Neurol Med Chir (Tokyo) 50, 67¿70, 2010

Intracranial Hemorrhage Associated With Convexity
Meningioma After Cerebral Angiography
—Case Report—
Yoshiteru MIYAJIMA, Hidehiro OKA, Satoshi UTSUKI,
Satoru SHIMIZU, Sachio SUZUKI, and Kiyotaka FUJII
Department of Neurosurgery, Kitasato University School of Medicine, Sagamihara, Kanagawa

Abstract
A 63-year-old female developed left hemiparesis caused by intracranial intratumoral and peritumoral
hemorrhage with cerebral herniation 4 days after cerebral angiography to evaluate right convexity and
petrosal meningiomas. The cerebral angiography procedure may have caused the tumoral edema and
intracranial hemorrhage because computed tomography on admission revealed the right convexity
meningioma as slightly low density compared to before the hemorrhage. Administration of contrast
medium is known to cause complications involving microcirculatory collapse and blood-brain barrier
dysfunction associated with brain tumors. Therefore, the contrast medium may have affected the
meningioma after cerebral angiography.
Key words: intracranial hemorrhage,
contrast medium

meningioma,

cerebral angiography,

side effect,

Introduction
Intracranial hemorrhage associated with brain tumor is
not uncommon, especially with glioblastoma and
metastatic brain tumor. The primary brain tumor most associated with hemorrhage is oligodendroglioma with an
incidence of 14.3%, but which increases to 29.2% in the
mixed type.5) The incidence of hemorrhage is 15.8% for
pituitary adenoma.11) The incidence of hemorrhage for
metastatic brain tumors is 3% overall,11) but the most
hemorrhagic tumor is melanoma, with an incidence of
35.7%.5) In contrast, the incidence of hemorrhage with
meningioma ranges from 0.5%–2.4%,4,5) reported as acute
subdural hematoma, chronic subdural hematoma,8) and
subarachnoid hemorrhage.6)
We treated a 63-year-old woman with severe intratumoral and peritumoral hemorrhage from a convexity
meningioma who required emergency surgery for cerebral
herniation 4 days after cerebral angiography.

Fig. 1 Computed tomography scans with contrast medium
showing right petrosal (A) and convexity meningiomas (B).

slightly high density compressing the surrounding parenchymal tissue. The tumors were located in the right convexity and the petrosal region, and computed tomography
with contrast medium revealed tumor enhancement (Fig.
1). The diagnosis was convexity and petrosal meningiomas.
The patient was taken to our hospital for preoperative
angiography on June 2, 2005. Cerebral angiography revealed that the right middle meningeal artery and internal
carotid artery fed the petrosal meningioma, and the right
middle meningeal artery and middle cerebral artery fed
the upper one third and lower two thirds of the convexity
meningioma, respectively. The middle cerebral artery
which fed the convexity meningioma was shifted downward (Fig. 2). These findings are typical of meningioma.

Case Report
A 63-year-old female experienced a falling episode in January 2005. She consulted a physician and was found to have
convexity and petrosal meningiomas. She could walk unaided in spite of her hemiparesis, had no disturbance of
consciousness, cognitive impairment, or coagulation disorder, and was not taking anticoagulant medication in
June 2005. Computed tomography revealed tumors as
Received

January 16, 2009;

Accepted

June 2, 2009

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Y. Miyajima et al.

The angiography procedure included administration of
iopamidol 75 ml (Iopamiron 300; Bayer AG, Leverkusen,
Germany) as a contrast agent and heparin natrium 1500
units. She was discharged from our hospital without incident on June 4, 2005.
Soon after discharge, she suffered sudden onset of severe headache and loss of consciousness while watching
television. On admission, she was semi-comatose with a
systolic blood pressure of 220 mmHg, anisocoria (rtÀlt),
and complete left hemiplegia. Computed tomography revealed intratumoral and peritumoral hemorrhages associated with the low density convexity meningioma (Fig. 3).

She underwent emergency surgery to remove the tumor
and hematoma, and decompression craniotomy. No subdural hematoma or subarachnoid hemorrhage was found
at craniotomy. The bleeding from the tumor was stopped
by blocking the branches of the middle cerebral artery
which were feeding the tumor. Histological examination
revealed transitional type meningioma.
The patient gradually regained consciousness and could
carry on a simple conversation, but hydrocephalus and
hemiparesis persisted. Thereafter, she underwent surgery
for the placement of a ventriculoperitoneal shunt on August 11, and cranioplasty on August 23. She was discharged from our hospital with hemiparesis.

