No. 4087.

DECEMBER 28, 1901.

A LectureON

HEMIPLEGIA.Delivered at the National Hospital for the Paralysed and

Epileptic, Queen-square, on Nov. 29th, 1901,

BY JAMES TAYLOR, M.A., M.D. EDIN.,F.R.C.P. LOND.,

PHYSICIAN FOR OUT-PATIENTS TO THE HOSPITAL; PHYSICIAN TO THENORTH-EASTERN HOSPITAL FOR CHILDREN, AND TO THE ROYAL

LONDON OPHTHALMIC HOSPITAL, MOORFIELDS.

GENTLEMEN,-The subject of my lecture this afternoon is Ihemiplegia, by which is meant that condition in which Ipower is impaired on the whole of one side of the body.In the common variety of this form of paralysis one arm, oneleg, one half of the face and of the tongue, and one half ofthe trunk are affected on the same side. In another varietyone arm, one leg, and one side of the trunk are affected onone side, while the face is affected on the other. The latterAs known as "crossed" " or "alternate" hemiplegia. There isanother form of crossed hemiplegia in which the arm, the

leg, and the trunk are affected on one side and the structuresinnervated by the third cranial nerve on the opposite side ;and still another in which the parts supplied by the fifthjierve are affected on one side, causing sensory impairment.on the same side of the face, while the motor power of theopposite limbs is affected. There is yet another kind of,paralysis to be considered called "double hemiplegia, "butithis in itself is scarcely a separate variety, only a condition1Ìn which paralysis of one side has been succeeded byparalysis of the other, and on account of the affection beinga two-sided one certain symptoms-especially the affec-tion of what are known as bilaterally associated muscles-are produced, in many instances causing a close re-

semblance to bulbar palsy, so that certain cases of double

hemiplegia are also spoken of as cases of "pseudo-bulbartparalysis." " In this lecture I shall only just refer to the con-.dition known as "functional" or hysterical hemiplegia-.a condition in which, without any, at all events discoverable,lesion, the symptoms of hemiplegia due to organic diseaseare very closely simulated. I have thought it best, in orderto obtain as comprehensive a view as possible of our subject,to divide the lecture into two main parts and to consider.(1) the character of the paralysis, the relative weakness or.disability produced in different parts of the body dependingupon the position of the lesion in the brain ; and (2) the- nature of the lesion producing the paralysis as determinedby the clinical history of the case. In conclusion, I shall- show you several cases which will illustrate at least some ofthe points to which I shall refer.

As regards the character of the paralysis, in the ordinaryform of hemiplegia there is weakness of one side of the.face and trunk and of one arm and of one leg. It is not

infrequently said that the paralysis of the face is of the,lower part only, but the whole of the one side of the face is.affected, although the weakness of the lower part is moreobvious ; in some cases of old hemiplegia it is hard to saythat there is any facial paralysis. The weakness of thetrunk on one side also is not as a rule very marked, althoughit is distinct enough, and the reason for this I shall refer topresently. In reference to the limbs, the arm is in the greatmajority of cases more paralysed than the leg. Why, then,with a lesion of one side of the brain causing paralysis of theopposite side of the body should the parts be affected in thisway-namely, the face and trunk less than the limbs, andof the limbs the leg less severely than the arm? The

.explanation of this peculiarity is to be found in the

hypothesis formulated in 1866 by Sir William Broadbent-ahypothesis which throws much light on obscure problems ofcerebral physiology and pathology, and one to which clinicalexperience gives almost daily stronger support. This hypo-thesis is that bilaterally associated movements are repre-sented on both sides of the brain, and the greater the

strength of this bilateral association the more nearly equal isthe representation on the two sides of the brain. Thus weknow that the two lower limbs are much more closely- associated in their movements than are the two upper. We

