No. 2768.

SEPTEMBER 16, 1876.

LecturesON THE

PHYSIOLOGICAL PATHOLOGY OFTHE BRAIN.

Delivered at the Royal College of Physicians of London,July, 1876,

BY C. E. BROWN-SÉQUARD,M.D., F.R.S., F.R.C.P.LOND., ETC.

LECTURE 1. - part VII.

ON A GREAT VARIETY OF FORMS OF PARALYSIS DUE TODISEASE IN ONE SIDE OF THE BRAIN.

A lesion in parts of the anterior or the middle lobes of the brain,outside of the supposed volltntary motor apparatus, can pro-duce complete and persistent hemiplegia-A lesion of centralparts of the brain or of the cerebellum, without the interven-tion of any marked alteration of or pressure upon parts ofthat apparatus, can also produce hemiplegia- Value of thosefacts against the admitted views concerning the causationof paralysis-Differences, as regards the power of producingparalysis, between parts of the brain belonging to the volun-tary motor apparatus and other parts of that nervous centre-Complete and persistent hemiplegia may appear, althoughdisease occupies but a part of the supposed voluntary motorapparatus in the brain-Facts relating to the corpora striataand to the pons Varolii-Contrast between two cases of dis-ease of the pons Varolii.THE parts of the brain of which I have not yet spoken

will not detain us long. I will only say a few words ofthe middle and the anterior lobes, then of the central parts,and lastly of the cerebellum, leaving aside the convolutions,because in another lecture I will revert to them in a com-

plete discussion of the facts showing how erroneous is thesupposition that in some small parts of the surface of thebrain there are distinct organs deserving the name of

psycho-motor centres. What I have said of the posteriorlobe cannot entirely be said of the anterior or of the middlelobes, on account of their containing those supposed centres,and also on account of their contiguity to the supposedvoluntary motor ganglions, and of the radiation into themof the fibres of the internal capsule and of the corporastriata. When a lasting and more or less complete paralysisis caused by even a not very extensive lesion located in theanterior or the middle lobes, it is invariably considered asdependent on some alteration of the corpora striata, or ofthe corona radiata, or of the so-called psycho-motor centres.But, as will be fully shown in another lecture, how can thisview be maintained in the presence of facts proving-1st,that a slight lesion of one of those lobes can produce a com-plete paralysis ; 2nd, that a considerable lesion of one orboth of those lobes can exist without any marked paralysis,3rd, that the paralysis due to a lesion in one or in both ofthose lobes can appear either on the opposite or on thesame side ?

Many facts show that a lesion in the most anterior partof one of the cerebral hemipheres-i. e., a part where no oneplaces any kind of voluntary motor centre-can producepara;ysis more or less complete, and lasting till death. Iwill mention but two cases, one of a tumour, the other ofhaemorrhage. In a case of Andral’s,* remarkable in manyrespects, there was a gradual paralysis, with ansesthesia, inboth right limbs, with right ptosis, caused by a smalltumour near the anterior extremity of the left hemisphere,the cerebral tissue remaining normal even near the tumour.A lesion such as that should not have produced hemiplegia,as the part of the brain it occupied does not belong to thevoluntary motor apparatus. The ptosis and the anaesthesiaare also symptoms in opposition to the admitted views. Itmay be said about this case as well as about any other in

* Clinique Médicale, fourth edition, Paris, 1810, vol. v., p. 1.

which paralysis appeared when no disease was found inother parts than in one of those which do not belong to thesupposed voluntary motor apparatus, that although notdiscovered it existed in some segment of that apparatus. Icannot, especially in cases of tumours, and of slow develop-ment of paralysis, deny that it is possible that there is someother alteration of the brain.* But, although possible,there is no proof that there is another alteration, and it isindeed an argument of very little value to maintain that oftwo lesions of the brain, one not only visible but sometimesa considerable one, and another which is not visible, it isthis last one which is the cause of a paralysis ! But thisargument, even if acceptable for cases of alterations of slowgrowth, cannot be used about cases in which a suddenlesion, well characterised by symptoms we know to belongto it, and besides found after death, coexists with a suddenparalysis which appears at the same time with those cha-racteristic symptoms. As a specimen of this I will mentionanother case of Andral’s.tCASE 9.-A man suddenly lost consciousness and fell. On

coming out of this apoplectic attack his speech was almostunintelligible, and his face and limbs were completely para-

lysed on the right side. He grew worse, and died nine daysafter the attack of apoplexy. The part of the substance of the

