Clinical Neurology and Neurosurgery 110 (2008) 71–74

Case report

Bilateral cerebellar infarction in the medial branches of posterior
inferior cerebellar arterial territory—Using endoscopic third
ventriculostomy to relieve acute hydrocephalus
Cheng-Yang Hsieh a , Jung-Shun Lee b , Chin-Yin Yu c , Chih-Hung Chen a,∗
a Department of Neurology, College of Medicine, National Cheng Kung University, No. 1, University Road, Tainan 701, Taiwan
b Department of Neurosurgery, College of Medicine, National Cheng Kung University, No. 1, University Road, Tainan 701, Taiwan
c Departments of Radiology, College of Medicine, National Cheng Kung University, No. 1, University Road, Tainan 701, Taiwan

Received 3 May 2007; received in revised form 17 August 2007; accepted 21 August 2007

Abstract
Simultaneous bilateral cerebellar infarctions in posterior inferior cerebellar arterial (PICA) territory, without brain stem involvement are
rare. We herein report a 51-year-old man developed sudden dizziness, nausea and vomiting. CT revealed hypodense bilateral lesions over the
cerebellum corresponding to the medial PICA (mPICA) branch territory. His mental state deteriorated 2 days after onset; repeated CT showed
severe third and lateral ventricular dilation. Endoscopic third ventriculostomy (ETV) was done to relieve the acute obstructive hydrocephalus.
The patient was later discharged with only mild residual ataxia. Compared with conventional surgical treatments (external ventricular drainage,
craniectomy and cerebellectomy), ETV has several advantages, including less risk and minimal invasiveness. However, further study is needed
on its safety and efficacy under such circumstances.
© 2007 Elsevier B.V. All rights reserved.
Keywords: Bilateral cerebellar infarction; Posterior inferior cerebellar arterial territory; Endoscopic third ventriculostomy; Hydrocephalus

1. Introduction

2. Case report

Cerebellar infarction usually occurs in posterior inferior
cerebellar arterial (PICA) and superior cerebellar arterial
territory. Simultaneous bilateral PICA infarctions are rare
because a PICA usually originates from the ipsilateral vertebral artery. There are only a few reported cases of cerebellar
infarction involving the medial PICA (mPICA) in both hemispheres [1–4]. However, the prognoses of such infarctions are
usually good as hydrocephalus is only occasional. This case
presented bilateral cerebellar infarction of mPICA territory,
leading to obstructed hydrocephalus, which was relieved by
endoscopic third ventriculostomy (ETV); this procedure has
been recently applied in such cases [5,6].

The subject was a 51-year-old male with a history
of tobacco and alcohol abuse. He developed acute nonvertiginous dizziness, nausea, vomiting and an unsteady gait
without specific lateropulsion. His medical history revealed
a surgically closed perforated peptic ulcer from 5 years
before. Except smoking, there were no risk factors for an
arteriosclerotic/atherosclerotic disease, i.e. diabetes mellitus,
hypertension or heart disease. He had been transferred from a
local hospital to our emergency department. He had an initial
blood pressure of 170/108 mmHg and heart rate of 76 bpm.
The patient was clearly conscious but had severe dizziness.
Neurologically, he did not exhibit findings attributable to
brain stem dysfunction, e.g. numbness, diplopia, dysphagia
and/or dysarthria, despite cerebellar signs. He did have bilateral dysmetria with intentional tremor, and was unable to
stand due to severe truncal dysbalance. Routine blood count,
biochemistry and coagulation profiles were all within norms.

∗ Corresponding author.

E-mail address: lchih@mail.ncku.edu.tw (C.-H. Chen).
0303-8467/$ – see front matter © 2007 Elsevier B.V. All rights reserved.
doi:10.1016/j.clineuro.2007.08.012

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Fig. 1. (A and B) Non-contrasting brain CT, 12 h after onset, showing typical hypodense triangular bilateral lesions of the caudal cerebella caused by acute
cerebellar infarction confined to bilateral mPICA territory. (C and D) CT after 53 h with deteriorated consciousness, showing infarcted cerebellar swelling and
dilated third and lateral ventricles suggestive for obstructive hydrocephalus.

Fig. 2. (A) MRI showing patent functioning and a flow void at the floor of the third ventricle after third ventriculostomy. (B) MRA showing stenosis in the
petrous portion of right internal carotid artery (arrow).

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73

Fig. 3. (A) Patent medial and lateral branches of the left PICA (arrow). (B) Total occlusion of the main stem of the right PICA (arrowhead) and a dominant
right AICA (white arrow).

Electrocardiography showed normal sinus rhythms. Computerized tomography (CT), 12 h after onset, showed bilateral
cerebellar infarction attributable to both mPICA territory
(Fig. 1A and B).
After 2 days, the patient deteriorated, and became agitated,
confused and disoriented. His Glasgow Coma Scale dropped
from full to E3V4M6. Repeated CT showed severe third and
lateral ventricular dilation suggestive for obstructive hydrocephalus (Fig. 1C and D). A neurosurgeon was consulted
and emergent endoscopic third ventriculostomy (ETV) was
done to relieve the obstructed hydrocephalus and an external ventricular drainage (EVD) was left. After operation,
the EVD was kept closed without drainage of cerebrospinal
fluid and functioned as an intracranial pressure (ICP) monitor.
Since the ICP was within normal limit on the following days,
the EVD was removed on post-operative day 3. The patient
regained consciousness 6 h after surgery; the endotracheal
tube was removed 12 h later. Magnetic resonance imaging, 11
days after onset, showed patent third ventriculostomy function, with no hydrocephalus remaining (Fig. 2A) and this was
also verified by a cine MRI. No significant abnormalities were
noted from magnetic resonance angiography except moderate stenosis of the petrous portion of right internal carotid
artery (Fig. 2B). Transthoracic echocardiography revealed no
intracardiac thrombus. Vertebral arteriography (Fig. 3A and
B) showed normal path and lumen size for the upper cervical
bilateral vertebral artery. The left PICA and bilateral anterior
inferior cerebellar artery were both normal. The main trunk
of the right PICA was completely occluded. The patient was
rehabilitated for ataxia and discharged 4 weeks after onset
with only mild residual dizziness.

