man subject to iits beginning in his right thumb 
 ■were to lose the right arm by amputation his firs would still seem to him to 
 begin in his thumb— to begin in his spectral thumb, tor eome time at least. 
 17 I have recorded a case of this kind, Medical limes aiid Gazette, June 5th, 
 
 1875. 
 28 Properly from most automatic to least automatic in evolution ; the opposite 
 in dissolution. " Most voluntary movement" is objectionable because it is a 
 mixture of psychological and anatomico-physiological language ; it is a popular 
 expression, equivalent to what is scientifically " least automatic movement." 
 
18 
 
 Munk and Krause * 9 in the dog, and Horsley and Semon 
 in the monkey, have investigated the cortical representa- 
 tion of the movements of the vocal cords. Krause in the 
 dog, Hor-ley and Semon in the moukey, 30 produced con- 
 vulsive seizures by excira r ion of the cortical "laryngeal 
 ceutre." Semon thinks that laryngismus stridulus in man 
 (the infant human being) is a cortical fit; but if so there is not an 
 exception to the statement that epileptiform fits begin in the 
 ammal parts, if we adopt Semon's views of, and inferences from, 
 the kind of representation of the vocal cords in the mutor cortex 
 ("purposive or volitional, since it is adduction, that is phoua- 
 tion "). 
 
 Although epileptiform seizures most often begin in the three 
 most animal parts of the animal parrs mentioned, yet as the fits go 
 on the organic held becomes involved. In a dog poisoned by 
 curara (respiration being artificially kept up) the animal parts 
 are excluded, and then we see that by excessive discharges ex- 
 perimentally induced in its " motor region," effects are produced 
 in, and are then limited to, the organic held. 
 
 There are Degrees of each variety corresponding to degrees of 
 the " severity " of the excessive discharge. Degrees are to be con- 
 sidered with respect to two factors, (1) amount of convulsion, and 
 (2) range of convulsion. I illustrate here quite arbitrarily by 
 Range only, and take the case of an epileptiform fit starting in 
 the thumb. Admitting that there are many ranges, it is allowable 
 to make arbitrary divisions (they must not be taken for real dis- 
 tiactions) into four Ranges : (1) Terminal 31 fit — the spasm involves, 
 say the hand, or some part of it only; (2) monospasm — the arm 
 becomes involved; (3) hemispasm; (4) bilateral convulsion— the 
 second 'ide being gained, the tit becomes universal. Observe the 
 use of the word " become." In the range (4) there is a March of 
 spasm from the part first seized all over the body, answering to 
 increased spreading of the central excessive discharge beginning 
 in some particular part of the motor region of the first half, aud 
 may be extending to the second half, of the brain. The second 
 side of the body (in 4) is affected later, and commonly less than, 
 the first side. 
 
 From (1) to (4) there is but a single variety of epileptiform 
 seizure in four different degrees. Otherwise stated, a man who 
 has had convulsion of the range (1) or (2) does not become subject 
 to another variety of epileptiform seizure when he has also fits 
 which, beginning in the same terminal part (hand, we are sup- 
 posing), have a more extensive range however much more extensive 
 it is; so to speak, that patient is subject to a fit, and has it in 
 different degrees on different occasions. However limited or how- 
 ever wide the range of convulsion, the corresponding discharge 
 begins in the very same centre of the motor region of but one, 
 the opposite half of the brain. This means that it is the place of 
 onset ('the signal symptom" which localises) 32 ; ir.pnint*" to the pir- 
 
 29 Sitzunysberichte dtr Kbniglichtn Academie der Wissensckaften uud Arctdv fur 
 
 Anatomit und Physiologic 1883. 
 
 3° Jouhnal, December 21 t, 18*9. 
 
 31 It maybe well said that a fit beginning by spasm o f the cheek does not 
 begin in & terminal part,; but the meaning of lue word terminal may, for my 
 present purpose, be used to include that onset. Peiipheral would have too 
 wide a meaning. I would suggest acro-epilepsy as a name for epileptiform 
 seizures were it not that it migtit mislead some to think that there are epilepti- 
 form seizures which begin in the nose. 
 
 3 2 The term aura is, I suppose, never used now in its original sense. When 
 a medical man speaks ot an aura in an epileptic fit starting from the epi- 
 gastric region, he is understood to mean that some sensation is referred by the 
 patient to that part of the body, and to believe that the sensation arises during 
 the incipience of a discharge of some central sensory elements. 
 
17 
 
 ticular part of the " motor region " of the cells of which part the 
 discharging lesion is made up. When a man's epileptiform fits 
 "get worse" — when we are supposing they become of greater 
 range — there is the same discharging lesion, but it has become of 
 more cells, or the cells of it have become still more highly unstable, 
 or perhaps there are both kinds of change; in consequence of this 
 purely local ingravescence, the induced discharges (compelled dis- 
 charges) of normal stable cells are more numerous. 
 
 Were A — and B — to be universally convulsed, they would have 
 different varieties of epileptiform seizures if in A — the onset was 
 by spasm of the hand, and in B — by spasm of the foot, however 
 much alike the fits looked at the acme of each ; the discharging 
 lesion in A — would be of some cells of his " arm centre," in B — of 
 his "leg centre." To note the "signal symptom" — to use Seguin's 
 term again, and therefrom to infer the seat of the discharging 
 lesion — is more important, obviously for " brain surgery," than 
 anything else about the paroxysms. 
 
 It has been implied, but it may be well to say explicitly, that 
 an epileptiform seizure does not, when become universal, turn 
 into the other kind of fit — the epileptic. I mention this because 
 I think a rapidly universal epileptiform seizure superficially 
 resembles an epileptic one, and a slowly developed epileptic 
 seizure superficially resembles an epileptiform seizure. 
 
 I have often urged that the Clinical Problem in every nervous 
 malady is of three elements: (1) Anatomical, (2) Physiological, 
 (3) Pathological. In other words, we have in every case to seek : 
 (1) the seat of the lesion, the structure damaged, (2) to infer the 
 kind of functional change of structure, and (3) to discover the 
 nature of the abnormal nutritive process of which the alteration 
 of composition of nervous matter producing the abnormal func- 
 tional state of structure is effected {vide infra). 
 
 It may be properly said that structure, function, and nutrition 
 never exist separately. It is quite obvious, taking for comment 
 normal conditions, that there would be no persistence of function 
 without continuous nutrition ; that function is not conceivable 
 apart from some structure, and that structure without function 
 is nothing for an organism. It is, however, convenient, if not 
 necessary, for clear exposition of nervous maladies, to consider 
 for a time each of the three separately. It will, however, be 
 impossible to consider one without frequent explicit and always 
 implicit reference to the others. Perhaps I use the term Anatomy 
 regarding the nervous system in an unusual sense ; I do not use it 
 convertibly with Morphology- A knowledge of the Anatomy of 
 any Centre is a knowledge of the parts of the body ivhich that centre 
 represents, and of the loays in which it represents them. 
 
 Anatomy. — (Localisation.) I shall say very little under this 
 head. The patient A. is subject to fits, every one of which begins 
 in his right thumb ; there is a lesion of the thumb centre of the 
 left middle level ("motor region") — this is the anatomical dia- 
 gnosis. (According to Beevor and Horsley, " the middle third of 
 the ascending parietal convolution is the focus of representation 
 of the movements of the thumb.") 
 
 Physiology.— Physiology deals with the dynamics of the 
 organism — that is, with its function. I use the term " function " 
 with regard to nervous diseases in a strict sense, and never in the 
 way it or its adjective is used when applied to the symptoms of a 
 hysterical woman, or to minute or transitory changes of struc- 
 ture. 33 I must now define the term. The function of organic 
 
 33 See an able paper by Dr. Allchin., Westminster Hospital Reports, vol. ii, 
 
18 
 
 matter and par excellence of nervous matter, to which I confine 
 further remarks, is to store up energy, 34 to liberate that energy 
 (nervous discharge) at different rates against resistances of differ- 
 ent amounts ; the energy liberated is dissipated or does work, or 
 there are both consequences according as the resistances en- 
 countered are or are not overcome, or are only partially over- 
 come. We have here to deal with abnormalities of this func- 
 tion — that is, with abnormal physiological states (I need not 
 always add the adjective abnormal). 
 
 There are two kinds of physiological or functional states in cases 
 of disease of the nervous system. (1) Function may be exalted, 
 and is, sometimes, as that of cells of a discharging lesion, very 
 greatly exalted ; these are superpositive functional changes — that 
 is, hyper-physiological states. (2) Function may be diminished 
 or lost ; these are negative physiological or functional states — 
 they are hypo-physiological states. Destructive lesions come in 
 this category, although there is in them loss, not merely of func- 
 tion, but of functionable material also. 
 
 The two kinds of functional changes — the hyper- and the hypo- 
 physiological — are opposites ; there are no degrees from one to the 
 other ; so to say, they depart from normal function, the one up- 
 wards, the other downwards. We shall have to speak later of a 
 negative functional change in temporary post-epileptiform pira- 
 lysis ; that negative change (there is temporary exhaustion of 
 nervous elements) is a direct result of the excessive discharge in 
 the prior paroxysm; the two opposite functional states of the same 
 nervous elements occur in immediate sequence. 
 
 Now I consider the inclusion of negative functional states in 
 cases of mere temporary exhaustion of nervous elements in the 
 same category with destructive lesions when nervous elements 
 and function are gone together. I dare say the former would he 
 called functional, because the alteration in the composition of the 
 material of nervous elements, whatever its nature, is no doubt 
 slight and is certainly temporary. But I call it a negative func- 
 tional change, because function is lost: the slight and temporary 
 alteration of composition is a pathological change. For the time 
 being fibres exhausted are not in effect nerve fibres at all ; with a 
 morphological plenum there is a functional vacuum as certainly 
 as there is when they are destroyed. Whether nervous elements 
 are f unctionless or gone altogether, the situation for the time being 
 is the same. I shall speak of both as "negative lesions." And 
 saying that the exhausted fibres recover soon is recognising fully 
 the vast difference in their condition from that of fibres destroyed 
 — properly, absence of fibres. 
 
 There are degrees of negative function from defect to loss. Of 
 these I will say nothing. There are two greatly different degrees, 
 if indeed we may not say two kinds, of superpositive (hyper- 
 physiological) function. We are concerned with both in this 
 inquiry ; it is imperative to distinguish them clearly. 
 
 There is (a) the vast exaltation of function of cells of a discharg- 
 ing lesion ; this degree is always produced by some pathological 
 process — that is, by morbid nutrition, a nutrition which alters the 
 composition of nervous matter. 35 This, the first degree of func- 
 
 si Assimilation of material having potential energy (anabr.lism) ; decomposition 
 of material (katabolism) with liberation of energy. 
 35 This is the definition I would suggest of a pathological process (morbid 
 nutrition) or of its result. I suppose that such poisons as strychnine alter the 
 composition of nervous elements, in consequence of which morbid nutrition (a 
 substitution nutrition) there is a functional change of the degree (a). It 
 seems more likely that strychnine enters into th6 very composition of matter of 
 nerve cells than that it stands outside the cells and " irritates " them. When a 
 
19 
 
 tional change, is of a highly explosive character; it issues in 
 paroxysmal discharges. 
 
 There is (6) a comparatively slight exaltation of function with 
 which we shall be particularly concerned when we consider post- 
 epileptiform conditions. In these conditions, besides paralysis 
 answering to a negative functional state of fibres of the second 
 segment of the kinetic route, there are increased tendon reactions 
 answering to a hyperphysiological state of this degree (b) of cells 
 of anterior horns (lowest motor centres). I believe that the second 
 degree of superpositive functional state is not — certainly not in 
 the case just alluded to — the direct result of a pathological pro- 
 cess, but that it is the indirect result of a negative functional state 
 of other, related nervous elements. (Here is, essentially, an appli- 
 cation of a principle long ago put forward by Anstie and Thomp- 
 son Dickson). This, the second degree of functional change, does 
 not issue in paroxysmal discharges, but in continuous discharges; 
 or discharge can at any time be evoked by appropriate slight exci- 
 tations. Returning to post -epileptiform conditions, the negative 
 functional state answering to the paralysis is alone produced by a 
 pathological process ; the abnormal condition of anterior horns 
 implied by increase of the tendon reactions is one of over-activity 
 of perfectly healthy nervous elements. There is simply the proper 
 activity of certain lowest motor centres, which is manifested at 
 its maximum when an obstacle has been removed, when control 
 has been taken off. I think, too, that cerebellar influx is no longer 
 antagonised (see Lecture I) ; and if so, the cerebellum is simply 
 unhindered in its activity, and is doing, now that an obstacle is 
 removed, what it was always " trying to do." Here, again, we 
 come across the principle that parts of the symp'omatologies of 
 nervous maladies are owing to activities or over-activities of per- 
 fectly healthy nervous arrangements. If this principle be valid, 
 it is evidently important to distinguish between the physiological 
 and the pathological factor in nervous maladies. Of course in- 
 creased activity of any nervous elements implies increased nutri- 
 tion, but there is not, I submit, in the case of elements answering 
 to the second kind of functional change, morbid nutrition. There 
 is not, then, what I call a pathological process; the composition 
 of the matter of the cells concerned is not altered. For the pre- 
 sent I shall speak only of the first degree (a) of superpositive 
 functional states — that which is of a highly explosive degree — and 
 is produced by a pathological process. 
 
