J Neurosurg 67:296-300,1987

Dissecting aneurysms of the anterior circle of Willis
arteries
Report of two cases
RYUICHI KITANI, M.D., TOORU ITOUJI, M.D., YATSUGI NODA, M.D.,
MAKOTO KIMURA, M.D., AND SATOSHI UCHIDA, M . D .

Departments of Neurosurgery and Medicine, Toyama Rousai Hospital, Uozu, and Departments of
Neurosurgery and Medicine, Kouseiren Namerikawa Hospital, Namerikawa, Japan
~" Two cases of spontaneous dissecting aneurysm extending from the supraclinoid portion of the internal
carotid artery to the middle cerebral artery are reported in two teenaged patients. Both patients collapsed with
a headache on the right side, left hemiparesis, and altered consciousness due to cerebral ischemia. One patient
became alert in 2 days; however, his condition rapidly deteriorated 4 days later and he died on the 8th day
from massive cerebral infarction. The other patient received a right superficial temporal artery (STA)-middle
cerebral artery (MCA) anastomosis 50 hours after his initial symptoms. He improved gradually and is able to
walk without help. Cerebral angiograms 3 months after the operation disclosed progressive attenuation of the
MCA and dilatation of the anastomosed STA. Artificial collateral flow demonstrated in the postoperative
angiogram may have been useful in preventing massive cerebral infarction.
KEY WORDS
9 dissecting aneurysm
9 internal carotid artery
middle cerebral artery
9 revascularization

ISSECTING aneurysms of the cerebral arteries in
the anterior circle of Willis are rare: to date,
approximately 30 cases have been reported.
These aneurysms have a propensity to occur in young
people. The initial clinical symptoms are the sudden
appearance of headache and the disturbance of consciousness with hemispheric functional loss. A few patients sustain intracranial hemorrhage. ~7 The salient
neuropathological feature in reported cases is occlusion
or stenosis of the arteries due to longitudinal dissection
by circulating blood entering outside the internal elastic
lamina of the arterial wall. The collapsed lumen of the
middle cerebral artery (MCA) and internal carotid artery (ICA) induces cerebral infarction? '8'H'22 Some patients escape massive cerebral infarction due to the
mildness of MCA narrowing or collateral flow, l'27 suggesting the usefulness of early bypass surgery.
We report the cases of two teenaged patients with
dissecting aneurysms. One patient received a superficial
temporal artery (STA)-MCA anastomosis, and his condition improved. The other patient was treated conservatively; he showed some improvement from the initial
condition but later deteriorated and died.

D

296

9

Case Reports

Case 1
This 14-year-old boy suddenly collapsed while participating in a physical education class on October 20,
1983. He complained of headache in the fight temporal
region and inability to move his left arm and leg. He
was transferred to the hospital 4 hours after the onset
of symptoms.
Examination. At admission, he had a severe left
hemiparesis and an associated left central facial weakness. His eyes deviated conjugately to the right. He was
somnolent but was able to speak well. There were no
abnormal physical signs on general examination, and
his blood pressure was 108/80 m m Hg. Lumbar puncture soon after admission yielded clear colorless cerebrospinal fluid (CSF) at normal pressure; CSF analysis
revealed 14 cells/cu mm, a protein level of 45 mg/100
ml, and a glucose content of 85 mg/100 ml. Computerized tomography (CT) on admission failed to identify
any cerebral lesion. Stenosis or occlusion of the MCA
was considered to be the cause of his condition.
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Dissecting aneurysms of the anterior circle of Willis arteries

FIG. I. Computerized tomography scans in Case 1. Left:
Scan obtained on the 2nd day after the ictus showing small
infarctions in the region of the fight basal ganglia. Right:
Scan obtained on the 6th day showing massive cerebral infarction in the distribution of the fight middle cerebral artery.

Course. It was decided to give the patient low-molecular dextran. On the 2nd day he became alert, and
neurological examination showed some improvement.
A C T scan disclosed small infarctions in the region of
the fight basal ganglia (Fig. 1 left). A right carotid
angiogram demonstrated occlusion of the distal end of
the ICA, with an eccentric stenosis of the MCA. The
lumen of the MCA was irregular at that point, but
smooth more distally. A distinct pooling of contrast
medium was seen above the dark-appearing anterior
cerebral artery (Fig. 2).
The patient's consciousness remained clear for 4
days, and his clinical deficits did not progress; however,
on the 6th day, he became drowsy and deteriorated
rapidly. A C T scan disclosed massive cerebral infarction
of the right hemisphere (Fig. 1 right). On the 7th day,
he was placed on a respirator when spontaneous respiration failed. He died 8 days after admission. Permission for a postmortem examination was not obtained.

