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CEREBRAL ISCHAEMIA ANDEXTRA-CEREBRAL VASCULAR DISEASE

EDWARD C. HUTCHINSON, M.D., M.R.C.P.Consulting Neurologist, Midland Centre for Neuro-Surgery and Stoke-on- Trent

PETER 0. YATES, M.D.Senior Lecturer in Neuro-Pathology,, University of Manchester

At a time when the problems of degenerativedisease and ageing are claiming the attention ofboth the clinician and the pathologist it is notsurprising that interest in cerebral vascular diseasehas been re-awakened. Lack of effective treat-ment in the past encouraged no great interest indefining critically the details of the variousclinical pictures and the corresponding variationsin the underlying pathological lesions. It is onlywithin the last 15 years that Aring (I945) andHicks and Warren (195-1) found it necessary to putforward vasospasm as a possible cause of cerebralischaemia in many of their cases of cerebral in-farction, since they were unable to demonstrateany adequate obstructive lesion of the appropriateintracranial vessel. The difficulties of acceptingvasospasm as a mnechanism of cerebral infarctionhave been summarised by Pickering (1959).Moreover, it is now realised that disease of thecarotid and vertebral arteries in their extracranialcourse is responsible for a proportion of previouslyunexplained cases of cerebral ischaemia encoun-tered by both the physician and the pathologist.

This review is concerned with the recentadvances in the aetiology, the clinical presentationsand the treatment of patients with extracranialcerebral vascular disease; the term ' extracranialvascular disease ' is used to emphasise the im-portant pathological fact that in these cases it is notunusual for more than one of the major vessels' inthe neck to be affected by disease. An apprecia-tion of the importance of extracranial arterialdisease, together with advances in vascularsurgery, anaesthesia and radiology, has en-couraged the successful surgical attack upon thesearterial lesions-a development which is the mostimportant recent advance in the treatment ofcerebral vascular disease.

PathologyIn the main the pathological changes in the

vessels in occlusive cerebral vascular disease arethose of athero-sclerosis although giant cellarteritis, polyarteritis nodosa, thrombo-angiitisobliterans, and the rare ' pulseless disease,' haveall been described. The clinical and pathologicalfeatures of the latter condition have been fullyreviewed by Kalmansohn and Kalmansohn (1957).

It is an accepted pathological observation thatthe pattern of vessel involvement in atheromavaries considerably from individual to individual-the pattern being determined- by the size of thevessel involved. In some cases the small, in othersthe large, vessels are predominantly affected. Sucha distinction is frequently seen in cerebral vasculardisease where the smaller intracranial arteries maybe free of disease when the changes are far advancedin the larger extracranial arteries. Indeed it isimportant in any study of cerebral ischaemia toappreciate that occlusive disease of the carotidartery occurs as frequently as occlusion of themiddle cerebral artery, and that occlusion of thevertebral artery occurs more frequently in itscervical course than does occlusion of either thebasilar or the posterior inferior cerebellar artery.A point of additional significance in the pathologyof these cases-important to the surgeon-is thefrequent localization of atheromatous disease in theinternal carotid artery at a point i cm. above itsorigin and in the vertebral artery to the portionlying between its origin from the subclavian arteryand the vertebral arterial canal. WVhatever thefundamental pathological lesion may be inatheroma haemorrhage into the base of theplaques in the carotid artery frequently occurs(Yates, I954) and Rob (I959) has emphasized theimportance of such an event in the pathogenesis ofclinical symptoms in carotid arterial occlusion.

Examination of any large series of patientscoming to autopsy with cerebral infarction showsthat between one-third and one-half of thesepatients have advanced disease of the carotid and

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the vertebral arteries in various combinations.Commonly, arterial disease is usually found in boththe carotid and the vertebral arteries producing inthe four vessels varying degrees of stenosis andocclusion. Less frequently the disease is confinedto the carotid artery alone and, least common of all,the atheromatous changes are present only in thevertebral arteries.

