Neurol Med Chir (Tokyo) 42, 560¿564, 2002

Dissecting Basilar Artery Aneurysm Growing
During Long-term Follow Up
—Case Report—
Shinya NABIKA, Shuichi OKI, Keisuke MIGITA, Naoyuki ISOBE,
Takahito OKAZAKI, Yosuke WATANABE, Kaoru KURISU*,
and Yuzo HAYASHI**
Departments of Neurosurgery and **Pathology, Hiroshima City Asa Hospital, Hiroshima;
*Department of Neurosurgery, Graduate School of Biomedical Sciences,
Hiroshima University, Hiroshima

Abstract
A 58-year-old male presented with a dissecting aneurysm of the basilar artery manifesting as dysarthria, left hemiparesis, and numbness of the left side. Angiography revealed a double lumen at the midportion of the basilar artery which was consistent with a diagnosis of dissecting basilar artery
aneurysm. The patient was treated conservatively, and remained neurologically stable for a 5-year
period following initial presentation, but serial magnetic resonance imaging revealed growth of the
aneurysm compressing the brain stem. His condition then worsened. Computed tomography revealed
obstructive hydrocephalus. Ventriculoperitoneal shunting was performed and the patient's symptoms
improved. However, he died of subarachnoid hemorrhage. Autopsy showed the patient had had a type 3
``dolichoectatic dissecting aneurysm.'' Surgical treatment should be seriously considered for treating
the patients with dissecting basilar artery aneurysm causing brain stem ischemia, especially if the
aneurysm is growing. High-flow bypass and proximal occlusion may be the choice in patients with poor
collateral circulations.
Key words:

basilar artery,

dissecting aneurysm,

dolichoectatic aneurysm

Introduction

Case Report

Recent developments in neuroimaging tools, such as
magnetic resonance (MR) imaging and digital
subtraction angiography, now allow the accurate
diagnosis of dissecting vertebrobasilar artery
aneurysms. Recurrence of bleeding is the most important prognostic factor for patients presenting
with subarachnoid hemorrhage (SAH), and surgical
treatment in the acute stage is recommended.2) Most
reviews focus on cases of dissecting vertebral artery
aneurysms, and considerably fewer reports describe
dissecting aneurysms of the basilar artery. We
treated a patient with a dissecting basilar artery
aneurysm which initially presented with brain stem
ischemia but subsequently caused fatal SAH.

A 58-year-old male with a history of hypertension
visited our hospital following sudden onset of dysarthria, left hemiparesis, numbness of the left side.
Computed tomography (CT) revealed a high density
area in the prepontine cistern (Fig. 1A). Left vertebral angiography revealed a double lumen at the
midportion of the basilar artery (Fig. 1B, C). These
findings were consistent with a diagnosis of dissecting basilar artery aneurysm. The patient was treated
conservatively to control his blood pressure. The left
hemiparesis gradually improved over the next 2
weeks and he was discharged to a rehabilitation
facility. Two days later, he showed neurological deterioration. He had alalia and quadriplegia, but he
was alert and ocular movement was unaffected,
namely the ``locked-in syndrome.'' The patient was
again treated conservatively and his condition gradually improved. MR imaging in 1995 revealed an infarction on the right side of the pons. The patient

Received

May 27, 2002;

Accepted

August 29, 2002

560

Dissecting Aneurysm of the Basilar Artery

Fig. 1

A: Computed tomography scan showing an area of high density in the prepontine cistern. B,
C: Left vertebral angiograms, frontal (B) and lateral views (C), showing a double lumen at the
midportion of the basilar artery, consistent with a diagnosis of dissecting basilar artery
aneurysm.

Fig. 2

Magnetic resonance (MR) images in 1995 (A) showing an infarction on the right side of the
pons. Serial MR images at yearly intervals (B–F: 1996–2000) illustrate the growth of the dissecting aneurysm which was starting to compress the brain stem.

became ambulatory and was discharged with mild
neurological deficit. Follow-up MR imaging revealed that the aneurysm was growing and had started to compress the brain stem (Fig. 2). However, the
patient remained neurologically stable. Six years after the initial attack, the patient was readmitted with
gait disturbance, and 5 months later his consciousness and dysarthria worsened. CT revealed obstructive hydrocephalus. Ventriculoperitoneal shunting
was performed and the patient's condition transiently improved. However, one month later he died of
SAH.
Autopsy revealed a giant fusiform aneurysm,

