Neurol Med Chir (Tokyo) 41, 271¿278, 2001

Dissecting Aneurysms at the A1 Segment
of the Anterior Cerebral Artery
—Two Case Reports—
Jun HIRAO, Hisayo OKAMOTO, Takashi WATANABE,
Shuichiro ASANO*, and Akira TERAOKA*
Department of Neurosurgery, Institute of Neurological Sciences, Tottori University School
of Medicine, Yonago, Tottori; *Department of Neurosurgery,
Teraoka Memorial Hospital, Hiroshima

Abstract
Two rare cases of dissections which involve the anterior cerebral artery (ACA) are reported. A 58-yearold woman presented with a ruptured dissecting aneurysm manifesting as sudden onset of severe
headache and consciousness disturbance followed by aphasia, right hemiparesis, paresis of the left lower extremity, and choreoathetotic movements of the upper arms and face. Computed tomography and
angiography revealed subarachnoid hemorrhage due to a dissecting aneurysm at the left A1 segment.
The dissecting aneurysm was trapped surgically on the day of onset. Her neurological deficits disappeared within a month. A 39-year-old woman experienced continuous dull headache from the day before onset, and then suffered right hemiparesis. Magnetic resonance (MR) imaging revealed cerebral infarction at the left globus pallidus. Angiography and MR imaging revealed a dissecting aneurysm at the
left A1 segment and occlusion of the left Heubner's artery. She received conservative treatment and her
neurological findings were improved. Dissections or dissecting aneurysms involving the ACA can be
classified into three types: Extension of a dissection to the ACA from the internal carotid artery, dissection at the A1 segment, and dissection at the A2–A4 segments. These types of dissection have distinct
uniform clinical features.
Key words:

dissection,

dissecting aneurysm,

A1 segment,

anterior cerebral artery

Introduction

Case Reports

Dissections or dissecting aneurysms of intracranial
arteries are rather rare35) and most frequently occur
in the territories of the middle cerebral artery (MCA)
or vertebrobasilar system.17,24) Dissections which involve the anterior cerebral artery (ACA) are extremely rare, with only five reported cases of dissections at the A1 segment.6,10,19,23,31) Four dissections
were identified by postmortem examination and one
by angiography. We report two cases of dissecting
aneurysms at the A1 segment of the ACA which were
identified by angiography and magnetic resonance
(MR) imaging.

Case 1: A 58-year-old previously healthy woman was
admitted to the Tottori University Hospital on January 23, 1995. She suffered sudden onset of severe
headache and lost consciousness. She was found by
her family members, and was transported to our
hospital by ambulance. On admission, she was confused and unable to speak due to motor aphasia, but
responded to simple verbal orders. Choreoathetotic
involuntary movements involving her bilateral upper extremities and face were apparent. Complete
paraplegia of the lower extremities as well as slight
weakness of the right arm was observed. Laboratory
findings were negative.
Computed tomography (CT) revealed diffuse
subarachnoid hemorrhage (SAH), especially in the
anterior part of the interhemispheric fissure which
was classified as Fisher's group 3 (Fig. 1). Left
carotid angiography disclosed the so-called string

Received
2001

October 10, 2000;

Accepted

March 7,

271

272

Fig. 1

Fig. 2

J. Hirao et al.

Case 1. Computed tomography scan on
admission showing diffuse subarachnoid
hemorrhage, especially in the anterior part
of interhemispheric fissure which suggests
a ruptured anterior communicating artery
aneurysm.

Case 1. Left carotid angiogram (oblique
view) on admission showing the so-called
string and pearl sign, and double contour
appearance in the aneurysmal dilatation at
the A1 segment of the anterior cerebral artery.

