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Neurol Med Chir (Tokyo) 48, 569572, 2008

Cavernous Malformation of the Ventral Midbrain


Successfully Removed Via
a Transsylvian-Transpeduncular Approach
Case Report
Tadahiro OHMURA, Katsuyuki HIRAKAWA, Mika OHTA,
Hidetsuna UTSUNOMIYA*, and Takeo FUKUSHIMA
Departments of Neurosurgery and *Radiology, Fukuoka University Faculty of Medicine, Fukuoka

Abstract
A 37-year-old woman presented with a rare cavernous malformation of the ventral midbrain with brainstem hemorrhage manifesting as sudden onset of headache and vomiting. The lesion was removed successfully through a transsylvian approach and a medial peduncular route. Postoperatively, her oculomotor nerve paresis worsened temporarily, but diplopia disappeared 2 months after surgery. We recommend the transsylvian-transpeduncular approach if the lesion is located in the ventral midbrain and
faces the ventral surface of the brainstem, because of the effective access with minimal neurological
deficits.
Key words: cavernous malformation,
transsylvian-transpeduncular route

ventral midbrain,

Introduction

vent re-bleeding is possible, but always difficult because of the depth and limited exposure of the lesion. In particular, ventral midbrain lesion is so far
from the brain surface that surgical treatment is
rarely indicated. Here we describe the successful
removal of a cavernous malformation in the ventral
midbrain via a transsylvian-transpeduncular approach.

Brainstem cavernous malformations are rare, but


account for 9% to 35% of all cavernous malformations.5,9,13,16) Supratentorial cavernous malformations tend to manifest as seizures, and infratentorial
cavernous malformations as cranial nerve paresis,
whereas brainstem cavernous malformations are
commonly associated with hemorrhage, and neurological deficits after hemorrhage are common.10,13,15)
Cavernous malformation is frequently associated
with venous malformation, which increases the incidence of hemorrhage.1,2,11) The associated venous
malformation must be preserved if the cavernous
malformation is resected because of the critical involvement in providing normal drainage.13)
Radiosurgery decreases the incidence of hemorrhage but often causes neurological deficits,12) and
can also reduce seizure frequency with time.8) No
histological evidence of vascular changes was found
in surgical specimens of vascular malformations after radiosurgery or conventional radiation.6)
Surgical treatment of such malformations to preReceived
2008

December 12, 2007;

Accepted

surgical approach,

Case Presentation
A 37-year-old woman presented at another hospital
with sudden onset of headache and vomiting. She
was referred to us 2 days later. On admission to our
hospital, neurological examination revealed right
dysesthesia, hypesthesia, mild hemiparesis, and left
oculomotor nerve paresis.
Computed tomography showed intrinsic hemorrhage extending from the right cerebral peduncle to
the periaqueductal gray matter in the ventral midbrain (Fig. 1). Magnetic resonance imaging revealed
a heterogeneous lesion with evidence of blood
products in various stages of degeneration (Fig. 2).
Cerebral angiography depicted a venous malformation lying anteriorly to the ponto-mesencephalic
junction, but no feeding artery or draining vein.

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Fig. 3

Fig. 1

Fig. 2

Computed tomography scan on admission


showing a large high-density area in the
ventral midbrain.

A: Preoperative axial T1-weighted magnetic


resonance (MR) image showing an intrinsic
mass lesion in the ventral midbrain. B:
Preoperative sagittal T1-weighted MR image
revealing a well-circumscribed mass lesion.

The patient underwent surgical resection of the


cavernous malformation via a transsylvian-transpeduncular approach on day 28 after the initial
presentation. A left pterional approach was used to
expose the left cerebral peduncle by a transsylvian
route. The sylvian fissure was widened to expose the
emergence of the left oculomotor nerve. The
cerebral peduncle was swollen, but neither hematoma nor cavernous malformation was observed on
the surface of the midbrain (Fig. 3). An anomalous
vein emerged from the lateral midbrain and coursed
ventrally to the ponto-mesencephalic junction, suggesting venous malformation. The posterior cerebral
artery and superior cerebellar artery were identified
just above and below the oculomotor nerve, respectively, then a 5-mm-long vertical cortical incision
was made between these arteries, just lateral to the
emergence of the oculomotor nerve and medial to

Intraoperative photographs showing the


ventral aspect of the midbrain exposed via
the transsylvian approach. A: A cortical
incision was made vertically in the area
delimited by the posterior cerebral artery
(PCA) below, the superior cerebellar artery
(SCA) above, and the emergence of the
oculomotor nerve (ON) laterally. B: Surgical view showing the relationship of the
PCA, SCA, ON, and ``fairly safe entry zone''
(arrow). ICA: internal carotid artery, S:
spatula.