Neurol Med Chir (Tokyo) 42, December, 2002

561

4.5 × 3.5 × 3.0 cm, arising from the basilar artery.
The aneurysm had caused compression necrosis in
the brain stem (Fig. 3A). The ruptured site had a diameter of about 3 mm (Fig. 3B). We could not identify the perforating arteries from the basilar artery.
The hemorrhage had extended into and completely
obliterated the third and fourth ventricles. The axial
section of the aneurysm showed a fresh hematoma
in most parts of the small true lumen, which had a
diameter of 1.0 cm (Fig. 4A). The aneurysm had a
very thin wall with partial fibrillary hypertrophy.
The aneurysm lacked intactness of the internal elastic lamina (IEL), with only a few fragmented area of

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562

Fig. 3

A: Postmortem photograph showing a giant fusiform aneurysm, 4.5 × 3.5 × 3.0 cm, arising
from the basilar artery, and causing compression necrosis at the brain stem. The hemorrhage
had extended into and completely obliterated the third and the fourth ventricles. B:
Postmortem photograph showing the rupture site (arrow) at the lower end of the aneurysm
and subarachnoid hemorrhage.

Fig. 4

A: Photograph of the axial section of the aneurysm showing a fresh hematoma in most parts
of the small true lumen (arrow). double arrow: Left vertebral artery. B: Photomicrograph
showing the aneurysm lacked intactness of the internal elastic lamina (IEL), but had a few
fragment area of IEL (arrowheads) and thickened intima (arrow). Elastica-van Gieson (EV)
stain, ×4. C: Photomicrograph of the dissection of the thickened intima showing an intimal
flap (arrow). EV stain, ×4.

IEL (Fig. 4B). Dissection of the thickened intima had
begun in the basilar artery aneurysm and formed an
intimal flap (Fig. 4C). No thrombus had formed in

and around the dissected intima. Atherosclerosis
was observed in the thickened intima of the basilar
artery except in the region of the aneurysm.

Neurol Med Chir (Tokyo) 42, December, 2002

Dissecting Aneurysm of the Basilar Artery

Discussion
Sixty-four cases of dissecting basilar artery
aneurysm have been reported.1–5,7,8,10,13,14,17,18,21) The
patients were aged from 15 to 77 years (median 42.8
years). Males slightly outnumbered females (29:23),
but 12 were of unknown sex. Thirty patients were
admitted with SAH, 24 were admitted with brain
stem ischemia, eight were asymptomatic, and two
had an unknown diagnosis. Most of intracranial dissections result in ischemia as the cause of death,6)
but we found that SAH slightly outnumbered ischemia as the main cause of death.4,17) Recurrence of
bleeding in the acute stage accounted for eight cases
(26.1%), which is similar to that reported for dissecting vertebral artery aneurysms (28%).23,24) Further
hemorrhaging tended to occur by the subacute
stage.16) The risk of second hemorrhage in the
chronic stage is very low.16) The mortality was quite
high at 38.3% among these 64 patients, compared to
the mortality of 8% among patients with dissecting
vertebral artery aneurysm.24) However, the mortality
was lower among patients who underwent surgery
than among those treated conservatively (24% vs.
44%).
Further bleeding of the aneurysm is the most important prognostic factor for patients with ruptured
dissecting aneurysms of the vertebral artery.15)
Therefore, treatments for preventing recurrence
of SAH are vigorously performed in such cases.
Reported surgical treatments for dissecting
aneurysms of the vertebral artery include proximal
occlusion (clipping), trapping, wrapping, clipping,
and reconstruction of arteries. However, the optimal
treatment for dissecting aneurysm of the basilar artery is not well established. We compared the treatment of patients that presented with SAH with those
that presented with ischemia among the 64 previously published cases.
Thirty patients presented with SAH, and 15 of
these underwent surgical treatment including proximal occlusion, neck clipping, and wrapping. Seven
cases among these 15 cases achieved good clinical
outcomes. Very recently, successful endovascular
embolization of a dissecting basilar artery aneurysm
which had caused repeated SAH was reported.12)
Prophylactic vascular reconstruction of the rostral
brain stem before the direct surgical treatment of
aneurysm is recommended.8) In particular, highflow bypass is suggested to enable collateral flow to
reach the brain stem after basilar artery occlusion.
Cases of serpentine basilar artery aneurysms have
been clipped under deep hypothermia with cardiac
arrest.9,20)
Some patients treated conservatively following