Fig. 3

Case 1. Right carotid angiogram (oblique
view) with digital compression of the left
common carotid artery on admission showing a dissecting aneurysm at the left A1 segment via collateral flow through the anterior communicating artery.

and pearl sign at the A1 segment of the ACA. The
aneurysmal dilatation had a double contour appearance, which suggested the presence of true and false
lumina in a dissecting aneurysm (Fig. 2). Right
carotid angiography with digital compression of the
left common carotid artery demonstrated the same
aneurysmal dilatation at the left A1 segment via the
collateral flow through the anterior communicating
artery (AcomA) (Fig. 3). Angiography detected no
other abnormal findings. The diagnosis was SAH
caused by ruptured dissecting aneurysm at the A1
segment of the left ACA. After cerebral angiography,
her neurological abnormalities such as motor aphasia, involuntary movement, and left leg paresis disappeared but she was still slightly confused. Her
preoperative World Federation of Neurosurgical
Societies grade was III, based on the Glasgow Coma
Scale score of 14 and the presence of right hemiparesis.
Trapping of the dissecting aneurysm was performed via the left pterional approach. After the sylvian fissure was opened, the left internal carotid artery (ICA) was identified and the A1 segment of the

Neurol Med Chir (Tokyo) 41, May, 2001

Dissection of ACA

273

"

Fig. 4

left ACA was exposed from the bifurcation of the
ICA to its distal portion. A reddish fusiform dilatation was seen 12 mm distal to the bifurcation (Fig. 4
right). The wall was so thin that the blood flow could
be seen. A perforating branch was observed arising
from the A1 segment proximal to the dissecting
aneurysm. A straight clip with a 7 mm blade was applied to the A1 segment just proximal to the dissection, causing the aneurysmal dilatation to collapse
(Fig. 4 left). The distal part of the A1 segment, the
AcomA, and the A2 segment of the left ACA were
exposed and identified, and a straight clip with a
7 mm blade was applied to the ACA adjacent to the
distal end of the dissecting aneurysm.
The postoperative course was uneventful. The
right hemiparesis improved gradually, and the
patient could walk 2 weeks after the surgery. CT
demonstrated no low-density areas during the
course, but single photon emission CT using technetium-99m hexamethylpropylene amine oxime
showed a low perfusion area at the medial and inferior part of the left frontal lobe. Cerebral angiography obtained 3 weeks after the surgery
showed the dissecting aneurysm had disappeared
(Fig. 5), and the left A2–A4 segments of ACA were
visualized via collateral flow through the AcomA.
The left A2 segment was narrowed compared to normal, probably due to delayed vasospasm. She was
discharged one month after admission without neurological deficit. She has since resumed her normal
activities.
Case 2: A 39-year-old woman was admitted to

Neurol Med Chir (Tokyo) 41, May, 2001

Fig. 5

Case 1. Operating microscope photographs showing a
reddish and fusiform dilatation at the A1 segment (right),
and the collapsed aneurysmal
dilatation after a straight clip
was applied to the A1 segment
just proximal to the dissecting
aneurysm (left).

Case 1. Left carotid angiogram (anteroposterior view) 3 weeks after the onset
showing the dissecting aneurysm has disappeared, and the left A1 segment terminates
with the perforating branch.

Teraoka Memorial Hospital on July 28, 1997. She
had suffered from dull frontal headache continuous-

274

J. Hirao et al.

ly for a day. Subsequently, she had spoken words
without meaning. She manifested right hemiparesis
one day later and then was transported to the hospital by ambulance. On admission, she was confused
slightly, but responded to simple verbal orders. She
had neither weakness nor numbness in her limbs
except for right facial nerve paresis. Laboratory
findings were negative, and lumbar puncture
showed clear cerebrospinal fluid.
MR imaging revealed a cerebral infarction at the
territory of left Heubner's artery (Fig. 6). Left carotid
angiography disclosed a fusiform aneurysm at the
A1 segment of the ACA (Fig. 7). There was no double contour appearance at the aneurysmal dilatation, nor any other abnormal findings. Axial MR imaging revealed double contour appearance in the
aneurysmal dilatation, which suggested the presence of true and false lumina in the fusiform aneurysm (Fig. 8). The diagnosis was cerebral infarction
caused by dissection at the A1 segment of the left
ACA and obliteration of the left Heubner's artery.
Her neurological deficits improved gradually after
conservative treatment. Follow-up MR imaging
demonstrated regression of the dissection. Repeat
cerebral angiography obtained 4 weeks after admission showed reduction of the dissection and no
progression to the distal portion (Fig. 9). Subsequently, She was discharged without neurological deficit
and has resumed her normal activities.

