of · brain-stem infarction was found in a review of over 100 cases of subclavian steal syndrome (North et al., 1962; Patel and Toole, 1965; Wheeler, 1967; Baker et al., 1973). The

Journal of Neurology, Neurosurgery, and Psychiatry, 1975, 38, 601-612

Role of cerebral angiography in vertebrobasilarocclusive disease

LOUIS R. CAPLAN AND ARTHUR E. ROSENBAUM

From the Departments of Neurology and Radiology, Harvard Medical School,The Beth Israel Hospital, and the Peter Bent Brigham Hospital, Boston, Massachusetts, U.S.A.

SYNOPSIS The authors attempt to separate clinical subgroups of patients within the larger categoryof vertebrobasilar artery disease, and to indicate the present role of angiography in their recognitionand management. Angiography is of use in separating posterior fossa occlusive vascular lesions fromspace occupying lesions. In addition, by defining the locus and nature of the occlusive process, it mayresult in more rational treatment and prognostication. Subgroups of vertebrobasilar ischaemia whichhave a favourable prognosis may be separable clinically or, in unclear cases, angiographically.

Recognition and description of clinical syn-dromes of brain-stem infarction flourished in thelate 19th and early 20th centuries (Weber, 1863;Jackson, 1864; Raymond and Cestan, 1901;Wallenberg, 1901). It was not until 1946, how-ever, that Kubik and Adams described occlusionof the basilar artery in postmortem examina-tions. These authors emphasized a dire prognosis.Subsequent reports described the clinical picture,which was called vertebrobasilar insufficiency(Denny-Brown, 1953; Siekert and Millikan,1955; Fang and Palmer, 1956; Williams andWilson, 1962; Williams, 1964); Browne andPoskanzer (1969), in a review of stroke treat-ment, also emphasized the grave nature of thedisease: 'If anticoagulation has value, it may bemore useful in the patient with vertebrobasilardisease, with its high mortality, than in otherforms of cerebral vascular thrombosis'.

Marshall's (1964) review of the natural historyof transient ischaemic attacks uncovered arelatively better prognosis for patients withvertebrobasilar ischaemic episodes than forthose patients with carotid ischaemia. Further-more, several groups of patients with ischaemicdisease of the posterior cerebral circulationseem to have a relatively good prognosis. Fisherdescribed several syndromes produced by lacunarAddress for correspondence: Dr Louis R. Caplan, Department ofNeurology, Beth Israel Hospital, Boston, Massachusetts 02215,U.S.A.(Accepted 10 February 1975.)

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infarction in the brain-stem related to smallvessel disease associated with hypertension: thedysarthria-clumsy hand syndrome (Fisher, 1967),pure motor hemiplegia (Fisher and Curry, 1965),pure sensory stroke (Fisher, 1965b), and homo-lateral ataxia and crural paresis syndrome(Fisher and Cole, 1965). These syndromes havea favourable outlook for recovery. Despitenumerous episodes of vertebral insufficiency, nota single case of pathologically documentedbrain-stem infarction was found in a review ofover 100 cases of subclavian steal syndrome(North et al., 1962; Patel and Toole, 1965;Wheeler, 1967; Baker et al., 1973). The puresyndromes of lateral medullary or lateral pon-tine infarction also have a good prognosis(Currier et al., 1958). Fisher (1970) has pointedout that occlusion of the vertebral artery in theneck commonly produces transient symptomsbut rarely produces brain-stem infarction unlessthe vertebral artery is occluded intracranially.Thus it must be clear that vertebrobasilar diseaseis not a homogeneous entity; some clinicalsubgroups have relatively better prognoses thanothers.The outcome in any given patient with poster-

ior circulation occlusive disease is dependent on:(1) the particular anatomy of the vertebrobasilarcirculation (developmental variations are verycommon); (2) the locus and rapidity of theocclusive process; (3) the physiological state of

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FIG. 1 Majorforms of vascular occlusion in the posterior circulation. 1. Medial hypertrophy ofsmall arteries.2. Obstruction of major vessel branches: a. atheroma in lumen ofparent vessel blocking orifice; b. atheromaextending into branch; c. thrombotic occlusion of branch. 3. Occlusion of vessel proximal to branch origin.4. Stenosis of large vessel by atheroma. 5. Embolic occlusion of vessel. 6. In situ thrombosis complicatingatheromatous stenosis ofa large vessel.

