Surg Neurol
1983;19:17-20

17

Complex Partial Seizures Associated
With Unruptured Thrombosed Basilar Artery Apex Aneurysm
Lyal G. Leibrock, Donald

R. Bennett,

and Solomon

Bloch

The Departments of Neurosurgery, Neurology and Radiology, University of Nebraska Medical Center, Omaha, Nebraska

Leibrock LG, Bennett DR, Bloch S. Complex partial seizures
associated with unruptured thrombosed basilar artery apex
aneurysm. Surg Neurol 1983; 19:17-20.

Complex partial seizures, an unusual presentation of a
thrombosed basilar artery apex aneurysm, are described.
The possible etiologies causing this presentation are
reviewed.
KEYWORDS: Aneurysm; Seizure; Basilar artery, thrombosed;
Emboli

Epilepsy is rarely caused by unruptured intracranial
aneurysms. In the collaborative aneurysm study only 4%
of the patients had seizures antecedent to their subarachnoid hemorrhage [5]. Suggested causative factors
are the hamartomalike action of the calcified wall of the
aneurysm or subclinical hemorrhage resulting in tissue
damage with subsequent development of a discharging
focus [8]. The case to be presented is o f interest in that
the temporal lobe epileptogenic focus was most likely
caused by ischemia secondary to embolization from an
unruptured thrombosed basilar aneurysm.
Case R e p o r t
A 60-year-old white female was admitted to the University of Nebraska Medical Center after a generalized
tonic-clonic seizure earlier in the afternoon of January
19, 1980. The patient related she had been sitting at a
table drinking hot chocolate, talking to her son, and had
suddenly felt faint. H e r son described the ensuing events.
His mother became "glassy eyed" and slumped to the
floor. She then developed a jerking motion of both upper and lower extremities. She was amnestic for the
episode, but she r e m e m b e r e d all events up to and immediately after the event. She had no tongue biting or
Address reprint requests to: Lyal G. Leibrock, M.D., Assistant Professor, Department of Neurosurgery, University of Nebraska Medical
Center, 42nd and Dewey Avenue, Omaha, Nebraska 68105.

© 1983 by Elsevier Science Publishing Co., Inc.

incontinence. After the event she had residual generalized headache and fatigue.
Approximately 4 - 6 years before admission she began
to experience very brief episodes characterized by the
abrupt onset of a "funny" feeling in the pit of her stomach, a fluttering of her chest, and the sensation of blood
running up the back of her head. This was followed by
a sense of ill being. The attacks lasted only several seconds, and they occurred with variable frequency. Two
years before admission an episode of loss of consciousness not associated with tonic-clonic movements was
reported. The convulsion before admission was preceded by a "small spell."
The patient had a long history of hypertension and
currently was taking Aldomet, 250 mg twice daily. H e r
father and sister died of strokes at early ages. Past operations included a cholecystectomy, stapedectomy and
tympanoplasty. She specifically denied a previous history of significant head trauma, meningitis, encephalitis,
or cerebral vascular accidents. T h e r e was no past history
suggestive of a prior subarachnoid hemorrhage or transient ischemic events of the anterior or posterior circulation. The remainder of her history was noncontributory.
On admission the patient was alert and oriented. There
was no evidence of laceration of her tongue. The blood
pressure was 178/94. The remainder of the vital signs
were normal. The general physical examination showed
normal results. Specifically no murmurs were heard over
the precordium or bruits over the carotid or supraclavicular areas. The results of the neurologic examination
were normal.
At the time of admission, the laboratory results for
hemogram, urinalysis, and electrolyte values were normal. An x-ray examination o f her chest showed arteriosclerotic vascular calcification of the aorta. Results of
electrocardiogram were within normal limits. A 24-hour
Holter monitor recording showed rare supraventricular
premature beats.
Tomography of the skull (Figure 1) revealed a calcified density just inferior to the pineal. Computed to0090- ~,019/83/01001 v-04503.00

18

Surg Neurol
1983;19:17-20

Leibrock et al

Figure 1. Lateral tomogram of the skull through the midline demonstrates
an oval collection of calcium with dense margins.

