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S U M M A R Y Ten patients with angiographically verified occlusion of the basilar or vertebral artery have
been followed for an average of 2.75 years. None has developed further ischemia after the initial stroke, and 4
patients survived without any clinical deficit. In occlusive disease of the posterior circulation, the critical period
for deficit acquisition is at the time of occlusion. Extent of the deficit depends on the rapidity of development of
adequate collateral circulation, and the presence of distal embolization at the time of occlusion. Some patients
survive basilar occlusion without permanent deficit.
Stroke Vol 10, No 3, 1979
OCCLUSION of the basilar artery is generally con- circulation. 46 No reference could be found on follow
sidered a very serious event incompatible with normal up of patients with angiographically documented
survival. Kubik and Adams 1 described 18 patients vertebrobasilar occlusive disease.
with brainstem infarction due to occlusion of the The author's files, and those of the Harvard Stroke
basilar artery discovered at postmortem examination Registry,7 were searched for patients meeting the
and emphasized the abrupt onset and frequent fatal following criteria: 1) patients who were examined and
outcome. Marshall2 subsequently pointed out that followed carefully by the author during hospitaliza-
many untreated patients with the clinical picture of tion for acute stroke; 2) technically satisfactory
posterior circulation vascular disease do not develop angiograms taken during the stroke which
serious deficits; however, the underlying vascular documented an occlusion of either a vertebral or the
pathology in this group of clinical patients was un- basilar artery; 3) patients who survived the acute
known. Occlusion of the vertebral artery, the most stroke and had been followed by the author more than
frequent cause of lateral medullary infarction iden- 6 months. The temporal profile of illness and clinical
tified at postmortem examination,3 has usually been outcome in this group of patients gave insights into the
associated with a relatively benign clinical course.4 In- pathogenesis of the clinical deficit and mechanisms of
frequent studies have attempted to correlate the compensation.
severity of the neurological deficit with angio-
graphically verified vascular pathology in the posterior Results
Case Material
From the Department of Neurology, Beth Israel Hospital and Ten patients (8 male, 2 female) from 26-71 years of
Harvard Medical School, Boston, MA.
Reprints: Louis R. Caplan, M.D., Chairman, Department of
age (average 52.2 years) were studied clinically and
Neurology, Michael Reese Hospital, 29th St. and Ellis, Chicago, IL angiographically. Six had occlusion of the basilar
60616. artery (2 proximal and 4 midportion beyond the
AICA branching). Four had an occluded vertebral weeks. In 4 of these 8 patients the clinical deficit fluc-
artery. All basilar occlusion cases had collateral cir- tuated with alteration of position in bed (3 when
culation involving the long circumferential cerebellar elevated, 1 when turned to the left side). Two patients
vessels (PICA, AICA, SCA) with late filling of the left the hospital without neurological abnormalities, 3
distal segment of the basilar artery. Patients with ver- had slight deficits, 4 moderate and 1 severe.
tebral occlusion had a patent contralateral vertebral Follow up ranged from Vi to 6 years (average 2.75
artery and basilar artery. Six patients had transient years). No patient developed a late increase in deficit
ischemic attacks (TIAs) prior to strokes. The time referable to the posterior circulation, and in 6 patients
between the initial TIA and the stroke ranged from 1 clinical deficits improved during the period of follow
week to 1 year (average 15 weeks). The last TIA up. Two patients with a slight deficit upon hospital dis-
always occurred within 1 month of the stroke (5 or 6 charge subsequently returned to normal. Six patients
within 1 week). TIAs were usually multiple (range have been treated with long-term warfarin; 2 patients
1-30, average 11). had temporary anticoagulant treatment (1 heparin for
After onset of stroke, 8 patients had either progres- 2 weeks, 1 warfarin for 6 months). No patient has had
sion of the deficit over a 2 or 3 day period, or had fluc- a new stroke, but 1 patient died of a myocardial in-
tuations of their clinical deficit during the first 2 farction 4 years after his pontine infarction.
Illustrative Cases
1. Patient 4
FIGURE 2. Patient 4: Retrograde filling of the basilar
A 46-year-old man with known coronary artery dis- artery (arrow) and superior cerebellar artery from a carotid
ease had 30 or more episodes of vertigo and diplopia injection.