It is now generally agreed that the developmentof symptoms in cerebral vascular disease may berelated in part to the available collateral circulation.The important sites in the development of a col-lateral circulation in cerebral vascular disease areas follows:-

i. Anastomoses over the cerebral hemispheresand the cerebellum between the superficialbranches of the major arteries-points where con-siderable anastomotic channels have been demon-strated by injection studies (Van der Eecken andAdams, I953). The importance of these anasto-moses in occlusion of the middle cerebral arteryhas already been demonstrated in life by angio-graphy (Rosegay and Welch, I954).

2. Anastomoses between the carotid and thevertebral arteries when one or other is occluded,and the most important site of anastomosis underthese circumstances is the Circle of Willis.

3. The potential collateral circulations betweenthe external and internal carotid arteries via theophthalmic arteries; the anatomy of these has beenfully defined by Weiss (1938).

4. When considering the collateral circulationin any given case the effect of congenital vascularabnormalities must be considered. Anomalies ofthe Circle of Willis, unimportant in health, may bevital in disease if the anomaly affects the establish-ment of an effective collateral circulation throughthe Circle of Willis when the carotid, vertebral orintracerebral arteries are occluded. Similarly,variation in size of the vertebral artery, present to asignificant degree in three-quarters of the patientscoming to post mortem (Stopford, I921) mayassume great importance if the larger of the two isoccluded by disease.

Areas of cerebral infarction in the brains ofpatients dying from ischaemic cerebral vasculardisease are frequently multiple, and may be presentin both the cerebellum and the cerebral hemi-spheres if both the carotid and the vertebralarteries are involved by disease. The infarct maybe found within the territory of an intracerebralartery if the atheroma is confined to the localvessel of supply but the infarct may also occur atjunctional territories-for example the junction ofthe middle and posterior cerebral arteries over theposterior parietal areas-if the cause of infarction isocclusion of the carotid and the vertebral arteries

which has led to a reduction of the total cerebralblood flow.

Clinical AspectsThere is already an extensive body of literature

on the neurological findings in cases of internalcarotid thrombosis and a detailed review hasalready appeared in this journal (Behrman, 1954);all the available literature emphasises the widevariations in the clinical presentation in these cases.These variations are in part determined by thedegree and distribution of the atheroma in theextracranial vessels so that the diagnosis of internalcarotid thrombosis applied to every case mayobscure the fact that the symptoms may also bedue to extensive disease of the other major vesselsof supply to the brain.

Surgical experience has shown that ligation ofone carotid artery may be carried out in theyounger patient without sequelae, and it is notsurprising, therefore, that occlusion of onecarotid artery by atheroma may be present withoutsymptoms. One of the most common presenta-tions of internal carotid thrombosis is for thepatient to present with symptoms and signs almostidentical with those of middle cerebral thrombosis.The usual sequence of events in these patients isfor the thrombus to extend from the site of diseaseat the origin of the carotid artery across the Circleof Willis and thus occlude the middle cerebraland frequently the anterior cerebral artery.Clinical difficulties may occur in these circum-stances when the infarcted brain becomes sooedematous as to produce signs of raised in-tracranial pressure (Clarke and Harris, 1958).

Extension of the thrombus from the internalcarotid artery directly into the intracerebralarteries has been observed, not only in athero-matous disease of the carotid artery, but also as acomplication of pregnancy in the postpartumperiod.

Case i.The patient, a woman of 24 years of age, had

been delivered normally of a child ten days beforeadmission to hospital. A week after delivery thepatient complained of a sudden attack of involun-tary movements of the right hand, and it wasprobable that during this first attack, she wasdysphasic. The attack lasted for some 20 minutes,and when she recovered she complained of head-ache over the left eye. Following this the patientwas depressed and confused, and it was clear thatfrom time to time she lost her speech for periodsof several hours on each occasion. The followingday she was transferred to hospital and she was seenfor the first time ii days after delivery. At thistime the patient was semi-conscious and totally

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aphasic. There was a dense right hemiplegia witha marked degree of sensory loss, but the modalitiesaffected could not be assessed in view of thepatient's mental state. The patient was of slightbuild and the neck was slim, so that examination ofthe cervical vessels could be carried out with ease.Normal pulsation of the carotid artery on the rightside could be felt, but on the left side there was nocarotid pulsation, and in addition a hard andthickened cord was pre'sent. The cerebro-spinalfluid showed a resting- pressure of I90 mm. ofwater, but the fluid was -clear and colourless andwas of normal cellular and protein content. Thepatient died in the early hours of the followingmorning, IX days after delivery.At post mortem the essential findings concerned

the central nervous system and the carotid arteries.There was a complete thrombosis of the left com-mon carotid artery from its point of origin in themediastinum extending into the middle cerebralartery within the skull. The left cerebral hemi-sphere was infarcted and oedematous. Therewere no other significant features in the generalpost mortem.