Discussion

Fig. 2 Right internal carotid angiograms, anteroposterior
view (A) and lateral view (B), showing the middle cerebral artery compressed downward, and contributing to the blood supply of the medial-inferior two thirds of the convexity meningioma. Right external carotid angiograms, anteroposterior view
(C) and lateral view (D), showing the middle meningeal artery
contributing to the blood supply of one third of the convexity
meningioma.

The present case of meningioma was associated with both
intratumoral and peritumoral hemorrhages. Hemorrhage
associated with meningioma after cerebral angiography
has not been described previously. Presumably the
hemorrhage with meningioma was caused by collapse
of the fragile arteries feeding the meningioma and draining vein,1,3) resulting in hemorrhagic infarction of the
tumor.1,3,7) Since the hematoma was in the same location
as the abnormal vascular network feeding the medialinferior two thirds of the convexity meningioma, this abnormal vascular network was suspected of being the
bleeding point (Fig. 4). Moreover, bleeding from the
meningioma at operation was stopped by blocking a
branch of the middle cerebral artery feeding the convexity
meningioma.
Since the hemorrhage occurred 4 days after cerebral angiography was performed, the hemorrhage was probably
caused by the cerebral angiography procedure. Four possible mechanisms of hemorrhage following cerebral angiography can be considered: Coagulopathy caused by
heparin administration; intratumoral infarction caused by
thrombosis induced by cerebral angiography; intratumoral infarction caused by microvascular failure induced by the contrast medium; and contrast medium-related osmotic changes acting on the fragile microvascular
network of the tumor-associated circulation. The first
mechanism is irrelevant, because the hemorrhage occurred 4 days after the cerebral angiography, and the half-

Fig. 3 Computed tomography scans showing a hematoma located inside and outside of the tumor, and intraventricular hemorrhage
without subarachnoid or subdural hematoma.

Neurol Med Chir (Tokyo) 50, January, 2010

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Fig. 4 Right internal carotid angiogram, anteroposterior view (A), showing the middle cerebral artery contributing to the supply of
the lower two thirds of the convexity meningioma. The location of the abnormal vascular network from the middle cerebral artery is
in accordance with the hematoma. Computed tomography scans showed the tumor as less dense after hemorrhage (B) than before
hemorrhage (C), suggesting intratumoral infarction. We assumed that the bleeding point was the abnormal vascular network. ITH:
intratumoral hematoma, LDA: low density area, PTH: peritumoral hematoma.

time of the heparin natrium is an hour. Intracranial
hemorrhage associated with meningioma after embolization is reported to be caused by proximal pulsation within
10 hours after occlusion of the vascular networks.2) Since
this hemorrhage occurred 4 days after cerebral angiography, the second mechanism is unlikely. In addition,
angiography did not seem to be the direct cause in this
case.
The effect of contrast medium on brain tumor is unclear. Brain tumors which are enhanced strongly are highly affected by the high osmotic pressure of the contrast
medium because of blood-brain barrier dysfunction. High
osmotic pressure induced by contrast medium may have
deleterious effects. For example, computed tomography
after coil embolization for a ruptured aneurysm revealed
that enhanced brain tissue and edema, with resultant neurological deficit.10) In addition, intratumoral hemorrhage
has occurred in a pituitary adenoma after cerebral angiography.9) Presumably cell achoresis, tearing of the tight
junctions, circulatory collapse of the microvascular elements, and vascular spasm are precipitated by the high osmotic pressure of the contrast medium. Therefore, the
high osmotic pressure of the contrast medium could affect
the meningioma through blood-brain barrier dysfunction
in part of the brain tumor, resulting in strong enhancement and brain edema. In the present case, we speculate
that the intratumoral and peritumoral hemorrhage associated with the meningioma originated from collapse of the
abnormal microvascular networks stretched by the swelling tumor volume, and precipitated by the high circulatory
osmotic pressure.

Neurol Med Chir (Tokyo) 50, January, 2010

The present case of intracranial hemorrhage associated
with meningioma after cerebral angiography was presumably caused by the effect of the high osmotic pressure of
the contrast medium on the meningioma through bloodbrain barrier dysfunction, resulting in enhancement of
part of the tumor and brain edema. However, this conclusion has no theoretical basis. This case illustrates the
necessity to consider the risks associated with cerebral angiography when performing evaluations of meningiomas.

Acknowledgments
This work was supported in part by Grants-in-Aid for
Scientific Research from the Ministry of Education (Nos.
10877218, 13671462, and 19591700) and a Parent's Association Grant from Kitasato University, School of Medicine,
Japan.

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Address reprint requests to: Yoshiteru Miyajima, M.D., Department of Neurosurgery, Kitasato University School of Medicine, 1–15–1 Kitasato, Sagamihara, Kanagawa 228–8555,
Japan.
e-mail: y_miya＠fc4.so-net.ne.jp

Neurol Med Chir (Tokyo) 50, January, 2010