 The hyperphysiological state (degree a) in the case of A — (vide 
 supra) is what I call a " discharging lesion." It is a crude hyper- 
 physiological state just as its diametrical opposite, loss of func- 
 tion, is a crude hypophysiological state. I continue to speak of 
 healthy cells as stable ; they are naturally unstable, of course, but 
 I mean by using the term stable that they are so in comparison 
 with those of discharging lesions, which I speak of as beiDg highly 
 unstable. The discharging lesion is of a few cells which have got 
 far above the rest of the cortical cells in degree of tension and 
 instability of equilibrium. That lesion is made up of cells of 
 nervous arrangements which represent some most special move- 
 ments of a particular muscular region ; the sudden and excessive 
 development of these movements from discharge of those cells is 
 
 rabbit's respiratory centres discharge excessively on withdrawal of blood, one 
 must suppose that before that discharge there is an abnormal metabolism 
 (pathological process) whereby matter of the cells of the centre becomes more 
 explosive. Certain " pathological processes," such as cerebral haemorrhage, are 
 really injuries ; hemiplegia resulting from clot is, so far as destruction of fir res 
 goes, like that caused by the prong of a pitchfork; there is no real pathological 
 process in either of these modes of destruction. 
 
20 
 
 the convulsion incipient (" signal symptom " of Seguin), or, if 
 there be no spreading of the spasm, it is the convulsion total. 
 
 The hyperphysiology of epileptiform seizures is the element of 
 the threefold clinical problem of which we are sure. We are quite 
 certain that normal movements are the results of liberation of 
 energy attending katabolism; thus the inference is irresistible 
 that that sudden and excessive development of many movements 
 at once, which we call convulsion, must be a result of an excess 
 of the same physiological process — of a sudden and excessive 
 energy-liberation attending great and rap'd katabolism. I will 
 give illustrations of the different effects of discharges of stable 
 cells (cells of comparatively low tension and of comparatively 
 stable equilibrium) in normal operations, and of those of cells of a 
 discharging lesion (cells of very high tension and very unstable 
 equilibrium) in a convulsion. 
 
 It would be most absurd to say that there is a Buttoning Centre, 
 but for convenience of illustration we may imagine such a centre. 
 I illustrate by motor elements only, although, of course, sensory 
 elements are concerned in all operations. In the operation of 
 buttoning there are slight and slow discharges of normal stable 
 cells (fibres are understood) of different nervous arrangements of 
 our supposed centre (lower centres and muscles being understood) 
 simultaneously and successively ; in consequence there is a har- 
 mony and a melody of the different movements of the hand and 
 arm by which the button is got into its hole. There is Harmony 
 by Contemperation 36 of different movements, and there is Melody 
 in that the compound contemperated movements follow one 
 another at proper time intervals ; there is what is commonly 
 called co-ordination, although the time element (melody) is not 
 much considered in most accounts of the process of co-ordination. 
 So much for the discharges of stable cells in the operations of 
 health. 
 
 Now let us suppose that the cells of the buttoning centre he- 
 come by some, any, pathological process, so highly unstable as to 
 constitute a discharging lesion. (For the present we shall speak 
 as if the excessive discharges of the highly unstable cells did not 
 provoke similar discharges of stable cells of collateral centres.) 
 The discharges are sudden and rapid, 37 and of all the cells nearly 
 at once; they do not cause a speedy and vigorous act of button- 
 ing, but a short, severe, and rapid contention of all the move- 
 ments of that operation ; this contention is convulsion of the hand 
 and arm. There is no harmony and melody ; on the contrary, in 
 the tonic stage, all contemplation is lost and all time-intervals are 
 merged, so that there is but one rigid state of the musculature of the 
 hand and arm, and, in the clonic stage, there is but a succession of 
 such rigid states. There are no movements properly so-called in 
 this convulsion ; but, if I may use the word for once, there is first 
 but a single big useless movement, and next a series of such so- 
 called movements which do nothing but " mark time." 
 
 The illustration, although the supposition of a buttoning centre 
 is grotesque, may render clear what presumably occurs when A — 
 is " attacked by his convulsion." The convulsion is a brutal de- 
 velopment of that man's own movements. I make this odd re- 
 mark because I do not think that it is always vividly realised 
 
 36 Contemperation is, says the Imperial Dictionary, an obsolete word. One of 
 its meanings given op. cit. is, " The act of reducing a quality by admixture of 
 the contrary." 
 
 87 I do not mean by using the word rapid, here or anywhere, that nerve im- 
 pulses travel more rapidly in the case of excessive discharges, but that more 
 occur in a given time than is normal — that there is a greater quantity of motion 
 in a given time. 
 
21 
 
 that an ordinary severe epileptic " attack " (to take that kind of 
 fit for a moment's illustration) is nothing more than a sudden ex- 
 cessive and temporary contention of very many of the patient's 
 familiar normal movements — those of smiling, masticating, arti- 
 culating, singing, manipulating, etc. A convulsion is not some- 
 thing altogether sui generis. Speaking figuratively and more 
 generally, and still of an epileptic paroxysm, there is the mad en- 
 deavour of the highest centres to develop the maximum of func- 
 tion of every part of the body, animal and organic, and of all 
 parts at once ; the phenomena of a very severe epileptic fit show 
 that this endeavour is nearly successful : the patient is almost 
 killed by the paroxysm, and is nearly dead (deeply comatose) after 
 it. 
 
 The cells of a discharging lesion are not to be thought of only 
 as occasionally discharging excessively; we have also to consider 
 their aspect of too easy dischargeability, otherwise their highly 
 unstable equilibrium. In health the cells of the " buttoning 
 centre " are made to discharge slightly on special excitations of 
 definite force, so that their discharges are in particular relations, 
 and in some degree of community with those of cells of other 
 centres (I will call them "collateral stable cells") with which 
 they are connected. The cells of the " buttoning centre," when 
 they have become highly explosive, are still integral parts or the 
 nervous system, and have the very same connections they had 
 before some pathological process so altered their nutrition that 
 they became highly explosive (and then, metaphorically speaking, 
 " mad parts "). Their equilibrium can be upset, they can be made 
 to discharge, and to discharge excessively, by less special excita- 
 tions of less definite force coming to them from collateral stable 
 cells — that is, theL. discharge depends on their own easy dis- 
 chargeability rather than on the particularity of the excitation 
 reaching them. Possibly their discharge is spontaneous when 
 tension is very great, and equilibrium very highly unstable. 
 
 I repeat that the cells which have become very highly " ex- 
 plosive" (those of the discharging lesion) continue to be elements 
 of the same nervous arrangements, and that these nervous ar- 
 rangements are still connected in the very same ways with the 
 remainder of the nervous system 38 as when their cells were stable. 
 Hence I do not speak of the highly explosive cells as being in any 
 motor centre, but as being of that centre. I submit that the 
 highly "explosive" cells of a discharging lesion will on their ful- 
 minating discharge overcome the resistance of, and thus produce 
 excessive discharge of, collateral stable nervous elements. The 
 epileptiform fit (excepting, perhaps, some slight terminal fits) is 
 not the result only of the discharge of the cells of the discharging 
 lesion, as was supposed for a limited illustration, when speaking 
 of the imaginary " buttoning centre." Making a purely arbitrary 
 limitation, we may imagine that the primary excessive discharge, 
 that of the fulminate of A.'s thumb-centre, only produces directly 
 the initial spasm, that of his thumb (the " signal symptom "); all 
 the rest of his convulsion will be indirectly produced by it, by 
 compelled excessive discharges of stable cells. Of these compelled 
 discharges I shall speak again later. 
 
 It will now be seen why the term physiological fulminate ia 
 occasionally used. I use it in almost a literal sense; the discharg- 
 ing lesion is supposed to be a detonator of collateral stable cells, 
 just as a fulminate (in the artillerist's use of the term) is of the 
 
 38 There is the obvious qualification that some nervous elements may have 
 been destroyed by the same pathological process which caused high instability 
 of other elements, and thus that some connections of the latter are cut. 
 
22 
 
 comparatively stable gunpowder in a cannon. I believe that the 
 only thing persistently physiologically abnormal in A. is that 
 some few cells of his thumb-centre have become fulminant. To 
 speak figuratively, this "mad part" compels many collateral 
 "sane" cells and cells of middle and lowest motor centres, and 
 ultimately the muscles, to co-operate in its occasional and sudden 
 excesses — makes them "act madly" for a time. If the few highly 
 explosive cells, those of the discharging lesion, could be destroyed, 
 the patient would be rid of his fits ; he would lose nervous ele- 
 ments which are doubtless never of value for co-operation with 
 the collateral stable cells in normal operations ; he would lose 
 eells of negative value and of positive injury — cells like those of 
 an animal poisoned by strychnine, whicb, on their discharge, 
 " run up " movements into useless contentions. The cells of A. 'a 
 fulminate, when called on to co-operate with normally stable cells 
 in any operation, function excessively, and so as, after the manner 
 of a detonator, to cause wide excessive discharges of many stable 
 cells. It is a pity that A. cannot be rid of these worse than use- 
 less cells ; but I know of no way of effecting this riddance. There 
 is the surgical question of cutting out part of the cortex. 
 
 I have, in the foregoing, used, regarding hyper-physiological 
 discharges, the term excessive, and, regarding the resulting con- 
 vulsion, the term severe ; the more excessive the discharge the 
 severer the fit. I now use more precise terms, and consider this 
 part of the subject a3 it was in effect, so it seems to me, long ago 
 considered by Herpin. I regret greatly that my ignorance of 
 physics renders me unable to deal with it adequately. 
 
 With regard to nervous discharges, or, as I shall here say, libera- 
 tions of energy by nervous elements, we have to consider two 
 aspects — quantity of energy liberated, and the rate of its libera- 
 tion ; the two varying factors both in normal and in " excessive " 
 nervous discharges. With regard to the convulsion, we have to 
 consider its degree, and the rate with which it is produced. 39 We 
 have to study the amount of convulsion, the range of convulsion, 
 and particularly the " deliberate " or " sudden " rate of onset. In 
 two liberations of equal quantities of energy at different rates 
 there is the same momentum or quantity of motion. But the 
 force of the more rapid but shorter liberation of energy will be 
 greater than that of the slower and longer liberation. Force only 
 exists while it lasts ; there is no doctrine of conservation of force. 
 The more rapid the liberation of energy by a discharging lesion 
 the greater resistances will be overcome, the more numerous 
 collateral stable elements will be compelled to discharge, and 
 thus the more the amount of convulsion and the greater its 
 range. 
 
 I suppose that there are degrees of instability of the cells of the 
 fulminates in different cases of epileptiform seizures and at diffe- 
 rent periods of the same case. When A.'s fits " get worse" (greater 
 amount of convulsion and greater range of convulsion), more cells 
 may have then become highly unstable, or those already highly 
 unstable may have become still more so ; his fulminate becomes 
 more fulminant, but that fulminate is made up of cells of the 
 same part of the " motor region," if not of the very game cells. I 
 now eonsider it must be taken hypothetically, the differences of 
 f ulmination of discharging lesions. Let me suppose two cases, in 
 each of which there is a discharging lesion constituted by cells of 
 the thumb centre. In the patient A. the cells are (1 am only able 
 
 39 Herpin, in his valuable work on Epilepsy, sums up several propositions as 
 follows (italics in original): — "En resume: plus le debut est long , moins lacrii* 
 ast violente, plus il est instantani, plusl'acces est intense." 
 
23 
 
 to distinguish vaguely) of lower degree of high instability (his 
 fulminate is much less of a fulminate) than in the case of A. A. In 
 both the first spa«m is of the thumb. I shall mention the cortical 
 discharges only; the sequent discharges of the lowest motor 
 centres and of the mu-cles are to be taken for granted. 
 
 In A — the primary discharge, that of the fulminate, is deliber- 
 ate, produces (secuudo-primary) discharges of few collateral stable 
 cells, and produces them slowly one after another ; the correspond- 
 ing convulsion sets in deliberately and spreads slowly ; is of little 
 range (very local; for example, of the arm only), is of long dura- 
 tion, and there is an easily traceable distinct sequence over the 
 range (all this, of course, comparatively with what occurs in the 
 next case). In A. A. the primary discharge is sudden, produces 
 (secundo- primary) discharges of many collateral stable cells, and 
 produces them rapidly and more nearly at the same time; the 
 corresponding convulsion sets in suddenly and spreads rapidly ; it 
 is of great range, is of short duration, and there is a less easily 
 traceable distinct sequence over the range. 
 
 The more rapid, though the shorter, of the two primary libera- 
 tions by the discharging lesions — supposing an equal quantity of 
 energy to be liberated by each — will overcome greater resistances, 
 and will thus compel discharges of a greater number of collateral 
 stable elements; the convulsion produced will be both of greater 
 amount and of greater range. Lines of many different degrees of 
 resistance will be overcome by such a primary liberation more 
 nearly at the same time ; the convulsion will more quickly attain 
 its maximum at every part affected, and will be more nearly of 
 the same degree in all parts affected. 
 
 We have not only to note how much of the body is ultimately 
 involved, but also the order in which the several parts involved 
 are affected — the March of the convulsion. There is not a simple, 
 but a compound sequence of spasm ; the convulsion does not cease 
 in one part when another is involved. To observe, to give a 
 simple example, how much of the arm has been involved when 
 convulsion appears in the face will, I think, help us to clearer 
 notions of localisation of movements of those two separate parts 
 of the body in the centre discharging (anatomical localisation) ; 
 or if not, at any rate as to the time relations of different elements 
 of different centres (physiological localisation). From increasing 
 discharge of a motor centre there is a double effect ; there is not 
 simply " more cunvulsion," there is (1) greater amount of con- 
 vulsion of the part first seized, and there is (2) extension of con- 
 vulsion to the next part of the same muscular region, or to some 
 other part represented in the centre discharging (or in another 
 centre connected with the one primarily discharging by particular 
 time relations). Most generally, the progress of the two dissolu- 
 tions — convulsion from increasing discharge of a motor centre, 
 and paralysis from increasing destruction of a motor centre — may 
 be rudely (and without the least pretence at exact quantification) 
 symbolised as (l) x, (2) x 2 y, (S)x 3 y 2 z; the order x, y, z, implies 
 the representation in the centre supposed of the time relations, 
 and of the degree of speciality of movements of the three parts. 
 Horsley and Beevor find Compound Order in their development 
 of " simple movements" by very slight excitations of small parts 
 of a monkey's " motor region." After developing what they 
 call the Primary Movement of a part, say one of the shoulder, 
 there follow, on increasing the excitation, secondary and ter- 
 tiary movements — that is, there is produced a sequence of move- 
 ments of segments of the arm. But when the secondary move- 
 ment comes the primary has not ceased ; on the contrary, it is 
 
24 
 
 intensified: the development may be roughly symbolised as p 
 and then p 2 s. 
 
