Epilepsia, 35(6):1317-1320, 1994
Raven Press, Ltd., New York
0 International League Against Epilepsy

Brief Communication

Intractable Complex Partial Seizures Associated with
Posterior Cerebral Artery Giant Aneurysm: A Case Report
Elza M. T. Yacubian, Sergio Rosemberg, Helga C. A. da Silva, Carmen L. Jorge,
Evandro de Oliveira, and Luis Marques de Assis
Departments of Neurology, Neurosurgery, and Pathology, Neuropathology Division, University of Sdo Paulo School
of Medicine, Sdo Paulo, Brazil

Summary: Giant aneurysms have rarely been reported in
association with intractable complex partial seizures
(CPS). We report a 30-year-old man with intractable CPS
since age 18 years. Seizure onset was electrically localized to right temporal lobe. Preoperative neuroimaging
studies showed a partially thrombosed giant aneurysm of
the right posterior cerebral artery. Selective arnygdalo-

hippocampectomy and occlusion of the posterior cerebral
artery did not cause deficits. The patient has been seizure-free for 15 months after operation. We review the
relevant literature on aneurysms as a cause of epilepsy.
Key Words: Epilepsy-Complex partial seizures-Giant
aneurysm-Hemosiderosis-Amy
gdalohippocampectomy.

In a population-based study, Annegers (1993) reported that the etiology in -70% of the cases of
epilepsy was unknown and for the remaining were
as follows: cerebrovascular disease 13.2%, developmental disorders SS%, head trauma 4.1%, brain
tumors 3.6%, CNS infections 2.6%, degenerative
CNS diseases 1.8%, and other causes 0.5%. In a
specialized neurology service, recognized etiologic
factors were detected in 44% of epileptic patients,
excluding hereditary seizures and symptomatic
neoplastic epilepsy (Bergamini et at., 1977). The
most frequent causes were birth injuries (17.8%),
craniocerebral trauma (12.2%), infections (1 1.9%),
and CNS malformations and congenital metabolic
encephalopathies ( I 3%)(Bergamini et al., 1977).
Swartz et al. (1 992) demonstrated neuropathologic
alterations in 93% of hippocampi in temporal lobe
epilepsy. Cerebral aneurysms have rarely been reported in association with temporal lobe epilepsy.
In a survey of 666 patients with this type of epilepsy, Currie et al. (1971) reported structural abnormalities in 169; only 1 had an aneurysm in the middle cerebral artery. In some large series of giant
unruptured intracranial aneurysms (Locksley ,

1966a,b; Morley and Barr, 1969; Drake, 1979;
Hosobuchi, 1985; Liang-fu and Da-jie, 1987; Battaglia et al., 1988) the main signs and symptoms were
related to bleeding or mass lesion. We report a 30year-old man with a 12-year history of intractable
complex partial seizures (CPS) who was diagnosed
as having a giant cerebral aneurysm of the posterior
cerebral artery, review the relevant literature on aneurysms as a cause of epilepsy, and discuss the possible pathogenetic mechanisms.
CASE REPORT
A 30-year-old man was admitted to the hospital
because of intractabIe CPS. When he was 15 years
old, he complained of episodes of diplopia and dizziness when he turned his head. At age 17 years,
after physical exercise, he experienced an episode
of headache, tonic posture of the limbs, vomiting,
and loss of urine. The headache persisted for 7
days , when he had a generalized tonic-clonic seizure (GTC). One year later, he began having recurrent spells (two or three times each day) characterized by loss of breathing, sialorrhea followed by
impairment of consciousness, and oral automatisms. During sleep, frequent GTC occurred. Despite treatment with 1,400 mg carbamazephine, 300
mg phenytoin (PHT), and 10 mg.clobazam daily, he
12 CPS a month.
experienced
General and neurologic examinations were nor-

Received March 1993; revision accepted November 1993.
Address correspondence and reprint requests to Dr. E. MArcia
Targas Yacubian at Department of Neurology do H.C.F.M.U.S.P.,
Av. Dr. Eneas de Carvalho Aguiar 255, Instituto Central-Sala
501I-A, 05403-SBo Paulo, SBo Paulo, Brazil.

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1318

E. M . T. YACUBIAN ET AL.

mal. Routine laboratory tests were negative. Videotelemetered interictal scalp/zygomatic EEG recording showed bursts of theta activity mixed with sharp
discharges over the right mesiobasotemporal region, and during the usual seizure the EEG showed
rhythmic 4-6-HZ sharp wave activity initially recorded on the right zygomatic electrode. Computed
tomography showed a small calcification in the ambiens cistern on the right side. Magnetic resonance
imaging (Figs. 1 and 2) disclosed a spherical mass
measuring 2.5 cm in diameter at the ambiens cistern, which compressed the right cerebral peduncle
and the right hippocampal formation. Axial spinecho T2-weighted MRI showed a partially thrombosed aneurysm with central high signal intensity,
which presumably represented methemoglobin and
a peripheral ring of low signal intensity consistent
with hemosiderin deposition. A lower intensity signal on the medial aspect consistent with a patent
lumen signal void was also observed. Cerebral angiography showed a partially thrombosed saccular
aneurysm at the origin of the right posterior cerebral artery (Fig. 3). Selective amygdalohippocampectomy and occlusion of the posterior cerebral artery proximal to the aneurysm were performed.
Pathologic findings included sever neuronal loss,
gliosis, and abundant macrophages with hemosider-

FIG. 2. Coronal T1-weighted magnetic resonance imaging.
The patent lumen is evident as a signal void in the medial part
of the aneurysm, which compresses the right cerebral peduncle (arrows). The thrombosed part of the aneurysm is
apparent laterally, deviating and compressing the right hippocampal formation (arrows).

in. The patient has been followed for 15 months and
has been seizure-free since the operation. He is
treated with 300 mg PHT daily.
DISCUSSION

Giant intracranial aneurysms, which are aneurysms > 2.5 cm in diameter, usually present with
clinical signs of subarachnoid hemorrhage or mass
lesion leading to chronic headache, visual disturbance, or cranial nerve palsies (Hosobuchi, 1985).