FIG. 3. Computerized tomography scans in Case 2. Left:
Scan obtained on the 2nd day after the ictus showing small
infarctions in the region of the right basal ganglia. Right:
Scan obtained 3 months after anastomosis showing no additional lesion.

Case 2
This 18-year-old man awoke with a severe right temporal headache at 9 a.m. on February 4, 1986. His
headache improved, but 30 minutes later he suffered
another severe headache and fell backward. He was
found by his family at 10 a.m. and was referred to us
as an emergency.

Examination. On admission the patient was drowsy
with a severe left hemiparesis including the lower half
of the face. Increased deep-tendon reflexes were noted
on the left side. A C T scan demonstrated no definite
lesion, and he was started on anticoagulant therapy. On
the 2nd day he was alert. Repeat CT showed the presence of small infarctions in the region of the fight basal
ganglia (Fig. 3 left). Carotid angiography demonstrated
spherical collapse of the right MCA at the first bifur-

FIG. 2. Right carotid angiograms obtained on the 2nd day after the ictus in Case 1. Left: Lateral view
showing a teardrop of contrast medium arising from the narrowed internal carotid artery (ICA) indicating a
pseudoaneurysm. Right: Anteroposterior view showing occlusion of the ICA and a diffuse, string-like
narrowing of the middle cerebral artery and pooling of contrast medium above the dark-appearing anterior
cerebral artery (arrow).

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R, Kitani, et al.

FIG. 4. Right carotid angiograms obtained on the 2nd day after the ictus in Case 2. Left: Lateral view
showing a diffuse attenuating branch of the middle cerebral artery (MCA, single arrow) and the irregular
lumen of the internal carotid artery (ICA, double arrows). Right: Anteroposterior view showing spherical
collapse of the MCA (single arrow) and the irregular lumen of the ICA (double arrows).

cation, attenuation of a branch just distal to it, and
luminal irregularity of the supraclinoid portion of the
ICA (Fig. 4).
Operation and Postoperative Course. An STAMCA anastomosis was performed on the 3rd day. Three
months after surgery a second angiogram showed severe
eccentric stenosis of the supraclinoid portion of the
ICA and MCA extending to a posterior branch. The
contrast medium in that branch showed a pair of
parallel lines. A teardrop of contrast medium extended
from the narrow supraclinoid portion of the ICA, where
the initial angiogram had shown an irregular lumen,
and the STA-MCA bypass was dilated (Fig. 5). Three
months after the operation, CT showed small infarctions, as were seen on the earlier study (Fig. 3 right),
and the patient's hemiparesis has improved. He can
walk without help, but has some left-arm paresis.
Discussion

Dissecting aneurysms of the cerebral arteries are
diagnosed by the angiographic or pathological findings.
Characteristic angiographic findings have been likened
to "string," "false and true lumen," "pearl and string,"
"pseudoaneurysm," and "tapered occlusion. "7 In Case
1, a string-like narrowing of the MCA was found.
Double density of the anterior cerebral artery was revealed on the anteroposterior view, and a pseudoaneurysm arising from the narrowed ICA was visualized on
the lateral view. These findings may indicate an intramural pooling of contrast medium in the anterior cerebral artery. On the initial angiogram in Case 2, the
MCA at the first bifurcation was pearl-shaped, and a
branch showed string-like narrowing. At angiography 3
months later, the MCA was narrower and a pseudoaneurysm was found in the supraclinoid portion of the
ICA where the initial angiogram had shown a mild
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irregular line of contrast medium. This irregular line
may indicate an elevated intima. A new dissection of
the internal elastic lamina might begin from this point,
extend to the MCA, and narrow the lumen of the MCA
even more. The follow-up angiogram in Case 2 showed
contrast medium in a branch of the MCA forming two
parallel lines on the lateral view. The parallel lines may
be due to a narrowing of the central part of lumen
caused by an elevated intima.
Twenty previous cases of dissecting aneurysms of the
circle of Willis arteries have been reported with sufficient clinical, pathological, and angiographic data to
form a basis for comparative study. Two of these were
apparently induced by head trauma, 3'5 while the others
had no clear etiology. These 20 cases may be divided
into three types according to the clinical course: in Type
1 the initial ictus was severe with rapid deterioration
and death in several days;6"x8'2~in Type 2 the initial
event was of moderate severity with obtundation and
hemiparesis (with or without aphasia), and the patients
showed some improvement for several days before rapid
deterioration and death; 9,24 and in Type 3 the patients
improved gradually after the onset but some hemispheric deficits remained.t6
The primary neuropathological finding in Types 1
and 2 is massive cerebral infarction caused by ischemia
resulting from the occlusion or stenosis of the MCA
and ICA lumina. ~8In one exception, a patient died due
to an intracerebral hemorrhage caused by anticoagulant
therapy.~~ Angiographic studies in Type 1 showed occlusion or severe stenosis of the MCA and ICA. Peripheral branches of the MCA were barely opacified; ~5'~9in
fact, peripheral blood flow in the hemisphere should be
minimal. Angiography was repeated in two Type 2
cases: the initial angiogram (when their deficit was
improving) showed moderate narrowing of the MCA
and ICA, and apparently sufficient perfusion of the

