No. 2671.

NOVEMBER 7, 1874.

Clinical LecturesON THE

COMMON FORMS OF PARALYSISFROM BRAIN DISEASE.

Delivered at University College Hospital,

BY H. CHARLTON BASTIAN, M.D., F.R.S.PHYSICIAN TO UNIVERSITY COLLEGE HOSPITAL, AND SENIOR

ASSISTANT-PHYSICIAN TO THE NATIONAL HOSPITAL

FOR THE PARALYSED AND EPILEPTIC.

LECTURE VI.-PART II.

WE have now to consider certain complications occasion-ally attendant upon lesions in the brain-regions last referredto, these complications being of sufficient importance to de-serve a separate study.HAEMORRHAGE INTO THE CORPUS STRIATUM OR THALAMUS,

FOLLOWED BY EFFUSION OF BLOOD INTO THE VENTRICLES.-An accident of this kind is often divided into two distinct

stages. Thus we may have at first to do with an ordinaryhemiplegic condition, commencing either by an apoplectic,an epileptiform, or a simple mode of onset. But, after aninterval of varying duration, a fresh haemorrhage occurs,and the blood then poured out tears its way through thebrain-substance into the lateral ventricles; so that a con-dition of profound coma, with stertor and general para-lysis, quickly supervenes. In other cases there is no pre-liminary attack of any kind. A large haemorrhage occurssuddenly, so that the blood at once lacerates the brain-substance and opens up a channel through which it is

copiously poured into the lateral ventricles. In such a casewe have from the first an apoplectic attack of the mostmarked kind, characterised by profound coma, generalparalysis of limbs, and dilated pupils.In each set of cases the laceration of brain-tissue and

pouring of blood into the lateral ventricle is associated witha decided lowering of the temperature of the body. Therectal temperature sinks to 96° or thereabouts, and remainsat this point for an hour or two, especially where the bleed-ing into the ventricles slowly continues. Should a fatalresult not speedily occur, we find that the primary depres-sion of temperature is followed after a time by a rapid rise,which slowly continues, in cases about to prove fatal, tillthe death of the patient. Such fatal result very often occursbefore the expiration of three days from the commencementof the attack, though occasionally not till a later period.In these cases of ventricular hsemorrhage we very fre.

quently indeed meet with tonic spasms of one, two, or morelimbs; or tonic may alternate with clonic spasms in the sameparts. In other instances we have a condition of rigidityin the limbs of one side, combined with clonic spasms in onor both extremities of the opposite side.

In this class of cases conjugated deviation of the eyes iisometimes present from the first, pointing to the side of thEbrain on which the haemorrhage with laceration has occurredAnd if the coma is not too profound, the conclusion aboulto be drawn from this indication may be confirmed by th(discovery of some slight signs of sensibility on the side oithe body towards which the eyes are turned. Touching thEconjunctiva on this side, for instance, may produce som<

closure of the eyelids, whilst irritation of the conjunctiva orthe other side (opposite to that of the brain lesion) give:rise to no corresponding reflex movements.The grouping of symptoms just described is tolerably dis

tinctive of hasmorrhage into the lateral ventricles. Wheithey are present we should in the majority of cases be justified in arriving at such a diagnosis. More rarely, howeverwe find these combinations of symptoms pretty closely imitated by the results of lesions in the pons Varolii, where wihave to do with injuries, either (a) small at first and subsequently increasing, or (b) large from the first, so as to resemble those cases in which a copious effusion of bloo(bursts at once into either of the lateral ventricles.In the former class of cases we might be guided to I

currect diagnosis if the hemiplegia which had previouslyexisted was of such a nature as to make it referable to a

lesion of the pons. And when the condition of coma withgeneral paralysis has become established as a result of anextensive lesion in the pons Varolii (whether this lesion isprimary or secondary), the condition itself is very apt to beassociated with contracted and motionless pupils, as in opiumpoisoning, whereas in cases of ventricular haemorrhage thepupils are usually dilated. The diagnostic indicationsafforded by the condition of the pupils in brain disease arefor the most part vague and indefinite, though the pointsabove stated, from their comparative uniformity, affordimportant exceptions to this general rule.

Tonic spasms are also more frequently absent in severecentral lesions of the pons than in cases where we have todo with ventricular heamorrhage. In those very severelesions of the pons which in their symptomatology other-wise closely resemble ventricular haemorrhages, muscularspasms are usually absent; we find instead a complete re-solution of all the limbs, and of the trunk muscles.Other cases of brain disease occasionally occur in which

the resemblance of the symptoms to those of secondaryventricular haemorrhage may be extremely close. I alludeto instances where a hemiplegic condition, from injury ofthe opposite side of the brain, becomes complicated by afresh lesion (either softening or haemorrhage) in the pre-viously sound hemisphere. I have seen such a case almostexactly simulate one of secondary ventricular haemorrhage.The power of diagnosing between these conditions is

occasionally a matter of some importance from the point ofview of Drosrnosis.LESIONS IN THE ANTERIOR, MIDDLE, AND POSTERIOR