 ■ Returning to epileptiform seizures, Compound Order is observed 
 on a small scale in fi f s involving limited regions of the body 
 (very well seen in the face), and on a large scale when such seiz- 
 ures become universal. There is a very intricate compound 
 sequence from the beginning of the fit to its universalisation. I 
 shall, however, make artificial separations, and say a fit which 
 becomes universal that excessive discharge beginning in some 
 cells of a part of the right middle motor centres produces convul- 
 sion (1) starting in the left hand and spreading up the arm and 
 down the leg (first side), (2) involving both sides of the trunk, and 
 (3) finally gaining the limbs of the right (second) side when all 
 parts of the body are in convulsion together. That the left limbs 
 are convulsed from discharge of the right middle motor centres, by 
 intermediation of the first set of fibres of the second segment, is 
 not doubted. I used to suggest that convulsion of both sides of 
 the trunk and of the right limbs is al30 produced by discharge of 
 that half by the second and (or rather as I should now say) third 
 sets of fibres. This was rash, for supposing that some convulsion 
 of the second (right) side is producible by discharge of that one 
 half (right), it does not follow that the convulsion which actually 
 occurs is produced by it alone. For my hypothesis of representa- 
 tion of both sides of the body in each half of the brain, it would 
 suffice if there were any degree of tonic or clonic convulsion of 
 the right (second) side, tor I only suppose that the right side is 
 represented le-s than and subordinately to the left side, and also 
 second in time in the right half. The subject is a difficult one. 
 Horf-ley finds that when the corpus callosum is divided, excitation 
 of the right (I continue to say " right " for convenience) middle 
 motor centres produces epileptic convulsion of the left limbs 
 only. 40 In the case of dogs, Franck and Pitres found that arti- 
 ficially induced dscharges of the right "motor region" caused 
 universal convulsion when the left motor region had been extir- 
 pated and the corpus callosum divided. I quoted them to this 
 effect in my third Croonian Lecture. 41 They, however, as I then 
 said, attribute the universalisation of the convulsion to the pons, 
 medulla, and cord (which together I call the lowest level). 
 
 Considering, then, the opinions of those who hold that the second 
 and third sets of fibres, as well as the first set (all the fibres of the 
 second segment of the kinetic route interconnecting the right 
 middle motor centres with the lowest motnr centres), end in the 
 left lowest motor centres, the researches of Franck and Pitres and 
 those of Horsley, and also the gr-at complexity of the subject, I 
 ought not to be dogmatic as to the process by which universal isa- 
 tionof an epileptiform convulsionisproduced. Most likely in severe 
 seizures the left middle motor centres are discharged, as Horsley 
 supposes, after the right by intermediation of ca<losal fibres, al- 
 though possibly some slight convulsion cf the right limbs is pro- 
 duced from discharge of the right half alone by intermediation of 
 the second and third sets of fibres. And most likely, too. the 
 anterior commissure of the pons, medulla, and cord (intrinsic 
 fibres of the lowest level interconnecting left and right lowest 
 
 40 In the abstract of " Brown Lectures," Lar.cet, December 25th, 1886, Mr. 
 
 Victor Horsley is reported : "The conclusions all round, therefore, were 
 
 very emphatic, to the effect that convulsions due to cortical discharge are 
 evoked in various groups of muscles by nerve energy proceeding from that 
 centre in each hemisphere which is in relation to each group of muscles, 
 and that in generalised epileptic convulsions both cerebral hemispheres are 
 involved. 
 
 41 Journal, March 23th, 1884. 
 
23 
 
 motor centres) are concerned. Probably the loss of consciousness 
 answers to excessive discharges of the highest centres caused by 
 the medium of sensory (upward) fibres. The process of universali- 
 sation of epileptiform seizures is a very intricate one, and deserves 
 more precise analysis than I am capable of making. 
 
 I stay here to say that, taking the case of A. in illustration, 
 when we have located his lesion we have done anatomical work 
 only ; when we have noted all we can about his convulsion (there- 
 from inferring that the lesion is a " discharging lesion "and the 
 effects of its discharge direct and consecutive), we have done phy- 
 siological work only. The experimenters on animals do the ana- 
 tomico-physiological work thoroughly well. 
 
 Taking up again the case of A., we have now the third element, 
 pathology, to consider. Here is the great difficulty. Being sure 
 that A. has a discharging lesion of this thumb centre, there may 
 be no evidence to show whether that lesion is produced (indi- 
 rectly) by tumour or not. Here I urge again the necessity of dis- 
 tinguishing between the physiology and pathology of cases of 
 nervous disease. 42 Having urged that there is a degree or kind 
 of functional change (6) which is not the result of any patho- 
 logical process, I am all the more wishful to urge the distinction. 
 I continue to speak of the first degree (a), and urge the distinc- 
 tion from this point. 
 
 It may be epigrammatically said, and with truth, that an epi- 
 leptiform seizure is " only a symptom." Nevertheless, it is always 
 symptomatic of one physiological thing, a " discharging lesion." 
 Otherwise put, an epileptiform seizure is not a symptom of 
 tumour, of " softening," or of meningitis ; it is a symptom of the 
 one thing — high instability of certain cortical cells, however pro- 
 duced — produced by any pathological process. Physiologically 
 speaking, there is but one " cause " of epileptiform seizures, 
 namely, high instability of some cells of some centre of the 
 Rolandic region ; but there are many " causes " of them if we 
 mean pathological processes leading to that instability. So that 
 in the case of A. (he being subject to fits), the question in patho- 
 logy is not the vague one : " What is the disease of a certain part 
 of his cortex "? but "What abnormality of the nutritive process 
 has produced such an alteration in the composition of the mate- 
 rial of cells in that part as to render them highly explosive, and 
 how was that abnormality set up?" Or, more generally and re- 
 garding all cases of epileptiform seizures (and epileptic too), we 
 put the question : " How are local persistent discharging lesions 
 established and kept up ?" 
 
 The first question is : " What is the most general nature of the 
 abnormal nutritive process of cells of discharging lesions in epi- 
 leptiform seizures ?" This we ask ourselves, whatever the par- 
 ticular gross pathology or morbid anatomy, tumour, " softening," 
 etc., may be in any case. 
 
 The cells of the discharging lesion, although ywasz-parasitical, 
 are not strictly parasitical ; for another purpose I urged that the 
 nervous arrangements into which they enter remain integral parts 
 of the nervous system, and now I urge that they are nourished 
 aloDg with the rest of the body. Their nutrition does go on in 
 some base fashion as certainly as that that of their stable neigh- 
 
 42 I have urged this many times for at least twenty years. " Functional 
 changes must not be confounded with pathological changes, although of course 
 the two necessarily co-exist" ("Study of Convulsions," "St. And. Grad. Rep.," 
 vol. iii, 1870). I mention this as I am said to have put forward the " theory of 
 discharges " as the pathology of epilepsy — a thing I earnestly repudiate. la 
 1870 I did not make two degrees of functional changes, and spoke only ef what 
 I now call the first degree (a). 
 
26 
 
 hours goes on in a proper way. By nutrition of some kind the 
 cells of the discharging lesion attain high tension and very un- 
 stable equilibrium, and occasionally discharge suddenly, exces- 
 sively, and temporarily ; their stability is alter their discharge 
 below normal ; by continuance of this abnormal nutrition they 
 reattain high tension, or no more fitswould ensue. What is the 
 " base fashion " of nutrition of these cells ? It does not follow 
 that the cells are more nourished, a lthough they are certainly 
 worse nourished. So to put it, they may be less nourished in 
 quantity and worse nourished in quality. The nutrition must be 
 such that it alters the composition of nervous matter of the cells, 
 and in such a way that it becomes more explosive. 
 
 I have so often spoken on this subject that I will only mention 
 the hypothesis that the nutrient fluid bathing the cells is com- 
 paratively stagnant, and that in consequence there is inferior 
 nutrition. I suggest that there is " substitution nutrition," phos- 
 phorus compounds becoming more nitrogenous, or nitrogenous 
 compounds more nitrogenised. I may illustrate by the well-known 
 case of glycerine becoming explosive (nitroglycerine) when some 
 of its hydrogen is replaced by nitric peroxide. The Composition 
 of this substance is altered, but its Constitution remains the same. 
 It may possibly be that the mass of the explosion of nerve ceils, 
 both in health and convulsion, is of non- nitrogenous matter, as is 
 the case in the normal discharges of muscle. But the suggestion 
 is that a nitrogenous substance is the " pivot" of the metabolism 
 of nervous matter both in physiological and in hyperphysiological 
 states. 43 I suppose the greater nitrogenisation of the material of 
 nerve cells makes it highly explosive, but that the constitution of 
 that material and the morphological structure of the cells remain 
 the same. If this hypothesis be valid, there are presumably de- 
 grees of substitution (as there are in the three chloracetic acids, 
 for example), and consequently degrees of high explosiveness. It 
 maybe that when a patient's fits "get worse," the original ful- 
 minate becomes more fulminant by still greater nitrogenisation, 
 as well as that more cells become part of his fulminate. The ab- 
 normal nutrition leading to change of composition is a patho- 
 logical process, whilst the high explosiveness it produces is a 
 functional change. Surely it is the change of function which 
 should be called a functional change. Whether these speculations 
 he valid or not, it is a warrantable inference that the nutrition of 
 the cells of the discharging lesion goes on, that it goes on wrongly, 
 and that some material of the cells does become highly explosive. 
 
 Now I consider differences in sizes of cells with regard to their 
 normal and morbid nutrition. 
 
 For theoretical reasons, and after the observations of Betz and 
 Mierzejewsky, I suggested 44 that those centres of the motor 
 region which especially represent small muscles (eyes, face, and 
 hands) will have a greater number of small cells than those which 
 especially represent the large muscles of the limbs. I think this 
 is generally true of the " motor region." And I suggest that it 
 accounts for the great frequency of onset of epileptiform fits in 
 the hand and face, for reasons to be given presently. The "leg" 
 centre contains many large cells, but it also contains some small 
 cells. Bevan Lewis's researches, to which I am very greatly in- 
 debted, show that the parts of the motor region representing small 
 
 43 "Whether the chief product of the metabolism of any tissue be a proteid 
 substance, or a fat, or a carbohydrate, proteid substance is the pivot, so to 
 speak, of the metabolism, and nitrogenous bodies always appear as the products 
 of metabolism." (Foster, Physiology, pt. ii, p. 828). 
 
 44 Medical Press and Circular, August 23rd, 1876. 
 
27 
 
 muscles have most small cells. He says — and this bears on the 
 remark I made on the leg centre — " that alongside the largest 
 pyramidal cells are numbers of others of the smallest dimensions " 
 (italics in original) 45 so that the discharging lesion of the " leg 
 centre " may be made up of small cells. 
 
 Although it is convenient for some purposes to say " small 
 muscles," the expression is not exact. For I urge once more that 
 nervous centres do not represent muscles, but movements. I will 
 substitute the expression " small movements " for " small muscles," 
 and that of "large movements" for "large muscles." As these 
 terms, the best I can think of, are vague, their meaning must be 
 taken as defined here. Most of the movements of the hand are 
 " small " according to the definition I now give of " small move- 
 ments." The parts moved have little mass, and in most of the 
 operations they serve in there is little more added mass. The 
 muscles are small and numerous, and in most operations by the 
 hand their movements are of little excursion, of short duration, 
 and rapidly changing. Short, prompt, and frequent liberations of 
 small quantities of energy ■will be required for these successions of 
 "small" different movements; I submit that the nervous arrange- 
 ments for these movements of the hand have small cells, and very 
 many small cells. Most of the muscles of the shoulder are " large 
 movements," according to the following definition. The muscles 
 are large and few ; there is much mass to move, the whole arm to 
 lift, and the added mass is often great in some of the operations 
 they serve in, as in lifting weights the hand takes up. In most 
 operations they serve in, the movements are of large excursion, of 
 comparatively long duration, and are comparatively little chang- 
 ing. They will require persisting and slow liberations of large 
 quantities of energy by, I suggest, comparatively few and large 
 cells. We may have " large " and " small " movements of different 
 parts of one limb in a single operation; When the arm h put 
 forth there are " large movements " of the shoulder, upper arm, 
 and forearm; and when the fingers, thus put forward, elaborately 
 explore an object, there are " small movements" ol the hand. 
 
 But although parts which most often engage in " large move- 
 ments " have large muscles, yet there may be " large movements " 
 of parts having small muscles. If we grasp an oar and pull a 
 boat, the whole of the musculature of the arm serves in a succes- 
 sion of similar large movements (and then subordinately to other 
 movements). For these, I suppose, will be discharges of large 
 cells, even for the movement of the bands grasping the oar; there 
 is. indeed, then but one unchanging movement of the whole hand, 
 a large movement as defined, all the small muscles serving to- 
 gether as if one muscle. 
 