The clinical presentation which has received themost attention in the literature is that in whichtransient episodes of neurological disturbance area feature of the history. The patient may besymptom free between these episodes or they mayoccur against a background of a progressiveneurological deficit. Disturbances of speech,motor power and sensation, may all-occur, as maytransient visual disturbances. These last areusually represented by attacks of monocularblindness affecting usually the same side as that ofthe diseased carotid artery. The attacks of dis-turbance of vision may last for minutes or severalhours, and they may disappear completely after atime or permanent impairment of vision maydevelop as a result of retinal artery occlusion.

These visual disturbances associated withcarotid artery stenosis have led to the measurementof retinal artery blood pressure with an ophthalmo-dynamometer. The results, in what may be apromising investigation in this condition, havebeen reviewed by- Hoyt (I959).

In this group of patients with recurring clinicalepisodes it is not uncommon at post mortem tofind atheroma causing stenosis in more than oneof the major arteries, and it seems reasonable tosuppose that many of these clinical episodes in thisgroup represent transient failures of the collateralcirculation-a circu-lation which may dependeither on the contralateral carotid artery or on the,vertebral arteries. Sudden failure of the cerebralcirculation as a whole may occur in these cases bythe sudden reduction of the cerebral blood flow by

the elevation of an atheromatous plaque in thecarotid artery by haemorrhage into the depths ofthe plaque as described by Rob -(959). Thefollowing patient is an illustration of the clinicalhistory and pathological findings in- this group ofcases where the atheroma involves both the carotidand the vertebral arteries:-

Case 2

The patient, a male aged 51 years, complainedthat one year before admission he had sudden;lydeveloped weakness of the right hand and, equallysuddenly, lost the sight of his right eye. Thesesigns cleared completely, but six months later henoted a further transient episode of weakness ofthe right arm and leg with some slurring of speech.A month after this he developed weakness of theleft arm, leg and face with a return of the speechdisturbance. When admitted to hospital theabnormalities in the nervous system comprised aleft homonymous hemianopia with sensory im-pairment down the left side of the body. Therewas also clear evidence on neurological examina-tion of a parietal lobe lesion.A right carotid angiogram showed complete

occlusion of the internal carotid artery. His sub-sequent progress was one of slow deteriorationwith occasional episodes of weakness of both theright and the left sides of the body. For the lasttwo months of his life the patient was confusedand agitated, sinking into coma in the last week ofhis life.At post mortem the significant abnormalities

were present in the brain and the cerebral vessels.The brain (Fig. i) showed patchy areas of infarc-tion throughout both the anterior cerebral andmiddle cerebral arterial territories. 'These changeswere estimated to be of two to three months'duration, and were most marked in the right hemi-sphere, but both the brain stem and basal gangliawere free of infarction. In the cerebellum therewas a recent bilateral infarction involving almostthe whole of the territory of the superior cerebellarartery.On examining the vessels the intracranial vessels

showed minimal atheroma only. In the extra-cranial portion (Fig. 2) both internal carotidarteries showed old, shrunken, re-organizedthrombus extending on both sides from the neckbeyond the origin of the ophthalmic arteries, butnot into the intracrariial vessels. In the sinusregion overlying the old organized thrombus fairlyrecent new thrombus had been deposited. Theleft vertebral artery: showed an old organizedthr6mbus from its origin to the level of the secondcervical vertebra. The right vertebral arteryshowed minor atheromatous plaques only.

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FIG. i.-Diagrams showing distribution of cerebral and cerebellar infarctsand the extent of occlusion of the major arteries supplying the brain.

