J Neurosurg56:766-776,1982

Posterior circulation revascularization
Superficial temporal artery to superior cerebellar artery
anastomosis
JAMES I. AUSMAN, M . D . , PH.D., FERNANDO G. DIAZ, M . D . , PH.D.,
R. A. DE LOS REVES, M.D., HOOSHANG PAK, M.D., SUnESH PATEL, M.D.,
BHARAT MEHTA, M.D., AND ROUSHDY BOULOS, M.D.
Departments of Neurological Surgery and Neuroradiology, Henry Ford Hospital, Detroit, Michigan
~/ Eight patients were evaluated for severe vertebrobasilar insufficiency (VBI). There were five males and
three females, with an average age of 60.2 years (range 42 to 67 years). Three were diabetic and five
hypertensive, including two patients who had both diseases. Seven of the eight had ongoing episodes of
VBI refractory to anticoagulant and/or antiplatelet agents. Symptoms included two or more of the
following in all patients: dizziness, diplopia, hemiparesis, hemihypesthesia, perioral numbness, bilateral
visual blurring, dysarthria, and ataxia. Angiography revealed severe atherosclerotic stenosis of the proximal
or midsection of the basilar artery in all patients.
A 10-cm segment of the anterior or posterior division of the superficial temporal artery (STA) was
anastomosed to a proximal segment of the superior cerebellar artery (SCA) through a right subtemporal
approach. Seven of eight (87%) postoperative angiograms demonstrated patency as evidenced by filling of
the SCA and, in most cases, of the basilar artery. Six of the eight patients were improved or asymptomatic
after the operation, one was unchanged, and one died. The average follow-up period was 14 months, with
a range of 4 to 23 months. Transient morbidity included temporal lobe swelling in four patients and a
subdural hematoma in one. Anastomosis of the STA to the SCA is a feasible therapeutic option in the
patient with VBI secondary to stenosis of the proximal or midsection of the basilar artery.
KEY WORDS
vertebral artery
9 basilar artery
cerebral angiography
9 superior cerebellar artery
~

T

HE syndrome of vertebrobasilar insufficiency
(VBI) may be caused by a variety of disorders,
both structural and nonstructural. The most
common structural lesions are atherosclerotic plaques,
which may occur anywhere from the proximal subclavian artery to the basilar bifurcation?
While stenotic lesions in the extracranial vertebral
system have been approached surgically for years,
those involving the intracranial vertebral and basilar
arteries awaited further refinements in microsurgical
techniques. These techniques, pioneered by Ya~argil,
et al., TM in the anterior circulation, were first applied
to the posterior circulation by us 4 in the form of an
occipital artery to posterior inferior cerebellar artery
(PICA) anastomosis. Sundt and Piepgras TM and Khodadad, et al., 13 reported their further experiences with
766

9 anastomosis
9 stenosis

9 microsurgery

9

this operation. A recent report by Allen, et al.,' describes microsurgical endarterectomy of the intracranial vertebral artery for stenosis proximal to the origin
o f the PICA. Thus, stenosis o f the intraca'anial vertebral artery proximal to the origin of the PICA became
surgically approachable.
There remained, however, the problem of stenosis
distal to the PICA. For vertebrobasilar junction stenosis distal to the PICA but proximal to the anterior
inferior cerebellar artery (AICA), we have reported
the technique of occipital artery to AICA anastomosisY Still to be resolved was the problem of midbasilar stenosis. That portion of the basilar artery
between the AICA's and the superior cerebellar arteries (SCA's) represents a very frequent site of atherosclerotic disease in the intracranial vertebrobasilar
J. Neurosurg. / Volume 56 / June, 1982

Anastomotic revascularization of posterior circulation
TABLE 1
Summary of course in eight patients with anastomosis*

Case
No.