J. Neurosurg. / Volume 67~August, 1987

Dissecting aneurysms of the anterior circle of Willis arteries

FIG. 5. Right carotid angiograms 3 months after the ictus in Case 2. Left: Lateral view showing two
parallel lines in a branch of the middle cerebral artery (MCA, single arrow) and the dilatation of the superior
temporal artery connected to a branch of the MCA (double arrows'). Right: Anteroposterior view showing a
teardrop of contrast medium extending from the narrowed internal carotid artery (single arrow) and eccentric
stenosis of the MCA (double arrows).

hemisphere; however, the second angiogram (during
the period of deterioration) disclosed severe stenosis or
occlusion of the MCA and ICA, 8'9 indicating further
progression of the dissection in the arterial wall. In
other Type 2 cases, angiography was performed only
when the patients' condition deteriorated and also
showed occlusion of the MCA and ICA. 26 This leads us
to the speculation that perfusion in the hemisphere
failed when the patients deteriorated. Angiograms performed in Type 3 cases showed sufficient perfusion
from spontaneous collateral circulation or via the moderately stenosed MCA and ICA. ~,27 A C T scan was
obtained in only one patient; that patient had a Type 2
disease. In this case, the admission CT scan showed no
definite lesion, but a repeat scan during deterioration
showed massive cerebral infarction in the distribution
of the MCA)
Both of our patients should be included in Type 2
based on the clinical course and/or the neuroradiological findings. The neuroradiological and neuropathological findings in these 22 cases may indicate that
if an anastomosis procedure is performed before the
second ictus, perfusion through the artificial bypass
may prevent massive cerebral infarction. In our Case
2, an STA-MCA anastomosis was performed to gain
enough peripheral perfusion before the second collapse. Fortunately, peripheral perfusion beyond this
bypass and the stenosed MCA was enough to prevent
an increase in cerebral ischemia. In patients with severe injury at the first bifurcation of the MCA, a single
anastomosis may not be enough to prevent the cerebral ischemia from worsening; in such cases, a double
anastomosis may be necessary. If the caliber of the
STA is small, an anastomosis using a venous graft
may be effective.23 We were not able to judge whether

J. Neurosurg. / Volume 6 7 / August, 198 7

proximal ligation of the ICA with the STA-MCA anastomosis was safe or useful. Such a surgical approach
should be effective if sufficient perfusion is obtained
through the bypass immediately after surgery.~2'14
The role of early operative revascularization for patients suffering from cerebral occlusive lesion remains
controversial. Some authors have indicated the potential hazards of this approach when brain damage has
progressed beyond a certain level. 2"4'25 Other authors
have reported that early operative revascularization is
effective for patients with peripheral perfusion through
collateral flow. They indicated that the adequacy of
collateral flow, as judged angiographically, is the best
predictor of outcome. 13 We suggest that early STAMCA anastomosis be considered for patients with peripheral perfusion beyond the dissecting aneurysm of
the MCA and ICA, even though this policy may lead
to unnecessary surgery for Type 3 patients due to the
difficulty in separating them from Type 2 patients at
an early stage. Perhaps emergency bypass surgery within
several hours after the onset of symptoms may be able
to save some Type 1 patients. 2~
References

I. Chang V, Rewcastle NB, Harwood-Nash DCF, et al:
Bilateral dissecting aneurysms of the intracranial internal carotid arteries in an 8-year-old boy. Neurology 25:
573-579, 1975
2. Crowell RM: STA-MCA bypass for acute focal cerebral
ischemia, in Schmiedek P (ed): Microsurgery for Stroke.
New York: Springer-Verlag, 1977, pp 244-250
3. DeVeer JA, Browder J: Post-traumatic cerebral thrombosis and infarction. Report of a case and discussion of
its bearing on the problem of immediate and delayed
post-traumatic apoplexy. J Neuropathol Exp Neurol 1:
24-31, 1942
299