very frequently use one arm quite independently of the other.A movement of one leg without some movement of the otheris comparatively uncommon, and in the habitual use of thelower limbs for purposes of locomotion the association of thetwo is a very close one. The same applies even more stronglyto the trunk movements. It is apparent that it is impos-sible for us to move one side of the abdomen or the chestwithout also moving the other. And so also with regardto the face. Facial movements in expression, &c., are nearlyalways bilateral. With regard to the forehead especially theyare inevitably so ; with regard to the eyes less so, althoughsome people find it impossible to wink with one eye ; and withregard to the lower part of the face-the part about themouth-the association is still less close, although still muchcloser than that between the two arms or even between thetwo legs. Given, then, a lesion of one side of the braincausing paralysis of the opposite side of the body-the face,the trunk, the arm, and the leg-and situated at such apoint (if such a point can be imagined) as to affectthe face, the arm, the leg, and the trunk areas or

fibres equally, we should expect to have the arm most

affected, the leg less affected, the face still less, espe-cially in its upper part, and the trunk least of all ; and this,as I have already told you, is what actually happens inthe ordinary form of hemiplegia. And I may just mentionin passing that this hypothesis explains also the phenomenawe meet with in double hemiplegia or pseudo-bulbar paralysisto which I have already referred. The symptoms by whichthis is allied to bulbar palsy are in the fact that swallowingand articulation are affected. The movements subservingthose actions are strong in their bilateral association andconsequently in their bilateral representation in the brain, sothat a lesion of one side of the brain if it affects them doesso only temporarily. But if, in addition to the weaknesscaused by a unilateral lesion, we have the weakness producedby a second lesion on the opposite side, it will at once beunderstood that considerable interference with these move-ments is not only likely but almost inevitable. And such isthe case, and as a consequence we have deglutition andarticulation so interfered with-to mention the two mostprominent symptoms-as to give rise to a condition closelysimulating true bulbar paralysis.

Let us now consider for a moment the position in which alesion will be situated in the brain to cause such a conditionas I have briefly sketched. Beginning with the cortex, wemay have the lesion situated there, causing so great a loss ofpower on the opposite side of the body as we have alludedto and you will easily understand that the lesion would haveto be one of very considerable extent. As the fibres of themotor tract proceed downwards and the area which theyoccupy becomes smaller and smaller they become more andmoe closely aggregated. There may be a lesion occurringat any part of their course. There may be one under thecortex, necessarily also a large one, or where the fibresare massed together in the posterior part of whatis known as the internal capsule, a tract of fibres

lying between the lenticular nucleus and the caudatenucleus and optic thalamus, and this is by far the mostcommon situation. Or we may have the lesion in the cruscerebri or in the pons, or even lower down in the medulla,although in the latter case, if it is low enough-i.e., belowthe trunk and nucleus of the facial nerve-the face will escapealtogether. But I have not seen a lesion so situated. In

any of these positions a small lesion may be sufficient tocause extensive paralysis. In determining the position of alesion it is necessary to remember that just as the centresfor the different parts occupy a definite position in the cortexso the fibres have a similar definiteness at least as low as thecrus. Thus in the internal capsule the face fibres are infront of the arm fibres, and those again in front of the legfibres. And it may incidentally be mentioned that behindthe leg fibres run the sensory fibres, and behind these againare the visual fibres subserving the two corresponding halvesof the retina---i. e., the field of vision of the opposite side,so that a patient with a lesion in this position on the leftside has right hemiplegia and cannot see to his right side-a condition known as "right hemianopia." Similarly in thecrus the face fibres are internal to the arm fibres, whilst theleg fibres are external to those for the arm. In the ponsthe same division cannot be distinguished, for the fibresare now collected into several bundles without any, at allevents discovered, topographical relation to function. Youwill also see that it is possible for a lesion to affect not thewhole of the opposite side of the body but only a part, and