Age (yrs),
Sex

Diabetic

Hypertensive

Lesion in BA

Graft
Patency

Operative
Complications

yes
yes
yes
yes
yes
yes
yes
no

TLS
TLS, SDH
TLS
TLS
none
none
none
BA thrombosis

1
61, M
yes
no
occlusion
2
63, M
no
yes
occlusion
3
64, M
no
yes
stenosis
4
67, F
no
yes
stenosis
5
60, M
yes
yes
stenosis
6
42, F
no
no
stenosis
7
58, M
no
no
stenosis
8
67, F
yes
yes
stenosis
* BA = basilar artery; TLS = temporal lobe swelling;and SDH = subdural hematoma.
system. 1~ We have attacked stenosis at this level by
performing a superficial temporal artery (STA) to
proximal SCA bypass? In this present paper, we
report our experience with eight such STA-SCA
anastomoses and review the indications, operative
technique, complications, and results o f this operation.
Summary of Cases
Superficial temporal artery to SCA anastomosis
was performed on eight patients between November,
1979, and December, 1980 (Table l). There were five
males and three females with an age range of 42 to 67
years. All except one (Case 7) were experiencing
ongoing episodes of VBI, despite treatment with anticoagulant a n d / o r antiplatelet agents. The patient in
Case 7 had suffered a completed brain-stem infarct
several months previously, and despite lack of persistent symptoms, underwent a bypass procedure because o f the precariousness of his posterior circulation.
There were three diabetic patients and five who were
hypertensive, including two patients who had both
diseases. Dizziness, although common, was not considered diagnostic of VBI unless associated with cranial nerve, sensory, cerebellar, a n d / o r motor symptoms. Table 2 summarizes the symptoms encountered
in our series of patients. Findings on neurological
examination on admission to the hospital were minimal in this series (Table 3); however, two patients
(Cases 2 and 8) deteriorated during the course of their
diagnostic work-up. Both patients had extremely tight
basilar stenoses which proceeded to occlusion (one
with fatal results) during hospitalization. These cases
will be considered in more detail below.

Case Reports
Case 1

This case has been reviewed in detail in a previous
paper? Briefly, this 6 l-year-old man presented with
episodes of light-headedness, near syncope without
loss of consciousness, and headache associated with
nausea; he also had episodes o f dysarthria and circum-oral paresthesias. Cerebral angiography performed elsewhere revealed mid-basilar artery stenosis
just distal to the origins of the AICA's (Fig. 1A). The
J. Neurosurg. / Volume 56 / June, 1982

TABLE 2
Occurrence of symptoms

Symptoms

No. of
Cases

dizziness
diplopia
hemihypesthesia
dysarthria
hemiparesis
ataxia
perioral numbness
tirmitus

7
6
6
5
5
3
2
2

TABLE 3
Findings on physical examination

Findings
none
Babinski sign
hemiparesis (mild)
ataxia
nystagmus

No. of
Cases
3
2
2
1
1

patient was started on intravenous heparin therapy
and referred to Henry Ford Hospital. Despite the
heparin, the patient continued to have episodes of
circumoral numbness, transient right lower extremity
monoparesis, and alternating numbness of the right
or left side of the body. A repeat cerebral angiogram
revealed complete occlusion of the previously stenotic
basilar segment (Figs. 1B-D and 4, Case 1). Due to
the persistence of his symptoms, the patient underwent a right STA-SCA anastomosis on November 26,
1979. The use of the posterior cerebral artery as the
recipient vessel was rejected because it was the only
visible source of supply to the basilar artery. Its temporary interruption during surgery was believed therefore to be contraindicated. The patient's postoperative
course was unremarkable, and he remains asymptomatic and off anticoagulant therapy 2 years following
the procedure. Postoperative angiograms demonstrate
patency, with enlargement of the anastomosis between
767

J. I. A u s m a n , et al.

FIG. 1. Case 1. A: Left vertebral angiogram, base projection, showing a high-grade stenosis of the
midportion of the basilar artery (arrow). B: Left vertebral angiogram, frontal projection, revealing
complete occlusion of the basilar artery (arrow) where previously there was a high-grade stenosis. C:
Right vertebral angiogram showing the fight vertebral artery (large arrow), which opacities a small right
posterior inferior cerebellar artery (small arrow). D: Left internal carotid artery, lateral projection. The
left posterior cerebral artery is opacified retrogradely from pial collateral anastomoses from the left middle
cerebral artery (dark arrow). The basilar artery is opacified retrogradely from the left posterior cerebral
artery (open arrow). E: Right external carotid angiogram 10 days postoperatively showing a patent
anastomosis (arrowhead) between the superficial temporal artery (STA, arrows) and the right superior
cerebellar artery (SCA). There is filling of the distal basilar and both superior cerebellar and posterior
cerebral arteries. F: Right external carotid angiogram 5 months postoperatively. The size and caliber of
the right STA has increased (arrows). The arrowhead shows the site of STA anastomosis to the fight SCA.
The distal basilar and posterior cerebral and superior cerebellar arteries are visualized.

the first and second postoperative angiograms (Fig.
1E and F).

