Transient

Neurological

Ischemic

Attacks

Deficits Simulating

in a Patient

with

Case Report—
Yasushi

UENO, Akira

Department of Neurosurgery,

TANAKA, and Yoshiya

Transient

Meningioma
—
NAKAYAMA

Fukuoka University, Chikushi Hospital, Chikushino , Fukuoka

Abstract
A 67-year-old female had a history of transient neurological deficits involving fainting and right-sided
hemiparesis. Magnetic resonance imaging showed a sphenoid ridge meningioma on the left , which had
encased the internal carotid and middle cerebral arteries. Carotid angiography showed occlusion of the
left internal carotid artery, a tumor stain, and engorgement of the surrounding cortical veins . Xenon-en
hanced computed tomography showed reduced cerebral blood flow and poor response to acetazolamide
in the surrounding brain tissue. The tumor was totally removed. Postoperatively,
the patient had no
more transient neurological deficts, and the response to acetazolamide
was fully restored. An in
tracranial tumor may cause transient neurological deficits by reducing the cerebral perfusion pressure .
This vascular insufficiency
may occur when the tumor occludes major cerebral arteries, steals flow
from the surrounding tissue, increases focal tissue pressure, and impedes regional venous outflow. The
latter two factors were probably responsible in this patient.
Key

words:

occlusion

transient
of cerebral

neurological

deficit,

meningioma,

Introduction

February

13, 1998;

blood

flow,

Case

Intracranial tumors often manifest as transient neu

rological deficits simulating transient ischemic at
tacks (TIAs).3-$,12'13 Several
pathophysiological
mechanisms have been postulated for such deficits,
including mass effect, Todd's paralysis, spreading
cortical depression, infarction or hemorrhage into
the lesions, coincidental
TIA, and vascular in
sufficiency.3-5,8,12 The latter may result from "steal
syndrome" or fluctuating intracranial pressure.3,12)
However, vascular insufficiency has not been ob
served by cerebral angiography or cerebral blood
flow (CBF) study as the cause of transient neurologi
cal deficits in a patient with an intracranial tumor.
We describe a case of sphenoid ridge meningioma
manifesting as transient neurological deficits based
on pre and postoperative cerebral angiography and
CBF studies.

Received

cerebral

arteries

Accepted

June 22, 1998

Report

A 67-year-old female had a 4-year history of tran

sient neurological deficits involving fainting and
right-sided hemiparesis lasting several minutes. She
never had a convulsive seizure. During the last sever
al months, the attacks had become more frequent, fi
nally occurring once a week. On admission, she was
slightly demented, with minimal hemiparesis on the
right, and quadrantic hemianopsia in the upper
right visual field. There was no papilledema. Com
puted tomography (CT) disclosed a huge and highly
enhanced tumor in the anterior and middle cranial
fossae on the left. Magnetic resonance (MR) imaging
in the coronal plane showed a homogeneous tumor
displacing the surrounding brain structures and en
casing the internal carotid and middle cerebral arte
ries (Fig. 1 left).
Carotid angiography demonstrated occlusion of
the left internal carotid artery and enlargement of
the perforating arteries in the early phase, and a rich
vascular stain of the tumor in the late phase, fed
primarily
by the recurrent
branches
of the
ophthalmic artery (Fig. 2A, B). The tumor was also

Fig. 1 Coronal
magnetic
resonance
images,
preoperatively
(left) showing a homogene
ous tumor arising from the left sphenoid
ridge, displacing
the surrounding
brain
structures
and encasing
the internal
carotid and middle cerebral arteries; and
postoperatively
(right) showing absence of
the tumor and brain displacement.

fed by the

middle

meningeal

and

ascending

pharyn

geal arteries
on the left. Engorgement
of the sur
rounding
cortical
veins,
and the superficial
and
deep sylvian
veins
was seen in the venous
phase

Fig. 2

(Fig. 2C). The superficial sylvian veins drained into

the cavernous sinus, and the deep sylvian veins
drained into the basilar vein and then into the inter
nal cerebral vein. The anterior and middle cerebral
arteries in the left hemisphere were perfused via the
right internal carotid artery and left posterior
cerebral artery (Fig. 2D). Xenon-enhanced CT meas
urements of the hemispheric CBF found 25.1 ml/100
g/min on the left and 30.8 ml/100 g/min on the right,
much lower than our control values of 38.0 5.4
ml/100 g/min (Fig. 3A, C, E). The CBF response to ad
ministration of acetazolamide was only 12.7% on
the left, much lower than our control values of 32.2
20.1%, but as high as 36.7% on the right. The CBF
and the increase after acetazolamide administration
around the tumor were as low as 24.2 ml/100 g/min
and 11.1%, respectively. Electroencephalography
de
tected slow waves in the left frontotemporal regions,
but no epileptic pattern.
Before surgery,
the tumor was partially
embolized
through
the left external
carotid
artery.
The emboli
zation
procedure
caused
no additional
neurological
deficits.
No CBF study was done at this point. At sur
gery, tumor
arose from the left sphenoid
ridge
extended
into the posterior
cranial
fossa through

Preoperative carotid angiograms, showing occlusion of the internal carotid artery and enlar
gement of the perforating arteries on the left in the early phase (A); a rich vascular stain
of the tumor, fed primarily by the recurrent branches of ophthalmic artery, in the late phase
(B); engorgement of the surrounding cortical veins, and the superficial and deep sylvian veins
in the venous phase (C); and perfusion of the anterior and middle cerebral arteries in the left
hemisphere via the right internal carotid artery and left posterior cerebral artery (D).

