Surg Neurol
1986;25:39-42

39

Basilar Artery Occlusion after Superficial Temporal
Artery-Superior Cerebellar Artery Anastomosis
Takashi Minakawa, M.D., Ryoji Ishii, M.D., Ryuichi Tanaka, M.D., and
Makoto Hayano, M.D.
Department of Neurosurgery, Brain Research Institute, Niigata University, Niigata and Mito Saiseikai Hospital, Mito, Japan

Minakawa T, Ishii R, Tanaka R, Hayano M. Basilar artery occlusion
after superficial temporal artery-superior cerebellar artery
anastomosis. Surg Neurol 1986;25:39-42.

Superficial temporal artery-superior cerebellar artery anastomosis for basilar artery stenosis was performed in a
patient who had experienced recurrent nonhemispheric
symptoms, and whose angiogram revealed a midbasilar
stenosis. Four months after the operation he was readmitred to our hospital complaining of transient motor
weakness and numbness of the left extremities. No neurological deficit was found on admission, but 1 hour later
the left-sided hemiparesis occurred again and progressed.
On the angiograms the upper basilar system was visualized via the superficial temporal artery, and the midbasilar
artery was occluded. This conversion seemed to be a natural course rather than the influence of the hemodynamic
change after the operation.
KEYWORDS: Anastomosis; Basilar artery; Occlusion; Stenosis;
Superior cerebellar artery; Superficial temporal artery

In recent years superficial temporal artery-superior cerebellar artery (STA-SCA) anastomosis for basilar artery
stenosis has been performed in patients suffering from
brainstem ischemia [1-3]. However, the management
of intracranial artery stenosis remains controversial, and
it is not known what effects the bypass surgery has on
the evolution of a bypassed arterial stenosis [9]. Re,
cently we encountered a patient who had suffered from
left-sided hemiplegia 4 months after S T A - S C A anastomosis for basilar artery stenosis, and whose angiogram
revealed occlusion of the basilar artery. This case is reported, and the possibility o f progression o f stenosis to
complete occlusion o f the arteries after revascularization
procedure is discussed.

Address reprint requests to: Dr. Takashi Minikawa, Department of
Neurosurgery, Brain Research Institute, Niigata University, Asahimachi 1, Niigata City, Japan 951.

© 1986 by Elsevier Science Publishing Co., Inc.

Case Report
A 53-year-old man was admitted to our hospital on November 22, 1983, complaining of motor weakness o f
the left extremities and double vision. For 1 year prior
to admission he had experienced motor weakness and
numbness of his left extremities, blurred vision, and dull
occipital pain almost every day. With rest, these symptoms disappeared within 30 minutes. The past history
included a 2-year history of hypertension, treated with
antihypertensive agents. Neurological examination revealed a right oculomotor palsy (limitation of ocular
movement and a slightly dilated pupil), left hemiparesis,
broad-based gait, and numbness of the left arm. Lumbar
puncture provided cerebrospinal fluid with a normal cell
count and protein content. The ophthalmoscopic examination demonstrated marked arteriosclerotic changes
in the retinal arteries. Computed tomography scans, with
and without contrast medium, suggested cerebral infarction of the medial surface of the right frontal lobe,
but no detectable lesion was found in the brainstem. As
it was supposed that he suffered from ischemia of the
brainstem, he was treated with the antiplatelet drug ticlopidine hydrochloride and intravenous low-molecularweight dextran starting on the day of admission. On
December 6 and 9, 1983, cerebral angiography was performed, but we could not insert the catheter via the
femoral arteries into the abdominal aorta, because of
tortuous iliac arteries. A left direct common carotid angiogram demonstrated the occlusion of the A2 segment
of the right anterior cerebral artery, whose territory was
supplied by retrograde filling from the right middle cerebral artery. A left retrograde transbrachial vertebral angiogram showed greater than 9 0 % midbasilar stenosis
at the part just distal to the origin o f the anterior inferior
cerebellar artery. The narrowed segment was about 10
mm long on the angiogram (Figure 1). The posterior
communicating arteries were not visualized on the carotid angiograms. About 3 weeks later he recovered
without neurological deficit, and no more ischemic episodes occurred. Because the patient was considered to
have a high risk of further brainstem infarction, a re0090-3019/86/$3.50

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Surg Neurol
1986;25:39-42

Minakawa et al

Figure 2. Right common carotid angiogram showing good filling of the
upper basilar system via the dilated superficial temporal artery (arrowheads).