Case 2
This 63-year-old man experienced several episodes
of transient dizziness in November, 1979. His local
physician found him to be hypertensive and started
him on antihypertensive drugs in December, 1979.
The patient then developed transient left amaurosis,
768

followed by a prolonged left hemihypesthesia and
mild left hemiparesis. Cerebral angiography revealed
a high degree of basilar artery stenosis. The patient
was anticoagulated with warfarin and referred to
Henry Ford Hospital. In spite of anticoagulation therapy, during the 10 days before admission the patient
continued to experience increasingly frequent episodes of dizziness, disorientation in space, loss of
balance, nausea, vomiting, headaches, and left hemiJ. Neurosurg. / Volume 56 / June, 1982

Anastomotic revascularization of posterior circulation

FIG. 2. Case 2. Upper: Frontal (left) and lateral (right) projections of the right vertebral (large
arrowhead) angiogram revealing complete occlusion (small arrowhead) of the basilar artery. There is reflux
of contrast material into the opposite left vertebral artery (small arrows), with opacification of the left
posterior inferior cerebellar artery (large arrows). Lower: Right external carotid angiogram, frontal (left)
and lateral (right) projections, revealing an enlarged-caliber right superficial temporal artery (small arrows)
anastomosed to the right superior cerebellar artery (large arrowheads). The small arrowhead points to the
site of anastomosis. Opacification of the basilar artery (large arrow) is seen, with visualization of both
superior cerebellar arteries. Note other areas of narrowing of intracranial vessels.

paresis. Neurological examination on admission on
March 2, 1980, revealed an alert, oriented man with
slightly decreased recent memory, a mild left hemiparesis, left hemihypesthesia, left hyperreflexia, and
poor tandem gait.
Because the original angiogram did not show the
origin of the great vessels or his STA, it was decided
to repeat the study. The patient was taken off heparin
and underwent repeat angiography on March 6. This

J. Neurosurg. / Volume 56 / June, 1982

study revealed occlusion of the previously stenotic
basilar segment (Fig. 2 upper) and other intracranial
stenoses (Fig. 4, Case 2). After the angiogram, the
patient experienced increased somnolence and some
progression of his left hemiparesis. An arterial line
and Swan-Ganz catheter were inserted, and arterial
blood pressure and pulmonary wedge pressures were
elevated by volume expansion, with improvement in
sensorium and motor strength on the left. Heparin
769

J. I. A u s m a n , et al.
anticoagulation was reinstituted. During the next several days, the patient's somnolence and left hemiparesis improved but continued to fluctuate, and it
was decided to proceed with the bypass because of his
unstable clinical state. On March 12, the patient underwent right STA-SCA anastomosis.
The postoperative course was stormy. Although
initially unchanged from his preoperative status, the
patient's level of consciousness and hemiparesis deteriorated on the 2nd day after surgery. A computerized tomography (CT) scan revealed right temporal
lobe swelling, and osmotic diuretic therapy was instituted. After this swelling had partially subsided, a
repeat CT scan showed a right temporoparietal subdural hematoma, which was evacuated on March 27.
Over the next several weeks the patient showed slow
but steady improvement. Repeat angiography on
April 4 revealed a patent anastomosis (Fig. 2 lower).
The patient was discharged to a rehabilitation center
on April 29, 1980, where he was given anticoagulant
therapy prophylactically. A follow-up visit in March,
1981, showed the patient to have a moderate left
hemiparesis and difficulty with recent memory. The
rest of the neurological examination was unremarkable, and the patient was free of transient ischemic attacks (TIA's) but still on anticoagulant drugs.
Comment

This case serves to illustrate two important points.
The first concerns the role of blood pressure in the
etiology and treatment of VBI. This patient's initial
symptoms (as well as those of Case 8) were exacerbated by the initiation or augmentation of antihypertensive therapy. Similarly, both patients required the
actual induction of hypertension to ameliorate their
ischemic symptoms during the course of their treatment. This pressure-dependence of the posterior circulation has been alluded to by others. 7 It is not our
intention to condemn antihypertensive therapy. We
would, however, like to point out that in the patient
with VBI, exacerbation of symptoms by lowering the
blood pressure with medication or position of the
patient is highly suggestive of high-grade stenosis in
the vertebral or basilar artery, with marginal perfusion
pressure across the stenosis, and requires prompt angiographic investigation.
The second point is in regard to angiography. All
of our patients tolerated their initial angiograms well.
In this patient, however, the basilar artery became
occluded prior to the second angiogram, resulting in
clinical deterioration. Whether this was caused by the
discontinuation of anticoagulant therapy in preparation for the angiogram, by technical factors during
angiography, or a combination of these, repeat angiography in patients with high-grade basilar stenosis
should be undertaken with extreme caution, and other
measures should be initiated to prevent coagulation,
such as partial heparinization, if angiography is
essential.
770