The clinical history in these patients may verywell suggest a vascular lesion as the underlyingcause, but sometimes the clinical diagnosis maynot be by any means so easy. Dementia maydominate the clinical picture from beginning toend as Fisher (1954) has already emphasized.Moreover the clinical history may be one of a slowand steadily progressive picture of disease of one orboth cerebral hemispheres so that the clinicalpresentation is indistinguishable without angio-graphy from an intracranial neoplasm.

Carotid and vertebral arterial disease may be

present without symptoms, but any illness pro-ducing sudden hypotension may unmask theinadequacy of the cerebral circulation. Haemate-mesis, coronary occlusion, post-operative shock,may all produce this effect, as may any other cause-of hypotension. Loss of consciousness or deathmay follow the episode of hypotension, or, if thepatient survives, transient or permanent neuro-logical signs may be apparent.

Disease of the vertebral arteries in their cervicalcourse may be the sole manifestation of cerebralvascular disease. Resulting ischaemia may give

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N4N4

FIG. 2(a).

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FIG. 2(b).FIG. 2.-Horizontal sections of the neck to show the state of the four major

cerebral vessels (a) just above the carotid bifurcation to show bothinternal carotids occluded by thrombus and the left vertebral by organizedthrombus, (b) to show both internal carotid arteries shrunken and fusedwith surrounding tissue at level of third cervical vertebra.

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rise to symptoms indicative of a brain stem, cere-bellar, or occipital lobe infarction (Hutchinson andYates, 1957; Crawford et al., 1958; Duffy andGrant, 1958). The clinical syndrome resultingfrom disease of the vertebral artery in its cervicalcourse bears a close relationship to the syndromeof basilar artery occlusion as it was defined byKubik and Adams (1946) and later by Millikanand Seikert (1955), a similarity which is not sur-prising since both ultimately supply approximatelythe same territory of the brain. Many points ofthe syndrome remain to be classified, one of themost important being the natural history of thedisease. As far as personal experience andpublished work will allow the patients may bedivided into two groups, the division dependingupon whether or not transient neurologicalsymptoms indicative of brain stem ischaemia occurbefore the final fatal illness.

If no such transient neurological episodes occurand the patient when seen by the physican, for thefirst time, is in coma-a not infrequent occurrencein these patients-then vertebral artery occlusioncannot be distinguished from any other form ofcerebral vascular disease. However, the loss ofconsciousness may be slow and if seen in the earlystages the signs of brain stem ischaemia may beelicited and the possibility of vertebral arterial oc-clusion may be considered, under these circum-stances. The diagnosis may be very much easierif transient neurological episodes occur before thefinal fatal illness. One may anticipate from thefact that the symptoms arise in the brain stem thatthe symptomatology may be very variable. Attacksof double vision, vertigo, unsteadiness and inco-ordination of the limbs and mental confusion, haveall been described. Visual disturbances too, arefrequent and this is not surprising, since occipitallobe infarction has been noted in these patients atpost mortem as a result of vertebral arterial oc-clusion. Crawford et al. (I959) mentioned bilateralblindness and hemianopia as occurring in theircases of vertebral arterial occlusion, and it may wellbe, as Symonds and Mackenzie (1957) havesuggested, that some examples of the syndrome ofthe bilateral posterior cerebral artery occlusionmay be due to disease of the vertebral arteries intheir cervical course. The following clinical ac-count gives the details of a patient who complainedof transient neurological episodes prior to the finalfatal episode.

Case 3The patient, a man of 57 years, was operated on

in 1945 for a mastoid infection and followingoperation remained well for I1 years. In 1958 hefirst complained of vertigo and vomiting. Inspite of the previous medical history no adequate

aural cause could be found for these attacks, andthey continued at frequent intervals until June of1959. In June 1959, an attack of vertigo andvomiting was accompanied by severe bifrontalheadache and over 48 hours the patient becamedrowsy and mentally confused. When he wasadmitted to hospital, in addition to the drowsinessand mental confusion, the patient was found to bemute. In addition, on formal examination of thecentral nervous system, there was well markednystagmus on lateral deviation of the eyes, a leftsided Horner's syndrome, and a left facial palsy.There was also evidence of a marked right hemi-plegia with sensory loss over the right side of thebody. The degree of sensory loss could not be de-termined in view ofthe patient's mental state. Un-fortunately, in view of the patient's mentalconfusion, the state of the visual fields could notbe assessed. The patient remained in this statewith minor fluctuations of consciousness for twoand a half months before he died.At post mortem the essential pathological