Fig. 6

Case 2. T2-weighted magnetic resonance
image the day after onset revealing cerebral
infarction in the territory of the left Heubner's artery.

Fig. 7

Case 2. Left carotid angiogram (anteroposterior view) disclosing a fusiform
aneurysm at the A1 segment of the anterior
cerebral artery. There was no double contour appearance in the aneurysmal dilatation.

Fig. 8

Case 2. Axial T1-weighted magnetic
resonance image 4 days after onset revealing double contour appearance in the
aneurysmal dilatation, which suggested the
presence of true and false lumina in the
fusiform aneurysm.

Neurol Med Chir (Tokyo) 41, May, 2001

Dissection of ACA

Fig. 9

Case 2. Repeat cerebral angiogram 4
weeks after onset showing reduction of the
dissection and no progression to the distal
portion.

Discussion
Only 32 cases of dissections which involve the ACA
have been reported (Table 1), including only five
cases of dissections at the A1 segment.6,10,19,23,31) Dissections or dissecting aneurysms involving the ACA
can be divided into three types based on the affected
site, the age of patients, the onset, progression, and
outcome of the disease. Type I dissection usually
originates at the ICA and extends to the ACA as well
as to the MCA. Type II dissection often occurs at the
A1 segment of the ACA. Type III dissection mainly
involves distal ACA, namely the A2, A3, and A4 segments.
Most type I dissections seem to occur in young
adults. All 10 patients were between 14–41 years
old3,5,7,13,15,18,25,26,30) except for a 75-year-old woman.1)
The mean age was 24 years. The etiology of type I
was speculated to be trauma in two cases, congenital
fragility of the vascular wall in two, atherosclerosis
in one, and unknown in five. Nine of the 10 patients
had cerebral infarctions and died within 8 days of
the onset. However, the 75-year-old woman1)
manifested SAH and survived with mild right

Neurol Med Chir (Tokyo) 41, May, 2001

275

hemiparesis and aphasia after surgical clamping of
the affected ICA. The high mortality associated with
type I dissections may be due to the sharp reduction
in collateral flow to the territory of the affected ICA
via the AcomA in the presence of the dissections of
the A1 segment of ACA. Occlusion at the earlier
stage may prevent farther extension of dissection
and/or possibly preserve more collateral flow
through the AcomA, so we suggest that intravascular occlusion of the affected ICA may be the best
treatment.
The five cases of type II dissections mostly occurred in young females except for one pediatric
case.6,10,19,23,31) Type II dissections often caused SAH.
A 26-year-old female suffered SAH but misdiagnosis
of ruptured AcomA aneurysm was made. After she
died on day 12, autopsy showed a ruptured dissecting aneurysm at the A1 segment of the ACA and an
unruptured AcomA aneurysm. A 5-year-old boy
manifested headache, right hemiparesis, and aphasia 3 days after minor head injury. Left carotid angiography demonstrated no filling of the left ACA.
He died after receiving decompressive craniotomy.
Postmortem examination revealed dissecting subintimal hematoma of the left ACA (A1, A2) and massive
infarction of left frontal lobe. The poor outcome may
have been due to the dissection of the A1 segment of
the ACA which extended to the A2 segment, as a
result of poor collateral flow through the AcomA. A
22-year-old pregnant female died of massive abdominal hemorrhage, and a 16-year-old female died of intracerebral hematoma (ICH) due to moyamoya disease. Autopsy of both cases disclosed unruptured
dissections at the A1 segments of ACA. A 48-yearold female experienced repeated bouts of severe
headaches. She eventually lost consciousness one
month after cerebral infarction at the territory of the
left ACA. Surgery identified a dissecting aneurysm
at the left A1 and A2 portions of the ACA. She recovered after the surgery. Our cases are considered
to be type II dissection based on the affected site
and the progression of the disease. Case I was the
first to be identified angiographically and treated
with trapping surgery.
Although only seven cases of type II dissection including ours have been reported, some dissections
or dissecting aneurysms at A1 segments may be misdiagnosed as such aneurysms. For example, 38 of
4295 aneurysms (0.88%) were aneurysms at the A1
segment of ACA and nine (0.2%) of these were
fusiform aneurysms or saccular aneurysms which
did not arise from a bifurcation.27) Two of 1000
aneurysms (0.2%) were fusiform aneurysms at the A1
segment.33) All of these cases may harbor type II dissection. Alternatively, type II dissection may be clas-