 A principle of representation is here in question ; we have not 
 only to do with sizes of cells, but also with numbers of cells, and 
 therefore with the volume of different centres. Schroeder van 
 der Kolk, illustrating by the case of the sturgeon, which has large 
 muscles and few cells in its spinal cord, pointed out that there is 
 not a mere relation between quantity of grey matter and size of 
 muscles, but that the grey matter is greater in proportion to the 
 compl-xity of. movements of muscles. This shows that we have 
 never to forget that centres represent movements of muscles, not 
 mere muscular masses. I have several times drawn attention to 
 Herbert Spencer's statements bearing on this question. 46 One 
 remark he makes is: " In proportion to the number, extensive- 
 ness, and complexity of the relations, simultaneous and successive, 
 
 * 5 A Text-book of Mental Disease, p. 106. 
 ^Psychology , 2nd ed., vol, i, pp. 35, 55, 67, 
 
23 ■% 
 
 that are formed among different parts of the organism, will be 
 tbe quantity of molecular action -which the nerve-centres are 
 capable of "disengaging " Spencer takes count of both impres- 
 sions and movements; I am illustrating by movements alone. 
 The much greater volume of the middle motor centres is in acroid 
 ■with the fact that they represent vastly more numerous different 
 movements than the lowest motor centres do ; the muscles repie- 
 sented by both levels are. of course, the same, being in each case 
 all the muscles of the body; hence the middle motor centres con- 
 tain 'many more cells and fibres than the lower centres do. Pie- 
 sumably the same principle applies in detail. According to Hoi 8- 
 ley and Beevor, the thumb and index finger, which have a great 
 number of different movements, chiefly " small movements," have 
 a large area of representation in the motor region. As to the 
 trunk area of the cortex, I quote what Horsley and Schafer say : 47 
 " It certainly is not a little remarkable that the numerous and 
 powerful muscles of the spine should be governed from so small a 
 portion of the cerebral cortex, but it is to be remembered that the 
 movements of which the spine is capable are comparatively few and 
 simple " (no italics in original). Tbe supposition is that parts hav- 
 ing many small and greatly changing movements are especially 
 represented by small cells and by many small cells, and that parts 
 having but few and little changing (''tonic") movements are re- 
 presented by large cells and by few large cells. 
 
 The size of cells is a very important matter with regard to their 
 nutrition. Both in health and in disease small 48 nerve cells will 
 he nourished more quickly than large ones when both are bathed 
 in the same nutrient fluid. (From diminished nutrient supply the 
 small cells will atrophy sooner than larye ones.) The smaller cells 
 wdl become highly unstable sooner than large ones during morbid 
 nutrition. It certainly is the fact that most epileptiform seizures 
 hegin in parts having " small movements," in parts represented by 
 areas of the cortex having most small cells. As I have pointed 
 out, they may begin in the large muscles of the upper arm ; it 
 would be begging the question to say that in these cases the 
 smallest cells of the "shoulder centre" are those which first be- 
 come highly unstable. The size of cells bears also on rates of dis- 
 charge. 
 
 Four hot iron balls will become cold much sooner than the same 
 mass of iron in one ball having the same quantity of heat as the 
 four balls together have. From discharge of four small cells, 
 which are together equal in mass to that of one large cell, there 
 will be, I submit, a liberation of energy in a shorter time than by 
 the large cell, supposing equal quantities liberated in the two 
 cases. Hence another reason for fulmination of the highly 
 unstable cells of discharging lesions if these cells are small. As 
 heing somewhat illustrative, I may refer to different sizes of 
 grains of powder used as ammunition ; slowly burning (pebble) 
 
 « Phil. Trans, vol. clxxix, 18S8, B. 
 48 " Other things equal, the smallest cells will soonest become unstable. A 
 mass of nervous matter in many small cells will 'present a much larger surface 
 to the contact' of nutrient fluid than the same mass in a few large cells" 
 (Harveian Lectures, Med. Times and Gaz., January 11th, 1879). My attention 
 was first directed to this subject on reading Spencer's Biology, where he ex- 
 pounds his theory of growth. A brief statement of Spencer's theory will be 
 found on p. 220 of The Evolution of Sex, by Geddes and Thomson, from which I 
 quote " In spherical and all other regular units the mass increases as the cube 
 of the diameter, the surface only as the square." I refer the reader to Ross's 
 great work, Diseases eflhe Nervous System, vol. i, p. 13, where he deals with the 
 significance of differences in eizes of nerve cells with regard to normal and 
 abnormal nutrition and its consequences. 
 
23 
 
 powder is required for large cannons, quickly burning (fine- 
 grained) powder for firearms. 
 
 To repeat the several hypotheses, Epileptiform seizures begin 
 most often in parts of the body having " small movements ;" these 
 movements are represented by nervous arrangements having many 
 small cells. 49 Small cells present a more extensive surface to 
 nutrient fluid than the small quantity of grey matter in large 
 cells, and will be more quickly nourished than large ones are. 
 Nerve cells become highly unstable from an abnormal nutrition, 
 such that, although their structure and the constitution of their 
 material is unaltered, that material becomes of more nitrogenous 
 composition, and thus more explosive. Small cells become highly 
 unstable more readily than large ones do; thus discharging lesions 
 are supposed to be especially of small cells. A rapid liberation of 
 energy overcomes greater and more numerous resistances than a 
 slower liberation of an equal quantity of energy. Small cells 
 liberate their energy in a shorter time than large ones; hence the 
 currents developed by fulminates of small cells overcome greater 
 and thus more numerous resistances than would fulminates of 
 large cells, and hence produce more convulsion and greater range 
 of convulsion. 
 
 We have assumed that the nutrition of the cells of the discharg- 
 ing lesion is continuous, and have supposed in effect that the 
 nutrient fluid is comparatively stagnant. But how is this com- 
 parative stagnation brought about ? This brings us to pathology, 
 commonly so-called. We have to distinguish between what I 
 may call the coarse pathology of a case and its immediate 
 pathology. 
 
 [Tn the remainder of the lecture the production of discharging 
 lesions by tumours and by arterial occlusion was considered.] 50 
 
 * 9 The movements, speaking most generally, represented by the cerebrum, 
 are, I suppose, numerous different punctuated movements (many and different 
 "small movements"). Presumably those represented by the cerebellum are, 
 in comparison, few and little different movements, movements as it were 
 gliding into one another (few and similar " large movements"). It is interest- 
 ing to observe that the structure of the cerebellum is more uniform than that 
 of the cerebrum, and that those of the cells of the cerebellum which are pre- 
 sumably motor are large and of nearly equal size. The movements for bracing 
 up the spine in standing or walking, and the separate movements of the lega 
 and arms in walking, will require comparatively continuous supplies of large 
 quantities of energy. (I believe, however, that the cerebrum and cerebellum 
 are both engaged by contemperation in at least all extensive operations.) 
 £° See Jouenal, July 21st, 1888. 
 
30 
 
 Lecture III. 
 
 After-Effects of Epileptiform Fits. — Paralysis due to Cortical Ex- 
 haustion. — Analysis of a Case. — Yariatiors in Degree and in 
 Range of Post- epileptiform Paralyses. — Hemiplegia, Povt-epilep- 
 tiform and from Destruction of Motor Part of Internal Capsule 
 contrasted. — Post- epileptiform Defects of Speech.— The Negative 
 and Positive Elements of these Defects. — The Psychical and 
 Physical. — The Concern of the Riyht and of the Left Half of the 
 Brain in Speech. 
 
 I hate now to consider the After Effects of excessive nervous 
 discharges in cases of epileptiform seizures. This part of our sub- 
 ject is of extreme importance ; the presumption is that from the 
 study of the comparatively simple post- epileptiform conditions 
 we shall obtain a basis for the interpretation of post-epileptic 
 conditions. It is for this reason that I go into some detail as to 
 the former. 
 
 There is not rarely after epileptiform seizures local temporary 
 paralysis; 51 and sometimes aphasia with it. For the present I 
 speak of paralysis only. In this inquiry we have no direct con- 
 cern with paralysis, temporary or permanent, owing to destruc- 
 tion (by clot, softening, or any other pathological process) of any 
 part of the brain, not even if the malady set in with a convulsion. 
 
 I must particularly mention cases in which there are both (1) 
 permanent paralysis— for example, imperfect hemipl. gia ; and (2) 
 occasional epileptiform seizures, the convulsion beginning in some 
 point of the muscular region paralysed and involving part or the 
 whole of it, and sometimes also parts beyond that region. In 
 these cases the two opposite functional states — destru< tion of 
 some nervous elements which represented complex movements, 
 and high instability of some otturs which still represent other 
 complex movements of the same muscles — are side by side in one 
 part of the cortex (or the latter of cortex and the foimer of fibres 
 passing down from it). After a paroxysm in such a case there may 
 be temporary increase of the paralysis. For my present purpose, 
 which is only an attempt to explain the nature of the sequence 
 (paralysis after convulsion), I shall exclude these cases, and deal 
 only with what I may call uncomplicated cases — that is, with 
 those in which there is only paralysis immediately when epilepti- 
 form seizures have ceased, such paralysis being temporary (un- 
 less, of course, the fits recur at short intervals). Something has 
 to be said, however, regarding certain of the so-called uncompli- 
 cated cases. 
 
 In some cases in which there is no discoverable paralysis in the 
 intervals of the fits, except for a short time after one there msy be 
 indirect evidence of a negative functional state of a few fibres of 
 the second segment of the kinetic route. That evidence is foot 
 clonus and exxggerated knee-jerk on the same side as that in 
 which the convulsion occasionally starts. I mean, of course, 
 cases in which these abnormal tendon reactions are producible at all 
 times, although in a greater degree just after a fit. It may be 
 that severely careful tests would show some quasi-trifi'mg paralysis 
 
 si This paralysis was long ago described by Todd under the name " Epileptic 
 Hemiplegia." 
 
31 
 
 — loss of a very few complex movements. I shall here ignore 
 this slight inferential paralysis, and speak of such cases as " un- 
 complicated." 
 
 Toe term post-epileptiform paralysis will be used to include all 
 paralyses tiie immediate sequels of epileptiform seizures. Arbit- 
 rary divisions may be made, speaking of range only. (1) Terminal 
 paralysis, as of a hand ; (2) monoplegia, as of an arm ; (3) hemi- 
 plegia; and (4) a range which is not generally admitted — some 
 degree of slight universal paralysis. I hold the hypothesis (essen- 
 tially that of Todd and Alexander Bobertson) that there is ex- 
 haustion of central nervous elements, including fibres of the 
 second segment of the kinetic route, and that this is produced by 
 the sudden and excessive discharge in the prior paroxysms 
 These nervous elements are exhausted, not otherwise injured, so 
 that recuperation is prompt, and the corresponding paralysis is 
 temporary. There is a sequence of two opposite functional states, 
 euperpositive of the first degree («) in the paroxysm, and then, 
 after the paroxysm, negative. But there is often more than a 
 negative functional state in the post-epileptiform condition. We 
 may find increased tendon reactions implying a superfunctional 
 state of the second degree (b) of lowest motor centres. The 
 duplex nature of these post-epileptiform conditions must be borne 
 well in mind. 
 
 The term "exhaustion" has been objected to; general bodily 
 prostration is, of course, not meant; but, as said, exhaustion of 
 nervous elements in a particular part ol the central kinetic route. 
 There are, I suppose, degrees of exhaustion, and no doubt of 
 different numbers of nervous elements of the kinetic route in 
 different cases. But illustrating by the extremest degree, the sup- 
 position is that nervous elements of the route, after their excessive 
 "exercise" in the fit, are left "fatigued" to the degree of u'ter 
 impotence. The nervous elements exhausted in post-epileptiform 
 paralysis are, I suppose, in the same state as are the motor nerve 
 fibres of the scintic nerve going to the cut-off leg of a frog after 
 strong faradisation of that nerve trunk ; the leg is convulsed by 
 the faradisation (stage analogous to epileptiform seizure), and is 
 next paralysed (stage analogous to post-epileptiform paralysis) 
 because its motor fibres are exhausted by the unnaturally high 
 functioning they have been artifically compelled into. A closer 
 analogy may be stated, although the case to be instanced is a com- 
 plicated one. The motor Derves of a frog, poisoned by a very large 
 dose of strychnine, lose function partly by the direct action upon 
 them of that poison, but partly (this is what is relevant) through 
 exhaustion — "the exhaustion of over-use due to the intense 
 activity of the nerve during the stage of spasm." 52 
 
 Not only the term, but the hypothesis itself is objected to. I 
 will consider other hypotheses. The paralysis has been ascribed 
 to cerebral congestion consequent on arrest of respiration in the 
 preceding seizure. It is difficult to see how cerebral congestion, 
 even if we grant that it can produce paralysis, could be so ex- 
 quisitely local as to produce what we sometimes observe, paralysis 
 of one arm only, or even of but part of one. Again, absolute para- 
 lysis of a limb is found after seizures nearly limited to that limb, 
 in which seizures there was no arrest of respiration and (if that is 
 thought to bear on the question) no loss nor even defect of con- 
 sciousness ; the patient may talk throughout an attack in which 
 an arm is involved, and after which it is temporarily paralysed. 
 There is the hypothesis that the temporary post-epileptiform para- 
 lysis is owing to a small extravasation of blood in the brain, 
 
 £ 2 See Wood's Therapeutics, 7th edition, pp. 258-9. 
 