findings were confined to the cerebral vessels andto the brain. On examination of the brain therewas a bilateral infarction in the distribution of thecalcarine fissure, but no occlusion of the posteriorcerebral vessels could be demonstrated. In thecerebellum there was bilateral infarction of theterritory of the superior cerebellar arteries andagain no occlusion of these arteries could befound. Both the infarct of the cerebellum and theoccipital lobes was considered to be of aboutbetween two and three months' duration. Onexamination of the vascular tree there was someminimal atheroma in the carotid arteries at theirorigin. Both posterior communicating arterieswere extremely small, and this congenital anomalywas probably important in the pathogenesis of theinfarction in this particular case. The examina-tion of the vertebral arteries in the vertebral canalshowed that there was a considerable difference insize between the two, the right being the larger.The left vertebral artery was partially occluded byatheroma at the level of the third cervical vertebra,but the right vertebral artery at the same level wascompletely occluded by both atheroma andthrombosis.The findings in this patient are in every way

typical of the syndrome of vertebral arterialocclusion.

The similarity between these patients and oc-clusion of the basilar artery has already beenstressed, but there is one set of circumstances inwhich the differentiation between the two may bemade, and that is where there is clinical evidenceof disease of the major vessels of the aortic arch.Signs of disease of the major vessels of the aortic

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arch in the older age groups are due to atheroma inthe majority of patients (Crawford et al., 1959).It is interesting to recall that Broadbent in I875 ina paper entitled ' Absence of Pulsation in bothRadial Arteries, the Vessels being full of Blood,'described a patient with absent radial pulses dueto atheroma of the subclavian arteries probablysuperimposed upon a congenital lesion. Thevertebral artery in the patient he described wasshown at post mortem to take an anomalousorigin from the aortic arch rather than its usualsite at the origin of the subclavian artery, and bydoing so it avoided the effects of atheromatousdisease at this site. Arterial occlusion andstenosis of the subclavian artery may frequently bepresent without symptoms, and in six patientsrecently observed with this condition only threecomplained of symptoms of ischaemia in the upperlimbs. Four of these patients developed anintracerebral lesion and in three of these theintracerebral lesion had all the characteristics of abrain stem lesion. The following patient whocame to post mortem is an example of this:-

Case 4The patient, a man of 57 years of age, com-

plained in 1957 of attacks of tingling in the lefthand and a constant feeling of coldness andnumbness of this limb. It was noted at the timethat the blood pressure in the left arm was verymuch less than that in the right arm, and thepulses in the subclavian and axillary artery on theleft were very much feebler than the right. Thediagnosis of subclavian arterial stenosis was madeat the time. He remained well for the next twoand a half years, apart from an occasional com-plaint of tingling in the left hand, particularly incold weather. In the spring of 1959 he com-plained of attacks of vertigo which came on quitesuddenly, and when present caused some ataxia inwalking. In August, 1959, he suddenly com-plained of an attack of weakness of the left arm,a weakness which recurred several times a day for afurther seven days. On the third day followingthe first of these attacks of weakness of the arm hecomplained of sudden weakness of the left legwhich lasted for 24 hours. On August 20, hedeveloped persisting weakness of the left hand,and he was then admitted to hospital. On admis-sion to hospital the blood pressure in the right armwas 145/95, but the left radial and brachial pulseswere totally absent. Pulsation in the left sub-clavian artery could be felt but was diminished;the carotid pulses were of equal volume to palpa-tion on both sides. Examination of the centralnervous system at that time revealed a left lowerfacial palsy, some increased tone in the left arm,together with impairment of response to pin prick

of the left hand, and probably also in the left leg.Position sense in the left fingers was also defective.Both plantar responses were extensor. Thereflexes in the left arm were considerably briskerthan in the right. The diagnosis of vertebralarterial occlusion at the level of its origin from thesubclavian artery was made, and the patient madea slow recovery. Two months after this episodehe was seized with sudden abdominal pain andadmitted to hospital where he died suddenly I2hours after admission. At autopsy the cause ofdeath was shown to be a mesenteric artery oc-clusion. The vessels at the base of the brainshowed a moderate degree of atheroma and bothposterior communicating arteries were extremelysmall. The left vertebral artery was occluded bya plaque of atheroma at a point 1.5 cms. distal to itsorigin from an atheromatous and narrowed sub-clavian artery. There was an old area of softeningon the left side of the brain stem. The carotid-and intracranial arteries were normal.