J. Hirao et al.

276
Table 1

Table 1 Classification of dissecting aneurysms involving the anterior cerebral artery

Type*

Author (Year)

Age/
Sex

I

Dratz and Woodholl (1947)5)
Anderson and Schechter (1959)3)

21/F
41/M

infarction
infarction

Wolman (1959)30)

16/M

infarction

Scott et al. (1960)25)

29/F

infarction

Nedwich et al. (1963)18)
Grosman et al. (1980)7)

30/F
23/M

infarction
infarction

Adams et al. (1982)1)

75/F

SAH

Steiner et al. (1986)26)

23/F

infarction

Linden et al. (1987)15)
Kitani et al. (1987)13)

23/F
14/M

infarction
infarction

Gherardi and Lee (1967)6)
Nelson (1968)19)

26/F
5/M

SAH
infarction

Pilz (1977)23)

22/F

incidental

Yamashita et al. (1983)31)

16/F

incidental

Honda et al. (1997)10)

48/F

infarction ª SAH

Present Case 1

58/F

SAH

Present Case 2

39/F

infarction

Nakazawa et al. (1984)17)

43/M

infarction

Amagasa et al. (1988)2)

44/M

infarction

Sasaki et al. (1991)24)

57/M

infarction

Terai and Matsubara (1991)29)

51/M

infarction

Guridi et al. (1993)8)

72/F

SAH + ICH

Nomura et al. (1993)20)

37/M

infarction

Yasukawa et al. (1993)34)

62/M

infarction + SAH

Kidooka et al. (1993)12)

45/M

infarction

45/M

infarction

Ishikawa et al. (1993)11)

42/M

infarction

Yano et al. (1995)32)

27/M

SAH + ICH

Nagata and Sato (1996)16)

43/M

infarction

Hayashi et al. (1996)9)

36/M

ICH

II

III

Manifestation

Symptoms and signs

Etiology

Outcome**

rt hemiparesis, semicoma
rt hemiparesis, aphasia,
rt hemianopia
headache,
nasal bleeding,
lt hemiplegia, aphasia
lt hemiparesis,
lt facial nerve palsy,
aphasia
lt hemiparesis
dysphagia,
rt hemiparesis
headache

trauma
arteriosclerosis

dead
dead

congenital defect of
the vessel wall

dead

trauma (surgical
complication)

dead

unknown
unknown

dead
dead

unknown

headache,
lt hemiparesis,
semicoma
lt hemiplegia, coma
headache,
lt hemiplegia
headache, coma
headache,
rt hemiparesis,
aphasia

congenital weakness
of elastic lamina

moderately
disabled
dead

headache,
rt hemiparesis
headache, paraplegia,
involuntary movement
of face and arms
headache,
rt hemiparesis
headache, vertigo,
involuntary movement
of legs,
convulsion,
rt hemiparesis
aphasia,
rt hemiparesis
headache,
weakness of lt leg
headache,
rt hemiparesis
headache, neck pain,
loss of consciousness,
rt hemiparesis
headache,
weakness of lt leg
rt hemiparesis,
dysarthria
headache,
rt hemiparesis
headache,
involuntary movement
of legs,
rt hemiparesis
headache,
weakness of lt leg
headache,
rt hemiparesis
headache,
weakness of rt leg
loss of consciousness,
weakness of lt leg

unknown
unknown

dead
dead

unknown
trauma

dead
dead

Guillain-Barr áe
dead
syndrome
moyamoya disease + dead
trauma
unknown
alive
unknown

good
recovery

unknown

good
recovery
good
recovery

unknown

trauma
unknown
unknown
arteriosclerosis
trauma
unknown
unknown
unknown

unknown
unknown
unknown
unknown

good
recovery
moderately
disabled
good
recovery
moderately
disabled
good
recovery
good
recovery
good
recovery
good
recovery
good
recovery
good
recovery
good
recovery
good
recovery
Contd.