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Role of cerebral angiography in vertebrobasilar occlusive disease

the systemic circulation and haematologicalsystem; and (4) the availability of adequatecollateral circulation; congenitally deficient orpreviously obstructed cranial and extracranialvessels may diminish available collateral vessels.

Six major types of vascular pathology may beseen in occlusive disease of the posterior cerebralcirculation (Fig. 1): (1) disruption of smallpenetrating branches of vessels as seen in hyper-tension or arteritis (Fisher, 1969); (2) obstruc-tion of branch vessels produced by atheromablocking the origin of the branches or byintrinsic atheroma or thrombosis of the largerbranches themselves; (3) occlusion of a vesselproximal to the origin of the branch (Fisher etal., 1961); (4) major stenosis of the intracranialvertebral arteries bilaterally or of the basilarartery; (5) thromboembolic occlusion of majorcerebral vessels arising from the heart, aorticarch, or vertebral arteries; (6) in situ thrombosisof the vertebrobasilar arteries themselves. Itseems likely that the last three pathologicalentities would be associated with more seriousinfarction and a more grave clinical outcome.Also these varying pathologies would probablyrespond quite differently to therapeutic endeav-ours such as anticoagulation. Castaigne et al.(1973) have reviewed the loci and nature ofvascular changes in patients with occlusions inthe vertebrobasilar system discovered duringpostmortem examinations.The clinical differentiation between small and

large vessel disease is frequently difficult.Occlusions of small, penetrating branch-vesselsgenerally occur in hypertensive patients. Theanatomy of the infarct is usually limited toterritories supplied by a single median, para-median, or circumferential vessel. Small vessellesions are usually not accompanied by promi-nent headache, and the duration of time betweenoriginal ischaemic symptoms and completedstroke is usually short (hours to weeks). In con-trast, large vessel disease-for example, basilarartery-often produces bilateral signs not pro-duced by occlusion of a single penetratingbranch: the symptomatic period may be pro-longed, the symptoms more variegated and lessstereotyped, and headache may be prominent.Branch occlusion may be attended by morewidespread signs, however, depending on the

integrity of other branches and the general stateof the circulation.With the frequent use of selective vertebral

angiography and magnification radiography, itis now possible to define the individual anatomyand vascular pathology in many cases ofposterior circulation occlusive disease. Bydefining the vascular lesion, angiography mayhelp the clinician not only to prognosticate butto select the most appropriate treatment. Angio-graphy also may help separate occlusive vasculardisease from haemorrhage or tumour of theposterior fossa. In this paper, we analyse 11recent cases of occlusive vascular disease of theposterior circulation studied clinically andangiographically to illustrate the role of angio-graphy in clinical management of vertebrobasilardisease.

CASE 1

S.M., a 55 year old insulin-dependent, diabeticgypsy man had a 14 year history of hypertension andthree previous myocardial infarctions. A stroke hadproduced left hemiparesis which cleared after a fewmonths. One day before admission, he awakenedwith dysarthria and right facial weakness which re-solved in 30 minutes. The next day dizziness, rightfacial weakness, and dysarthria recurred but fluc-tuated during the day until right hemiplegia devel-oped. Examination revealed complete right hemi-plegia and shivering of his left limbs. The next day hebecame quadriplegic and developed bifacial paresis,dysphagia, and severe dysarthria. Electroencephalo-graphy was normal. Transfemoral cerebral angio-graphy (Figs 2a-c) demonstrated no filling of thebasilar artery above the level of the anterior inferiorcerebellar arteries. The left posterior inferior cere-bellar artery filled the left superior cerebellar arteryresulting in retrograde opacification of the upperbasilar artery. Bilateral carotid angiography showedno supratentorial circulatory abnormality. He wasplaced on anticoagulation therapy and was able towalk with help 11 months later. No additionalischaemic episodes have occurred in the 33 monthssince the original stroke.