. brain at the anterior extremity of the left hemisphere con-tained a clot of blood as large as a hen’s egg. The clot wasat about half an inch from the anterior point of that side ofthe brain and an inch from the upper part of the surface,and it did not extend to the lateral ventricle, which, as alsothe corpus striatum, was uninjured. No alteration in anyother part of the brain.In this case no part of the supposed voluntary motor

apparatus can be considered as having caused the paralysis,which must have been produced by the lesion found-i. e.,

. a lesion of a part not endowed with the function of originatingvoluntary movements. It is clear, then, that paralysis may bedue to other causes than a mere loss of function of the partdiseased.The same reasoning leads to the same conclusion when

we find that paralysis can appear and last till death in casesof inflammation, tumour, or haemorrhage in those parts ofthe middle lobe of the brain which do not belong to thevoluntary motor apparatus. There are many such cases inwhich a small amount of blood effused either in the lower orthe lateral part of the middle lobe has caused a more orless complete hemiplegia, which lasted till death. Atrandom I take out of my notes on this point three cases-oneof tumour, the second of inflammation, and the third ofcapillary apoplexy, in parts of the middle lobe not belongingto the voluntary motor apparatus, and in which there wascomplete hemiplegia. The first of these cases was publishedby Moutard-Martin,:j: the second by Brachet,§ the third byR6dier. 11As regards paralysis caused by disease in the central parts

of the brain, especially the walls of the third and fifthventricles, it is difficult to say that the neighbouring parts,the so-called motor ganglia and the crura cerebri, have nota great share in its causation, as almost always the diseaseextends to these last parts. Still hemiplegia can appeareven when the lesion seems to be equal on the two sides,"or greater on the side of the paralysis.** In a case mentionedby Abercrombie,tt paralysis of the left arm occurred in apatient in which no lesion was found, but a clot in the iterad quartum ventriculum.As regards paralysis coexisting with disease of the cere-

bellum, I will only say now that in a number of cases it isabsolutely impossible to admit that a pressure on the ponsVarolii, and still less on the medulla oblongata or the cruracerebri, has existed, so that it is clear that that part of theencephalon, although not being either a psycho-motor centre

* Besides other kinds of alteration, there is one which everybody knowsto be rather frequent in old cases of disease of the brain; it is the secondarydegeneration which extends all along the base of the brain in certain parts.I am so well prepared to admit that this degeneration, and not the lesionwhich produced it, may be the real cause of a paralysis, that I will, in an-other lecture, describe as a distinct form of paralysis oae which seems tedepend altogether on that degeneration.t Loc. cit., p. 300.$Bulletins de la Société Anatomique, vol. xxxiv., 1859, p. 98.§ Quoted by Gintrac, loc. cit., vol. vii., p. 265.11 In Recherches sur les Paralysies, par Rendu. Paris, 1874, p. 162.If As in a case of small tumour of the corpus callosum (Aluers, quoted by

Ladame, loc. cit., No. 174, p. 184).** As in a case of Queene (Bull, de 1a So c. Anat., vol. iv., 1829, p. 35).fit Loc. cit., p. 2e6.

388

- or a motor centre like the corpus striatum, or a place of than what he saw (perhaps the plugging of branchespassage of voluntary motor conductors, can give rise to of the basilar artery); nothing was found, however, butparalysis.* "disease of that artery in one spot," and by its side

After this long examination of facts to show that parts perhaps a somewhat softened spot "no larger than aOf the brain not belonging to the voluntary motor apparatus barleycorn." There had been " palsy of the right side tocan give rise to paralysis, it is necessary, before I pass to such an extent that even the intercostals of that side didanother argument, to survey, at least summarily, the whole not act," and convulsions of the left limbs, with loss offield, and to discuss some points of a general character. vision, and other symptoms.As there cannot be the least doubt that a number of parts Andral* relates a case of complete right hemiplegia.- Of the brain which are not motor (for the sake of brevity I allied with, if not caused by, no other discovered lesion but