Neurol Med Chir (Tokyo) 41, May, 2001

Dissection of ACA
Table 1,
Type*
III

277

contd.
Author (Year)

Age/
Sex

Manifestation

Araki et al. (1996)4)

52/M

infarction

Okuno et al. (1996)22)

50/M

Koyama et al. (1996)14)

45/M

hemorrhagic
infarction
infarction

44/M

infarction

Symptoms and signs
headache,
weakness of lt leg
headache,
urinary incontinence
dizziness,
weakness of lt leg
rt hemiparesis,
dysarthria

Etiology
unknown
unknown
unknown
unknown

Outcome**
good
recovery
good
recovery
good
recovery
good
recovery

*Our classification was assigned as follows: type I, extension of dissection to anterior cerebral artery from internal
carotid artery; type II, dissection at A1 segment of anterior cerebral artery; type III, dissection at A2–A4 segments of
anterior cerebral artery. **According to Glasgow Outcome Scale. ICH: intracerebral hematoma, SAH:
subarachnoid hemorrhage.

sified as SAH with unknown etiology, because dissections or dissecting aneurysms are often difficult
to identify angiographically. MR imaging may be
useful to demonstrate dissection or dissecting
aneurysm.
The 17 cases of type III dissections were mainly
found in middle-aged males, aged between 27–72
years (mean age 47 years).2,4,8,9,11,12,14,16,17,20,22,24,29,32,34)
The patients were Japanese except for one.8) The etiology was presumed to be trauma in two cases, arteriosclerosis in one, and unknown in the others.
Twelve of the 17 type III dissections caused cerebral
infarctions, one SAH and infarction, two SAH and
ICH, one hemorrhagic infarction, and one ICH. Fifteen patients had hemiparesis or weakness of the
lower extremities. Nine of 12 patients who suffered
only ischemic attacks were treated conservatively
and two were operated with wrapping surgery of
dissecting aneurysms at the chronic stage, whereas
one was treated with trapping with A3-A3 anastomosis. Trapping and resection of the dissection was
performed in one patient with SAH, trapping with
bypass surgery in one, and conservative treatment
in one. All 15 patients showed complete improvement of neurological abnormalities with exceptions
of moderate hemiparesis in two patients. However,
one patient died suddenly of massive and recent
gastric bleeding caused by acute erosive gastritis 6
weeks after the onset.8)
Headache is a common symptom even in patients
with dissections of the ACA causing ischemia
without SAH. All 16 patients who showed cerebral
ischemia and were able to speak on admission complained of headache at the onset. Our first patient
had aphasia, right hemiparesis, paresis of the left
lower extremity, and choreoathetotic movements of
the upper extremities and face after recovery of consciousness. Thus, hemiparesis and/or paresis of the
lower extremities is also a characteristic of type II

Neurol Med Chir (Tokyo) 41, May, 2001

dissection of the ACA. Two cases of type III dissection showed transient involuntary movements at the
onset.12,17) Involvement of the extra-pyramidal system which is perfused by the ACA might cause such
involuntary movements.
We selected trapping surgery for the first patient
with SAH, because angiography indicated collateral
flow through the AcomA, based on reports that trapping surgery is a good treatment for a fusiform
aneurysm at the A1 segment,21,33) when collateral
flow through the AcomA was sufficient. Treatment
for a dissecting aneurysm at the A1 segment is likely
to be similar to treatment for fusiform aneurysm.28)
Our two cases of dissecting aneurysms at the A1
segment of the ACA were identified by angiography
and MR imaging, and one was treated by trapping
surgery. We classified dissections or dissecting
aneurysms involving the ACA into three types based
on the affected site. Type I dissection occurs in relatively younger patients and causes fatal brain infarctions. Type II dissection tends to occur in females
and causes SAH or cerebral infarction, although
there were only seven cases of this type. The outcome seemed to depend on the sufficiency of collateral flow through the AcomA and the amount of
subarachnoid clot in the case of SAH. Type III dissection occurs in middle-aged males and causes
transient ischemic attacks and/or rather mild SAH.