COMMENT The presence of hypertension anddiabetes suggested either small or large vesseldisease in this patient. The clinical picture, how-ever, was more compatible with large vesselocclusion of the basilar artery. He was a sub-optimal candidate for anticoagulation because

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FIG. 2 Case 1. Near total occlusion of the basilar artery between the superior cerebellar and anterior inferiorcerebellar branchings. Collateral flow from posterior inferior cerebellar artery (PICA) to superior cerebellarartery (SCA). (a) Lateral projection: transient filling of the rostral basilar artery (arrow) is via the stenoticsegment. (Distal basilar artery, BA.) (b) Lateral projection; two seconds later: greater filling of the superiorcerebellar artery has resultedfrom flow through SCA branches (superior vermian and marginal). The posteriorcerebral artery isfaintly filled(white arrows). (c) 450 cross-table oblique projection: the central ray coursesfromlaterally between the petrous pyramids and shows the superior limit of the basilar artery (BA) occlusion justbelow the origin of the superior cerebellar arteries.

of his hypertension and nomadic nature. Asthere was arteriographic confirmation of basilarocclusion, anticoagulant therapy was useddespite relative contraindications.

CASE 2

D.S., a 78 year old mildly hypertensive widow, gave asix month history of intermittent dizziness withstaggering. On one occasion she recognized transientdysarthria associated with faintness. Six days beforeadmission she noted weakness of her legs on rising.Later the same day her left face, arm, and leg wereweak. The weakness gradually increased, and on themorning of admission there was diplopia on rightgaze and paraesthesiae of the left hand. Examinationrevealed a partial right sixth nerve palsy, a moderateleft hemiparesis, diminished palatal motion, dys-arthria, and bilateral extensor plantar reflexes. Theright sixth nerve palsy gradually cleared. Selectiveleft vertebral angiography demonstrated normalvertebral arteries and a minimally irregular basilarartery without stenosis or occlusion. She made anexcellent recovery clinically and remains self-sufficient at home two years later without furthertreatment.

COMMENT The clinical findings fit best with abasilar artery branch occlusion producing a

right median pontine infarction. The reducedpalatal movement, extensor plantar reflexes, bi-lateral leg weakness, and six month history oftransient ischaemia with dizziness did raise thequestion of disease of a larger vessel. Arterio-graphy failed to reveal serious large vesselpathology and led to the decision not to useanticoagulants.

CASE 3

A.W., a 46 year old mildly hypertensive Chineseman had had a myocardial infarction a year earlier.During the two weeks before admission, he hadthree transient episodes of nausea, vertigo, andataxia. Examination revealed a right sixth nervepalsy and a tendency to fall to the right while erect.In the hospital, he developed left hemianopsia. Rightvertebral angiography filled the posterior inferiorcerebellar arteries bilaterally but the basilar arterywas only faintly opacified (Fig. 3a). Left internalcarotid arteriography (Fig. 3b) showed retrogradefilling of the superior portion of the basilar arterywith excellent filling of the superior cerebellarvessels. The basilar artery was occluded for a shortsegment between the level of its anterior inferiorcerebellar and superior cerebellar artery branches.The patient did well on anticoagulant therapy andhas had no recurrent episodes.

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FIG. 3 Case 3. Focal occlusion of basilar artery below the origins of the superior cerebellar arteries. (a) Selec-tive right vertebral arteriography-lateral projection: the right posterior inferior cerebellar artery filled welldespite the prominent stenosis at its origin. Contralateral posterior inferior cerebellar branches subsequently fillwell. Above the level of the right PICA origin, the basilar artery (solid arrow) diminishes in calibre and washoutfrom this segment is slow. Only the posterior inferior surface of the cerebellum opacifies. (b) Left internalcarotid angiography-lateral projection: via a small posterior communicating artery, the ipsilateral posteriorcerebral and both superior cerebellar branches (SCA) fill well; the contralateral posterior cerebral artery isopacified, but less densely. The segment of occlusion between the proximal (Fig. 3b) and distal (Fig. 3a) portionsof the basilar artery is short.