the pyramidal tract. The 5-mm incision did not expose the hematoma cavity, so the incision was extended 3 mm rostrally after the posterior cerebral artery was displaced inferiorly. The hematoma cavity
was found 3 mm below the surface. The hematoma
contained brownish, liquefied material and clotted
blood, and was aspirated and removed with
microdissectors and a suction tip, exposing a dark
vascular conglomerate resembling a mulberry. The
conglomerate was removed after being dissected
from the surrounding gliotic tissue.
Histological examination of the specimen showed
vascular spaces of various sizes lined with a single
layer of endothelial cells, multiple hemosiderin
deposits, and widespread gliosis, which were consistent with cavernous malformation.
The patient's oculomotor nerve paresis worsened
temporarily, but later improved, and diplopia disappeared 2 months after surgery. The right sensory disturbance and hemiparesis also improved, and she
returned to normal life as a housewife. Postoperative magnetic resonance imaging confirmed total
removal of the vascular lesion and disappearance of
the mass effect (Fig. 4).

Discussion
Brainstem cavernous malformation is associated
with increased frequency of bleeding or re-bleeding,
so treatment should be designed to prevent acute
bleeding, especially if a hemorrhagic episode has already occurred. Surgical treatment has an overall
morbidity and mortality rate of 35%, a permanent or

Neurol Med Chir (Tokyo) 48, December, 2008

Surgical Approach to Midbrain Cavernous Malformation

Fig. 4

Postoperative axial (A) and sagittal (B) T1weighted magnetic resonance images showing that the cavernous malformation had
been totally removed.

severe morbidity rate of 12%, and a temporary complication rate of 23%.13) However, conservative
management resulted in death in 20% or more of
patients and severe disability in 7%, mostly due to
hemorrhage or progressive growth of the cavernous
malformation.5) However, no operative mortality occurred and 99 patients (72.3%) either improved or
remained clinically stable among 137 cases of surgically treated brainstem cavernous malformations.18)
The pterional-transsylvian approach,14) bifrontal
approach through the lamina terminalis, transcallosal approach,17) subtemporal approach, and lateral
transpetrous approach have been reported as surgical approaches to ventral midbrain lesions. Relatively early surgery within 4 to 6 weeks of the
hemorrhage has been recommended because the
procedure will be easier if the hematoma is still unorganized and no significant amount of fibrous
perilesional gliotic tissue has developed.4,7) Most
previous reports used a cortical incision at the focal
bulge and/or discolored part of the cortical surface.
Cavernous malformation in the cerebral peduncle
required a minimal 3-to-5 mm incision parallel to the
fiber tracts initially.7) Surgical access to the ventral
mesencephalon can be obtained through a ``fairly
safe entry zone'' delimited above by the posterior
cerebral artery, below by the superior cerebellar artery, medially by the emergence of oculomotor nerve
and the basilar artery, and laterally by the pyramidal
tract (Fig. 3B).3) We used a 5-mm long vertical incision in the cortical surface through this entry zone,
and added a 3-mm upward incision to reach the
hematoma cavity by displacing the posterior
cerebral artery.
The cerebral peduncle consists of corticospinal,
corticonuclear, and corticopontine fibers.2) The corticospinal and corticonuclear tracts occupy only the
middle two-thirds or so of the peduncle, and the cor-

Neurol Med Chir (Tokyo) 48, December, 2008

Fig. 5

571

Surgical field drawing of the midbrain


showing the topographical anatomy of the
oculomotor nerve (ON) and cerebral peduncle. Arrow: approach, 1: fronto-pontine
fibers, 2: pyramidal fibers, 3: temporo-pontine fibers.

ticopontine fibers form the rest. The center sixth of


the peduncle consists of frontopontine fibers, and
the most lateral sixth consists of temporopontine
fibers.2) Therefore, there is a window between the
emergence of the oculomotor nerve from the median
groove and the pyramidal fibers in the peduncle that
affords surgical access to the ventral midbrain
through the more medial part of the peduncle and
prevents injury to the motor tract (Fig. 5).3) In our
case, we made an 8-mm vertical incision in the medial part of the peduncle by the emergence of the
oculomotor nerve and removed the cavernous malformation without permanent disruption of any neurological function.
The present case shows that a cavernous malformation in the ventral midbrain can be successfully
removed via a transsylvian-transpeduncular route
without additional permanent complications.

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Address reprint requests to: Tadahiro Ohmura, M.D.,


Department of Neurosurgery, Fukuoka University
Faculty of Medicine, 7451 Nanakuma, Jonan ward,
Fukuoka 8140180, Japan.
e-mail: tadaohmfukuoka-u.ac.jp

Neurol Med Chir (Tokyo) 48, December, 2008

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