3. Discussion
Tada et al. [1] reported the first clinicoradiological case of
bilateral cerebellar mPICA territorial infarction. There were

several possible contributing factors, in that case and this
one, such as both PICAs arising from the basilar artery, both
mPICAs arising from a single PICA on one side, emboli
to bilateral PICA, or pressure effects exerted by a large
PICA infarction compressing the cerebellar cistern arteries,
inducing a smaller opposite-side infarction. Since vertebral
angiography showed the medial and lateral branches of the
left PICA to be completely patent, and the right PICA totally
occluded, we believe that the left mPICA territory must have
been mainly supplied by a more dominant right medial PICA,
and the right lateral PICA territory is mainly supplied by a
right dominant AICA, as supported by the angiogram. This
would most likely explain the CT and angiographic findings.
According to Kang et al. [3], the etiology of such infarctions
includes stenoocclusive PICA and extracranial vertebral arterial disease. An arteriosclerotic etiolgy or embolic disease
cannot completely be ruled out, since the patient showed
findings attributable to atherosclerotic stenosis of the right
internal carotid artery as shown in the MR angio. However,
classical risk factors were not present. Regarding an embolic
disease, the findings were also not contributive, at least as
evidenced by the electrocardiography and the transthoracic
echo. A 24 h long-term ECG and a transesophageal echo were
not performed.
Obstructive hydrocephalus can be derived from various
processes, like the aqueduct stenosis, tumors from pineal
area or cerebellum, and cerebellar infarction or hematoma.
Permanent ventriculoperitoneal shunt or a 1–2-week period
EVD is the treatment of choice for the obstructive hydrocephalus. However, the risks of post-operative ventriculitis
and meningitis are high and problems of shunt dependency
and dysfunction can pose significant additional morbidity to
the patient. One study indicated that the overall infection rate
after EVD is 8.6% in a setting of neurosurgical care unit [7].
The obstructive hydrocephalus secondary to a cerebellar
infarct ranges from 13 to 30% [8,9] and is transient in nature.
As long as the tissue swelling resolves, the CSF passage will

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regain patency. The “transient” feature offers the rationale
for ETV as an alternative for suboccipital craniectomy and
EVDs or VP shunts in selective conditions. From the literature, only 13 cases receiving ETV have been reported in the
scenario of cerebellar infarction [5,6]. Except for one patient
who receiving suboccipital craniectomy due to progressive
brain edema after ETV [5], the remaining 12 cases were well
tolerant to ETV and had uneventful courses. However, not all
patients with obstructive hydrocephalus secondary to cerebellar infarct are candidates for ETV. According to the series
from Baldauf et al., they excluded the comatous patients
which implicated the brain stem compression, and the mean
Glasgow Coma Scale is 11.2 before surgery [5]. We inserted
an EVD for monitoring the ICP with the fear of the unexpected increasing ICP. Besides, this short-term (3 days) EVD
does not increase the risk of ventriculitis compared to the
longer period (1–2 weeks).
In conclusion, the subject suffered bilateral cerebellar infarctions confined to mPICA vascular territory; ETV
successfully relieved the resulting hydrocephalus. These
infarctions may have been caused by occlusion of the right
PICA, but this anatomical variation cannot be proven. In
selective cases, ETV is a rational treatment modality for
cerebellar infarction-induced hydrocephalus.

References
[1] Tada Y, Mizutani T, Nishmura T, Tamura M, Mori N. Acute bilateral
cerebellar infarction in the territory of the medial branches of posterior
inferior cerebellar arteries. Stroke 1994;25:686–8.
[2] Han SW, Cho GC, Baik JS, Park JH, Kim JY, Heo JH. Bilateral cerebellar
infarction caused by dominant medial posterior inferior cerebellar artery.
Neurology 2006;66:1125–6.
[3] Kang DW, Lee SH, Bae HJ, Han MH, Yoon BW, Roh JK. Acute bilateral
cerebellar infarcts in the territory of posterior inferior cerebellar artery.
Neurology 2000;55:582–4.
[4] Gurer G, Sahin G, Gekirge S, Tan E, Saribas O. Acute bilateral cerebellar
infarction in the territory of the medial branches of posterior inferior
cerebellar arteries. Clin Neurol Neurosurg 2001;103:194–6.
[5] Baldauf J, Oertel J, Gaab M, Schroeder HW. Endoscopic third ventriculostomy for occlusive hydrocephalus caused by cerebellar infarction.
Neurosurgery 2006;59:539–44.
[6] Ramos-Zuniga R, Jimenez-Guerra R. Rational management of transient
obstructive hydrocephalus secondary to a cerebellar infarct. Minim Invas
Neurosurg 2006;39:302–4.
[7] Park P, Garton HJ, Kocan MJ, Thompson BG. Risk of infection
with prolonged ventricular catheterization. Neurosurgery 2004;55:594–
699.
[8] Macdonell RA, Kalnins RM, Donnan GA. Cerebellar infarction: natural
history, prognosis, and pathology. Stroke 1987;18:849–55.
[9] Raco A, Caroli E, Isidori A, Salvati M. Management of acute cerebellar infarction: one institution’s experience. Neurosurgery 2003;53:
1061–5.