COMMENT This patient's clinical picture ofcerebellar signs and symptoms along with aright sixth nerve palsy and right occipital lobelesion was confusing. Angiography demon-strated the serious nature of the vascular pro-cess, a clinically unsuspected basilar occlusion.These findings led to the choice of anticoagulanttherapy.

CASE 4

F.B., a 77 year old female with peptic ulcer disease,had a three week history of dizziness with falling andfrontal headache. Two days before admission shenoticed episodic dizziness, dysarthria, and inabilityto stand. On the day of admission, there were sixepisodes of dysarthria and quadriparesis. Examina-tion during a spell revealed severe dysarthria, bi-facial paresis, tongue protrusion to the left, quadri-paresis greatest in the left limbs, and bilateralextensor plantar reflexes. Between spells only a mildleft facial weakness and slight left ataxia were seen.Countercurrent right brachial arteriography showed

severe irregularity and stenosis in the superiorextreme of the right vertebral artery and the adjacentinferior portion of the basilar artery. She wastreated with anticoagulants and had not had a subse-quent stroke in two years of follow up. When theanticoagulant was stopped temporarily a year afteradmission, she again became vertiginous and fell onseveral occasions. These symptoms ceased upon re-institution of the therapy.

COMMENT This elderly woman had a relativecontraindication to anticoagulation (peptic ulcerdisease) with intermittent but severe symptomsof bilateral brain-stem dysfunction. Angio-graphy corroborated the serious nature of theunderlying pathology and led to anticoagulationwith special attention to ulcer management.

CASE 5

H.T., a 49 year old man with a gastrectomy forpeptic ulcer disease, had no history of hypertensionor cardiac disease but complained of intermittent

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606 Louis R. Caplan and

pain and coldness in his feet. For two weeks beforeadmission, he had intermittent blurred vision andheadache. Ataxia, dizziness, a weak feeling in thelegs, dysarthria, perioral paraesthesiae, and a feelingthat his eyes were turning were variably present atthe time of visual blurring. Examination betweenattacks was normal. Intravenous heparin therapywas instituted. Vertebral angiography showed nor-mal vertebral and basilar arteries with slow flow andsome delayed emptying. A careful haematologicalsurvey revealed a haemoglobin level of 16.7 g/dl, andan elevated platelet count of 360 OOO/mm3 but nodefinite clotting disorder. Aspirin (1 g per day) led toa remarkable alleviation of his neurological andperipheral vascular symptoms.

COMMENT The clinical history clearly sug-gested vertebrobasilar ischaemic spells andperipheral vascular disease. The absence ofsignificant vessel disease on cerebral angio-graphy resulted in a careful systemic search.The haematological disorder was uncovered butis still poorly characterized. The remarkable

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benefit from aspirin was believed to be related toits effect on platelet agglutination.

CASE 6

S.S., a 60 year old man had complained of inter-mittent headache, dizziness, and nausea for sixmonths. A month before hospitalization he had aspell of left-sided weakness lasting for several hours.On the day of admission he had felt weak at workand fell. Examination revealed a complete left hemi-plegia. Cranial nerves were normal except for persis-tent burning pain and tingling in his face bilaterally,worse on the right. A glucose tolerance curve showeddiabetes. Left vertebral angiography (Fig. 4) revealeda normal left vertebral artery with transient refluxinto the right vertebral artery. A few millimetres ofthe caudal portion of the basilar artery filled (Figs4a and c). The superior cerebellar artery filled fromhypertrophied hemispheric branches of the posteriorinferior cerebellar artery (Fig. 4b), resulting inopacification of the rostral basilar artery. Carotidangiography was normal with no opacification of the