during a 3 month period. He awakened during
December, 1975, with poor hearing and slurred speech
and staggered when he attempted to walk. Recovery a few seconds. He was placed in the Trendelenburg
occurred within hours, but later the same day he position and an intravenous infusion of heparin was
became mute and quadriplegic while awaiting ex- begun. By the next morning, a right internuclear
amination in the office of an otologist. Neurological ophthalmoplegia (INO) and slight left hemiparesis
examination within minutes revealed ocular bobbing remained; by day 7, examination showed return to
and no voluntary or reflex horizontal gaze. There was normal. Angiography revealed occlusion of the prox-
severe facial, palatal and lingual paralysis bilaterally. imal basilar artery; the left posterior inferior
The left limbs were flaccid, but the patient could cerebellar artery (PICA) filled the left superior
feebly lift his right arm and right leg from the bed for cerebellar artery (SCA) by branches coursing over the
cerebellar hemispheres, leading to delayed filling of
the distal basilar artery (figs. 1 and 2). A transient
brief deficit (right INO and left hemiparesis) followed
angiography. During hpspitalization the patient was
treated with intravenous heparin, subsequently
changed to warfarin. He has had no further attacks or
central nervous system deficits in the 2Vi years since
hospitalization. After 1 year, warfarin was discon-
tinued. He has been maintained on dipyridamole 150
mg, aspirin 20 grains and clofibrate 2 gm daily.
2. Patient 1
A 65-year-old male with a remote myocardial in-
farction (20 years) complained of intermittent
claudication of his legs. A year before hospitaliza-
tion, he had a brief episode of dizziness with diplopia.
Two weeks before admission an episode of diplopia
lasted 5 minutes. During the week before hospitaliza-
tion, there were 4 brief spells of dizziness with
diplopia; on one other occasion he suddenly slumped
to the ground without paralysis. An ophthalmologist
whom he consulted discovered weakness of the right
FIGURE I. Patient 4: Vertebral angiogram lateral view. lateral rectus muscle. On the morning of admission in
Filling of the PICA and cerebellar branches of the vertebral December, 1974, he noted dizziness, slurred speech
artery without filling of the basilar artery. and numbness, and weakness of his right limbs. A left
Discussion
5
FIGURE 3. Patient 5: Right vertebral angiogram revealing Meyer et al. described the angiographicfindingsin
filling of the PICA but no distal vertebral opacification 35 patients with occlusive disease of the posterior cir-
(arrow) culation and emphasized the frequency of abnor-
malities in the basilar artery itself. Clinical course and (sometimes after death of cerebral tissue, i.e., stroke)
follow up data were not included in the report, which which is generally resistant to further hemodynamic
excluded "critically ill patients" or those with severe crises. In addition, stabilization of the clot (days to
brainstem infarction. Nonetheless, angiography in 2 weeks) is usually associated with a cessation of late
patients revealed clinically unsuspected complete emboli arising from the region of thrombosis.
occlusion of the basilar artery. Archer and In some patients, e.g., group 3 (patient 10) throm-
Horenstein6 discussed the angiographic findings in 20 bosis may produce a progressive clinical course over
patients with basilar occlusion. Their clinical group days without preceding TIAs. In our experience, in
consisted of patients with severe clinical deficits in patients with progressing stroke due to lacunar infarc-
contrast to Meyer's criteria for selection.3 Fifteen of tion or internal carotid artery occlusion, the prognosis
Archer and Horenstein's patients were stuporous or is poorer than for those patients with TIAs or fluctuat-
comatose at the time of angiography and 2 were ing course. The recovery phase of a TIA or fluctuat-
"locked-in"; 15 patients died, 4 were severely disabled ing thrombotic stroke may be due, at least partially, to
and 1 patient had a moderately severe deficit the presence of adequate collateral circulation.
(hemiparesis). These authors defined the locus of Progressing stroke may indicate poor collateral poten-
occlusion and the pathways of collateral circulation tial, and so a worse prognosis. The single patient in
and sought to correlate the anatomy of the clinical group 3 in this report had the most severe deficit of
deficit with angiographic findings. Caplan and Rosen- any of our 10 patients.
baum4 pointed out the utility of vertebrobasilar Jones, Millikan and Sandok11 described the tem-
angiography in differentiating severe obstructive dis- poral profile of 37 patients with a clinical diagnosis of
ease of the vertebral or basilar artery from "small vertebrobasilar system infarction. None of the
vessel" disease within the posterior circulation, and patients had angiographic definition of the underlying
emphasized the frequent benign outcome of many vascular pathology, but all 10 patients who died had
patients with clinical vertebrobasilar symptoms who occlusion of a vertebral or basilar artery at post-
had no major vascular lesions seen angiographically. mortem examination. Twenty-two of their 37 patients
Caplan and Rosenbaum also pointed out that patients had reached maximum deficit within 24 hours, and
with known basilar occlusion may survive without dis- some other patients progressed over a period of 4
abling neurological sequelae. The present report seeks days. No patient had progression of signs after 1
to extend and explain that finding. week, and there were no known late exacerbations.