References
1)

Adams HP Jr, Aschenbrener CA, Kassell NF,
Ansbacher L, Cornell SH: Intracranial hemorrhage
produced by spontaneous dissecting intracranial
aneurysm. Arch Neurol 39: 773–776, 1982
2) Amagasa M, Sato S, Otabe K: Posttraumatic dissecting aneurysm of the anterior cerebral artery. Case
report. Neurosurgery 23: 221–225, 1988
3) Anderson R, Schechter M: A case of spontaneously
dissecting aneurysm of the internal carotid artery. J

278

4)

5)

6)

7)

8)

9)

10)

11)

12)

13)

14)

15)

16)

17)

18)

19)

20)

J. Hirao et al.
Neurol Neurosurg Psychiatry 22: 195–201, 1959
Araki T, Ouchi M, Ikeda Y: [A case of anterior
cerebral artery dissecting aneurysm]. No Shinkei
Gega 24: 87–91, 1996 (Jpn, with Eng abstract)
Dratz HM, Woodholl B: Traumatic dissecting
aneurysm of left internal carotid, anterior cerebral
and middle cerebral arteries. J Neuropathol Exp Neurol 6: 286–291, 1947
Gherardi GJ, Lee HY: Localized dissecting hemorrhage and arteritis. Renal and cerebral manifestations. JAMA 199: 219–220, 1967
Grosman H, Fornasier VL, Bonder D, Livingston KE,
Platts ME: Dissecting aneurysms of the cerebral arteries. Case report. J Neurosurg 53: 693–697, 1980
Guridi J, Gallego J, Monzon F, Aguilera F: Intracranial hemorrhage caused by transmural dissection of the
anterior cerebral artery. Stroke 24: 1400–1402, 1993
Hayashi H, Fukuda O, Endo S, Takaku A: [Intracerebral hemorrhage secondary to dissecting
aneurysm of the anterior cerebral artery]. No Shinkei
Geka 48: 1053–1056, 1996 (Jpn, with Eng abstract)
Honda N, Yuge T, Miyagi J, Shigemori M: [A surgical
case of dissecting aneurysm of the anterior cerebral
artery]. No Shinkei Geka Journal 6: 634–638, 1997
(Jpn, with Eng abstract)
Ishikawa R, Sunagawa S, Itoh I, Iwashita K: [An experience of dissecting cerebral aneurysm of the anterior cerebral artery]. No Shinkei Geka 21: 355–359,
1993 (Jpn, with Eng abstract)
Kidooka M, Okada T, Sonobe M, Nakazawa T, Handa
J: Dissecting aneurysm of anterior cerebral artery.
Report of two cases. Surg Neurol 39: 53–55, 1993
Kitani R, Itouji T, Noda Y, Kimura M, Ueda S: Dissecting aneurysms of the anterior circle of Willis arteries. J Neurosurg 67: 296–300, 1987
Koyama S, Kotani A, Sasaki J: Spontaneous dissecting aneurysm of the anterior cerebral artery; Report
of the two cases. Surg Neurol 46: 55–61, 1996
Linden MD, Chou SM, Furlan AJ, Conomy JP:
Cerebral arterial dissection. A case report with
histopathologic and ultrastructural findings. Cleve
Clin J Med 54: 105–114, 1987
Nagata K, Sato K: [Surgical treatment for the dissecting aneurysm of the anterior cerebral artery ]. No Socchu No Geka 24: 80–84, 1996 (Jpn, with Eng abstract)
Nakazawa T, Saito A, Watanabe K, Matsuda M,
Handa J: [Dissecting aneurysm of the anterior
cerebral artery: Report of a case]. No Shinkei Gega 12:
1211–1216, 1984 (Jpn, with Eng abstract)
Nedwich A, Haft H, Tellem M, Kauffman L: Dissecting aneurysms of cerebral arteries. Arch Neurol 9:
477–484, 1963
Nelson JW: Dissecting subintimal hematomas of the
intracranial arteries. Report of a case. J Am Osteopath Assoc 67: 512–527, 1968
Nomura H, Nishijima M, Hounoki S, Oka N, Takaku
A: [A dissecting aneurysm of the anterior cerebral artery. A case report and a review of literature]. No
Shinkei Geka Journal 2: 152–155, 1993 (Jpn, with Eng