FIG. 4 Case 6. Excellent posterior inferior cerebellar to superior cerebellar collateral circulation in distalbasilar artery occlusion. (a) Selective, left vertebral arteriography-lateral projection: the junctional segmentbetween the distal basilar artery and the origin ofthe posterior inferior cerebellar artery (PICA) fills transiently.The PICA is well developed and, via the inferior vermian branches, rapidly opacifies the superior vermianterritory ofthe superior cerebellar artery. Vertebral artery, VA. (b) One second later: both superior vermian andmarginal branches of the superior cerebellar artery (SCA) have opacified without basilar artery filling. (c)Chamberlain-Townes projection: only the distal extreme of basilar artery (BA) is shown on selective vertebralangiography. The hemispheric branches of the posterior inferior cerebellar artery (PICA) are hypertrophied andconnect with hemispheric branches of the superior cerebellar artery. The PICA to SCA vermian connections liein the midline.

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vertebrobasilar system. He has done well on anti-coagulants.

COMMENT Clinically, the lesion seemed toinvolve a penetrating branch of the basilarartery. However, the long duration of symptomsand persistent bilateral facial paraesthesiaeraised the question of large vessel disease. Thelatter diagnosis was confirmed by angiography.

CASE 7

J.L., a 72 year old man, had complained of recentsevere lethargy and vomiting felt to be related todepression. Examination revealed a lethargic manwith horizontal nystagmus and left limb ataxia.Subsequently bilateral limb and facial paresisdeveloped with bilateral extensor plantar signs andstupor. An electroencephalogram was diffuselyslow. Angiography revealed an obliterated leftvertebral artery and severe narrowing of the rightvertebral artery with no intracranial basilar arteryfilling. Heparin was administered, but the patientbecame comatose and died.

COMMENT The initial clinical impression ofmetabolic encephalopathy was unlikely becauseof the lateralized cerebellar signs. Angiographydefined a bilateral block of vertebral artery flowand clarified the diagnosis of infarction in theposterior cerebral circulation rather than hae-morrhage or mass lesion. The patient succumbeddespite the use of heparin.

CASE 8

M.B., a 58 year old man, suddenly became vertigin-ous, veered to the left, and felt an odd sensation inhis left limbs a month before admission. Thesesymptoms cleared after two days, but two weekslater he noticed pain in his left eye and nose and anodd metallic taste in his mouth as well as left-sidedweakness. At another hospital, left sixth nerve palsy,nystagmus, and left hemiparesis were found. Rightcarotid angiography was normal. He developedstiffness of his legs and transient stupor which im-proved after heparin administration. Examinationrevealed a left Horner's syndrome, decreased leftcorneal reflex, a left sixth nerve palsy, diminishedhearing on the left, left ataxia, and bilateral extensorplantar reflexes. The left vertebral artery could not becatheterized from either the left subclavian artery oraortic arch. The thyrocervical trunk was injected andmuscle branches of the left vertebral artery opacified

with opacification of the near inferior extreme of theleft vertebral artery. Right vertebral angiographyrevealed normal posterior inferior cerebellar arteriesand basilar artery with retrograde flow down the leftvertebral artery. He has done well on anticoagulanttreatment.

COMMENT This patient had two sudden episodesof brain-stem dysfunction, one thalamic and theother lateral pontine. Angiography revealed anoccluded inferior extreme of the left vertebralartery in the neck which was the likeliest sourceof embolization to the posterior circulationintracranially. Anticoagulation was used to pre-vent subsequent embolization.