Case 3

This 64-year-old man was admitted on August 26,
1979, with a 4-week history of transient episodes of
dizziness, left hemihypesthesia, and diplopia, increasing in frequency to one per day on the several days
prior to admission. These spells had been refractory
to aspirin therapy.
Neurological examination on admission was negative. The patient underwent angiography which revealed approximately 90% stenosis in the midportion
of the basilar artery just distal to the AICA's, and
other cerebral vascular lesions (Fig. 4, Case 3). He
was placed on warfarin anticoagulation therapy and
sent home. However, he continued to have vertigo
and diplopia increasing to approximately one to two
times a week associated with nausea and vomiting.
On March 2, 1980, repeat angiography revealed no
change in the lesions. The patient underwent a right
STA-SCA anastomosis on March 17. The postoperative course was complicated by the development of a
right sixth nerve palsy and lethargy secondary to right
temporal lobe edema. These signs gradually resolved.
A postoperative angiogram on April 1 revealed a
patent anastomosis. The patient continued to improve,
complaining only of slight difficulty with memory and
a few episodes of diplopia. These symptoms cleared
prior to his discharge. On his last clinic visit on March
26, 1981, 1 year after surgery, the patient was neurologically intact and had no further episodes of VBI.
Case 4

This 67-year-old hypertensive woman presented
with a 3-month history of intermittent dizziness and
a 2-week history of intermittent right-sided facial and
hand numbness, dysarthria, and ataxia, with a tendency to veer to the right. Neurological examination
on admission was normal. Angiography revealed midbasilar stenosis and other cerebral vascular lesions
(Fig. 4, Case 4).
She was placed on a course of oral anticoagulant
drugs and was discharged; however, her symptoms
increased in frequency and she was hospitalized again
2 months later. On April 14, 1980, the patient underwent a right STA-SCA anastomosis. The initial postoperative angiogram revealed only marginal filling of
the anastomosis, but a subsequent angiogram on
November 14, 1980, revealed better filling. At her
last clinic visit on January 13, 1981, the patient was
asymptomatic except for occasional right-sided tinnitus, which was thought by the ear, nose, and throat
consultant to be due to high-frequency hearing loss.
Case 5

This 60-year-old man experienced three episodes of
transient dizziness, diplopia, dysarthria, and left hemiparesis and hemihype~the'sia in the 2 months prior to
admission. The episodes lasted approximately 20 minJ. Neurosurg. / Volume 56 / June, 1982

Anastomotic revascularization of posterior circulation
utes and then completely cleared. Cerebral angiography performed elsewhere revealed a high-grade stenosis of the basilar artery between the AICA and
SCA, and other cerebral vascular lesions (Fig. 4, Case
5). Warfarin was prescribed, but this was subsequently
discontinued due to gastrointestinal bleeding. The
patient experienced another similar TIA on discontinuation of anticoagulation therapy, and was referred
to Henry Ford Hospital for further evaluation and
treatment.
The neurological examination on admission was
negative. The patient underwent a right STA-SCA
anastomosis on July 21, 1980. The postoperative
course was uneventful. Angiography performed 10
days after surgery revealed a patent anastomosis with
filling of the upper basilar system. The patient complained of slight difficulty with recent memory postoperatively, but was otherwise asymptomatic. He remained free of symptoms at his last clinic visit in
February, 1981.
Case 6