quality them so, meaning that they do not belong to any a very small (size of a pea) tubercle in the ancyroid cavity,part of the voluntary motor apparatus,) have, however, the with redness of several convolutions of the left hemispherepower of producing a paralysis, I think we can consider near the median fissure.as proved that a loss of voluntary movement may be due to Aberorombief gives a case in which aphasia and a completequite another cause than the cessation of the function of right hemiplegia, followed after three months by a markedthe diseased part. This being established, it is interesting amelioration of the power of motion in the leg, while theto know if there are differences between the motor parts of arm remained absolutely motionless, so long as the patientthe brain (those which belong to the voluntary motor appa- lived (fifteen years). The autopsy showed that there was aratus) and the parts which are not motor, as regards their good deal of fluid in both lateral ventricles, but no morbidrespective power of producing paralysis. Facts in very appearance in the brain, except that the meninges adheredgreat number clearly show that there are great differences. to it and to each other, at a spot the size of a shilling, on1st. Lesions of motor parts of the brain produce paralysis the upper part of the right hemisphere. No doubt it willmore frequently than lesions of the other parts. 2nd. Le- be objected that in this case there must have been an un-^&bgr;ions of motor parts generally produce more considerable seen lesion in the left side producing at the same timeand more lasting paralysis than lesions of the other parts. aphasia and a crossed hemiplegia; but, on the one hand,3rd. ParalyEis due to lesions of motor parts is more fre- aphasia can appear from disease of the right side of thequently allied with or followed by spasmodic rigidity than brain even in people who are not left-handed, and, on thethat which is caused by lesions of other parts. other hand, paralysis may appear on the side of a brain

Are we to find in these differences any proof of the cor- lesion. So that it is quite possible that the alteration foundTeotness of the old views concerning the mode of production in this case at the surface of the right hemisphere was theof paralysis in brain disease ? P Certainly not, as the motor cause of the paralysis of the right limbs and of the loss ofparts are only more able than the parts which are not motor speech. But, in case it is supposed that in the left hemi-to produce paralysis. And if we look at other facts, we find sphere there was a lesion, which, although too slight to bethat direct paralysis-the existence of which is a death blow seen, had produced the symptoms, I will say that if I admitto the admitted views about the causation of paralysis-can that supposition my argument becomes perhaps more power-occur as well from disease of the motor parts as from lesions ful, as then a lesion too small to be seen had been able firstof the other parts. Besides, we find that considerable to produce, and then to maintain for fifteen years, a completealterations and even complete destruction of parts can exist paralysis of the right arm and an incomplete paralysis ofwithout the appearance, or at least any marked degree, of the right leg.paralysis, whether the lesion exists in motor parts or in the It would be very easy to show that with limited altera.-- other parts, or in both simultaneously. And if the supposi- tions (due to inflammation, tumours, embolism, &c.) of thetion is made that each half of the brain has the power to intra-ventricular corpus striatum, the crus cerebri, and theact in place of the other-to replace it in case of alteration pons Varolii, there is often a complete and persistentpreventing it from fulfilling its functions, so that the ab- paralysis. Those cases are too frequent to deserve proofs.sence of paralysis, when one side of the brain is alone dis- I, therefore, will now give a few cases of hsemorrhage in theeased, would not show that the old views rejuvenated by corpus striatum and the pons Varolii, showing that a limitedthis supposition must be given up,-then I will say, and alteration of each of those parts can produce a complete andwill show by and by, that there are cases of considerable persistent hemiplegia. Dr. R. B. Toddt gives a case ofalterations of motor parts of the brain on the two sides sudden and complete paralysis of the left side, followed bywithout any marked paralysis. death after several weeks. In the centre of the rightFrom this discussion, and from the facts mentioned about corpus striatum there was a small cavity containing blood

parts of the brain which are not motor, it results clearly and softened cerebral tissue. With the view now generallythat paralysis can appear otherwis’3 than as an effect of loss of -admitted that the conductors of the orders of the will tofunction of the part diseased. If paralysis in such cases is muscles only partly pass through the corpora striata, hownot such an effect, it must be due to some influence exerted was there such a paralysis when the lesion not only did notby the part diseased or its neighbourhood on other parts exist outside of the right corpus striatum, but only occupiedendowed with the power of giving rise to voluntary move- a part of that ganglion?ments, arresting or restraining that power. Jacquet§ relates that a man was attacked with paralysis

5. Complete and persistent hemiplegia may appear, although of the left side, which persisted till he died, three months<KMCtse occupies but a part of the supposed voluntary naotor after. A cyst, the size of a filbert, containing a rust-colouredapparatus in the brain.-This is a most powerful argument ,fluid, was found in the centre of the right corpus striatum.against the admitted views, especially when it is remem- The rest of that corpus striatum was healthy, as were alsobered that considerable disease of parts of that apparatus the other parts of the brain. How, I will ask again, canmay exist without paralysis, or with paralysis occurring in there have been such a persistent paralysis when, as it wasthe wrong place-i. e., on the side of the lesion. I am fully in the case of Dr. Todd, but still more evidently here, theaware that a complete paralysis may be supposed to be due lesion was so inconsiderable, and when such a great part ofto a pressure upon parts of the voluntary motor apparatus the channels between the volitional centres and the musclesappearing healthy, or to an unfound alteration of those remained normal ? Pparts, and I have no doubt that such suppositions are often As regards the pons Varolii, I will also only mention atrue. But what of cases in which a suddenly produced few cases. Ollivierll gives the case of a woman attackedlesion causes all the phenomena which we know to depend with complete right hemiplegia, which persisted severalonbsemorrbagein the brain, including a complete hemiplegia, years. In the middle part of the left half of the ponsand in which the autopsy shows that there really was an Varolii a cicatrix was found, which interrupted the con-effusion of blood in that great nervous centre? Before tenuity of a part of the longitudinal fibres. The medullarygiving the indication of some such cases in which the substance around that remnant of a lesion due to hsmor-alteration was not very great, I will mention a few other rhage had its normal consistency. Here again, then, westriking, although not so decisive, facts. find a complete and long-persistent paralysis caused by a