CASE 9

D.T., a 72 year old diabetic hypertensive female,complained of headache and difficulty with walkingfor several months. Examination was normal exceptfor a shuffling gait, bilateral extensor plantar signs,and inconsistent horizontal nystagmus. A day afteradmission, lethargy, bifacial weakness, verticalnystagmus, and vomiting were noted. The clinicaldiagnosis was uncertain, but a space occupying lesionof the posterior fossa was suspected. Angiographyrevealed arteriosclerosis and delayed washout fromthe (smaller) right vertebral artery (Fig. 5a). Bloodflow through the (larger) left vertebral artery wasgreatly diminished (Fig. Sb). An occlusion of themidportion of the basilar artery was present. Bothposterior cerebral and superior cerebellar arteriesfilled via leptomeningeal anastomoses after middlecerebral artery opacification (Fig. 5c-d). Subse-quently she developed bilateral decorticate posturingand died despite anticoagulation therapy. Post-mortem examination revealed an old, partiallyrecanalized occlusion of the basilar and rightvertebral arteries. Extensive recent infarction affectedthe cerebral peduncles, pons, cerebellum, and medialoccipital lobes. The mid-pons was almost totallynecrotic.

COMMENT A confusing clinical picture of head-ache and shuffling gait suggested a mass lesion.Angiography demonstrated bilateral slowing ofvertebral blood flow and mid-basilar arteryocclusion and clarified the diagnosis. She dieddespite anticoagulation.

CASE 10

D.V., a 62 year old hypertensive diabetic man, after aday of chills and malaise, suddenly became un-

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FIG. 5 Case 9. Acute caudal basilar artery occlu-sion with thrombosis involving vertebral arteries.(a, top left) Right subclavian arteriography-frontal oblique projection: although the subclavianartery is densely opacified, flow through the rightvertebral artery (arrows) is slowed. The vertebralartery is tortuous and irregular in calibre and lessdensely opacified than the subclavian or internalmammary arteries. Washout from it is slowrelative to that of other cervical and subclavianbranches. (b, top right) Left vertebral arterio-graphy-frontal oblique projection: at the time ofinjection, considerable reflux of the 6 ml bolusoccurred into the subclavian artery but disappearedquickly. This angiogram (obtained seven secondsafter injection) shows filling of only the proximalportion of this vertebral artery (arrows). (c, left)Left carotid angiography-lateral projection, mid-arterialphase: diffuse advanced changes ofarterio-sclerosis affect the anterior and middle cerebralbranches. Posterior temporal branches (MCA) ofthe middle cerebral artery are well filled peri-pherally. (d, right) Left carotid angiography-latearterial phase. Retrograde filling of posteriorcerebral branches peripherally (PCA, whitearrows) from the middle cerebral artery vialeptomeningeal anastomosis results in filling of thesuperior portion of the basilar artery with inferiorflow into the superior cerebellar branches (SCA).

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FIG. 6 Case 11. Collateral circulationz via large anterior inferior cerebellar arteries in inferior basilar arteryocclusion. (a) Left vertebral arteriography lateral projection, early arterial phase. Excellent opacification ofthe left vertebral artery results in reflux into the right vertebral artery (RV) with demonstration ofan irregularlymarginated basilar obstruction just beyond the origin of the large AICAs. No posterior inferior cerebellarbranches were visualized. (b) Frontal projection arterial phase similar to (a). Hemispheric branches com-municating with the superior cerebellar territory are visualized. The occlusion of the basilar artery is again seen(arrow). Right vertebral, RV.

responsive while defaecating. Pneumococcal pneu-monia with high fever was recognized and treatedwith antibiotics. On the fourth day of illness, he wasalert but memory function was poor. When asked todescribe a picture, the patient would omit parts ofthe picture and would have difficulty in comparingsizes and distances within the picture. He would alsoomit words and sentences within a paragraph.Bilateral extensor plantar reflexes were present aswell as a minimal left arm weakness. After initialimprovement, a left gaze palsy and somnolencedeveloped. Electroencephalography revealed diffusedelta slowing. On the eighth hospital day, he becamedeeply comatose. Examination revealed small reac-tive pupils, no reflex eye movements, and bilateraldecerebrate posturing. Left vertebral angiographyrevealed delayed flow with no opacification abovethe left posterior inferior cerebellar artery. Byanalysing the plain radiographs of the neck andcomparing foramina transversaria, it was clear thatthe left vertebral artery was dominant. Basilar occlu-sion was suggested. He died despite rapid hepariniza-tion. Postmortem examination revealed occlusion ofthe right vertebral artery and lower basilar artery inan area of considerable atheroma. There was

extensive infarction involving the midbrain, pons,thalami, and bilateral temporal and occipital lobes.

