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Case Reports
J Korean Neurosurg Soc 29：
： 426-429, 2000
Ruptured Posterior Communicating Artery Aneurysm Causing
Bilateral Abducens Nerve Paralyses
-Case Report Chea Heuck Lee, M.D., Young Cho Koh, M.D.
Department of Neurosurgery, Seoul Paik Hospital, College of Medicine Inje University, Seoul, Korea
= Abstract =
양측성 외전신경 마비를 보인 파열성 후교통동맥 동맥류
- 증례보고 인제대학교 의과대학 서울백병원 신경외과학교실
이 채 혁·고 영 초
rare case of bilateral abducens nerve paralyses after rupture of a left posterior communicating artery(PcomA)
aneurysm with multiple unruptured aneurysms in a 46-year-old female is presented. Sudden left abducens
nerve paralysis followed by progressive right abducens nerve paralysis were present without additional neuroophthalmological signs. Postoperatively, bilateral abducens nerve paralyses gradually recovered and disappeared in
2 weeks. The authors reviewed and discussed the possible mechanisms involved in this uncommon neuro-ophthalmological manifestation.
A
KEY WORDS：Bilateral abducens nerve paralyses・Ruptured posterior communicating artery aneurysm・Unruptured
aneurysm.
Introduction
Neuro-ophthalmological abnormalities frequently follow
the rupture of intracranial aneurysm. They are generally
classified into visual field defects, disturbances of ocular
movement, and ptosis10). In most cases presenting with
disturbances of ocular movement, the location and direction
of the aneurysm to the 3rd and 6th cranial nerves(CN) is
closely related. However, aneurysms located far from the
oculomotor systems may sometimes cause disturbance of
ocular movement. In such cases, the manifestations are
unilateral or bilateral and appear to be a false localizing
sign secondarily to increased intracranial pressure9).
The authors report a case of bilateral abducens nerve
paralyses developing immediately after the rupture of a left
posterior communicating artery(PcomA) aneurysm with
unruptured left anterior choroidal artery(AchA) and right
426
PcomA aneurysms. Possible pathogenesis are reviewed and
discussed.
Case Report
A 46-year-old female patient suffered from sudden severe
headache and double vision on left lateral gaze without
disturbance of consciousness for two days before admission. She visited local clinic and took the computed tomographic(CT) scan, which showed no specific abnormalities.
Even treating with some medications, her symptoms were
persisted and followed by new double vision on right
lateral gaze.
On admission, she was somewhat drowsy but oriented,
complained of severe headache. Bilateral abducens nerve
paralyses without other cranial nerve palsies were noted.
Bilateral extensor plantar responses and nuchal rigidity
were also apparent. Brain CT scan revealed slight obliteraJ Korean Neurosurg Soc/ Volume 29 / March, 2000
Chea Heuck Lee · Young Cho Koh
tion of the left sylvian fissure and mild ventricular enlargement(Fig. 1). Diagnostic lumbar puncture revealed bloody
cerebrospinal fluid. Left AchA, PcomA, and right PcomA
aneurysms were found on the four-vessel cerebral angiography. Left PcomA aneurysm was elongated and projecting
to postero-infero-laterally. And other aneurysms were small,
ovoid, and projecting dorsolaterally(Fig. 2, 3).
Because sudden left abducens nerve palsy developed
first, it strongly suggested that left PcomA aneurysm was
one that had ruptured. A left frontotemporal craniotomy
was performed and successful clippings of the ruptured left
PcomA aneurysm and unruptured left AchA aneurysm
were done. Blood clots were in the perimesencephalic cistern.
Postoperative course was uneventful and bilateral abducens
nerve paralyses gradually improved and disappeared by the
14th postoperative day. The second operation for the unruptured right PcomA aneurysm was performed with successful
clipping 1 month later(Fig. 4).