Figure 1. Left transbrachial retrograde angiogram disclosing a severelongsegmented stenosis, about I 0 mm long, just distal to the origin of the anterior
inferior cerebellar artery (arrow).

vascularization procedure-anastomosis between the superficial temporal artery and the superior cerebellar
artery-was planned.
On February 23, 1984, the patient underwent the
revascularization procedure. An end-to-side anastomosis was performed between the distal end of the frontal
branch of the right superficial temporal artery and the
ambient portion of the right superior cerebellar artery.
Postoperatively he was neurologically normal except for
a right trochlear nerve palsy that disappeared 2 months
later. The pulsation of the right superficial temporal
artery was distinctly palpable. He was maintained on the
antiplatelet drug, and the inhibition of the platelet aggregation was well controlled. He was discharged on
March 16, 1984.
On July 9, 1984, he experienced a sudden motor
weakness of the left extremities while working and fell
to the ground. He could not move his left extremities,
and complained of numbness of the left arm, nausea,
and dull occipital pain. Immediately after the onset he
was transferred to our hospital.
On readmission there were no neurological deficits,

but the episode suggested a transient ischemic attack.
One hour later the left hemiparesis occurred again and
progressed. The neurological examination revealed conjugate deviation to the left, left facial palsy, dysarthric
speech, left hemiplegia, and bilateral Babinski reflexes.
On the next day, the neurological deterioration progressed further: horizontal nystagmus and palsies of the
right abducens and right facial nerve were added to the
previous symptoms. Palatal and lingual pareses were also
noted bilaterally, but no evidence of involvement of the
third cranial nerve was found. A computed tomography
scan demonstrated no abnormal lesion in the brainstem.
On July 13 and 20, 1984, cerebral angiography was
performed. A right common carotid angiogram showed
excellent filling of the upper basilar system via the superficial temporal artery (Figure 2). A left retrograde
transbrachial vertebral angiogram disclosed complete
occlusion of the previously stenotic basilar artery segment just distal to the origin of the anterior inferior
cerebellar artery (Figure 3). He was treated with urokinase and low-molecular-weight dextran, and his neurological deficits gradually improved. Although he remained paretic 2 months after the onset, he could walk
without a stick, and continued to improve slowly.

Discussion
Occlusion of the bypassed artery after STA-MCA anastomosis for middle-cerebral-artery or internal-carotid-artery stenosis has been reported recently. The
occlusion occurred asymptomatically in some cases [4],

Basilar Artery Occlusion

Figure 3. Left transbrachia/ retrograde angiograms showing complete occlusion of the pre24ous stenotic lesion (arrow). (A) Anteroposterior z,ieu:
(B) lateral z'iew.
but in almost all cases was associated with neurological
symptoms, and the angiograms generally showed good
filling of the bypasses [4,8,9]. Most of the patients suffered from neurological symptoms within a few days
after their bypass operations. It was postulated that the
vascular stasis and the decrease of blood flow through
the stenotic artery after the bypass surgery would predispose the stenosis to occlusion in the immediate postoperative period.
Ausman et al [2] first reported a successful surgical
procedure, superficial temporal artery-proximal superior cerebellar artery anastomosis, for a patient with
upper-brainstem ischemia. In their report the patient
showed recurrent nonhemispheric episodes, and repeated angiograms showed the progression ofmidbasilar
stenosis to occlusion. The bypass surgery was performed
for ischemia o f the upper brainstem because of the midbasilar occlusion. In the literature these surgical procedures were done in patients with upper-brainstem
ischemia because of basilar-artery occlusion or stenosis
[3], and in the latter case postoperative occlusion of the
bypassed artery, as occurred in the intracranial internal
carotid artery system, could be expected. Little information is available regarding the natural history of patients with basilar-artery stenosis, but it seems more

Surg Neurol
1986;25:39-42

41

severe than other intracranial-artery stenoses [5-7,10,11].
The prognosis of basilar artery stenosis depends on collateral circulations involving the long circumferential
cerebellar vessels with late filling of the distal segment
of the basilar artery. Our case had no angiographic visualization of the posterior communicating artery or other
collaterals, and severe long-segmented stenosis was
present at the midbasilar artery. H e experienced transient nonhemispheric symptoms, almost every day for 1
year prior to admission. In our opinion he had a high
risk of major brainstem infarction; consequently, we
adopted a revascularization procedure as appropriate
treatment. As a result, he developed brainstem infarction 4 months after the bypass surgery. However, the
residual symptoms were not severe, and oculomotor
nerve palsy, which meant ischemia o f the midbrain, was
not present during the second hospitalization. The progression of the stenosis to occlusion seemed to be a
natural course because the preoperative angiogram revealed a long segment of severe stenosis o f the midbasilar artery, and the occlusion occurred 4 months after
the surgery. We conclude that S T A - S C A anastomosis
plays an important role in the prevention o f fatal brainstem infarction.
References
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1986;25:39-42

2. Ausman Jl, Diaz FG, Reyes RA, Pak H, Patel S, Boulos R. Superficial temporal to proximal superior cerebellar artery anastomosis for basilar artery stenosis. Neurosurgery 1981;9:56-60.
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M i n a k a w a et al

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