and
the

Fig. 3

Computed tomography scans (A, B) and xenon-enhanced computed tomography images (C-F),
before surgery (A, C, E) showing reduced cerebral blood flow, especially on the left side (C),
and impaired acetazolamide-induced
response on the left side (E); and after surgery (B, D, F)
showing further reduced blood flow on both sides (D), probably reflecting postoperative
depression of cerebral metabolism, but normal response to acetazolamide (F).

tentorial
notch.
The tumor
encased
the internal
carotid
and middle
cerebral
arteries,
which
were
atrophic
and discolored
yellow. The tumor was total
ly removed
in a piecemeal
fashion.
Histological
ex
amination
showed
a meningotheliomatous
menin
gioma.

Postoperatively, her hemiparesis deteriorated and

motor aphasia appeared, but these deficits fully re
covered 2 months later. The transient neurological
deficits have never occurred during 11 months of fol
low up. MR imaging showed that both the tumor and
brain displacement
were absent (Fig. 1 right).
Carotid angiography revealed that the tumor stain
and engorgement of the surrounding cortical veins

were gone, and the collateral circulation persisted

(Fig. 4). The hemispheric CBF had further fallen to
19.0 ml/100 g/min on the left and 26.1 ml/100 g/min
on the right (Fig. 3B, D, F). However, the CBF
response to acetazolamide administration was fully
restored to 61.1% on the left and to 73.6% on the
right.
Discussion

Symptoms resembling classical TIAs due to in

tracranial tumors are most commonly associated
with supratentorial meningiomas.3) Seventeen (8%)
of 210 patients with supratentorial meningiomas ex

Fig. 4

Postoperative carotid angiograms, showing absence of the tumor stain and engorgement of
surrounding cortical veins (A, B), whereas the left internal carotid artery remained occluded
(A) and the collateral circulation persisted (C).

perienced intermittent and transient impairment of

cerebral function, occurring as stereotyped deficits
of varying complexity and lasting from a few
minutes to more than a day.') Three (7.5%) of
another series of 40 patients who underwent CT for
transient episodes of focal neurological dysfunction
had meningiomas.13) Supratentorial meningioma is
probably the most common cause of such symptoms
because of its slow growth and the remarkable abil
ity of the brain to accomodate invasion without
manifesting fixed signs of cerebral deficits or in
creased intracranial pressure until the tumor has
been present for years.")
A possible pathophysiological
explanation for tran
sient neurological
deficit simulating
TIA in in
tracranial
tumors is that the mass has impinged on
the cerebral blood vessels to a degree sufficient to
cause partial impairment
of CBF. When systemic
blood pressure falls or tumor size increases critical
ly, the CBF is decompressed,
causing temporary cor
tical ischemia and paralysis of function. With a read
justment
Although

in CBF, the cortical

function
unverifiable,
such an explanation

returns.
is appar

ently tenable.')
Furthermore,
episodes
of spontane
ous increase
in intracranial
pressure
are associated
with
a variety
of intracranial
lesions,")
and
are
known
to occur
during
plateau
waves.
However,
such hypothesis
of vascular
insufficiency
has never
been substantiated
by cerebral
angiography
or CBF
study.
Reduced
cerebral
perfusion
pressure
was substan
tiated by a decrease
in cortical
CBF value to as low
as 24.2 ml/100 g/min
and
a poor
response
to
acetazolamide
as low as 11.1% near the tumor in our
patient.
Misery perfusion
is present
when the CBF is
near the critical
level of 19-20 ml/100 g/min, below
which
neuronal
function
is impaired.lo,ll)
A CBF
study of patients
with TIAs but normal
CT findings
using
positron
emission
tomography
showed
that
the minimal
CBF value was 22.10 ml/100 g/min
in
the symptomatic
hemisphere
and
36.85 ml/100 g/
min in the asymptomatic
hemisphere.")
Four factors
seemed
to be involved
in the CBF reduction
in our
patient:
Occlusion
of the internal
carotid
artery
on
the left; steal of CBF from the surrounding
brain tis
sue by the highly vascular
tumor;
mass effect on the

brain structures
increasing
the focal tissue pressure;
and a regional
increase
of venous
pressure
due to
the impediment
of venous
outflow
around
the tumor
seen on carotid
angiograms.
Postoperative
restora
tion of cerebral
perfusion
pressure
was indicated
by
the relief of transient
neurological
deficits
and the
full recovery
of vascular
response
to acetazolamide.
Cerebral
circulation
is impaired
in patients
with
mass effect,') and impediment
of regional
venous out
flow is hemodynamically
not negligible.''')
Accord
ingly, the mass effect of the tumor
and the possible
increase
of venous
pressure
were
suspected
to be
greatly
responsible
for the CBF decrease
in our
patient.
The misery
perfusion
state must have been
the background
to her transient
neurological
defic
its. The additional
intracranial
pressure
increase
and the resulting
the deficits.

CBF

decrease

may

have

induced

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Address reprint requests to: A. Tanaka, M.D., Department

of Neurosurgery,
Fukuoka
University,
Chikushi
Hospital,
377-1
Ohaza-Zokumyoin,
Chikushino,
Fukuoka 818-0067, Japan.