CC c

1780

then it will give rise to what is known as "monoplegia "-a small lesion in the leg area of the cortex, e.g., may causeonly weakness of the opposite leg. It will scarcely causecomplete paralysis by reason of the bilateral representationalready referred to. A limited lesion in the arm area may,however, cause practically complete paralysis of the oppositearm alone. From the closer aggregation of the fibres lowerdown the lesion to cause a monoplegia would have to be anexceedingly small one, and as a matter of fact monoplegiafrom any lesion lower than the cortex, or just underneath it,is very rare for this reason. :

We may have, then, an ordinary case of hemiplegia-we Ishall say "left hemiplegia" for reasons which will be obvious 1further on. Such a condition as that described may be due ito a lesion in any of the places mentioned and without Ifurther symptoms it is impossible to say where. Sometimes,however, we find that the leg is more affected than the arm, I

that, for example, movement of the foot is completelyabsent while the hand can be moved. In such a case the é

face is as a rule slightly if at all visibly affected and the (

lesion will of course be one the focus of which is in the leg 1area of the cortex or among the leg fibres of the internal i

capsule or the crus. It is, indeed, a condition, as it were, 1

midway between monoplegia and ordinary hemiplegia. In 1

many cases, also, in which the leg is more affected than the !"arm there is anaesthesia of the paralysed side present and tthen the lesion is situated in all probability at the hinder c

part of the posterior two-thirds of the internal capsule. As o

we have already mentioned, the leg fibres are the most n

posterior of the motor fibres in the capsule and lying close to c

them are the sensory fibres. If, in addition to the anaesthesia, a

there is also hemianopia (loss of the corresponding half of n

the field of each eye) the probability of the lesion being of bthe hinder end of the capsule becomes a certainty, and con- v

versely, where, in a case of hemiplegia you find hemianopia Iand hemiansesthesia, the leg, as a rule, is more affected than t:the arm. VI

I have hitherto purposely spoken of left hemiplegia, as bthere is frequently associated with paralysis of the right side e:

the condition known as aphasia, in which the patient is c

unable to speak or perhaps even to understand what is said Tto him. According to current doctrines permanent aphasia r(

is always due to a cortical lesion or to a lesion lying imme- f(

diately under the cortex, and it is said that any lesion irsituated lower is not capable of causing at least permanent paphasia. The reason for this is said to be that speech pro-cesses can be conducted across through the corpus callosum c

and reflected down from the opposite hemisphere. c

It is the rule with right hemiplegia to have some degree of c

aphasia. If there is none, then either the patient is left- a:handed or the lesion is situated at some distance from the ir

speech centre and in such a way as not to interfere with the CI

conduction of speech processes. Thus a lesion of the internal is

capsule may cause right hemiplegia without aphasia and ojeven a cortical lesion may do so if the speech centre is not ti

injured. If, for example, you have the focus of a unilateral bcerebral lesion near the middle line it is quite likely that m

the third frontal convolution may escape, and Dr. J. Hughlings m

Jackson has for years been in the habit of pointing out that g-in cases of right hemiplegia without aphasia or with slight as

and transient aphasia the leg as a rule is more affected than althe arm. I am able to show you to-day two cases illustrating ttthis st

But besides these ordinary forms in which the affection of tcone-half of the body is all on the same side, a condition of 0:crossed hemiplegia is met with, as I have already stated. The himost common form is that in which the face on one side is ca

affected and the limbs on the other. In such a case the re

lesion is situated in the lower part of the pons affecting the th

pyramidal tract before it has decussated and involving thefibres of the facial nerve as they pass from the nucleus to to

emerge as the facial nerve. The affection of the face in such isa case is, as a rule, more severe than in ordinary hemiplegia geand partakes much more of the characters of the paralysis or

known as "peripheral facial palsy" or "Bell’s paralysis." " di:In other words, the upper part of the face is much more ofaffected than is usual in cerebral paralysis. The sixth an

nucleus also is often affected in such a case, and this will henot be surprising when you think of the relation of such a se:

lesion in the position I have described to this nerve and co

the close connexion of the nuclei of the sixth and seventh winerves. Similarly we may have hemiplegia in a patientassociated with anxsthesia of the face, and in such a case ca

also the lesion must be pontine, the anaesthesia bein due tho

to affection of the fifth nerve or its nucleus. Sometimes irie a case of hemiplegia, in other respects of the ordinary typee —namely, affection of the face, the arm, the leg, and then I trunk on one side-we have paralysis of the third nerve of, the opposite side. Such a condition, if it is the result of

e only one lesion, can result from a lesion in only one situationr —namely, in the crus cerebri of the side on which the thirdi nerve is paralysed. It is a very uncommon forml ofi hemiplegia., We shall now proceed to the second part of the subject

and consider how to determine the nature of the lesioncausing hemiplegia, whether hemorrhage, thrombosis, em-

3bolism, or tumour. The two factors to be taken account of) in such consideration are the mode of onset of the paralysisand what may be called the clinical pathology of the indi-

vidual, meaning by this the state of his arteries, pulse, heart,kidneys, and organs generally.

1. As regards haemorrhage the onset of the paralysis is, asi a rule, sudden and may take place during exertion. Perhaps: one of the commonest forms of exertion with which cerebral. hemorrhage is associated is straining at stool. There is

usually loss of consciousness, and if the hemorrhage is alarge one there may be profound coma with stertorousbreathing or the irregular respiration known as Cheyne-Stokes respiration. If the hfemorrhage is superficial,that is cortical, the onset is usually signalised by a

convulsion starting in the limbs opposite to the siteof hemorrhage and usually becoming universal. Theremay be a series of such convulsions the result of thecortical irritation. The pulse may be full and tense and theartery hard and obviously atheromatous. Healthy vessels donot readily rupture, whereas atheromatous ones do, and,besides, atheroma of arteries is not uncommonly associatedwith the presence on them of small aneurysmal dilatations.The heart also may be hypertrophied and there may be con-tracted kidneys. It does not necessarily follow that therewill be albumin in the specimen of urine you may examine,but this does not exclude kidney change, and it is well toexamine for the presence of vascular changes usually asso-ciated with kidney disease besides those already mentioned.The most important of these are the changes in theretina and its vessels, the condition known as I I albuminuricretinitis," and I have known this frequently present in caesin which repeated examination has failed to reveal the

presence of albuminuria.2. The presence of these retinal changes is not absolutely

conclusive that the condition giving rise to the symptoms iscerebral hemorrhage, for it must be remembered that thecondition of vessels which makes them liable to rupture isalso that which tends to give rise to clotting in them and soinduce the second condition which we have to consider as acause of hemiplegia-viz., thrombosis. When this conditionis present in the old the onset as a rule occurs during rest,often the rest which follows undue exertion The commonesttime of onset is during the night and the paralysis may onlybe realised when the patient gets up, or tries to get up, in themorning. Loss of consciousness may or may not take place-more frequently it does not; the pulse is slow and the conditiongenerally not apparently one of such urgency and seriousnessas in hemorrhage. As will have been evident from what has

already been said, visceral changes may be present similar tothose mentioned as associated with hemorrhage, for, as alreadystated, the atheromatous condition of the arteries rendersthem not only liable to rupture but also to become blocked.One thing is worth remembering, and that is that when thehemiplegia is on the right side and aphasia is present thecause is more likely to be thrombosis than hemorrhage. Thereason of this, from what has been said about the situation ofthe lesion in aphasia, will be apparent.What I have said so far about thrombosis refers particularly

to that condition as occurring in the aged. But hemiplegiais not confined to the aged, and in young adults or peoplegenerally under the age of 40 years in whom no heart diseaseor kidney disease is present hemiplegia is almost invariablydue to thrombosis occurring in diseased vessels. The natureof such disease is the thickening which results from syphilis,and this is no doubt the usual condition giving rise to

hemiplegia in those who have not reached the age at whichsenile atheroma may occur or in whom there is no cardiaccondition likely to give rise to embolism or diseased vesselswith kidney affection.