This combination of arterial insufficiency in anupper limb, coupled with a brain stem lesion,makes a distinctive clinical picture and importantto recognize, since it is clear that surgical treatmentof atheroma at the origin of the vertebral arterymay be as effective as that of the surgical treatmentof carotid arterial disease (Crawford et al., 1958).No mention has so far been made of one

clinical sign which is of considerable importance inthese lesions-the cervical bruit. Rob (I959),in emphasizing the value of the sign, estimated thata bruit was present in over 25 per cent. of caseswith stenosis of the carotid artery and sometimesaccompanied by a palpable thrill. The bruit isoften harsh in quality, systolic in timing, and con-ducted into the skull, with a maximal intensitydirectly over the site of occlusion. When presentsuch a bruit may be heard clearly over the orbit.A bruit in the supraclavicular fossa of similarquality may be present with subclavian arterialdisease.

RadiologyRoutine radiology of the skull has little positive

information of value to contribute to the diagnosisof extra- or intracerebral vascular disease. It isimportant, however, since by demonstratingpineal shift or changes in the bony contours of theskull an indication of other intracranial pathologymay be given. Cerebral angiography, a techniquewhich made possible the demonstration ofthrombosis of the carotid artery in life, still remainsthe most important single investigation. Notonly has it added certainty to the diagnosis ofocclusion of the major vessels, but it has provideda rapid means of differentiating these lesions from

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other intracranial lesions. The increasing use ofanigiography in vascular disease has emphagizedthe frequent difiiculties of differentiating with anycertainty on clinical grounds between intracranial.and extracranial vascular occlusion.

Routine percutaneous carotid angiography willadequately demonstrate atheromatous disease atthe origin of the internal carotid artery and oc-clusion of the larger arteries within the skull.Disease of the vertebral artery is more difficult todemonstrate because of the intrinsic difficulties inobtaining angiograms of the artery itself. It isgenerally agreed that direct puncture of thevertebral arteries when atheroma is suspected is un-desirable, in view of the risk of precipitatingthrombosis. Catheterisation of the brachial arteryis satisfactory in expert hands (Sutton, I959;Pygott and Hutton, I959) or the alternative methodof injecting through the subclavian artery in thesupraclavicular fossa (Crawford et al., 1959;Morris, I959). Pneumothorax occurs in IO to 20per cent. of patients with the latter procedure,but it may be that this risk is preferable to directpuncture of the artery with its attendant danger ofprecipitating vascular occlusion. The most dif-ficult technical problem is the demonstration ofstenosis or occlusion of the origin of the majorvessels of the aortic arch. Crawford et al. (I959)have used the method of Robb and Steinberg(I939) for visualizing the origin of these vessels,and they report that they have used this methodsatisfactorily on 2,o patients for a variety of lesionswithout mortality or significant complications.

TreatmentAt the present time a patient cannot be offered

dietetic or other measures which will prevent withcertainty the development of atheroma. Therefore,in the foreseeable future, treatment of extracranialvascular disease will be concerned with medical orsurgical treatment of these lesions.

Medical treatment must include the manage-ment of the patiernt with the' acute stroke,' and therecovering hemiplegia. Little need be said aboutthe well-tried general principles of the treatmentof such patients, but there is no doubt that success,in terms of recovery of function of the affectedlimbs, will in part be determined' by the standardof efficiency of the nursing and physio-therapywhich the patient receives in the acute stages.The other major problem in the treatment of thesepatients is the question of anti-coagulant therapy.Earlier reports on the treatment of cerebralthrombosis and embolism with anti-coagulanttherapy (Foley and Wright, I950) were hopeful,and the later observations of Millikan, Siekert andShick (1955), Carter (I957) and Fisher (1958)encouraged their continued use. Millikan and