Discussion
Cranial nerve palsies accompanying intracranial aneurysms are not uncommon, but there appear to have been few
cases with bilateral abducens nerve paralyses. Disturbances
of ocular movements, caused by unilateral oculomotor nerve
paralysis, are observed most frequently with ICA and basilar artery(BA) aneurysms8). BA or vertebral artery aneurysms may also cause unilateral abducens nerve paralysis1)2)5).
Pathologic mechanisms causing these paralysis are 1) direct contact to the nerve of the aneurysmal sac, 2) secondary effect of hemorrhage from the aneurysmal rupture,
3) remote effect due to increased intracranial pressure, and
Fig. 1. Computed tomographic scan revealing a mild ventricular enlargement without subarachnoid hemorrhage on the basilar cistern.
Fig. 3. Right carotid angiogram showing a round sacular
posterior communicating artery aneurysm directing
dorsolaterally.
Fig. 2. Left carotid angiogram showing an elongated sacular
aneurysm originating from the junction of the internal
carotid and posterior communicating artery(arrow
head), and junctional dilation on the proximal anterior
choroidal artery(arrow).
J Korean Neurosurg Soc/ Volume 29 / March, 2000
Fig. 4. Post-op. CT scan showing bilateral aneurysm clips in
situ without any specific intracranial abnormality.
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Ruptured Posterior Communicating Artery Aneurysm Causing Bilateral Abducens Nerve Paralyses
4) vasospasm of the basilar artery pontine branches. Most
direct compression of the nerve is ascribed to unruptured
aneurysm and usually involving the oculomotor nerve.
Neuro-ophthalmological abnormalities related to ocular movements are seldom reported after the rupture of intracranial aneurysms10). However, the incidence of direct cranial
nerve involvement by the aneurysm is nearly equal to that
of indirect involvement secondary to hemorrhage or intracranial hypertension3).
There are clinical and pathological reports on the directly compressed cranial nerves by the aneurysm itself only
in optic, oculomotor, and abducens nerves. The location of
the aneurysm was usually the anterior part of the circle of
Willis, most commonly in relation to the internal carotid
artery. However, few authors reported that over three fourth
cases had definite evidence of small amount of blood
extravasation, suggesting leakage of blood. Clinically this
evidence indicated that functional impairment of the nerve
by an adjacent aneurysm occurs most frequently in conjunction with hemorrhage3). While there is no doubt that gradual compression by dilatation of a pulsatile aneurysm sac
will damage nerve tissue, this nerve is evidently capable of
functional adjustment for a considerable time. An abrupt
dilatation without rupture could impair nerve function by
mechanical stretching or it might lead to edema or hemorrhage in the involved nerve through venous obstruction, which
would account for a sudden onset of the nerve paralysis3).
Increased intracranial pressure readily causes abducens
nerve paralysis. This is generally considered as a falselocalizing sign. The abducens nerve has a long intracranial
course at the base of the brain, and is consequently vulnerable to injury, especially where it crosses the petrous apex
and traverses the sharp edge of the petrous temporal bone6)9).
However, such damage generally results in unilateral abducens nerve paralysis.
Bilateral abducens nerve paralyses in neurosurgical patients is rare and may occur secondary to subarachnoid
hemorrhage or increased intracranial pressure4). A few ruptured AcomA aneurysm causing bilateral abducens nerve
paralyses were reported7)12). It probably results from the
symmetrical filling of the basal cisterns with blood and
followed by stretching of the structures lying between the
brain and skull in the subarachnoid space7). The acute
hydrocephalus and brain swelling that accompany subarachnoid hemorrhage may also causes the paralyses.
Several authors reported that the mechanism might also
428
be due to vasospasm of the basilar artery pontine branches
affecting the abducens motor nucleus6). However, other
accompanying signs have to be observed in these cases.
Bilateral abducens nerve paralyses of the nuclear type is
usually associated with gaze abnormality and/or bilateral
facial paresis due to the close anatomical relation-ship between the abducens nuclei, the medial longitudinal fasciculus, and the facial nuclei.