3. This leads us to the consideration of the third condition

causing hemiplegia-viz., embolism. In embolic hemiplegiathe onset is sudden, consciousness may or may not be lost,

1781

and if it affects the right side aphasia-transitory it may be-is usually present. The sudden onset and the presence ofobvious heart disease, especially of mitral stenosis, are

usually sufficient to indicate the nature of the lesion,although even then the rule is not absolute, and I have]mown thrombosis occurring in an artery affected with

endarteritis due to syphilis cause hemiplegia in a patientwith mitral stenosis.

4. Another cause of hemiplegia is tumour and in this the.clinical history is of immense importance. If there is or hasbeen headache, sickness, and optic neuritis with unilateralweakness, of course the cause is almost certainly tumour, butyou may justifiably diagnose tumour when not one of thoseso-called classical symptoms is present, if there is hemiplegiaof slow onset-i.e., affecting first one limb slightly andgradually increasing its effect both in degree and in extent,the wedkness occupying months or even longer before it canbe definitely described as hemiplegia. If the tumour is- situated beneath the cortex or in the vicinity of the central,ganglia you may have only the slow onset to guide you ; ifit is in the cortex you may have in addition fits of localcommencement and the hemiplegia may at first be only atemporary one occurring after the fits.

I need scarcely consider the question of abscess which mayalso cause hemiplegia. If abscess is present you will prob-ably have a history of traumatism, or ear disease, or

empyema, or suppuration in some other part. I have known,however, cases of abscess in which none of those were

present and in which the clinical history and condition didnot give rise to any suspicion that the cause was other thanan ordinary vascular one. Yet in the great majority of casesof abscess you will have one of the three conditions I havementioned-ear disease, suppuration elsewhere, or a historyof injury.

I would just mention the hemiplegia which occurs in child-hood. This may be of two kinds. 1. You may have a birth

palsy hemiplegic in type, although in this form of paralysisthe symptoms are usually bilateral. As the onset occursduring birth, usually in first-born children, and in cases inwhich the labour is long and difficult, often instrumental,and as the cause of it is meningeal haemorrhage, you canunderstand that the affection is usually bilateral in itssymptoms, the haemorrhage extending on each side of thevertex. But you can also understand how the symptomsmay be hemiplegic if the hsemorrhage is confined to oneside of the vertex. 2. The other form of hemiplegia inchildhood is the ordinary so-called infantile, hemiplegiaoccurring in the early years of life, commencing usually witha unilateral fit or a series of convulsions. The cause of thisis uncertain ; according to some it is an inflammation of the

grey matter, according to others a thrombosis in arteries,while Sir William Gowers believes that it is determined by avenous thrombosis. The hemiplegia is often severe, there issometimes present the peculiar mobile spasm known as

athetosis, and the patient is often subject to fits starting onthe paralysed side. One point also is of interest, and that isthat mal-development of the hemiplegic side nearly alwaysresults, so that it is smaller in every way than its fellow.I am able to show you an excellent example ofthis.The treatment of hemiplegia divides itself into two natural

parts-the treatment at the onset and the later treatmentundertaken with the view of restoring function as much aspossible. The great point in reference to the treatmentat the onset is to determine the cause of the paralysis. <

If it is embolism, absolute rest, light food, and extreme 1care in avoiding any strain on the heart are the essentials ; ]

if it is haemorrhage, free purgation, light, easily digested 1

food, leeches to the temples if there is pain, and abso- <

hite rest are the main things; if it is thrombosis in <

the old, gentle aperients, together with cardiac stimu- ]lants and liquid nourishment, are best ; if thrombosis in (

the young, then mercury and iodide of potassium must be 1

energetically administered. It is unnecessary to go into the

subject of the treatment of tumour or abscess. Anti- 1syphilitic remedies or operation are the only means openfor the former, operation for the latter is the only treatment 1to be considered. Treatment in the later stages is directed 1to improvement of the condition. Loss of power and rigidityare the two things to be considered. Gentle rubbing is 1certainly useful in overcoming the rigidity, faradisation <applied to the extensors-e.g., of the forearm-may diminish (

the flexor spasm and will also exercise the affected limbs.Fresh air, gentle exercise, and light, easily-digested food are 1the other means for securing the best results. a