R. Kitani, et al.
4. Diaz FG, Mastri AR, Ausman JI, et al: Acute cerebral
revascularization after regional cerebral ischemia in the
dog. Part 2: Clinicopathologic correlation. J Neurosurg
51:644-653, 1979
5. Dratz HM, Woodhall B: Traumatic dissecting aneurysm
of left internal carotid, anterior cerebral and middle cerebral arteries. J Neuropathol Exp Neurol 6:286-291,
1947
6. Duman S, Stephens JW: Post-traumatic middle cerebral
artery occlusion. Neurology 13:613-616, 1963
7. Friedman AH: Arterial dissections, in Wilkins RH, Rengachary SS (eds): Neurosurgery. New York: McGrawHill, 1985, Vol 1, pp 1297-1300
8. Grosman HG, Fornasier VL, Bonder D, et al" Dissecting
aneurysm of the cerebral arteries. Case report. J Neurosurg 53:693-697, 1980
9. Hegedtis K: Dissecting intracranial aneurysm. Arch Psychiatr Nervenkr 232:25-32, 1982
10. Hochberg FH, Bean C, Fisher CM, et al: Stroke in a 15year-old girl secondary to terminal carotid dissection.
Neurology 25:725-729, 1975
11. Johnson AC, Graves VB, Pfaff JP Jr" Dissecting aneurysm
of intracranial arteries. Surg Neurol 7:49-52, 1977
12. Lawner PM, Simeone FA: Treatment of intraoperative
middle cerebral artery occlusion with pentobarbital and
extracranial-intracranial bypass. Case report. J Neurosurg
51:710-712, 1979
13. Meyer FB, Piepgras DG, Sundt TM Jr, et al: Emergency
embolectomy for acute occlusion of the middle cerebral
artery. J Neorosurg 62:639-647, 1985
14. Mohr G, Martinez SN" Prophylactic microvascular anastomoses in the management of large and giant intracranial
aneurysms, in Spetzler RF, Carter LP, Selman WR, et al
(eds): Cerebral Revascularization for Stroke. New York:
Thieme-Stratton, 1985, pp 356-371
15. Nedwich A, Haft H, Tellem M, et al: Dissecting aneurysms of cerebral arteries. Review of the literature and
report of a case. Arch Neurol 9:477-484, 1963
16. Norman RM, Urich H: Dissecting aneurysm of the middle cerebral artery as a cause of acute infantile hemiplegia.

300

J Pathol Bacteriol 73:580-582, 1957
17. Ramsey TL, Mosquera VT: Dissecting aneurysm of the
middle cerebral artery. Ohio State Med J 44:168-170,
1948
18. Robert F, Maltais R, Giroux JC: Dissecting aneurysm of
middle cerebral artery. J Neurosurg 21:413-415, 1964
19. Sato O, Bascom JF, Logothetis J: Intracranial dissecting
aneurysm. Case report. J Neurosurg 35:483-487, 1971
20. Scott GE, Neubuerger KT, Denst J: Dissecting aneurysms
of intracranial arteries. Neurology 10:22-27, 1960
21. Seelig JM, Marshall LF, Zovickian J, et al: Emergency
extracranial-intracranial bypass with barbiturate protection for acute symptomatic middle cerebral artery occlusion, in Spetzler RF, Carter LP, Selman WR, et al
(eds): Cerebral Revascularization for Stroke. New York:
Thieme-Stratton, 1985, pp 386-391
22. Sinclair W Jr: Dissecting aneurysm of the middle cerebral
artery associated with migraine syndrome. Am J Pathol
29:1083-1091, 1953
23. Spetzler RF, Rhodes RS, Roski RA, et al: Subclavian to
middle cerebral artery saphenous vein bypass graft. J
Neurosurg 53:465-469, 1980
24. Spudis EV, Scharyj M, Alexander E, et al: Dissecting aneurysms in the neck and head. Neurology 12:867-875,
1962
25. Tamura A, Asano T, Sano K: Correlation between rCBF
and histological changes following temporary middle cerebral artery occlusion. Stroke 11:487-493, 1980
26. Wisoff HS, Rothballer AB: Cerebral arterial thrombosis
in children. Review of literature and addition of two cases
in apparently healthy children. Arch Neurol 4:258-267,
1961
27. Wolman L: Cerebral dissecting aneurysms. Brain 82:
276-291, 1959
Manuscript received October 30, 1986.
Address reprint requests to: Ryuichi Kitani, M.D., Department of Neurosurgery, Toyama Rousai Hospital, 992
Rokuromaru, Uozu 937, Japan.

J. Neurosurg. / Volume 67~August, 1987