PARTS OF THE CEREBRAL HEMISPHERES.&mdash;It is a rule towhich, as you know, there are only very few exceptions,that a lesion in either hemisphere of the brain, if ofsufficient extent, induces a paralysis of the limbs on theopposite side of the body. Whilst we may, therefore, incases of hemiplegia, at once arrive at a conclusion as to theside of the brain injured, it is by no means easy for us, inthe great majority of cases, to determine in what precisepart of the hemisphere the lesion is situated. In the recordsof cases of brain disease we mostly find the site of lesionroughly described-it is spoken of as being in the anterior,the middle, or the posterior lobe; and anyone who examinessuch records carefully will soon find that the " middle lobe"is cited much more frequently as the site of lesion thaneither of the other lobes. How is this apparent selection tobe explained ? There can be little doubt, I think, that itis principally attributable to the fact that a very muchlarger bulk of brain-tissue is included under the designationmiddle" lobe than enters into the formation either of the" anterior" or of the " posterior" lobe. What is roughlyspoken of as the middle lobe is a mass of brain-tissue havingboth greater depth and breadth than the portions of thehemisphere in front or behind, and it includes what in morescientific phraseology we should term the "parietal" andthe 11 temporo-sphenoidal" lobes.To discriminate duringlife betweenlesions occupyingthese

different situations is at present often extremely difficult, ifnot impossible, though doubtless, as time goes on and morecareful attention is given to this subject by a numerousband of workers, our knowledge will increase. Now, how-ever, a few hints only can be given towards the solution of

, such difficult problems in cerebral diagnosis.Anterior or frontallobe.-Large lesions in the anterior lobe

,

may either actually implicate the olfactory bulb on one side,, or may interfere with its functional activity by bringing, about an undue pressure upon the part of the brain in which

it is situated. Thus such lesions are often associated with, the very significant sign of loss or decided impairment in

the sense of smell on the side of the body on which thebrain lesion occurs, and, therefore, on the side opposite to

. that in which the limb-paralysis exists. Such a sign may

. be encountered in association with haemorrhage into the, anterior lobe, or with softening of the same part caused by. embolism or thrombosis of the anterior cerebral artery-by, some of the branches of which the olfactory bulb is fed.

Again, lesions of the posterior part of the frontal lobe on. the left side, where we have to do with right-sided hemi-l plegia, are frequently indicated by the coexistence of a

typical aphasic condition., On the other hand, there is no one sign or set of signs, sc

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far as I know, which would point at all conclusively to anacute lesion in the form of haemorrhage or softening in theparietal or in the temporo-sphenoidal lobe. Almost the samekind of statement has to be made in respect to lesions in theposterior or occipital lobe. I say" almost" because there iscertainly one exception to this rule. Owing to the fact thatthe corpora quadrigemina are fed ’by arterial twigs whichcome off on each side from the posterior cerebral artery, itnot unfrequently happens that a softening of the posteriorlobe of the brain, due to occlusion of the correspondingposterior cerebral artery, gives rise to some loss of sight inthe eye of the opposite side, as well as to paralysis of theopposite limbs. The unilateral loss or impairment of sightand the hemiplegia being different results of the same cause(the cutting off of blood-supply from the territory of theposterior cerebral artery), it is important to note that thetwo become established simultaneously. Should the im-

pairment of sight not be extreme, its existence may escapethe notice of the patient. It is a sign, therefore, for whichyou should inquire whenever a doubtful case presents itself.

After a time we may perhaps learn something more defi-nite than we at present know concerning the degree andkind of impairment in the mental powers due to lesions inthe anterior, middle, and posterior parts of the brain re-spectively. Now there is nothing certain to be said on thissubject. I will merely add that various reasons led me,some years ago, to the conclusion that the posterior lobes ofthe brain had more to do with higher intellectual functionsthan the anterior lobes-a conclusion which, however con-trary it may be to generally received opinions, has sincebeen strengthened by observations made independently indifferent directions and by different persons. Dr. HughlingsJackson and other authorities on the subject of brain diseasehave also come to the conclusion that mental impairment orderangement is apt to be more especially marked where wehave to do with injuries of the posterior lobe of the brain-that is, such signs are apt to be more marked than withlesions of the anterior lobe of the brain, notwithstandingthe more popular notion as to the overwhelming importanceof this part in respect to intellectual functions. Dr. Hugh-lings Jackson also considers that injuries of the right pos-terior lobe produce more marked impairments in intellectualfunction than similar injuries of the left posterior lobe.More extended observations, however, seem needed beforewe can safely arrive at a positive conclusion on this difficultsubject. ’