COMMENT The early clinical picture was puzzlingbecause of the prominence of hemispheral signs(diminished alertness with poor visual andmemory function) and the absence of clinicalsigns of brain-stem dysfunction. Fever and sepsiswere complicating issues. Metabolic encephalo-pathy, infection of the central nervous system, orinfarction of watershed zones of the brain wereearly possible diagnoses. Angiography clarifiedthe diagnosis of occlusive disease of the posteriorcerebral circulation. Careful scrutiny of plainradiographs of the neck aided in confirming thatdelayed emptying involved the dominant verte-bral artery.

CASE 11

V.I., a 58 year old hypertensive man, had sufferedintermittent spells of dizziness, diplopia, andgeneralized weakness for one week. On the day ofadmission he awakened with dizziness. A right hemi-

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paresis and later transient apnoea occurred while hewas being examined in the Emergency Ward.Examination revealed bilateral partial sixth nerve

palsies and a slight right hemiparesis. Heparintherapy was instituted. While he was in hospital,the symptoms fluctuated considerably and were

worse when he sat or stood. Left vertebral angio-graphy revealed occlusion of the basilar artery justdistal to the bilaterally large anterior-inferior cere-

bellar artery branches (Fig. 6a-b). The posterior-inferior cerebellar arteries were not visualized.Anterior-inferior cerebellar artery branches filledthe superior cerebellar artery and distal basilarartery. He was placed on anticoagulants and had nosymptoms 15 months later.

COMMENT The clinical picture of bilateralabducens palsies and fluctuating weakness indi-cated vertebrobasilar artery disease. Because ofthe possibility of basilar aneurysm and hyper-tension, which represents a relative contra-indication to long-term anticoagulation, angio-graphy was performed. The presence of a totalbasilar occlusion led to anticoagulation.

DISCUSSION

Meyer et al. (1960) published their findings on 35patients in whom angiography of the posteriorintracranial circulation was performed by percu-

taneous subclavian or vertebral injection or byretrograde injection into the carotid artery. Ahigh incidence of stenosis of the basilar artery(seven out of 35) and stenosis of the cervicalvertebral artery were found. They commented:'In the majority of patients with insufficiency of thevertebral basilar system, the main site of disease is inthe basilar artery itself, and in those with disease ofthe cervical portion of the vertebral artery there isoften associated atherosclerosis of the basilarartery.'Since that time there have been several importantadvances in the clinical-pathological correlationof posterior circulation strokes, and many

advances in angiographic technique and capa-bilities. Fisher (1965a, 1967) has delineated theclinical and pathological picture related tobrain-stem lacunae, and Fisher and Caplan(1971) have discussed the pathology of basilarbranch occlusions.The advent of low-toxicity contrast media and

advances in the technique and experience of the

personnel performing vertebral angiographyhave made this procedure safer. A review ofseveral large recent series indicates that seriouscomplications are surprisingly rare. In a largeScandinavian series of over 200 cases of vertebralangiography (Torma and Fogelholm, 1967),seven of 249 patients undergoing vertebralangiography had serious neurological complica-tions all of which cleared within 72 hours.Weibel and Fields (1966) reported on 846 patientswho underwent trans-subclavian vertebral angio-graphy. Of these, 900 developed complications,all of which were local and minimal. There wereno deaths and no cerebral complications.Pribram (1965) cites two serious complicationsin 357 vertebral studies: an asymptomaticocclusion of the vertebral artery and the other acerebellar syndrome.The Seldinger technique for selective catheteri-