32 
 
 caused, I suppose it is meant, by congestion consequent on arrested 
 respiration in the preceding seizure. I admit that very small 
 clots may cause local paralysis, and that such paralysis may be 
 transitory. But the post-epileptiform paralysis is — that is in my 
 experience — always of the parts which were first and most con- 
 vulsed in the prior fit ; it would be marvellous if a small haemor- 
 rhage happened locally in one-half of the brain, so as to produce 
 temporary paralysis of the parts first and most convulsed, and 
 happened in the same place in every fit the patient had. Besides, 
 if arrested respiration could cause cerebral haemorrhage by leading 
 to sudden great congestion of the brain, we should find very local 
 paralysis after fits of the epileptic kind, and we do not ; according 
 to current opinion there is no paralysis at all after seizures of 
 this kind. I shall exclude the two hypotheses just dealt with. 
 
 Post-epileptiform paralysis has been ascribed to inhibition by 
 some medical men whose hypotheses deserve respectful consider- 
 ation. Growers believes that discharges in epileptic fits some- 
 times inhibit ; he thinks that temporary paralysis is found in some 
 cases after a purely sensory discharge which does not next dis- 
 charge motor centres, but inhibits them. In some cases of epilepti- 
 form seizures the patient tells us that his arm " falls dead," there 
 being no spasm in it, whilst the face of the same side is being con- 
 vulsed. This, so far as I can learn, is a paroxysmal, not a post- 
 paroxysmal paralysis, but possibly it remains for a short time 
 after the convulsion of the face has ceased. I express no decided 
 opinion as to the validity of the inhibition hypotheses. I think it 
 possible that there may be discharge spreading slowly in a motor 
 centre of the middle level, excessive enough to cause slight after- 
 exhaustion of some of its elements, although not one strong 
 enough to overcome the resistance of lowest motor centres, and 
 thereby to produce actual convulsion. I have spoken of " feelings 
 of convulsion " in which there is no actual convulsion, but do not 
 know whether there was any degree of post-paroxysmal paralysis 
 of the parts " ideally convulsed." I go on to consider how far the 
 hypothesis I hold, essentially that of Todd and Robertson, accounts 
 for the facts of different cases. 
 
 There is exhaustion of the cortex after artificially induced epi- 
 leptiform fits in some lower animpls, as Franck and Pitres 53 have 
 shown; th^v use the term " Epuisement cortical post-6pileptique." 
 They write : 5i " Le phe"nomene de l'6puisement cortical conse"cutif aux 
 acces d'epilepsie partielle (what I call epileptiform seizures) est 
 tres facile a constater." The " 6puisement " is transitory ; it lasts 
 a quarter or half an hour. By artificial excitation of the part of 
 the cortex in question, as the exhaustion diminishes, simple move- 
 ments are first producible, and later epileptiform seizures, but 
 not, for some time, is an attack provoked so intense as before 
 the " epuisement." I think that the researches of these dis- 
 tinguished physicians countenance the inference 1 have drawn that 
 the exhaustion in post-epileptiform conditions, although local, is yet 
 widespread in the "motor region;" that besides "running down" 
 of the cells of the fulminate there is also running down of the col- 
 lateral normal (stable) cells which were compelled by the fulmi- 
 nate to discharge excessively. Franck writes : 55 " Cet Epuisement 
 ©5t tout local, non point qu'il se borne exclusivement a la portion 
 circonscrite du champ moteur excit6 en premier lieu, mais il est 
 limited lazonemotricedececoteV' Exhaustion in the sense of general 
 bodily prostration is not meant, for Franck and Pitres point out 
 
 53 Arch, de Phys., 1883. 
 
 5* Op. cit. 
 
 55 Fonctions Motrict-s du Cerveau, pp. 90, 91. 
 
3S 
 
 that excitation, without effect on the exhausted part of the motor 
 region, when transferred to the motor region of the opposite hemi- 
 sphere, produces severe convulsions. 
 
 I will here mention an objection to the hypothesis of exhaustion 
 made to me by a physician whose opinion 1 respect highly, that 
 during post-epileptic coma there may occur a convulsion affecting 
 all parts of the body, which I say are then paralysed. But what 
 I mean by paralysis in post-epileptic coma is loss of some most 
 complex movements, represented by the highest centres of all or 
 very many parts of both sides of the body ; there is retention of 
 other most complex movements represented by those centres ; 
 most of the complex (middle centres) and simplest movements 
 (lowest centres) being also retained. Further, it is quite certain 
 that an arm which the patient is quite unable to move in the 
 slightest degree after an epileptiform seizure may be suddenly 
 seized with another severe convulsion (I am supposing a case in 
 which neither in nor after the paroxysm consciousness is lost). 
 This, however, is only reasoning by analogy, and I admit that the 
 interpretation of the last-mentioned case is to me most difficult. 
 
 I will now give an illustration of post-epileptiform paralysis. 
 It may be taken to be an artificial one, but it is essentially that of 
 a patient whose case I reported. 56 
 
 A man, B., was seemingly (1) quite well when he arrived at my 
 house after a walk of about a mile. (It is convenient to speak of 
 this as the "first stage," not, of course, of the fit, but of the 
 dramatic occurrence I am relating.) (2) (a) A fit began in the toes 
 of his left foot. 57 (5) The whole leg was gradually involved, the 
 spasm passing up the limb. In about eight or ten miantes the 
 convulsion ceased, when (3) the leg was found to be (a) paralysed, 
 and (b) there was exaggeration of its knee-jerk and clonus of the 
 foot. (4) In six hours or less he was seemingly well again, cer- 
 tainly he was then rid of his paralysis; and next day (I did not 
 test his tendon reactions before) his knee-jerks were normal and 
 there was no foot-clonus. Let me consider the four acts of this 
 drama. 
 
 (1) The patient was not really well when he arrived at my 
 house. He had a persistent discharging lesion, presumably of a 
 few cells of his leg centre (perhaps only of some of those of the 
 hallux centre); so to say, he always carried it about with him, or, 
 to speak more precisely, it was a persistent ^wasz-parasitical 
 hyper-functionable part of himself. 
 
 (2) (a) The discharging lesion did function and that excessively, 
 and possibly produced the initial spasm (of the toes) by its sole dis- 
 charge; but (b) next, as a fulminate, by overcoming the resistance of 
 (discharging) other cells of the leg centre it compelled these nor- 
 mal stable cells to discharge — compelled them to co-operate in its 
 excess. 58 So much for the discharges (primary and secuudo-primarj ) 
 
 56 Medical Times and Gazette, February 12th, 1881. 
 
 57 Referring to the real case {op. cit.) the patient said that in all his seizures 
 the first " sensation " was to the outer side of the ball of the gre*t toe; very 
 likely I missed a very earliest stage, one possibly of spasm limited to the big 
 toe. 
 
 58 In the real ease {op. cit.) the left arm was slightly convulsed. The current 
 hypothesis would be that, in causing this part of the fit, the discharge spread 
 from the leg centre to the arm centre. This I cannot disprove. Yet I think it 
 an equally legitimate hypothesis that the discharge causing the slight move- 
 ments ot the arm in this case was of those elements of the " leg centre" repre- 
 senting subordinate movements of the arm. No doubt, of course, in a severer 
 fit other centres of the motor region would be discharged. As implied in several 
 parts of these Lectures, I do not accept the current doctrine of Localisation. 
 The minute investigations of the monkey's cortex by Horsley and Beevor go 
 strongly against it. To me the "leg cen;re" is only a part of the "motor 
 region" where most special movements of the leg are represented, and where 
 
34 
 
 of the cortex (middle motor centres). That there was a super- 
 normal activity from cortex excessively discharging to and of the 
 mn-cles of the leg convulsed is certain. The route of the nu- 
 merous and rapidly succeeding nerve impulses from the hyper- 
 physiological cortical process would be certain fibres of the 
 corona radiata, of the internal capsule, of the crus cerebri, pons, 
 and medulla of the right side, then of fibres of the left lateral 
 column (possibly also of the second and third sets of interconnect- 
 ing fibres, both of which I shall ignore here) up to the anterior 
 horns (some lowest motor centres) ; so far the second segment of 
 the kinetic route is concerned. The resistance of the cells of 
 these lowest motor centres would be overcome (secondary dis- 
 cbarges), and the impulses (presumably increased in number) 
 would then he of fibres of the nerve roots from those centres, 
 thence of the continuing fibres of nerve trunks and their branches 
 to the end plates of the muscles (third segment of the kinetic 
 route); the resistance of the muscles would be overcome, and 
 there would finally be great " explosive decomposition" of muscle 
 substance (tertiary discharges). 
 
 (3"! The paralysis signified exhaustion of nervous elements pre- 
 viou»ly excessively functioning in the paroxysm. There would be 
 exhaustion of cells of the cortex, not only of those of the dis- 
 charging lesion, but also of tho.-e collateral stable cells which it, 
 as a fulminate, compelled to discharge excessively. There would 
 he exhaustion, too, of the fibres passing down from both sets of 
 cells. The hyper-kinetic route, or at least part of it, would now 
 he a hypo-kinetic tract. There would be exhaustion as low down 
 as certain lowest motor centres; these centres were therefore 
 exalted in function (second degree of superpositive functional 
 change), hence the increased tendon reactions. 
 
 (4) The paralysis had passed off; the patient could walk well. 
 Next day the knee-jerks were normal. There was recuperation 
 of the exhausted nervous elements. No doubt the cells of the 
 discharging lesion (after the fit, stable below normal) began at 
 once by gradual morbid nutrition to re-attain high tension and 
 "very unstable equilibrium — " began to prep»re for the next fit." 
 
 So far as I have seen, post-epileptif orm paralysis is always most 
 of the parts which were first and most convulsed in t'e pre- 
 ceding paroxysm, as in the case of the patient B. This corre- 
 spondence is denied by some eminent physicians; further obser- 
 vations will settle the matter. It is an important one, for, 
 according to the view I take, post-epileptiform paralysis adds no 
 evidence to that afforded by the prior convulsion as to the seat of 
 pathological changes in the cortex. If, however, there is not the 
 correspondence I suppose, the case is very different and the situa- 
 tion is a most difficult one. 
 
 I think there is a relation of proportionality between the 
 severity of the epileptiform fit (severity of the discharge) and 
 the subsequent temporary paralysis (amount of exhaustion). I 
 should have thought this a truism if it had not been expressly 
 denied. It is averred that whilst, after the epileptiform tind of 
 
 subordinate movements of the arm and of other parts of the body are also repre- 
 sented (the same, muta'is mut ndis, for other centres). The researches of Sher- 
 rington (Journ. of Physiology, vol. x. JVo. 5 seem to me to be counter to the cur- 
 rent doctrine. He writes, " after lesion in the leg area, enrioaching little 
 
 if at all upon the cortex of the arm area, the degeneration in the cord s'opped 
 short in great part in the cervical region, especially in the cervical enlargement. 
 Again, after lesion in the arm area, encroaching li.tle if at all upon the cortex 
 of the leg area, the degeneration in the cord extended down through the dorsal 
 into the lumbar and even throughout the sacral region of the cord." He sug- 
 gests, however, that the fibres descending from the arm area into the lumbar 
 region are visceral, 
 
35 
 
 seizure there is often decided paralysis, there is not, as a matter 
 of fact, any whatever after the severer fits of the epileptic kind. 
 I demur to the "fact," believing that whilst after a limited 
 epileptiform seizure there is often great local paralysis, loss of 
 many movements of a small part of one side of the body, there is 
 after a severe epileptic fit widespread paralysis, loss of few 
 movements of most, if not of all, parts of both sides of the body. 
 Indeed, I submit that the whole condition of bodily impotence 
 after a severe epileptic fit is paralysis, and that, speaking gene- 
 rally, there is really more paralysis than is found after severe 
 epileptiform seizures. 
 
 The relation of an epileptiform fit to the sequent paralysis, or, 
 more exactly, the relation of the two opposite functional states, 
 discharge, and subsequent exhaustion, is not a simple relation. 
 
 According to the hypothesis I hold, there should always be some, 
 however little, paralysis after an epileptiform seizure, at least some 
 in the parts first and most convulsed, however slight the attack 
 miy have been. Trifling degrees of paralysis are easily over- 
 looked. This deserves remark. Once more I urge that more or 
 less paralysis from negative central lesions is always loss of more 
 or fewer movements ; it is not to be thought of merely as loss of 
 power in muscles. There may, for example, be loss of the most 
 special (the most "delicate") movements of the muscles of the 
 hand with retention of other, the next most special (the 
 " coarser") movements of those muscles. I will illustrate by a case 
 of imperfect post-epileptiform paralysis. 
 
 After a slight epileptiform seizure starting in the hand, the 
 patient may have difficulty in picking up a pin, and may yet be 
 able to gra-p strongly. There is clumsiness of movement, or per- 
 haps some may say " loss of muscular sense." These terms must 
 not let us overlook the fact that the slightly abnormal motor con- 
 dition of the hand is a double condition one of two opposite ele- 
 ments. There is in the case supposed difficulty in picking up the 
 pin, because a few most special movements of the hand are lost 
 (so far paralysis, negative element) ; the pin has to be picked up 
 by the next most special movements remaining, which are now 
 the most special of the movements (positive element) ; they do not 
 serve so well as the most special would have done ; hence the 
 operation is " clumsy." 59 
 
 From such quad- trifling paralysis as that indicated, loss of a few- 
 most special movements of the muscles of the hand, there are met 
 with after severer epileptiform seizures beginning in the hand 
 degrees of loss of next and next most special (or, equivalently, of 
 the next and next more general) to loss of all movements of the 
 muscles of it, and of some movements of the rest of the arm too ; 
 there is then no " clumsiness," for no movements of the hand re- 
 main to do anything. 
 