his colleagues were particularly impressed with thevalue of anti-coagulant therapy in the treatment ofthe basilar artery insufficiency. Clearly there aretwo aspects to the problem which must be con-sidered separately-the use of anti-coagulants inthe acute phase and the use of long term anti-coagulant therapy to prevent further occlusions-inthe cerebral vessels.In considering the use of anti-coagulants in the

acute phase of cerebral vascular disease there aretwo major difficulties. It has already beenemphasized that the increasing use of angiographyhas underlined the difficulty, not only in dif-ferentiating between intra- and ext-ra-cerebralvascular occlusion, but also in differentiatingbetween cerebral thrombosis and a circumscribedcerebral haemorrhage. This clinical differentia-tion is essential in the safe use of anti-coagulants inthe patient suffering from an acute cerebralvascular lesion. McKissock, Richardson andWalsh (1959) have recently reported an extensivestudy of spontaneous 'intracerebral haemorrhage,and illustrates in doing so the clinical difficultiesencountered. The other problem in the acutephase is the theoretical possibility, which has someexperimental support, that infarcts may becomehaemorrhagic with the use of anti-coagulants(Woods et al., I958; Sibley et al., I958).The whole problem of anti-coagulants in cere-

bral vascular disease has recently been reviewed byMarshall and Shaw (I959). They emphasizethat an estimate of the use of long term anti-coagulants presents difficulties sinice so little isknown of the natural history of the various types ofcerebral vascular disease. They report theirinterim results of a controlled trial of anti-coagulants in an acute cerebral vascular lesionand also the long term results of such treatment.It is to be hoped that this and other planned trialswill finally answer the difficult but importantquestion on the correct place of anti-coagulantsin the treatment of cerebral vascular disease.The surgical treatment of extracranial vascular

disease is on firmer ground. Originally thesurgical treatment was confined to arterectomy(Chao et al., 1938) or to sympathectomy (Johnsonand Walker, 195I), but the results obtained bythese methods were not very different from whatone might reasonably anticipate in the naturalhistory of the disease. The first successfularterial reconstruction was reported by Eastcott,Pickering and Rob (954), and Rob (I959) hasreviewed his later experience with 70 cases. Hisstatement that ' good results usually followsurgery when the occlusion is partial and poorresults when it is complete' summarizes his views.This clear cut difference between the results ofsurgery in partial and complete occlusions em-

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phasizes-the importanceef early-diagnosisr in thepatient with extracranial vascular disease. Although the surgery of complete occlusion of thecarotid artery has been disappointing Rob makesthe-important point that operation -on completeocc-lusions, if carried out early as arni emergencybefore the thrombus has timeto become adherent-tothe vessel wall, may very well be attended bygreater success. Sutrgery of the vertebral arteryhas not advanced to the same degree as- that of thecarotid, but it is to be hoped that with improvedradiological techniques reconstruction of thevertebral artery at its origin may also be possibleas described by Crawford et al. (1958).

Summaryi. The pathology of extracranial vascular dis-

ease, as it affects the clinical picture of cerebralischaemia, is described.

2. The clinical syndromes resulting from extra-cranial carotid and vertebral arterial disease aredescribed.

3. The place of anti-coagulants in the treatmentof cerebral vascular disease is discussed and thesurgical treatment of carotid occlusion andstenosis is briefly reviewed.

AcknowledgmentsWe wish to thank Professor D. A. K. Black and

Mr. R. T. Johnson for permission to publish theclinical details of cases 2 and 3 respectively.

REFERENCESARING, C. D., (I945), Brain, 68, 28.BEHRMAN, S. (I954), Postgrad. med. J., 30, 570.BROADBENT, W. H. (I875), Trans. clin. Soc. Lond., 2, I65.

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A Clinic for the diagnosis and treatment of Internal Diseases (except Mental or Infectious Diseases). TheClinic is provided with a staff of doctors, nurses, technicians, modern Radiological and Physiotherapydepartments.

The surroundings are beautiful. The climate is mild. There.is central heating throughout. The annualrainfall is 30.5 inches, that is less than the average for England.

The Fees are inclusive and vary according to the room occuDied.For particulars apply to THE SECRETARY, Ruthin Castle, North Wales.

Telegrams: Castle, Ruthin Telephone: Ruthin 66

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