A Clinical LectureON

THE EARLY DIAGNOSIS OF PULMONARYCONSUMPTION, WITH ESPECIALREFERENCE TO THE VALUE

OF TUBERCULIN.Delivered at the Brompton Hospital for Consumption on

Nov. 6th, 1901,

BY ARTHUR LATHAM, M.A., M.B. OXON.,M.A. CANTAB., M.R.C.P. LOND.,

ASSISTANT PHYSICIAN TO THE HOSPITAL, AND TO ST. GEORGE’SHOSPITAL.

GENTLEMEN,-I make no apology for discussing with youthis afternoon the grounds upon which we are justified inmaking a positive diagnosis of early pulmonary consumption,more especially as I hope to bring under your notice amethod of diagnosis which has been strangely neglected inthis country-namely, the use of Koch’s old tuberculin.The early diagnosis of tuberculosis is a question of supremeimportance, perhaps the most important that the physicianhas to face, as anyone must realise when he grasps the factsthat one person out of ten dies in this country from thisdisease, that a large proportion of those who die from otherdiseases are afflicted with consumption in one or other of itsforms, and that in the early stages we can, owing to ourgreatly increased knowledge of the pathology’ and treatmentof the disease, almost certainly bring about complete arrestof the tuberculous process, whilst in the later staes ourefforts must ’often be largely palliative. 1am not; I think,making too strong a statement when I assert that the largernumber of cases of pulmonary tuberculosis,’ which are

undetected in the early stages, end fatally within three -’orfour years from the first onset of the disease. There can,therefore, be no question as to the importance of the diseasebeing detected at the earliest possible stage.

I have here 15 or more patients who are in ah early stageof consumption, but before you examine’them I will brieflyrefer to the methods we employ to arrive at a definitediagnosis in the early stages of this disease. There are,fortunately, several ways in which we can achieve our object.We are, I think, justified in making.a ’positive diagnosis inthe vast majority of cases under the following circumstances.

1. When we find diminished resonance and increasedresistance to the finger associated with the presence ofpersistent crepitations or fine rales in those situations inwhich tuberculosis usually starts in the lungs&mdash;namely,the apices of the upper lobes, ’more’ especially towardstheir posterior aspect. For example, the year before lastI saw a patient at Sawstn with Mr F. Edwards. She waswell nourished and there was no family history of tubercu-losis or history of exposure to infection ; she had enjoyedprevious good health, save that she had been troubledfor a few months by a dry hacking cough. Therewas no loss of weight and no rise of temperature. The

sputum had been examined on several occasions, but notubercle bacilli were found. On physical examination Ifound slightly diminished resonance and increased resistanceto the finger, together with feeble respiration and a fewcrackles at the end of inspiration above the left clavicle andto a less extent in the left supra-spinous fossa. The other

portions of the lungs were healthy. I made a positive diagnosisof tuberculosis notwithstanding the absence of tuberclebacilli and the patient regulated her life in accordancewith that opinion. She is now practically well, the only signspresent being slight dulness and diminished breath soundsat the left apex, together with definite though slight con-traction in that position-signs, that is, of a healed tuberculouslesion.

If there is no diminished resonance we cannot make apositive diagnosis, for we meet with cases in which there is noalteration of the percussion note but such physical signs asdiminished breath sounds and fine rales, associated perhapswith slight fever. These rales eventually clear up and areprobably due to local catarrh of the smaller tubes. Nor,again, can we make so positive a diagnosis in the absence