 59 Here is an illustration of the principle of duplex symptomatology of nervous 
 maladies, a'l.d that the positive element is often owing to activity or to over- 
 activity of nervous arrangements umouched by any pathological process. The 
 movements by which the pin is picked up are theoutcome of activity of bealthy 
 nervous arrangements. To blame thfse, to speak figuratively, for the clumsi- 
 ness of the operation is to ignore that they are doing their best in the evil cir- 
 cumstances. The piinciple is most important, if it applies, as I think it dues, 
 throughout the nervous system, from the symptomatology of a case of paralysis 
 of an ocular muscle to that of cases of insanity ; in the former case it is quite 
 certain that most of the symptomatology answers to activity of perfectly healthy 
 nervous arrangements of the highest centres ; the negative mental symptoms 
 in cases of insanity alone correspond to disease; they signify Dissolution of 
 part of the highest centres ; the coexisting positive mental symptoms signify 
 Evolution going on on a lower level of those centres. The very same principlels 
 displayed in cases of aphasia. 
 
56 
 
 The last remark introduces another part of our subject. It ina- 
 plies that post-epileptiform paralysis varies in a double way, (a} 
 in degree (number of movements lost) and (b) in range (number 
 of parts of which movements are lost). 1 think, in harmony with 
 what was said in Lecture II, on compound order of spreading of 
 convulsion, that degrees of difference between what may be called 
 little and great paralysis after epileptiform seizures are not 
 simple degrees of more or less amount of paralysis, nor simple 
 degrees of more or less range; there are degrees of both, there are 
 differences of Compound Degree. After the slight epileptiform 
 seizure alladed to in the foregoing, there was slight paralysis 
 limited to the hand. If that patient had had a somewhat severer 
 fit, he would have had after it more paralysis of the hand (loss 
 of more movements of it) and greater range of paralysis (loss of 
 some movements of the nest part, say the forearm). 
 
 That there was exhaustion lower than the cortex in B.'s case, 
 exhaustion also of fibres of the second segment of the kinetic- 
 route, that is, up to the lowest motor centres, is signified by the 
 exaggerated tendon reactions. I have spoken of the lowest motor 
 centres and of the third segment of the kinetic route (fibres from 
 them to the muscles) and of the muscles as not being exhausted in 
 B. at the time when his leg was paralysed. It would, however,, 
 be remarkable if a few elements of these lowest parts of the 
 kinetic route were not hypo-kinetic to some trifling degree after 
 the hyper-kinesis during the convulsion — if there were not after 
 their excessive exercise some exhaustion of a few of their ele- 
 ments. No doubt, being more strongly organised structures, the 
 lowest motor centres and muscles are less easily exhausted by the 
 discharge, and, if exhausted, recuperate soonest of all parts of the 
 route. After some epileptic fits (Westphal, Gowers, Beevor) the 
 knee-jerks are temporarily lost; in these cases some lowest motor 
 centres, the lumbar nuclei (as Gowers suggests) are probably tem- 
 porarily exhausted. For my part, I think it likely that during 
 the post-epileptiform paralysis in B., although his knee-jerks were 
 exaggerated, there was some trifliDg hypo kinesis of the lowest 
 part of the route, that the hypo-kinetic tract was from cortex up 
 to and of the muscles, although, no doubt, elements of the cortex 
 and of the first segment of the kineticroute were most exhausted. 
 The muscles in such cases act to faradisation (I did not test B. 
 this way) as well as do those of the fellow leg. But if we were to 
 take a case of paralysis, such as that of a man a few years age 
 under my care who had nineteen hundred and forty-five fits — each 
 beginning in his left thumb, involving the left arm, fixing his 
 ehest, and turning his head to the left — in about fourteen days, 
 and whose left arm was absolutely paralysed in the intervals, we 
 might find by fine testing (what we did not find in that patient by 
 ordinary testing) some slight degree of reduction of faradic reaction 
 of the muscles, or, if not, of reduction of faradic or galvanic re- 
 action in their nerve-trunks, of the part paralysed. In B. the 
 exaggeration of the knee-jerk would not show that all the cells of 
 the anterior horn which is concerned with that jerk were intact; 
 a few of the smallest cells may have been exhausted. 
 
 In a case of amyotrophic lateral sclerosis there is wasting of 
 some cells of anterior horns (hence the atrophy of some muscular 
 elements) and increased activity of other cells of the same horns 
 (hence the increased tendon reactions of the same muscles). Thia 
 case shows that the functional condition of different cells of the 
 same anterior horns may be diametrically opposite, and that the 
 symptomatology in the muscular region which the horns supply 
 znay be of two correspondingly opposite elements. I shall pui 
 
57 
 
 aside the hypothesis of exhaustion of a Tery few elements of the 
 lowest motor centres, and of the third segment of the kinetic 
 route, and of the muscles in such cases as that of B. for the present, 
 but yet do not abandon it. I shall speak of the hypo-kinetic tract 
 in such cases as that of B., as if it extended no lower than fibres 
 of the lateral column, and as not involving any cells of the lowest 
 motor centres in which they end. It would be reasonable to grant 
 that it was at least of that depth in B.'s case. 
 
 It will be well to draw attention to resemblances and differences 
 between post-epileptiform hemiplegia and the hemiplegia which 
 is the result of destruction of the motor part of the internal cap- 
 sule; for the moment assuming that the explanation given of the 
 former is correct, and that the statements accepted by most phy- 
 sicians as to the latter are accurate. I will call the former Hemi- 
 plegia E, the latter Hemiplegia D. 
 
 First, for resemblances, taking to begin with, for comparison 
 and contrast, recent Hemiplegia D. The regional (paralytic) affec- 
 tion is the same as in Hemiplegia E, and in each depends on a 
 negative state of the same strand of fibres, those interconnecting 
 the right middle motor centres and the left lowest motor centres. 
 (I shall speak only of what I called the first set of fibres.) .Now 
 for differences. In Hemiplegia E (as in the case of the patient B.) 
 there is exaggeration of the tendon -eactions, in Hemiplegia D 
 they are, we shall suppose, normal. Correspondingly for the nega- 
 tive lesions; in Hemiplegia E the negative lesion is of the whole 
 length of the interconnecting fibres mentioned (and spoken of be- 
 fore as the second segment of the hyper-kinetic route become a 
 hypo-kinetic traet) up to, but not involving, the lowest motor 
 centres. In recent Hemiplegia D the negative lesion is quite 
 local, a breaking up of the capsular part of the interconnecting 
 fibres ; the rest of the segment, its wnole extent below the capsular 
 break, being normal, 
 
 Now for old cases of Hemiplegia D ; in these there are increased 
 tendon reactions ; in them a negative lesion secondary to the cap- 
 sular one has been established; there is then a negative state (de- 
 struction) of the fibres (lateral sclerosis) below, and added on to, 
 the local capsular lesion ; 60 that is to say, in the case of Hemi- 
 plegia E there is established at once the state of things which 
 only occurs late in Hemiplegia D. So long as the exhaustion lasts 
 (so long as the central kinetic route is hypo-kinetic) in Hemiplegia 
 E, the situation is the same as in old cases of Hemiplegia D ; it is 
 the same for the time being whether the nervous elements in 
 question are functionally dead, as in the former, or actually dead 
 (broken up and wasted away), as in the latter. 
 
 In a popular use of the word cause, these negative conditions 
 may be said to cause the increased tendon reactions, just as, popu- 
 larly speaking, opening floodgates is said to cause water to flow. 
 But using the word cause properly, it is an impossibility that the 
 negative functional state in either Hemiplegia E or D can cause 
 anything ; a nothing cannot cause the something, the superposi- 
 ive condition for exaggeration of the knee-jerks. If Bastian be 
 right in his conclusions as to the effect of absolutely complete 
 transverse lesion of the dorsal or cervical cord (see Lecture I), the 
 hypothesis of a change in the anterior horns, produced hy any sort 
 of pathological process, is no longer tenable, as he has pointed out. 
 I shall, however, consider other arguments against that hypo- 
 thesis, which are supplied by cases of post-epileptiform paralysis. 
 
 It is agreed upon that the increased tendon reactions in cases 
 
 69 Sherrington has traced the " descending wasting" in the lateral column o5 
 the cord of the monkey as low as the coccygeal nerve roots, 
 
38 
 
 of hemiplegia depend on exalted " excitability " (a superpo°itive 
 functional .state) of nervous elements of some anterior horns. 
 There are different hypotheses as to the process by which that 
 exaltation is produced, and thus as to the exact state of the cells 
 of the anterior horns concerned. Two questions may be asked. 
 Is the abnormal condition of the cells the result of any patho- 
 logical process involving the horns themselves, or are the cells 
 healthy although in greater activity ? I reply to the first question 
 negatively, and to the second affirmatively. 
 
 I take, for further consideration, an old case of Hemiplegia D, 
 one in which lateral sclerosis is established. Ard now I consider 
 rigidity as well as increase of the knee-jerk (limiting illustration 
 to that one tendon reaction), both of which superpo-itive pheno- 
 mena it is agreed upon imply exaltation of function of cells of 
 anterior horns. One hypothesis as to the production of exaltation 
 of function of the anterior horns (some of the lowest motor centres) 
 is that the same process which leads to destruction of fibres of the 
 lateral column produces, when come to the horns with which 
 they are in physiological union, increased " excitability" of their 
 cells ; the same process, on this hypothesis, produces loss of func- 
 tion (destruction) of fibres and its physiological opposite super- 
 function of cells. The hypothesis of Charcot deserves to be re- 
 ceived with profound respect. Eeferring to the condition of the 
 cells of the anterior horns, as it corresponds to rigidity in hemi- 
 plegia, he considers it the theory which best accounts for facts 
 we daily witness in cerebro-spinal diseases, that there is a purely 
 dynamic lesion of their ganglion cells— a state analogous to that 
 produced by strychnine. If this state of the cells be produced by 
 an extension to them of the same process as that which has de- 
 stroyed fibres, it (however slight the alteration effected may be, 
 and however insusceptible of microscopical demonstration the 
 change may be) must be considered to be the result of a pathological 
 process. 
 
 This hypothesis cannot apply to Hemiplegia E ; in this case it 
 is not likely that there are caused by the excessive discharge a 
 negative state of fibres, and a super-positive one of cells. All the 
 more that after some epileptic fits there is found exaltation of the 
 knee-jerk, and after others loss of it ; differences, explainable on 
 differences, in the severity of the discharge in the paroxysm, and 
 on the different " depths" of exhaustion after it ; there is a nega- 
 tive functional state in both, but lower down in the kinetic route, 
 of cells of anterior horns, when the knee-jerks are absent,. 
 
 My hypothesis is that both in Hemiplegia E and in old cases of 
 Hemiplegia D, the cells of the anterior horns are perfectly healthy. 
 They are, I submit, untouched by the pathological process causing 
 the lateral sclerosis or by any other, and are simply over-active, 
 partly from loss of control, and partly from non-antagonised cere- 
 bellar influx (second degree (b) of superpositive functional change). 
 But I do not state the hypothesis of loss of control as I used to 
 do. There is sometimes exaggeration of the knee-jerk in recent 
 cases of hemiplegia, and this may be owing to sudden loss of cere- 
 bral (middle motor centres) control. I shall, however, speak as if 
 the current opinions were correct — that both the increased tendon- 
 reactions and rigidity "wait for" the descending degeneration in 
 cases of Hemiplegia D. I now adopt an hypothesis put forward 
 by Gowers, which is to the effect that close upon the anterior 
 horns there are small inhibitory centres, the anterior horns being, 
 in his nomenclature, "muscle- centres." 
 
 In cases of recent Hemiplegia D, before the degeneration in the 
 ateral column, these local inhibitory centres are intact, and the 
 
knee-jerks are not exaggerated. But I suggest that in such 
 cases of Hemiplegia E as that of the patient B., they are ex- 
 hausted as well as are fibres of the lateral column ; after those epi- 
 leptic fits, when the knee-jerks are lost, both the inhibitory centres 
 and the muscle centres are exhausted. Now taking old cases of 
 Hemiplegia D, and dealing with rigidity as well as with the ex- 
 aggerated knee jerk, I would say that the " descending" process, 
 when it reaches the anterior horns, destroys the small local in- 
 hibitory centres ; the anterior horn proper, " the muscle centre" 
 now bereft of its inhibitory centre, is uncontrolled. The cells of 
 the " muscle centres " are not invaded by any pathological pro- 
 cess ; they are healthy, but yet over active from loss of control 
 This hypothetis as to old cases of Hemiplegia D invokes but one 
 mode of action — destruction. That hypothesis brings the facts of 
 Hemiplegia E into harmony with those of long-standing cases of 
 Hemiplegia D ; it accounts for the absence of increased tendon re- 
 actions in recent cases of Hemiplegia D. Certainly cases of Hemi- 
 plegia E have to be considered as well as ca-*es of recent and old 
 Hemiplegia D in all hypotheses as to the nature of increase of the 
 knee-jerk in cases of brain disease. 
 
 Of any degree of rigidity of muscular regions paralysed — 
 during the paralytic stage or part of it I mean of course — after 
 epileptiform seizures I know nothing. Possibly I have overlooked 
 it. But Franck and Pitres have made very important observa- 
 tions on a muscular rigidity after epileptiform seizures produced 
 in dogs and cats. Of course i; might be said that this active 
 muscular condition is owing to a slighter degree of the same cor- 
 tical discharge which produced the obvious fit — that it is not 
 post-paroxysmal, but a great attenuation of the paroxysm itself. 
 But these distinguished observers tell us that the rigidity is alto- 
 gether different from the convulsion in the attack itself. And 
 what is decisive is that ablation of the whole motor zone does not 
 cause disappearance of the rigidity. 61 It seems to me that the 
 hypothesis I have taken from Gowers, exhaustion of inhibitory 
 centres, and consequent over-activity of the muscle-centres of 
 the anterior horns to which they belong, best explains these 
 phenomena. 
 