Our patient had multiple aneurysms including ruptured
left PcomA aneurysm. With the review of the clinical
history, we could conclude that the left abducens nerve
paralysis was secondary to hemorrhage and the right abducens nerve paralysis was due to increased intracranial pressure. Therefore, unilateral or bilateral abducens nerve paralyses may occur after ruptured or unruptured aneurysms.
Precise history taking and more meticulous neuro-ophthalmologic or neuroradiologic examination should be done to
evaluate cranial nerve paralysis.
• 논문접수일：1999년 8월 17일
• 심사완료일：1999년 11월 14일
• 책임저자：이 채 혁
411-410 경기도 고양시 대화동 2240
인제대학교 의과대학 서울백병원 신경외과학교실
전화：0344) 910-7315, 전송：0344) 910-7319
E-mail：[email protected]
References
1) Coppeto JR, Chan YS：Abducens nerve paresis caused by
unruptured vertebral artery aneurysm. Surg Neuro 18：385387, 1982
2) Dumas S, Shultz WT：Abducens paresis：A rare presenting
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sign of posterior-inferior cerebellar artery aneurysm. J Clin
Neuro Ophthalmol 2：55-60, 1982
Hyland HH, Barnett HJM：The pathogenesis of cranial nerve
palsies associated with intracranial aneurysm. Proc Roy Soc
Med 47：141-146, 1957
Keane JR：Bilateral sixth nerve palsy. Arch Neurol 33：681683, 1976
McKinna AJ：Eye signs in 611 cases of posterior fossa aneurysm：The diagnostic and prognostic value. Can J Ophthalmol
18：3-6, 1983
Miller NR：Topical diagnosis of neuropathic ocular motility
disorders, In Miller NR(ed)：Walsh and Hoyt’s clinical Neuroophthalmology, Vol 2. Baltimore, Williams & Wilkins, 1985,
pp652-784
Nathal E, Yasui N, Suzuki A, et al：Ruptured anterior communicating artery aneurysm causing bilateral abducens nerve
paralyses -Case report-. Neuro Med Chir(Tokyo) 32：17-20,
J Korean Neurosurg Soc/ Volume 29 / March, 2000
Chea Heuck Lee · Young Cho Koh
357
1992
8) Raja IA：Aneurysm-induced third nerve palsy. J Neurosurg
36：54-551, 1972
9) Sachsen weger R：Clinical localization of oculomotor disturbances, in Vinken PJ, Bruyn GW(eds)：Handbook of Clinical
10) Sato T, Sakurai Y, Suzuki J：Neuro-ophthalmological findings
following the onset of rupturing of cerebral aneurysms, in
Suzuki J(ed)：Cerebral Aneurysms, Tokyo, Neuron-Sha, 1979,
pp95-100
Neurology, Vol 2. New York, John Wiley & Sons, 1969, pp286-
양측성 외전신경 마비를 보인 후교통동맥 동맥류 출혈
- 증례보고 인제대학교 의과대학 서울백병원 신경외과학교실
이 채 혁·고 영 초
= 국문초록=
뇌 지주막하출혈에서 흔치않은 임상양상인 양측성 외전신경마비와 두통을 주소로 내원한 46세 여자환자에서 혈
관조영술을 시행하여 좌측 후교통동맥 동맥류, 전맥락동맥 동맥류, 그리고 우측 후교통동맥 동맥류등 다발성 뇌동맥
류가 발견되어 수술시행 하였다. 양측성 외전신경마비 이외에 시력 및 시야장애는 보이지 않았다.
수술시 상당한 뇌압증가의 양상을 보였고, 좌측 후교통동맥 동맥류 출혈흔적과 기저조에 소량의 혈종이 있었으며,
첫번의 좌측 수술 후 2주 정도에 안구운동장애가 서서히 회복되어 정상화되었다.
저자들은 뇌동맥류 출혈에서 드물게 보는 양측성 외전신경마비 환자를 경험하였기에 문헌고찰과 함께 증례보고
한다.
중심 단어：양측성 외전신경마비・후교통동맥 동맥류출혈・다발성 뇌동맥류.
J Korean Neurosurg Soc/ Volume 29 / March, 2000
429