This 42-year-old diabetic hypertensive woman presented with a 1-year history of increasingly frequent
episodes of dizziness, tinnitus, diplopia, and left hemiparesis. For other medical reasons she could not be
given oral anticoagulant therapy. The episodes were
unaffected by therapy with aspirin and dipyridamole.
Neurological examination revealed slight left-sided
hyperreflexia and bilateral extensor plantar responses,
but was otherwise unremarkable. The patient underwent angiography, which revealed proximal basilar
stenosis and other cerebral vascular lesions (Fig. 4,
Case 5). She underwent a right STA-SCA anastomosis
on August 20, 1980. The postoperative course was
unremarkable. Postoperative angiography revealed a
patent anastomosis. On her last clinic visit on March
26, 1981, the patient stated that she had experienced
two further episodes, of a lesser magnitude, of dizziness and left-sided face and hand numbness since the
operation. She was otherwise neurologically intact
and asymptomatic. She was admitted to the hospital
and underwent angiography the following day. This
revealed enlargement of the STA and increased filling
of the basilar artery and its branches.
Comment

This patient's episodes of VBI were not entirely
halted by the surgery. They have, however, decreased
in both magnitude and frequency, while at the same
time the angiographic appearance of the bypass graft
has enlarged. Further follow-up review is necessary
to see whether her episodes will cease altogether.
Case 7

This 58-year-old man experienced three episodes of
dizziness, diplopia, dysarthria, and right hemihypesthesia in November, 1979. The first two episodes were
J. Neurosurg. / Volume 56 / June, 1982

transient, and the last resulted in a prolonged deficit.
At the time of his last episode he underwent cerebral
angiography, which revealed a right vertebral artery
occlusion, a left vertebral artery which ended in the
PICA, and evidence of mid-basilar stenosis (Fig. 4,
Case 7). The patient was placed on aspirin and
dipyridamole therapy and referred to Henry Ford
Hospital.
It was uncertain whether he should be followed
medically or undergo a surgical bypass procedure. It
was elected to follow him clinically , and a repeat
angiogram was planned to evaluate the status of his
vertebrobasilar circulation and its collaterals. Angiography was repeated on November 5, 1980, revealing
no change in the angiographic lesions. Because it was
thought that the patient was at risk for a major brainstem infarct due to his severely compromised circulation, and because of the patient's concern about the
possibility of a subsequent infarction, he was admitted
for a basilar artery revascularization. The neurological
examination on admission was negative except for
bilateral extensor plantar responses. The patient underwent a right STA-SCA anastomosis on November
11, 1980. Postoperative angiography on March 2,
1981, revealed a patent anastomosis but poor filling
of the posterior fossa vasculature through the anastomosis. At his last clinic visit on March 6, 1981, the
patient remained asymptomatic (as he had been preoperatively) and neurologically intact.
Comment

This patient underwent an essentially "prophylactic" bypass. In spite of anatomically significant lesions, the lack of demand for extra circulation (as
evidenced by his lack of ongoing symptoms which
implied adequate circulation) may explain the poor
filling through the anastomosis.
Case 8

This 67-year-old diabetic hypertensive woman presented to the emergency room on October 16, 1980,
with a 1-day history of transient nausea, vomiting,
bifrontal headache, left upper extremity paresis, and
dysarthria. She had experienced a transient episode
of bilateral visual blurring 1 week previously. In the
emergency room, the patient was noted to have an
elevated blood pressure (182/110 mm Hg). She was
told to increase her antihypertensive medication.
Later that day, she experienced another transient
episode of all of the same symptoms plus bilateral
blurred vision. She returned to the emergency room
and was admitted to the medicine service.
Neurological examination on admission was normal. Shortly after admission the patient developed
cardiac dysrhythmias which required that she be
transferred to the coronary care unit for prolonged
evaluation and treatment. After her cardiac status was
stabilized, she continued to have episodes of VBI.
On November 3, 1980, the patient underwent angi771

J. I. Ausman, et al.

FIG. 3. Case 8. Left: Left vertebral angiogram, lateral projection, demonstrating high-grade stenosis
of the basilar artery (arrowhead). The marked irregularity of the basilar artery indicates atherosclerotic
changes. Right: Postoperative left vertebral angiogram showing complete occlusion of the basilar artery
(arrowhead).

ography which demonstrated a high degree of basilar
artery stenosis and other cerebral vascular lesions
(Figs. 3 left and 4, Case 8). She was placed on full
intravenous heparin anticoagulation therapy but, despite this, developed episodes of dizziness and visual
blurring. On November 4, she experienced a transient
(5-minute) episode of quadriparesis and unresponsiveness. She was transferred to the neurosurgical
intensive care unit and underwent intravascular volume expansion in addition to anticoagulation, and
was taken off her antihypertensive medications. During the following month, numerous attempts were
made to decrease the patient's blood pressure, which
was in the range of 180/110 to 200/130 mm Hg.
However, each time this was done she became symptomatic, requiring re-elevation of her blood pressure.
Because of this refractoriness to medical therapy,
basilar artery revascularization was thought to be the
only alternative. On December 9, 1980, the patient
underwent a right STA-SCA anastomosis. Postoperatively, she never regained consciousness. A repeat
angiogram revealed occlusion of the entire basilar
artery (Fig. 3 right). The patient had a progressive
downhill course and died on January 4, 1981. An
autopsy was refused by the family.