 Although heyond mentioning it I have not in this Lecture 
 spoken of cerebellar influx, I believe it to be a factor in the causa- 
 tion of the exaggerated tendon reactions in Hemiplegia E, and of 
 these and the rigidity in old cases of Hemiplegia D — that in both 
 there i3 loss of control and unantagonised cerebellar influx, and 
 thus that the two positive symptoms are owing to the unhindered 
 activity of perfectly healthy structures. 
 
 In some cases of epileptiform seizures at, or close upon their 
 onset, there is loes or, at least, defect of speech with very little local 
 spasm. (We have, of course, no concern in this inquiry with any 
 cases of le petit mal). I shall, however, speak only of temporary 
 abnormal affections of speech, not in, but after the paroxysms — of 
 what is present when all convulsion is over. 62 I explain post- 
 epileptiform defects of speech in the same way as I did post-epi- 
 leptiform paralyses, supposing there to be in the former exhaus- 
 tion of nervous arrangements of " Broca's region." 
 
 Just as the e are cases of epileptiform seizures with permanent 
 paralysis of the side of the body in some part of which the con- 
 vulsion starts and in which there is more paralysis, temporarily, 
 
 61 Les Fonctions Moines du Cirveau by Francois Franck pp. 88, 89. 
 62 " There is a peculiar class of cases of epileptic hemiplegia in which the 
 exciting cause of the epileptic fit at the same time damages or greatly injure* 
 voluntary power and speech." (Todd, Nervous Diseases, lecture xv.) 
 
40 
 
 of that side after a paroxysm, so in some cases of epileptiform 
 seizures there may be permanent defect of speech and a temporary 
 increase of that defect after a paroxys n. I shall omit considera- 
 tion of these important cases. So far as I have seen, abnormal 
 affections of speech are found after fits with right-side " signal 
 symptoms." They certainly occur after left-sided fits, as Dr. Herman 
 Weber has pointed out. 63 
 
 I have only once known abnormal affection of speech to occur 
 after a fit beginning in the foot (rigbt); that case is of no particu- 
 lar value in localisation, as at the necropsy two large blood cysts 
 were found, causing extensive compression of each cerebral hemi- 
 sphere. Temporary defect of speech after epileptiform seizures 
 beginning in the (1) right hand or (2) right side of face or tongue, 
 or Doth, is not rare. 
 
 The " abnormal talking " after some eleptiform seizures has long 
 seemed to me 64 not to be what couli commonly be called aphasia; 
 it often sounds like a melange of an articulatory defect and of a 
 speech defect. It may be that in these cases there is not only ex- 
 haustion of some elements of Broca's region, but also of elements 
 of the corresponding lowest (bulbar) motor centres ; if so, the situ- 
 ation is analogous to cases where, after epileptic fits, the knee- 
 jerks are absent, from, presumably, exhaustion of (lumbar) lowest 
 motor centres. I think the "abnormal talking" referred to most 
 likely to occur after epileptiform fits beginning in the cheek or 
 tongue. What may be distinguished as "pure aphasia" is itself, 
 physically regarded, a paralytic affection in the sense of loss of 
 complex ('' articulatory ") movements of the tongue, palate, lips, 
 etc. ; so the melange spoken of, if the hypothesis suggested be 
 valid, is physically a mixture of loss of some complex (middle 
 lesrel) and some simplest (lowest level) movements of those 
 parts. The subject is not a simple one, because along with right 
 hemiplegia from destructive lesions we sometimes meet with a 
 difficulty of articulation (I used to call it " ataxy of articulation") 
 when there is no obvious disability in the tongue, palate, lips, 
 etc. 65 There is one thing which must be mentioned in this con- 
 nection. We should not consider that the inability of a patient 
 who is more or less aphasic after an epileptiform seizure to put 
 out his tongue when told is evidence of implication of lowest 
 motor (bulbar) centres ; for in these cases the tongue moves well 
 in other and simpler operations. Moreover, this inability is often 
 found in cases of aphasia from desrructive cerebral lesions, and 
 lasts too long in those cases for the easy explanation of " shock ;" 
 in them implication of bulbar centres is out of the question. This 
 curious symptom is loss of a most special movement from a corti- 
 cal or sub-cortical lesion; in that sense it is paralysis. It is no 
 way regarded a speech or articulatory defect. To put out the 
 tongue when told is what is called a " voluntary " movement, just 
 a* lifting the arm when told, or the card-sharper's shrug (Lecture 
 II) is. 
 
 I shall ignore the hypothesis mentioned, and deal only with 
 eases which would be admitted by all to be defects of speech 
 proper, that is to be " of an aphasic character" — cases in which 
 mucti speech of an imperfect kind remains, the utterances being 
 
 63 Trans. Inte-national Med. Congress, 1881, vol. ii, p. 19. 
 
 ^''Stidy of Convulsions," St. And Med. Grad. Assoc, vol. iii, 1870; Rey- 
 noVis'j System of Medicine, vol. ii, second edition, p. 287 ; see also Gowers' 
 Epdeusy. p. 101. 
 
 ,° 5 Dr. Charles K. Mills, of Philadelphia, relates, University Medical Medicine, 
 November, 1889, a very important case of "Softening of the Face-area with 
 Oro-lingual Monoplegia." 
 
41 
 
 clearly articulated. In most of these the prior convulsion starts in 
 the right hand, and, I have thought, most often, not in the thumb 
 or index finger, but in the hand generally or in the ulnar fingers. 
 Of course there are many degrees of abnormal affection of speech 
 of this kind, and it varies according to the time elapsed since the 
 cessation of the fit. 
 
 I have not observed post-epileptiform loss of speech, but only 
 defect of speech (" partial aphasia"). I shall use the term Defect of 
 Speech E, or Partial Aphasia E. The term " defect of speech" is 
 equivocal, as is also the term " partial aphasia;" it really covers two 
 opposite elements, negatively loss of some speech, and positively re- 
 tention of the rest of speech. 66 The patient gets words out clearly, 
 and may even get out simple appropriate replies, such as "Very 
 well," and may answer correctly by "Yes" or "No," or both. This 
 is the positive element : it is the inferior speech to which the 
 patient is reduced. But he is not able to reply correctly except 
 by " Yes " and " No," and by other simple and very general ex- 
 pressions; he is not able to converse properly on simple subjects; 
 he is unable to explain anything at all complex. These statements 
 give the negative element : the speech lost. It is of extreme 
 importance to distinguish the two opposite elements of the 
 symptomatic condition. It is plainly impossible that the 
 post-epileptiform exhaustion {vide supra), which I suppose 
 there is of part of Broca's region, can answer to the 
 patient's utterances — to the positive element : that negative 
 functional state of nervous elements of the region answers to the 
 patient's loss of some speech. His utterances, positive element, 
 however inferior as speech, answer to activities of nervous 
 arrangement of Broca's region which are healthy — which are in 
 all ways normal except possibly for slight " loss of control." Here 
 is another illustration of the statement that part of the symptom- 
 atology of nervous maladies is the outcome of activity of healthy 
 nervous arrangements. 67 
 
 We must bear well in mind that speech is a psychical process. 
 Nowhere is it more important to distinguish the psychical from 
 the physical. I say once more that psychical symptoms are to 
 medical men only signs of what is wrong in a material system. Our 
 task as physicians is to ascertain the nature of the physical pro- 
 cess correlative with speech, or more exactly the nature of the 
 
 66 My present concern with aphasia is only a very limited one. I need not 
 always supply the obvious qualifications to statements made in the text. The 
 expressions "loss of some speech" and " retention of the rest of speech" must 
 not be taken literally as if they meant that the patient had lost certain words or 
 propositions of the (his) English language altogether, and had retained the rest 
 of them intact. Such is an impossible condition of things when an aphasic 
 patient corrects his mistakes. But the statements may be taken literally for 
 the mere purpose of a limited illustration. I do not suppose that there are fixed 
 nervous arrangements— some for these words or syllables (properly movements 
 corresponding to syllables) only and some for those only. I would rather than 
 hold this mechanical doctrine go to the other extreme, and say that there are 
 no nervous arrangements for movements in any centres except at the time when 
 these and those motor nervous elements are functioning together in a particular 
 temporary grouping. 
 
 67 It is one thing to locate the negative lesion which destroys speech (renders 
 a person unable to speak aloud), and quite another thing to say that " speech 
 resides "in any particular part of the cortex. Words, or some other symbols, 
 serve us during thought ; when a man is thinking " gold is yellow," words in 
 propositions are as certainly concerned as they are when he says that aloud. I 
 submit that the highest centres ("organ of mind") must be engaged during 
 speech, whether external or internal, notwithstanding that a negative lesion of 
 a part of the middle motor level produces aphasia. Not believing in abrupt 
 localisations, I do not mean by using the term "Broca's region" to limit the 
 negative lesion productive of aphasia to that part of the lowest frontal convo- 
 lution which enters into the " motor region." As is the custom, I shall neglect 
 
 concern which the highest centres must have with speech. 
 
42 
 
 anatomical substrata of words (syllables). No one denies that the 
 physical basis is of cells and fibres, but this is a morphological 
 account of it. The anatomical basis is, I submit, of morphological 
 elements so grouped as to form certain sensori-motor nervous ar- 
 rangements. These, I presume, are audito-articulatory — that is, 
 they are nervous arrangements representing certain auditory im- 
 pressions along with certain corresponding complex (articulatory) 
 movements of the tongue, palate, lips, etc. We suppose the motor 
 elements of these sensori-motor arrangements to be of Broca's 
 region. In the case of Defect of Speech E our ultimate concern 
 is with the two opposite functional states of these motor ele- 
 ments which answer respectively to the two opposite psychical 
 elements of the double symptomatic condition, which is unfor- 
 tunately named (defect of speech or partial aphasia) after the 
 negative element only. The motor elements alone of the sensori- 
 motor substrata of speech are damaged. I submit that in Defect 
 of Speech E there is correlative with its negative psychical ele- 
 ment exhaustion of some nervous arrangements of Broca's region, 
 which is productive of loss of some of the complex movements 
 of the muscles of the tongue, etc. (" articulatory muscles "). And 
 I submit that the speech remaining possible is correlative with 
 integrity of other nervous arrangements of that same region for 
 other complex movements of the same muscles; these healthy 
 nervous arrangements function during the inferior speech remain- 
 ing possible to the patient, and produce the corresponding articu- 
 latory movements. I have now to support the conclusion that 
 the inferred exhaustion of some elements of Broca's region in 
 Defect of Speech E produces paralysis in the sense of loss of com- 
 plex movements of the tongue, etc. 
 
 There is often with Defect of Speech E some temporary decided 
 paralysis of (loss of many movements of) the right arm. This 
 statement, however, although allowable clinically, is not a scientific 
 one. "We should not in a realistic inquiry group together a 
 psychical symptom and a physical one as if when so considered 
 they were symptoms of the same order. In harmony with what 
 I have said, the things really comparable are respectively loss of 
 some complex movements of the muscles of the tongue, etc. (cor- 
 responding to the negative element in the defect of speech), and 
 loss of some complex movements of the muscles of the arm (in 
 both of movements represented by the middle motor centres). In 
 this sense the two co-existing things are paralyses. On this basis 
 alone is their concurrence intelligible and their comparison and 
 contrast possible. With regard to the defect of speech, it is to be 
 vividly kept in mind that the fellow part of the right middle 
 motor centres (centres of the left half of the brain) for other com- 
 plex movements of the muscles of the tongue, etc., and that the 
 right and left lowest (bulbar) motor centres for simplest move- 
 ments of those muscles are intact. 
 
 Those who do not follow me in distinguishing the psychical from 
 the physical will, perhaps, think that I am confounding difficulty 
 of articulation, a physical symptom, with a mental symptom (with 
 "aphasia"). The fact is that lam making an absolute distinc- 
 tion between speech, which is a psychical process, and its corre- 
 lative anatomico-physiological process, which is purely physical. 
 It is only the physical bases of words (or properly of syllables) 
 which I assert to be sensori-motor nervous arrangements repre- 
 senting complex movements of the muscles of the tongue, etc., in 
 association with complex combinations of auditory impressions. 
 I only say that correlative with the negative psychical element in 
 defect of speech there is the physical loss of some complex move- 
 
43 
 
 ments of the tongue, etc. Still, it may be thought that I have no 
 clear ideas on the difference between aphasia, a mental defect, and, 
 for example, " bulbar paralysis." In reality I have said that the 
 " bulbar centres" (some lowest motor centres) are quite intact in 
 Defect of Speech B. In bulbar paralysis there is loss of the 
 simplest movements of the tongue, etc., and the negative lesion 
 is bilateral (of certain motor centres of both halves of the lowest 
 level), whereas in all cases of aphasia there is loss of complex 
 movements of tbe tongue, etc., and the negative lesion is of 
 motor centres of but one (left) half of the middle level, and the 
 lowest motor (bulbar) centres are intact. Is not this difference 
 enough ? 
 
 The objection may be made that, whilst in the case of post- 
 epileptiform paralysis with partial aphasia there is obvious 
 paralysis of the arm, there is, as a matter of fact, none of the 
 tongue, palate, lips, etc. It will be well in further exposition to stop 
 speaking of Defect of Speech E, and to take in illustration a simpler 
 (although much more serious) case, one of loss of speech (" com- 
 plete aphasia ") from a destructive lesion, say from softening of 
 Broca's region. I shall suppose, however, that there is retention 
 of " yes " and " no." 68 Here the negative element is loss of 
 nearly all speech ; the positive element being only retention of 
 " yes " and " no." I shall call this case Loss of Speech D, or 
 Complete Aphasia D ; but the word K loss " is to be taken as 
 qualified by " except for retention of ' yes ' and ' no.' " We 
 shall suppose there to be, as there nearly always is, right 
 hemiplegia. 
 