The initial period of TIAs, in group 1 patients, Since little data exist concerning the clinical tempo
likely represents diminished flow referable to vascular of angiographically verified vertebrobasilar occlusion,
stenosis. When occlusion of the vertebral or basilar it will be useful to compare the clinical course of our
artery becomes complete, a hemodynamically un- patients with that of patients with known occlusion of
stable situation develops in which collateral circula- the internal carotid artery (a vessel of comparable size
tion must develop quickly or there will occur irreversi- and length). Fourteen patients, personally examined,
ble ischemia of brainstem, cerebellum, or posterior with angiographically documented occlusion of the in-
cerebral territory hemispheral tissue. During this ternal carotid artery were followed an average of 3
period of development of collateral circulation (1-21 years. Eight had TIAs, 2 sudden onset deficits, and 4
days), hemodynamic changes (arrhythmia, bleeding, gradually progressive onset over days. Fluctuations of
or hypotension) and alteration of position may be clinical deficit occurred during the first 2 weeks but the
critical. 8 ' 9 The slight changes in cerebral blood flow patients remained stable thereafter irrespective of
which occur on sitting may be enough in these patients treatment (8 untreated). Two of these patients had late
with marginal vascular compensation to produce (greater than 1 year post-stroke) episodes of
clinical ischemia. Positional ischemia has been limited amaurosis fugax; each, in addition to the carotid
to patients with basilar or bilateral vertebral occlusion occlusion, had severe stenosis of the ipsilateral exter-
and has not been seen in patients with unilateral nal carotid artery and 1 had, in addition, stenosis c{
vertebral occlusion, presumably because of an ade- the ophthalmic artery. No patient developed a late
quate contralateral vertebral supply. As thrombosis permanent or transient central nervous system deficit
occurs, embolization distally within the vertebro- on the side of prior carotid occlusion. Barnett and
basilar system may lead to sudden posterior circula- Aldis12 specifically studied the question of delayed
tion clinical deficit. Embolization distally is the cerebral ischemia distal to occlusion of a major
presumed mechanism of presentation in our group 2 cerebral artery. Of 426 patients, there were only 12 oc-
patients with sudden onset deficits, and in patient 5 currences of subsequent events, 4 within the first 2
with a sudden deficit following TIAs in whom nonfill- weeks (1.9% late occurrence). Of the late occurrences
ing of the left superior cerebellar artery (a clinically 3 were amaurosis fugax alone, 6 were cerebral alone
affected vascular territory) favored an embolic and 3 were amaurosis fugax and cerebral. One patient
mechanism. Embolization in the posterior circulation had common carotid stenosis ipsilateral to an internal
has been documented on postmortem examination by carotid artery occlusion but episodes ceased after
others.10 Meyer et al.6 and Sundt, Whisnant et al.9 complete common carotid artery occlusion. In 3
have also emphasized the role of emboli arising from patients documented hemodynamic changes occurred
proximal vertebrobasilar occlusion. After a period of (2 postural hypotension and 1 ventricular arrhythmia).
several weeks, a stable collateral circulation develops Barnett13 subsequently reported that 25 of 235 patients
enrolled in a cooperative study of antiplatelet aggrega- (weeks or a few months) anticoagulation may be
tion drugs had cerebral ischemia subsequent to known hypothetically useful in preventing embolization or
occlusion. One of these patients had a basilar artery acute extension of the clot. A clinical trial of conserva-
occlusion, and another a bilateral vertebral artery tive medical therapy with short term anticoagulation
occlusion in the neck. Barnett and Aldis12 and or agents which decrease platelet agglutination (e.g.,
Barnett13 expressed the belief that late episodes aspirin, dipyridamole, or sulfinpyrazone) seems
represented embolic material breaking off from the worthy of consideration as opposed to the present
top of the prior occlusion, or, more commonly, em- practice in many centers of long term warfarin
bolization from diseased external or common carotid therapy. Intracranial bypass grafts (e.g., occipital to
collateral supply. In other series of patients with PICA shunts) might be reserved for those unusual
carotid occlusion reported in the literature late patients with documented extensive stenosis of major
episodes occasionally occurred but insufficient details vertebral or basilar vessels with repeated episodes of
were given regarding the nature and locus of the late ischemia unresponsive to conservative treatment.
ischemia.
The patient population reported herein represents a References
selected group of patients with vertebrobasilar disease
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1) Some patients with occlusion of the basilar vertebrobasilar arterial system. Arch Neurol 2: 27-45, 1960
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Our data suggest that in the group of patients with mortem data. Brain 96: 133-154, 1973
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Stroke. 1979;10:277-282
doi: 10.1161/01.STR.10.3.277
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright 1979 American Heart Association, Inc. All rights reserved.
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