Comment
This case reinforces the point made in the comment
on Case 2 concerning the role of hypertension in
772

posterior circulation insufficiency. This patient required not only full anticoagulation therapy but hypertension greater than 100 mm Hg diastolic (a potentially dangerous combination) in order to remain
asymptomatic. It was believed that surgical treatment
offered her the only chance to avoid a potentially
catastrophic stroke. Nevertheless, her entire basilar
artery thrombosed perioperatively. Whether this occlusion was related to the discontinuation of heparin
anticoagulation in preparation for surgery or to the
operation itself is speculative. However, the fact that
the entire basilar artery as well as the bypass graft
became thrombosed would tend to support the former
conclusion. It is quite possible that in a patient with
a critically tight stenosis such as this, thrombosis is the
inevitable result. However, if faced with the same
situation in the future we would consider tapering the
patient's heparin while administering intravenous
low-molecular-weight dextran and possibly a vasopressor, such as dopamine, before and during surgery.
Only further experience with similar patients will tell
us whether this is a reasonable approach.

Operative Technique
Prior to intubation, an arterial line is inserted
to constantly monitor blood pressure. In neurologically unstable patients, a Swan-Ganz flow-directed
balloon-tipped catheter is placed percutaneously to

J. Neurosurg. / Volume 56/June, 1982

Anastomotic revascularization of posterior circulation
closely monitor fluid balance and cardiovascular function during and after the operation. The catheter is
usually placed just before the operation in those patients whose heparin anticoagulation has been discontinued several hours prior to surgery. A Foley catheter
is inserted to monitor urinary output and to allow the
use of osmotic diuretics during the surgery. A lumbar
catheter is inserted for intraoperative cerebrospinal
fluid (CSF) drainage. It is critical that the CSF drainage be functional because of the necessity for retraction and elevation of the temporal lobe in order to
reach the tentorial incisura.
The patient is placed supine with the right shoulder
and hip elevated and the head horizontal, hyperextended, and the left side down. The right side is always
used to avoid retraction of the temporal lobe on the
dominant side. Both anterior and posterior branches
of the STA are traced on the scalp with the use of a
directional flow Doppler probe. The anterior branch
is preferred for use in the anastomosis. It is traced
from the area anterior to the pinna to the most distal
portion visualized on the angiogram, usually for 8 to
10 cm or more. The scalp is shavedand prepared with
povidone-iodine solution in the usual manner. A direct incision is made over the STA, and approximately
10 cm of the vessel is dissected under the microscope,
from its most distal to its most proximal location. All
side branches are individually cauterized and transected. Anatomical continuity is maintained only at
the proximal and distal ends of the vessel. The incision
is then extended posteriorly from the pinna above the
ear in a parieto-occipital direction so that the incision
from anterior limb to posterior limb represents a V,
with the apex of the V at the pinna. The flap is
reflected and retracted superiorly. The temporalis
muscle is incised in a cross-bow fashion and the flaps
are retracted laterally. A free bone flap is raised by
placing a single burr hole on the anterior inferior
temporal region just above the ear at the point through
which the STA will enter. With the electrical drill, a
quadrangular free bone flap is elevated. The inferior
portion of the flap is brought down to the base of the
middle fossa by extending the craniectomy with a
Leksell rongeur. After hemostasis is achieved, the
dura is tacked to the bone to prevent intraoperative
bleeding. The spinal drain is opened at this time, and
the patient is given 40 mg of furosemide intravenously,
followed l0 to 15 minutes later by a 50-gm bolus of
intravenous mannitol.
A dural incision is made at the base of the craniotomy and the dura is reflected superiorly. The temporal lobe is elevated until the tentorial incisura is
identified. Care is taken not to compromise the vein
of Labb6 or posterior temporal veins as they enter the
sigmoid sinus. Self-retaining retractors are placed.
The edge of the tentorium is elevated, cauterized, and
transected to provide more exposure. The microscope
is again utilized and the arachnoid over the brain stem
is picked up and opened, revealing the SCA. The flap
J. Neurosurg. / Volume 56 / June, 1982