Dr. Duncan gave to Abercrombiet the details of a case in lesion occupying only a part of the motor tract.which it may seem that there was more extensive disease &mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;’&mdash;-&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash;&mdash; * Loc. cit., p. 41. t Loc. cit., p. 249..* I say paralysis-i,e., a loss of voluntary movement, and not a disorder :t Clinical Lectures, p. 629 aud 640.in the voluntary movements from any supposed defect of co-ordination. &sect; Quoted by Gintrac, loc. cit., vot. vii., p. 157.

t Loc. cit., p. 208. ’11 Trait6 des Maladies de la MoeUe Epmi&egrave;re, vol. ii., p. 164.

389

In the well-known case of Mr. W. F. Barlow’s* there wa

right hemiplegia and anseatbeaia, with paralysis of the lefside of the face from a haemorrhage which was not considerable. Mr. Barlow says :&mdash;" On examination no effusionwas found in the cerebrum or cerebellum, but a section othe pons Varolii discovered a clot in it as large as a filbershell, with a slightly softened boundary of nervous tissueA section of the pons in the mesial line passed nearly thi-ougithe centre of the effusion." As in this case the patient seemto have been examined carefully, and as she remained conscious, even intelligent, until within two or three hours oher death (which occurred five days after the attack), ther1is great value in the statements that the right limbs wer1paralysed, and that the left ones were moved by her willI have already alluded to this case when I spoke of thos1instances in which an alteration in the centre of the ponproduces an altern hemiplegia. I give now more detailabout it as it shows clearly that injury to only a part othe motor tract can produce considerable paralysis, beside:showing also that the same lesion on the other side manot engender paralysis.A case of Dr. Roger’st deserves to be mentioned just afte:

that of Mr. Barlow’s. A clot in a cavity, the size of Ipigeon’s egg, was found by Dr. Roger in the posterior ancsuperior part of the left side of the pons Varolii. I

hardly extended into the right side. Still the patient, aftelhaving been attacked with complete paralysis of the righside, very soon after became paralytic also on the left sideSo that if we contrast this case with that of Mr. Barlow’!we find that in this last a lesion occupying nearly the samEextent on the two sides of the pons produced paralysis o:only one side, while in the other case a lesion which waialmost altogether in one half of the pons caused paralysein the two sides of the body. Is it not evident from thesEcases that paralysis does not always depend on the loss o:function of the part diseased, but on the influence!exerted by an irritation of the diseased tissue acting orother parts to produce a cessation of their activity ?In the case of Roger’s it may be supposed that there wal

a pressure over the whole pons Varolii exerted by thEeffused blood. Considering, first, that the tissue of thai

organ is hard, comparatively to that of other parts of thEbrain; secondly, that the amount of blood was not ver3great; and thirdly, that the effusion took place in the uppetand posterior part of the pons-i. e., very near the fourthventricle and far from the place of passage of the con.

ductors of the orders of the will to muscles, this explanationis not to be accepted.From the above facts and a number of others that I could

mention, it is clear that, parts of the voluntary motor appa.ratus being left healthy, there may be a complete and long.persistent paralysis caused by disease occupying only a

portion either of the motor tract or of the so-called motoicentres. According to the admitted theories concerningthe production of paralysis in brain disease, a lesion of onlya part of the tract should not produce more than a partialparalysis, or if at first the paralysis were complete (in con-sequence, as is supposed, of pressure on other parts), itshould cease to be so when the pressure diminishes or

ceases-by absorption of effused blood, for instance. There-fore, the completeness of paralysis in some cases, and itslong persistence, with or without absolute completeness, inother cases, clearly show how erroneous are the admittedviews.

CHRONIC DIARRH&OElig;A OF INDIA ANDTHE TROPICS.