mography scan (Figure 2) showed a calcified mass near
the basilar summit. Angiography (Figure 3) revealed a
thrombosed basilar artery apex aneurysm. The posterior
cerebral arteries were patent and of normal appearance.
The initial electroencephalogram (EEG) obtained the
day after admission was normal while awake and during
drug induced light sleep states (Figure 4A). Small sharp
spikes were seen independently over both hemispheres,
a finding considered a normal variant. An EEG after
sleep-deprivation, obtained 2 months after discharge from
the hospital, revealed low-to-moderate bursts of theta
activity with mixed sharp waves over the left temporal
region (Figure 4B). In-phase cancellations were noted
between the F7 and T3 electrodes while instrumental
phase reversals occurred between the T3 and T5 electrodes. The small sharp spikes were also seen (Figure
4C). These EEG abnormalities were compatible with an
irritative focus within the left temporal lobe.
The patient was placed on a regimen of 300 mg of
phenytoin daily; blood levels of 10-20 mg% were maintained. The patient has been followed 2.5 years since
the diagnosis. There has been a marked decrease in the
frequency of her spells. Over the past 6 months she has
only had three brief episodes.

Discussion
In the older age group, cerebral vascular disease is reported to be a leading cause of epilepsy [27]. The type
of vascular disease is often not documented or the as-

Figure 2. (A) A computed tomography scan without contrast-medium
enhancement. A well-defined area of calcification is intimately related to
the distal end of the basilar artery. (B) A computed tomography scan after
injection of contrast medium. The film demonstrates a collection of contrast
in the proximity of the calcified area seen in the study without contrast
medium.

sociation made merely because of the age of the patient.
The present case is unusual in that this patient with
complex partial and generalized seizures was found to
have an unruptured thrombosed aneurysm at the apex
of the basilar artery. Although this finding may have
been incidental, complete cardiovascular, metabolic, as

Seizures with Unruptured Aneurysm

Surg Neurol
1983;19:17-20

Figure 3. Lateral vertebral angiotomography. The calcified area h located
at the distal end of the basilar artery, and probably represents a clot-filled
aneurysm of the basilar artery (arrows).

well as four-vessel cerebral angiography failed to uncover other causes. Specifically, the extracranial as well
as the intracranial carotid arterial system was normal.
Seizures secondary to ruptured aneurysms have been
previously reported; however, the aneurysms have been
located more commonly on arteries of the anterior cir,
culation [5].
In this case the aneurysm was thrombosed, which is
an unusual occurrence [3,7]. T h r o m b o s e d aneurysms

rarely cause subarachnoid hemorrhage or the mass effect
of giant aneurysms, but they can embolize. Embolization
from aneurysms is considered rare [9], but cerebral infarction related to emboli from intracranial aneurysms
has been reported in several cases [1,4,11]. A prior
report has described temporal lobe electroencephalographic disturbances associated with major and minor
syndromes of vertebral basilar insufficiency [6].
In our patient it seems reasonable to postulate that
emboli from this aneurysm traveled through the posterior cerebral artery and its branches to the temporal
lobe with resultant microinfarction and the subsequent
development of an epileptigenic focus. By history there
were no symptoms suggestive of intermittent posterior
circulation ischemia; however, destruction of temporallobe tissue supplied by distal branches of the posterior
cerebral artery may not cause immediate clinical signs.
O f interest and support o f this mechanism is the report
by Stewart et al [ 10]: his case 4 had symptoms suggestive
of complex partial seizures and later suffered a generalized convulsion. Other transient symptoms present in
the patient suggested that they were secondary to embolization of a clot from the aneurysm. Seizures occurring acutely with embolization are well documented.
Infarction after epilepsy does occur; however, the frequency has not been adequately investigated.

References
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A

C

8

A I -F 7

Fp I - A I

FT-'I~ I

FP2-A2
F3-A i

Figure 4. Electroencephalogram samples
from tracings performed." A initial, B and
C 2 months after discharge. See text for
interpretation.

19

~-'ee

Ts-Cz

F4-A 2

F8-A 2

Oi-Cz

C3-A I

FP2-Cz

C4-A2

-A, ~1

FS.-~
T4--~
T6"Cz

o2--cz

02-A 2
I~ t ~

H~-70
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12

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20

Surg N e u r o l
1983;19:17-20

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Leibrock et al

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