of the tentorium is retracted and reflected, and is
anchored to a more lateral aspect of the tentorium
with a single suture. Care is taken not to damage the
fourth nerve. The SCA is identified in its lateral circum-mesencephalic portion. The vessel generally has
no perforating branches as it traverses from the lateral
portion of the midbrain to the superior portion of the
cerebellum. However, if it does have branches to the
brain stem, a portion of the artery beyond the area
with the brain-stem branches is selected for the anastomosis. This artery can be single but frequently
divides into rostral and caudal branches. 15The larger
of the two branches is identified, and all arachnoid
adhesions are carefully dissected under the microscope. The vessel is generally fairly loose and can be
gently elevated by placing a small cotton ball or a
small piece of Gelfoam underneath the vessel. A
rubber dam is placed on top of the Gelfoam and
underneath the vessel to isolate the segment of the
artery to be used. The self-retaining retractors are
now temporarily removed as attention is again directed to the STA. The distal portion of the STA is
transected and its proximal portion clipped with a
broad Mayfield damp, partially sprung to prevent
STA endothelial damage. The vessel is irrigated thoroughly with heparinized saline. The STA is used in
its entirety and only the most distal portion is carefully
cleaned of all adventitial tissue. The vessel is brought
down to the area of the SCA, and a fish-mouth stoma
is made in the STA.
Now the patient is given 120 mg of intravenous
thiopental for cerebral protection, and Kleinert-Kutz
clamps are placed on the SCA. A longitudinal elliptical arteriotomy is made on the SCA to equal the
length prepared on the STA. A Silastic stent is placed
inside the SCA after the vessel is irrigated with heparinized saline. With the aid of the long bayonet
microinstruments, including locking needle holders
and fine-tipped forceps, an end-to-side anastomosis is
completed with interrupted 10-0 nylon sutures. To
facilitate suturing in this depth, half-circle needles are
utilized. The stent is removed before completion of
the sutures, and the area of the anastomosis is once
again irrigated with heparinized saline. The temporary clips are removed by first taking off the distal
SCA clip, then the proximal SCA clip and, last, the
STA clip. A small amount of bleeding is generally
observed and, if necessary, an additional suture is
added to the area of the anastomosis. The operative
field is thoroughly irrigated with normal saline, and
the retracted temporal lobe is carefully inspected for
bleeding points or contusions. Hemostasis in this area
and on the proximal portion of the STA pedicle is
achieved. The incision is closed in layers in a routine
manner. Care is taken to allow sufficient room for the
STA to enter the dura and bone undisturbed. A major
portion of the dura is closed and the bone flap is
replaced. The skin and muscle are dosed in a routine
manner.
773

J. I. Ausman, et al.

/i

~.

6

7

1

FIG. 4. Diagrams of the major extracranial and intracranial vessels, anteroposterior view, in all eight
patients. Dark areas represent areas of occlusion or stenosis. Arrows represent collateral circulation.

Postoperative Management
Concern for temporal lobe swelling is paramount.
A CT scan is usually performed within the first 6
hours after surgery to ensure that there is no temporal
or subtemporal clot. None was found at this stage.
Swelling of the temporal lobe was found in four of
these eight patients within 3 days of surgery, and was
treated with steroids a n d / o r mannitol, if necessary,
with complete resolution of the edema. Otherwise,
routine postoperative management is given. The patients are not restarted on heparin therapy. All patients were started on aspirin postoperatively, 5 grains
four times daily.
Follow-up angiograms were obtained in all patients.
Six had angiograms within 2 weeks of surgery and the
remainder within 5 weeks of the operation. Five patients had two postoperative angiograms and one
patient three. Patency, defined as any intracranial
filling through the anastomosis, was found in seven of
the eight cases. Filling of a single SCA branch was
seen in two cases, and filling of the basilar artery and
774

usually some or all of its branches to the site of the
stenotic occlusion was seen in five of eight cases. In
the six patients with two or more postoperative angiograms, increased filling of the recipient vessel tree was
demonstrated in two cases. To properly visualize the
STA and SCA, a selective external carotid injection
was usually necessary because the internal carotid
artery was usually patent in these patients. A Townes
projection with this injection, directed as if looking a t
the vertebral basilar circulation, is necessary to visualize filling of the system through the STA-SCA
anastomosis. Figure 4 summarizes the angiographic
results.