BY SIR J. FAYRER, M.D., F.R.C.P.

ONE of the most troublesome, tedious, and often dan-gerous results of residence in India, is a form of diarrhoea,which is liable to be as intractable and obstinate in charac-ter as it is exhausting in its effects. Though generallyseen in those who have spent many years in hot climates, itoccasionally occurs in others who have been there but a shorttime. It is known as 11 diarrhoea, alba," or white flux-so

* Transactions of the Pathol. Society, London, vol. iv., 1853, p. 28.t Bulletins de la Soci&eacute;t&eacute; Anatomique, Paris, 1837, p. 156.

.s called from the grey, whitish, light or clay-coloured evacua-’t tions, which are frequent, copious, fluid or semi-fluid, oftenl. frothy, and occasionally lienteric, especially after any indis-)f n cretion in diet; or mixed with mucus tinged with blood, when.t any fresh source of enteric irritation or congestion may3. have been induced.h This form of diarrhoea is an evidence of broken-downs health in those who have been exposed to certain climatic

rf r- influences, and may exist irrespectively of obvious diseasee of liver, spleen, or other abdominal viscus. Its origin il:1b

e often insidious, commencing with simple looseness of theI. bowels, with little or no pain, and producing rather a feelinge of relief than of suffering; and it may be, not until thes

subject of it finds he is losing flesh, strength, and energy,.f that he realises the serious nature of the complaint. It

IS seems to be the result of climatic influences in which9y probably, malaria (whatever that may be) is not uncon-

cerned, and is due rather to a general derangement of the,1’ hepatic, splenic, and gastro-intestinal functions, than to-a the usual irritant or eliminative causes of diarrhoea; no-t doubt these disturbed functions are accompanied by de-r generation of structure.t The white or clay-coloured appearance of the dejections i&J. suggestive of deficient or altered hepatic secretion; buts this, probably, may be accounted for by the general statee of ansemia to which all the organs and the body are reducedf rather than by any actual disease of the liver itself. It is,a indeed, only as the disease progresses that the pale colours of the excretions becomes so marked, for in the outset theye resemble those of diarrhoea from other causes. The balancef between exhalation and absorption seems to be disturbed...s and much of the large quantity of fluid that is poured out,a or ingested into the intestine, and which, in the natural

osmotic circulation of intestinal fluids, should be reab-s sorbed, is hurried on and, as it were, prematurely expellede the absorption of nutrient matter is thus interfered witht and diminished, and wasting results, as may be seen ine the attenuated and exhausted frames of those who havey suffered for any.time from the disease.r The appearance of persons suffering from this disease is,i characteristic. They are pale and emaciated, with loose,- dry, flaccid, flabby skin, which often in later stages is dis-i coloured as by chloasma or Addison’s disease. The fat

disappears; the eyes are pearly; the lips and conjunctive1 are blanched; the tongue is dry and smooth, and in ad-- vanced stages it appears contracted and shrunk, its papilBae’- are obliterated, the surface is red as a raw beefsteak, glazedi and dry, at times its edges are excoriated, and the mouthr and its mucous membrane are the seat of aphthous spots or-

epithelial proliferation, and so tender and sensitive as to,be intolerant of wine or any substance or fluid in the least.

1 pungent or stimulating, on account of the burning pain its- contact gives rise to.t The earlier phases of the disease are characterised byr general malaise-perhaps some evidence of malarious poi-- soning,-such as fever, neuralgia, or myalgia-distension of3 the abdomen, especially after food, dyspepsia, irritability ofi the bowels, which are provoked by the reflex irritation ofi anything taken into the stomach to expel their contents.

There is general languor and feeling of debility both men--tal and physical, disinclination for work, and all exertionis difficult and distasteful. As the diarrhoea gradually in-creases, these symptoms may to a certain extent be miti-gated, and the patient think himself better; but as thedisease insidiously progresses, the strength fails, and sooneror later he finds himself compelled to give up work, and.seek recovery in change of climate. The state becomes

. one of extreme ansemia, and as it goes on, dropsical effusions,.

take place in the areolar tissue of the lower extremities,,

and may indicate an approaching fatal termination.A very similar, perhaps identical, form of disease is knownr

r in some of the hill stations of India as U hill diarrhoea," andj has been well described by Twining, A. Grant, E. Goodeve,.; and other medical officers of the Indian Service. It often, proves intractable, and even fatal, especially to those who.have been long in the country, and whose health has pre-

viously suffered from malarious poisoning; and occasionally,I fear, it is the result of an injudicious selection of climate:,