21)

22)

23)

24)

25)

26)

27)

28)

29)

30)
31)

32)

33)

34)

35)

abstract)
Oba M, Suzuki M, Onuma T: [Two cases of ruptured
fusiform aneurysm of proximal anterior cerebral artery (A1 segment)]. No Shinkei Geka 17: 365–368,
1989 (Jpn, with Eng abstract)
Okuno S, Ochiai C, Nagai M: Dissection aneurysm of
the anterior cerebral artery causing hemorrhagic infarction. Surg Neurol 45: 25–30, 1996
Pilz P: Dissezierendes Aneurysma der Arteria cerebri
anterior und Guillain-Barre-Syndrom in der Schwangerschaft. J Neurol 214: 295–299, 1977
Sasaki O, Koike T, Takeuchi S, Tanaka R: Serial angiography in a dissecting anterior cerebral artery
aneurysm. Surg Neurol 36: 49–53, 1991
Scott GE, Neubuerger KT, Denst J: Dissecting
aneurysms of intracranial arteries. Neurology (Minneap) 10: 22–27, 1960
Steiner H, Lammer J, Kleinert R, Schreyer H: Dissecting aneurysm of cerebral arteries in congenital vascular deficiency. Neuroradiology 28: 331–334, 1986
Suzuki M, Onuma T, Sakurai Y, Mizuki K, Ogawa A,
Yoshimoto T: Aneurysms arising from the proximal
(A1) segment of the anterior cerebral artery. A study
of 38 cases. J Neurosurg 76: 455–458, 1992
Tamura M, Tsukahara Y, Yodonawa M: [Fusiform
aneurysm of anterior cerebral artery (A1 segment). A
case report]. No Shinkei Geka 13: 1337–1340, 1985
(Jpn, with Eng abstract)
Terai S, Matsubara T: [A case of dissecting aneurysm
involving solely anterior cerebral artery]. No Socchu
13: 159–164, 1991 (Jpn, with Eng abstract)
Wolman L: Cerebral dissecting aneurysms. Brain 82:
276–291, 1959
Yamashita M, Tanaka K, Matsuo T, Yokoyama K,
Fujii T, Sakamoto H: Cerebral dissecting aneurysm
in patients with moyamoya disease. J Neurosurg 58:
120–125, 1983
Yano H, Sawada M, Shinoda J, Funakoshi T: Ruptured dissecting aneurysm of the peripheral anterior
cerebral artery. Case report. Neurol Med Chir (Tokyo)
35: 450–453, 1995
Yasargil MG: Operative anatomy, in Yasargil MG
(ed): Microneurosurgery, vol I. Stuttgart, Georg
Thieme Verlag, 1984, pp 92–98
Yasukawa K, Kamijou Y, Momose G, Kobayashi S,
Ikeda A: [A case of anterior cerebral dissecting
aneurysm presenting subarachnoid hemorrhage and
cerebral infarction at the same time]. No Socchu No
Geka 21: 461–466, 1993 (Jpn, with Eng abstract)
Yonas H, Agamanolis D, Takaoka Y: Dissecting intracranial aneurysms. Surg Neurol 8: 407–415, 1977

Address reprint requests to: T. Watanabe, M.D., Department of Neurosurgery, Institute of Neurological
Sciences, Tottori University School of Medicine,
36–1 Nishi–cho, Yonago, Tottori 683–8504, Japan.

Neurol Med Chir (Tokyo) 41, May, 2001