Discussion
The syndrome of vertebrobasilar insufficiency
(VBI) is predicated upon a history of transient episodes indicative of ischemia in the brain stem, cerebellum, or occipital cortex) This posterior circulation
insufficiency may be characterized by a variety of
symptoms, including cranial nerve dysfunction such
J. Neurosurg. / Volume 5 6 / J u n e , 1982

Anastomotic revascularization of posterior circulation
as diplopia or dysarthria, cerebellar findings such as
ataxia or dysmetria, occipital cortex symptoms such
as bilateral amaurosis or hemianopsia, and motor or
sensory alterations involving any combination of the
four extremities. Dizziness, although probably the
most common single symptom seen in VBI, rarely
occurs in isolation, and, when unaccompanied by
other symptoms, is usually the result of labyrinthine
disease and not vertebrobasilar ischemia. '2 Table 1
lists the symptoms, in order of frequency, observed in
our series. This is generally representative of their
incidence in other series in the literature? ,12,14
The incidence of VBI appears to be approximately
half that of carotid circulation TIA's. s Although some
studies have suggested a worse prognosis for carotid
than vertebrobasilar TIA's, TM this appears to be a
function of the rigidity of criteria for the diagnosis
of VBI: if dizziness alone is considered indicative of
VBI, the subsequent "stroke" rate will be lower than
that for carotid TIA's. Cartlidge, et al., s using strict
criteria for the diagnosis of VBI, found no significant
difference in the probability of the occurrence of
stroke between patients (without angiography) who
suffered TIA's related to the carotid or the vertebrobasilar circulation. Both were in excess of 35% over 5
years.
Atherosclerotic stenosis or occlusion in the posterior
circulation is the most frequent cause o f VBI. 9 These
atherosclerotic plaques may occur anywhere from the
proximal subclavian artery to the distal basilar artery.
While some present as distinct clinical syndromes
(such as subclavian steal or "top of the basilar" syndrome 6) which suggest the etiology, the vast majority
require cerebral angiography for localization of the
lesion.
Modern angiographic techniques allow accurate diagnosis with an acceptable risk in the patient with
VBI. O f 88 consecutive vertebral angiograms performed for posterior circulation insufficiency syndromes at Henry Ford Hospital, five (5.6%) have been
associated with worsening of the patient's neurological
status, with three of these (3.4%) resulting in persistent
minor deficits. There have been no deaths. This compares favorably with the complication rate in the
literature, which has mostly been reported to be in the
range of 3% to 9%. 11 Both surgical and angiographic
risks appear to be increased in the patient with highgrade stenosis, but one would also assume that these
are the patients who are at the greatest risk of infarction in the natural history of the disease.
Anticoagulation has been the treatment of choice
for basilar artery stenosis in the past, but its long-term
value has not been documented. There is, additionally, a high risk of hemorrhage associated with its
use. 17Five of these patients were experiencing ongoing
symptoms while on heparin or warfarin. For these
patients, there was no medical alternative to the operation. For those patients with less severe symptoms,
a choice could be made between medical and surgical
J. Neurosurg. / Volume 5 6 / J u n e , 1982

therapy. Whether these patients would have been
better treated medically can be debated but, considering the severity of the vascular compromise, the
mortality rate (13%, or one of eight cases) and the
permanent morbidity rate in this series was quite
limited.
While the angiographic and surgical morbidity in
this series might, at first glance, seem excessive, it
should be recalled that many o f the patients were
suffering from unstable VBI secondary to critically
tight stenoses. Although there are no available data
on the natural history of a similar (untreated) population, one would expect that the stroke rate in this
group would be extremely high.
As more experience is gained in the surgical treatment of basilar artery stenosis, perhaps a clearer
definition of the criteria for surgery will emerge. For
the present time, this series stands as a point of
reference with which to compare a similar group of
patients on strictly medical therapy.
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Manuscript received August 6, 1981.
Accepted in final form January 19, 1982.
Address reprint requests to: James I. Ausman, M.D.,
Ph.D., Department of Neurological Surgery, Henry Ford
Hospital, 2799 West Grand Boulevard, Detroit, Michigan
48202.

J. Neurosurg. / Volume 56 / June, 1982