Neurol Med Chir (Tokyo) 42, December, 2002

563

basilar artery dissection causing brain stem ischemia have achieved good outcomes.17,18) However,
most patients treated conservatively had poor outcomes. Twenty-one of the 24 patients who presented
with ischemia were treated conservatively. Three
patients had a good outcome and 12 patients died.
Therefore, aggressive treatment should be considered even in patients with ischemia. Especially, in
patients with progressive dissection at radiographic
follow up, further treatment seems to be necessary
to prevent subsequent bleeding13) as in our own case.
In our case, the right vertebral artery was aplastic
and there was no flow from the posterior communicating artery. Therefore, simple proximal occlusion of basilar artery was not a choice for treatment.
Recently, high-flow bypass and proximal occlusion of the basilar artery have been reported for
large aneurysms in the posterior circulation.8,12,19,22)
Radial artery bypass grafts were used between the
intracranial vertebral artery and posterior cerebral
artery to treat large basilar artery aneurysms and
achieved good results.8) Therefore, high-flow bypass
surgery and proximal occlusion might have been the
only option to rescue our patient. However, we
should keep in mind that there is a risk of occlusion
of the perforating arteries and the growing
aneurysm.
Fusiform and dissecting aneurysms can be classified into four categories, type 1 to type 4.11) Damage
to the IEL is often an associated factor in the pathogenesis of aneurysm formation and there is a strong
relationship between the pathological features of the
aneurysm and the clinical course.11) In the present
case, intimal thickening compensated for the weakness of the arterial wall caused by the damaged IEL.
In addition, adaptive and multiple dissections had
occurred in the thickened intima, with a thrombus
forming in and around the dissected intima. This
type of aneurysm is pathologically characterized by
fragmentation of the IEL, multiple dissections of the
thickened intima, and organized thrombus in the
lumen. According to the classification by Mizutani
et al.,11) our patient had a type 3 dolichoectatic dissecting aneurysm. This type of aneurysm is exclusively located on the basilar artery and appears angiographically as a tortuous fusiform aneurysm with
irregular contrast as seen in our case. Patients with
such aneurysms usually present with non-SAH
symptoms and aneurysm growth to giant size. The
patients may die of SAH, three of eight in Mizutani's
series. The present case also suggests that the natural course of angiographical type 3 basilar artery
aneurysm is ominous and intensive treatment
should be performed.

S. Nabika et al.

564

Surgery should be seriously considered for treating a patient with dissecting basilar artery aneurysm
causing brain stem ischemia, especially if the
aneurysm is growing. High-flow bypass and proximal occlusion should be the choice in patients with
poor collateral circulation.

13)

14)

References
15)
1)

2)

3)

4)

5)

6)

7)

8)

9)

10)

11)

12)

Amin-Hanjani S, Ogilvy CS, Buonanno FS, Choi IS,
Metz LN: Treatment of dissecting basilar artery
aneurysm by flow reversal. Acta Neurochir (Wien)
139: 44–51, 1997
Berger MS, Wilson CB: Intracranial dissecting
aneurysms of the posterior circulation. Report of six
cases and review of the literature. J Neurosurg 61:
882–894, 1984
Boulanger TH, Aymand A, Urbain E, Merlamd JJ,
Labasse H: Diagnosis and endovascular treatment of
midbasilar dissecting aneurysm. JBR-BTR 79:
171–174, 1996
Farrell MA, Gilbert JJ, Kaufmann JC: Fatal intracranial arterial dissection: clinical pathological
correlation. J Neurol Neurosurg Psychiatry 48: 111–
121, 1985
Hosoda K, Fujita S, Kawaguchi T, Shose Y,
Yonezawa K, Shirakuni T, Hamasaki H: Spontaneous
dissecting aneurysms of the basilar artery presenting
with a subarachnoid hemorrhage. J Neurosurg 75:
628–633, 1991
Kawaguchi S, Sasaki T: Management of dissecting
aneurysms of the posterior circulation. Acta Neurochir (Wien) 131: 26–31, 1994
Kishiguchi T, Yamada K, Ito M, Taneda M,
Hayakawa T: [Histopathological analysis of
dolichoectatic basilar artery]. No Socchu No Geka 22:
491–494, 1994 (Jpn, with Eng abstract)
Kobayashi N, Kamiyama H: [Reconstruction of the
basilar arterial system: Methods of high flow bypass
in posterior cranial fossa]. No Socchu No Geka 27:
270–276, 1999 (Jpn, with Eng abstract)
Lawton MT, Raudzens PA, Zabramski JM, Spetzler
RF: Hypothermic circulatory arrest in neurovascular
surgery: evolving indications and predictors of
patient outcome. Neurosurgery 43: 10–21, 1998
Miwa Y, Ooe N, Murase S, Nokura H, Ohkuma A:
[Clinical study of dissecting and fusiform aneurysm
of the vertebro-basilar system]. No Socchu No Geka
22: 241–246, 1994 (Jpn, with Eng abstract)
Mizutani T, Miki Y, Kojima H, Suzuki H: Proposed
classification of nonatherosclerotic cerebral fusiform
and dissecting aneurysms. Neurosurgery 45: 253–260,
1999
Nagasawa S, Ohta T, Kajimoto Y, Tanaka H,
Kawanishi M, Tada Y: Giant thrombosed vertebral
artery aneurysm treated by extracranial-intracranial
bypass and aneurysmectomy. Case report. Neurol