 To say that the patient Aphasia D is speechless because he 
 has lost the memory of words is to give no explanation of his 
 inability to speak, any more than it is an explanation of tbe 
 paralysis of his right arm and leg to say that it is owing to loss 
 of volition. All psychological explanations of physical inabilities 
 are merely verbal. Admitting for the sake of argument only that 
 loss of memory of words is a correct description, our concern as 
 physicians is with the physical condition correlative with that 
 psychical loss. A part of the patient's brain has disappeared, pro- 
 bably the hinder part of the lowermost (left) frontal convolution 
 (and no doubt more brain adjacent) has been changed to defluent 
 stuff which is brain no longer ; we shall speak of this as " destruc- 
 tion of Broca's region." I repeat that the lesion causes paralysis. 
 I admit that there is no disability in the muscles of the tongue, 
 palate, lips, etc., in their commonplace services, as in eating, 
 drinking, swallowing, etc. ; I admit it readily, because I only 
 mean that there is loss of the complex articulatory movements of 
 those muscles. There is nothing discoverably wrong with these 
 muscles except for the slight facial and lingual paralysis which is 
 a part of hemiplegia, right or left. The case illustrates that we 
 may have loss of some movements of certain muscles without dis- 
 coverable disability of those muscles. The seeming paradox in the 
 particular case under remark is easily explained by Broadbent's 
 well-known hypothesis. 
 
 In our speechless patient, not only are the lowest most motor 
 centres of both halves of the bulbar part of the lowest level for 
 simplest movements of the muscles of the tongue, etc., intact, but 
 
 68 To speak is not merely to utter words, but to propositionize. The patient 
 spoken of in the text, although not absolutely speechless, is so, except that he 
 has only the use of the two most general of all propositions ; I say "the u=e of" 
 supposing that in the case taken for illustration the patient can assent and 
 dissent by them. If he only uttered them at random, or if they were only signs 
 of emotion, they would not serve propositionally, they would then be of no 
 speech value. 
 
44 
 
 also, what is most important, complex movements of these 
 muscles of both sides remain represented in the right half of the 
 brain (middle motor centres). Hence, on account of those re- 
 maining representations, there is no obvious disability of the 
 muscles of the tongue, etc., in their commonplace services. Taking 
 the simple representation by the lowest level for granted, the as- 
 sumption is that the muscles of both sides of the tongue, palate, 
 lips, etc., are represented by complex movements in each half 
 of the brain, though no doubt more especially in Broca's 
 region than in the fellow-region of the right. Here is an 
 exemplication of Broadbent's hypothesis. Horsley and Schafer 
 write : " The face area, although we have so called it for conveni- 
 ence sake, actually gives rise to movements not only of the facial 
 muscles, but also of the whole of the upper part of the aliment- 
 ary tube (mouth, throat, and larynx) It is physiologically 
 
 remarkable from the fact that many of the movements which 
 result from its excitation are apt to be executed bilaterally, which 
 is only exceptionally the case with excitation of the other areas 
 (except that for the head and eyes)." 69 Hence destruction of 
 neither Broca's region nor its fellow-part of the right middle 
 motor centres produces disability in the commonplace services of 
 the muscles of the tongue, etc., although beyond all question some 
 movements of them are lost. But destruction of part of both 
 halves does, 70 as some cases of double hemiplegia show, notably 
 one recorded by Dr. Thomas Barlow. 71 
 
 So that, so far from " confounding cases of aphasia with cases of 
 bulbar paralysis," I am making a very definite distinction. So far 
 am I from comparing loss of speech, considered as a negative 
 psychical symptom, with the physical symptoms of bulbar para- 
 lysis, that I urge that there is not even a basis for any reason- 
 able contrast of the two ; psychical symptoms and physical sym- 
 ptoms are " not on the same platform." Eegarding the physical 
 condition correlative with the aphasia and that of the case of bulbar 
 paralysis, the cases are alike in that there is in each loss of move- 
 ments of the same muscles ; on this basis I urge their resemblance 
 as cases of paralysis. At the very same time I urge the differences 
 between loss of complex movements of the tongue, etc., repre- 
 sented by certain middle centres of but one half (left) of the brain 
 in cases of Loss of Speech D, and loss of simplest movements of 
 those parts represented by certain lowest (bulbar) centres of both 
 halves of the lowest level in cases of bulbar paralysis. 
 
 Furthermore, the tongue, palate, and lips not only act well in 
 eating, drinking, swallowing, etc., in Loss of Speech D, but also 
 when the patient says " Yes " and " No." He may have a stock 
 utterance, as " Awful," " Oh, my God! " etc. He may when excited 
 swear or get out other elaborate ejaculations; none of these are 
 speech proper — they are not propositions, but compound inter- 
 jections ; the patient cannot repeat (" nay ") what he ejaculates. 
 The articulation of all these utterances is perfect, and I presume 
 that no one would deny that the articulatory movements are 
 effected by perfectly healthy nervous arrangements. They are 
 effected, I submit, by those of the undamaged right half of the 
 brain, of course with subagency of lowest (bulbar) motor centres 
 of both halves. Still neglecting, as everybody else does, the con- 
 cern of the highest centres with speech and with morbid affec- 
 tions of it in disease, I submit that as regards speech the right 
 
 69 Phil. Irans., 1888. 
 
 tft §u,ch cases are sometimes called cases of cortical bulbar paralysis ; they ay& 
 
 double cortical ; the bulbar centres are intact, 
 
 Ti Jovrnai.1877. 
 
45 
 
 half of the hrain is the automatic half, and that the left is that 
 half in which automatic action ceases into what we call voluntary 
 
 aC The"positive condition of our patient, Loss of Speech D, is that 
 he retains the propositional use of " yes " and " no," physically two 
 complex articulatory movements of the tongue, etc. 
 
 Now I draw attention to the fact that the patient who never 
 speaks, never does make (with the exceptions stated) the complex 
 movements of articulation, which I say are lost Instead ol ex- 
 SSg that he does not do so because he has lost « the memory 
 of words," I submit that he never makes them because the 
 nervous arrangements for those movements have disappeared— 
 that he has not got those complex movements. Once more I urge 
 that what is psychically aphasia is physically paralysis. 
 
 Moreover, the part destroyed in the case of aphasia is motor, 
 no one denies since the researches of Hitzig and Ferner that the 
 homologous part in lower animals is motor. Hence, there is 
 nothing for destruction of it to produce in these animals except 
 paralysis. Mark that although destruction of that part of the 
 "motor region "on the left in man produces no disability of .the 
 muscles of the tongue, etc., of either side (beyond the slight right 
 facial and lingual paralysis spoken of as part of hemiplegia) dis- 
 charge of that part develops movements ot these muscles ol both 
 sides ; by subagency, of course, of certain lowest motor centres ol 
 both halves of the lowest level, develops a contention of complex 
 and of simplest movements of those muscles. From discharge ol 
 the part on the left are revealed the movements, the loss ol which, 
 upon destruction of that part, is masked by compensation by the 
 fellow part of the right half of the brain. Yet there may be dis- 
 charge (impulses passing by route of the callosal fibres) ol the 
 fellow part on the right consequent on the primary discharge ol 
 the left. I mention again that Sherrington has traced degenerated, 
 fibres from a unilateral lesion of the lower end of the fissure ol 
 Eolando into bath halves of the pons and medulla. 
 
 Hence I conclude that the patient hemiplegic and speechless 
 (aphasic) has not only lost very many complex movements ol the 
 muscles of the right arm and leg, but that he has also lost many 
 complex movements of muscles of both sides of the tongue, lips, 
 etc. ; the conclusion is that his whole physical condition is, and is 
 nothing else than, paralysis in the sense of loss of movements 
 
 The condition is fundamentally the same in the Defect ol Speech 
 E but the negative element (loss of some speech) is less, and the 
 positive element (retention of much speech) is greater. Here, 
 again, it will be well to illustrate by the case of a destructive 
 lesion (a much smaller one than in Loss of Speech D), by softening, 
 destroying but little of Broca's region ; I will call this case Delect 
 of Speech D. There is not rarely from such a pathological 
 process a condition essentially like that in some eases ol Detect ; oi 
 Speech E. Let us suppose that in the case of Defect ol Speech D the 
 patient frequently makes mistakes when he talks, either by using 
 wrong words or by being reduced to very " automatic utterances, 
 such as " Very well," or that he often uses roundabout expressions 
 such as " It won't come out here" (which, eked out by appropriate 
 pantomime, meant "I can't make water"). And yet, to simplify 
 exposition, I will take the patient's saying "hat for carpet 
 only, that to be a sample of the whole of his condition. Here we 
 see the necessity of distinguishing the two elements, negative 
 and positive. It is certain that the softened brain (really what is 
 brain no longer; there is a hole filled with detritus of nervous 
 elements^ cannot be the cause of the patient's saying " hat ; that 
 
46 
 
 is the speech left, and is owing to activity of the part of Broca's 
 region which remains perfectly healthy. 72 This, his positive con- 
 dition in speech, is sampled by his saying " hat." His negative 
 condition is alone owing to "disease," and is sampled by his in- 
 ability to say " carpet." 
 
 The negative element in Defect of Speech D is a minor degree 
 of that in Loss of Speech D ; the positive element is a major de- 
 gree of the positive element (" Yes " and " No " only) in Loss of 
 Speech D ; in the former the dissolution of Broca's region is 
 shallow and the level of evolution high, whilst in the latter the 
 dissolution is very deep and the level of evolution very low, if 
 there be any in that region. The two cases differ in double de- 
 gree. In the Defect of Speech D there is much speech left, and 
 there are very many mistakes ; in the Loss of Speech D there is 
 very little speech left, and there are no mistakes, the patient cor- 
 rectly assenting to and dissenting from (by " Yes " and " No ") all 
 statements made to him. 
 
 Now for the physical condition in Defect of Speech D. Answer- 
 ing to the slight negative element, there is loss of but a few com- 
 plex articulatory movements represented in Broca's region ; 
 answering to the positive element there is retention of many other 
 such movements ; or we may say, limiting illustration to the 
 samples, there is loss of the complex movements answering to in- 
 ability to say " carpet," and retention of the complex movement 
 answering to saying " hat." If anyone says that a word (pro- 
 perly a syllable) is not a movement he is agreeing with me; for I 
 am contending that activity of nervous arrangements represent- 
 ing certain complex movements (with, of course, corresponding 
 impressions) of the tongue, etc., is only the anatomico-physiolo- 
 gical process going on during the appearance of what are the 
 psychical things — words. I need only say that the softening in 
 Defect of Speech D is the negative lesion equivalent to the ex- 
 haustion in Defect of Speech E. The utterances both in Defect of 
 Speech E and D are the outcome of activities of perfectly healthy 
 nervous arrangements. The negative lesion in both is dissolution ; 
 in each the speech, however imperfect, as certainly signifies evolu- 
 tion going on on a lower level, as the speech of healthy persons 
 does evolution going on on the normal level. 
 
 I have admitted that the patient in Defect of Speech E and D may 
 correct his mistakes — that after saying the wrong word "hat " he 
 may immediately say the right word " carpet," — and I will here 
 admit that when he says " hat " he knows that the word is not the 
 right one. But this does not invalidate the principle of the 
 explanation. For convenience of exposition I made the arbit- 
 rary assumption that there are fixed and unalterable nervous 
 arrangements for particular movements, in this case for com- 
 plex movements of the tongue, etc., corresponding to syllables. 
 I think the seeming difficulties could be met if, abandoning that 
 assumption, I were to go into detail as to the constitution of 
 nervous centres. At any rate, the attempt is to give a 
 materialistic explanation of the physical condition in aphasia, 
 without confounding the concomitant psychical states with that 
 physical condition. I submit that the explanation is, at any rate, as 
 good as the psychological explanation. If we do invoke the latter 
 so-called explanation, we have not only to account for, to take the 
 samples again, " loss of memory " for " carpet," but also for the 
 
 72 To give another example, surely it is impossible that when the patient re- 
 ferred to in the text said, " It won't come out here," there was engagement of 
 nervous arrangements which were " diseased " in any way whatever ; the " dis- 
 ease" was the cause of his inability to say " I can't make water." 
 
47 
 
 " over-memory " for " hat." "When the patient cannot say "carpet," 
 why does he utter anything ? Why does " hat " come out instead ? 
 And admitting that the " loss of memory " for " carpet " is only 
 temporary, and that next moment the patient can say " hat," we 
 have to account for the temporary defect of " memory " and for 
 its sudden restoration for that case. Moreover, if the patient says 
 " hat " and knows that it is wrong, he can only know it by there 
 being revived in him the word " carpet " at the very same time ; 
 certainly these two words must be revived mentally; there is then 
 "verbal diplopia." If it is admitted that the psychological state- 
 ments as to the aphasic conditions are correct descriptions, those 
 who make them are just as much bound as anyone else to seek 
 the abnormal material conditions of the several phenomena of 
 " amnesic aphasia." And bearing in mind the proof given by 
 Ferrier, Horsley, Scbafer, Beevor, Sherrington, and many others, 
 that the region damaged is motor, a merely morphological account 
 of the physical condition in aphasia will not suffice. If anyone 
 says that he cannot understand how activities of motor nervous 
 arrangements can correspond to words, I would remind him that, 
 except the popular psychologist, no one pretends to understand 
 how any material conditions correspond to any psychical states. 
 
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