LESIONS LIMITED TO THE CORTICAL GREY MATTER, ORCAUSING PRESSURE UPON THIS SUBSTANCE.-It is only to beexpected that the precise combinations of symptoms pro-duced by lesions of the cortical substance should vary im-mensely, according to the nature, and also according to theextent, of the injury in different cases. The groupings ofsymptoms due to lesions in this situation are indeed, as a 1matter of fact, most varied in their nature. I cannot iattempt to describe one tithe of the different modes of com-bination which may present themselves, and shall thereforemerely proceed to indicate the kind of symptoms most

I

frequently present, as well as those which are most free Iquently absent, where we have to do with lesions of thecortex of the hemispheres.As in dealing with other parts of this subject, the state-

ments I am about to make will be based partly upon my ownobservations, and partly upon a careful study of a largenumber of cases recorded by other observers, both in thiscountry and abroad. The published cases to which I havereferred have been recorded by their respective observersunder the head of cortical haemorrhage or cortical softening,of meningo-encephalitis, and of submeningeal haemorrhage.

Cephalalgia is often present to a notable degree where themeninges are especially implicated, though it is much morefrequently absent when the lesion is limited to the corticalsubstance itself.Loss of consciousness, more or less prolonged, may mark

the onset of a superficial affection of the brain, though justas frequently delirium manifests itself as one of the initialsymptoms. At other times we have to do merely withobtuseness of intellect, or more or less marked stupor.

Convulsions may usher in an acute affection of the corticalgrey matter, though this does not seem to be so frequentlythe case with such affections of the cortex as the recent ex-periments by Hitzig and Ferrier on lower animals mighthave led us to expect. More limited tonic and clonic spasms,

without loss of consciousness, are, however, frequent accom.paniments of such affections, in some part of their courseAnd actual convulsive attacks also occur with great fre.quency in a class of cases with which we are not at presentconcerned-namely, in association with new growths in.volving the cortex.No definite paralysis exists in some cases; there may bE

merely great general weakness, with a slow vacillatingmode of walking, or actual inability to stand. In othercases there are signs of partial hemiplegia-that is, we mayhave more or less complete paralysis of one arm, togetherwith a very slight lowering of the angle of the mouth onthe same side, though there is no appreciable weakening ofthe leg.Should the lesion occupy the third left frontal convolution

or parts immediately adjacent, aphasia is met with, eitheralone or in association with partial hemiplegia. With in.juries of the grey matter in other parts of the hemispheres,the power of speech and of intellectual expression generallymay be variously interfered with. We may meet with well-marked amnesic defects, or there may be merely a slow andlaboured utterance, with or without some amount of mentalincoherence.In other instances we have defects of speech belonging to

some one of these categories in association with a muchmore complete hemiplegic condition-that is to say, theparalysis in the arm and in the leg may be well marked,and present the usual peculiarities, though paralysis ofthe face is either absent or so slightly marked as to bescarcely appreciable. This last is a sign which occasionallyhas great significance.The loss of sensibility, again, in these cases of hemiplegia

due to superficial lesions, is generally very slight, and oftenscarcely appreciable even within a few days from the dateof onset of the malady. In some instances, instead of aloss of sensibility, there may be even slight hypersesthesiain parts of the paralysed limbs.Another point worthy of note is, that the difference in

temperature between the paralysed and the non-paralysedside of the body is rarely very marked, seldom exceeding1&deg; F., and tending soon to disappear.

If we bear in mind, therefore, the peculiarities I havementioned with regard to the distribution of the motorparalysis, its frequent association with mental changes,and with tonic or clonic spasms in the limbs, theabsence of distinct loss of sensibility, or of any notableelevation of temperature on the paralysed side where wehave to do with lesions of the surface of the brain, we getan assemblage of signs and symptoms which frequently provevery characteristic of the hemiplegic condition thus induced.It is not to any one of these signs singly, but to a combina-tion of them, that we must look for guidance. Thus, if wefind a patient showing some amount of mental incoherenceor delirium suffering from a partial hemiplegia, with littleaffection of the leg or face, and if at the same time thereare muscular twitchings in one or more limbs, or rigidityabout the neck or other parts of the body, our regionaldiagnosis becomes comparatively easy. Such a combinationof symptoms would point strongly to the existence of alesion involving the surface of the brain on the side oppo-site to that on which the motor paralysis exists.

I Looking upon such a case as I have just referred to asone of medium severity, many other groups of symptoms ofa slighter kind may present themselves, as well as com-binations of a more serious nature. In the slighter caseswe may have no actual paralysis, but rather tonic or clonicspasms in association with symptoms indicative of slightmental disturbance. And, although we seem advancing onthe road towards a more definite localisation in some ofthese cases, the efforts which have been made must be con-sidered to be still merely tentative.In instances of more severe superficial lesions-cases due

to wide-spread embolisms, or to very copious arachnoidhsemorrhages&mdash;a profound apoplectic condition is producedin which nearly all differential characters are for the timelost, and during the continuance of which the patient oftenrapidly sinks.

CHOLERA lately broke out in the prison at Singapore,but according to the most recent accounts its progress hadbeen checked.