zation of individual brachiocephalic arteriesallows safe and more extensive study of theposterior circulation. Radiographic magnifica-tion provides greater resolution and bettervascular detail and is used routinely in our cases.Radner (1951), Schechter and Zingesser (1965),and Pochaczevsky et al. (1971) have reviewed theradiological anatomical details of posteriorcirculation angiography and have pointed outsome pitfalls in analysis of these studies. Othershave commented extensively on the radiographicfeatures of vertebrobasilar occlusive disease.Extensive analysis of the venous anatomy of theposterior fossa has not only corroborated arterialfindings but can be equally or more valuable inthe diagnosis of space-occupying vascular lesionsin the posterior fossa (such as cerebellar haemor-rhage or an oedematous cerebellar infarction).Since both cerebellar infarction and cerebellarhaemorrhage can produce death by brain-stemcompression and are often successfully treatedby decompressive surgery (Lehrich et al., 1970),differentiation of them and appropriate surgicalplanning can be life-saving.The occlusive nature of the pathology in our

patients was identified angiographically in cases7, 9, and 10, in whom the suggested clinicaldiagnoses were a metabolic disturbance or aspace-occupying lesion. In other cases, clinicallyconsidered to be vascular in nature, angio-graphy was instrumental in defining whether thedisturbance involved small or large vessels.

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Several patients with rather minor signs weresurprisingly found to have complete basilarocclusions (cases 3 and 6). Two patients withrather ominous clinical complaints and signsproved to have very little large vessel pathologyangiographically (cases 2 and 5) and were sparedlong-term anticoagulation. Four other patients(cases 1, 3, 4, and I 1) who were poor anti-coagulant risks had the diagnosis of severebasilar obstruction verified and were treatedwith anticoagulants despite the risks involved. Asource of posterior circulation embolization wasidentified in another patient (case 8) in the formof an occluded vertebral artery. A disturbance inflow without anatomical obstruction was sug-gested in case 5 and was perhaps related to ahaematological disorder. The remarkable re-sponse to aspirin is of interest in this case andwas considered to be related to its effect onplatelet agglutination. Four of our patients withverified basilar artery occlusion are alive at 30,29, 33, and 15 months after the stroke (cases 1, 3,6, 11). One of the patients has a residual para-paresis and another a mild hemiparesis; theother two patients have only minimal residualsigns and are essentially well. It is not wellappreciated that patients may indeed survive fora prolonged period after a total basilar occlusionwithout disabling neurological sequelae. Two ofthe patients (cases 7 and 9) had bilateral verte-bral artery occlusion. In our experience, bilateralocclusion of the intracranial vertebral artery hasoften presented a confusing clinical picture ofataxia, visual disturbance, and altered mentalfunction which has generally terminated fatally.The diagnosis may not be evident until arterio-graphy of the posterior circulation has been per-formed.

Unfortunately, optimal therapy of occlusivedisease of the posterior circulation remains anunsettled question. Early studies of anticoagula-tion in vertebral basilar disease did indicate somepossible benefit (Millikan et al., 1955, 1958;Hill et al., 1960). However, these early clinicalstudies grouped brain-stem ischaemia as asingle entity and only occasionally consideredtransient ischaemic attacks, strokes in evolution,and completed strokes as separate subgroupswithin this larger group. The underlying vascularanatomical and pathological derangements werenot considered. Little knowledge of the natural

history of the disease was then available forcomparison with the treated group. The role ofheparin and other anticoagulants needs clarifica-tion especially in those patients with seriousvascular lesions. The vascular anatomy, andtemporal state of the stroke (transient ischaemicattack, stroke in evolution, or completed stroke)should be important factors in deciding the typeof therapy instituted. The role of agents whichdiminish platelet agglutination-for example,aspirin and dipyridamole-in the therapy ofvertebral basilar disease has not been analysed.

REFERENCES

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of · brain-stem infarction was found in a review of over 100 cases of subclavian steal syndrome (North et al., 1962; Patel and Toole, 1965; Wheeler, 1967; Baker et al., 1973). The