16)

17)

18)

19)

20)

21)

22)

23)
24)

Med Chir (Tokyo) 34: 311–314, 1994
Nakahara T, Satoh H, Mizoue T, Kawamoto H,
Kohmo Y, Kurisu K: Dissecting aneurysm of basilar
artery presenting with recurrent subarachnoid
hemorrhage. Neurosurg Rev 22: 155–158, 1999
Oki S, Shima T, Ishikawa S, Uozumi T, Yamane T,
Hara H: [A case of intracranial arterial dolicho-ectasia]. No To Shinkei 31: 593–600, 1979 (Jpn, with Eng
abstract)
Ono J, Yamamura A, Kobayashi S, Sugaya Y, Toritani
H, Hirai S, Kobayashi E: [Management of 62 patients
with ruptured dissecting aneurysms of vertebrobasilar system]. The Mt Fuji Workshop on CVD 18: 95–98,
2000 (Jpn, with Eng abstract)
Ono J, Yamamura A, Kubota M, Hirai S, Miyata A:
[Management of 42 patients with ruptured dissecting
aneurysms of vertebrobasilar system]. No Socchu No
Geka 24: 51–55, 1996 (Jpn, with Eng abstract)
Pozzati E, Andreoli A, Padovani R, Nuzzo G: Dissecting aneurysms of the basilar artery. Neurosurgery 36:
254–258, 1995
Ross GJ, Ferraro F, De Riggi L, Scotti LN: Spontaneous healing of basilar artery dissection: MR findings.
J Comput Assist Tomogr 18: 292–294, 1994
Sundt TM Jr, Piepgras DG, Marsh WR, Fode NC:
Saphenous vein bypass grafts for giant aneurysms
and intracranial occlusive disease. J Neurosurg 65:
439–450, 1986
Uede T, Ohtaki M, Tanabe S, Hashi K: [Direct surgical management of giant and large intracerebral
aneurysms, associated with intraluminal thrombus
and/or atherosclerotic thickening of aneurysmal
neck]. No Shinkei Geka 25: 1007–1015, 1997 (Jpn, with
Eng abstract)
Vishteh AG, Spetzler RF: Evolution of a dolichoectatic aneurysm into a giant serpentine aneurysm during
long-term follow up. Case illustration. J Neurosurg
91: 346, 1999
Wakui K, Kobayashi S, Takemae T, Kamijoh Y,
Nagashima H, Muraoka S: Giant thrombosed vertebral artery aneurysm managed with extracranialintracranial bypass and aneurysmectomy. J Neurosurg 77: 624–627, 1992
Yamamura A: Diagnosis and treatment of vertebral
aneurysms. J Neurosurg 69: 345–349, 1988
Yamamura A, Watanabe Y, Saeki N: Dissecting
aneurysms of the intracranial vertebral artery. J Neurosurg 72: 183–188, 1990

Address reprint requests to: S. Nabika, M.D., Department
of Neurosurgery, Hiroshima City Asa Hospital,
2–1–1 Kabeminami, Asakita–ku, Hiroshima 731–
0293, Japan.
e-mail: noge＠asa-hosp.city.hiroshima.jp.

Neurol Med Chir (Tokyo) 42, December, 2002