FIG. 1. Proton density image of partially thrombosed giant
aneurysm of right cerebral posterior artery showing heterogeneous signal intensity. Central high signal intensity presumably represents methemoglobin, and the low signal intensity peripheral ring is consistent with hemosiderin deposition, except in the medial aspect of the aneurysm, where a
lower intensity signal represents the patent lumen signal void
(arrows).

Epilepsia, Vol. 35,No. 6 , 1994

FIG. 3. Vertebrobasilar arteriogram shows in right cerebral
posterior artery the vertically oriented residual patent lumen
of the giant aneurysm (arrow). The thrombosed portion of the
aneurysm is not documented by the arteriogram.

CPS AND CEREBRAL GIANT ANEURYSM
When a patient has epileptic seizures, the possibility of an intracranial aneurysm is rarely raised. Only
4% of the 2,621 patients reported by Locksley
(1966a) who had a first subarachnoid hemorrhage
had epilepsy before bleeding. In 151 cases of unruptured aneurysms, epilepsy was detected in 36% of
the middle cerebral and 8% of the posterior communicating cerebral artery (Locksley , 1966b), although the characteristics of the seizures were not
described.
In a series of 28 patients with giant aneurysms
reported by Morley et al. (1969), 3 had epilepsy.
Two of them had seizures for many years before
undergoing successful operation for the aneurysm.
In all, the aneurysms were located at the middle
cerebral artery. In this series, there were no posterior cerebral artery aneurysms, probably because of
their precocious tendency to rupture.
Liang-fu and Da-jie (1987) reported epilepsy in 2
of 21 cases of giant aneurysms, both located at the
middle cerebral artery. Sengupta et al. (1978) described 6 cases of epilepsy and aneurysms. The interval between onset of seizures and diagnosis varied from 1 day to 30 years. Five patients had partial
seizures (1 focal motor, 1 versive, 1 psychic, I vertiginous, 1 CPS with automatism) and I had GTC.
In all patients, the aneurysms were located at the
middle cerebral artery. EEG in 4 patients showed
temporal lobe foci. Five patients who underwent
operation with obliteration of the aneurysms were
seizure-free, although they continued to be treated
with antiepileptic drugs (AEDs). The only patient
who was not operated on because epilepsy was the
only complaint died six months later of severe subarachnoid hemorrhage. Liang-fu and Da-jie (1987)
reported that although the mechanism of epilepsy
due to intracranial aneurysm is not known, in 2 of
their patients the calcified walls of the aneurysms
might have acted as hamartomas, causing epilepsy.
Another possibility is that aneurysms may leak
without producing clinical manifestations of subarachnoid hemorrhage. These minor leakages may
produce localized damage to brain and cause an epileptogenic focus. Whittle et al. (1985) described 4
patients with CPS for several years who were
shown to have giant aneurysms of the middle cerebral artery. None had a history of subarachnoid
hemorrhage. Operative findings included compression of mesiotemporal cortex and evidence of previous hemorrhage from the aneurysms. In 2 patients, clipping of the aneurysm with decompression of the adjacent temporal lobe cured the seizure
disorder. In the other 2 patients, the aneurysms
could only be wrapped and the seizures continued.
Leibrok et al. (1983) reported a patient with auto-

1319

nomic partial seizures followed by GTC owing to a
thrombosed basilar artery apex aneurysm. They
postulated that emboli from this aneurysm traveled
through the posterior cerebral artery and its
branches to the temporal lobe, with resultant microinfarction and subsequent development of an epileptogenic focus.
Our patient showed strong evidence of a relation
between epilepsy and giant aneurysm of the posterior cerebral artery. Clinically, onset of the seizures
occurred 1 year after an acute episode characterized by sudden headache followed by vomiting,
tonic posture of the limbs, and loss of urine, which
might have been consecutive to bleeding. Hosobuchi (1985) reports that patients with giant aneurysms who do not present with recent subarachnoid
hemorrhage show evidence of a more remote history of bleeding that probably occurred when the
aneurysm was smaller.
Whether patients with a temporal lobe lesion
should undergo removal of hippocampus in addition
to resection of the lesion is still controversial.
Added to the uncertainty about the role of hippocampus in generation of seizures in such patients is
the concern about the neuropsychologic sequelae,
especially with regard to memory function after resection of a healthy hippocampus (Fried et al.,
1992). Fried et al. (1992) suggested that patients
with mesiotemporal lesions and a history of early
seizure onset have profound cell loss in all hippocampal fields except CA2 and that this structure
therefore may be included in the resection. During
the surgical procedure, we noted that aneurysm
walls and the mesiotemporal lobe structures were
yellow; we then performed selective amygdalohippocampectomy .
The neuropathologic examination in our case
confirmed the findings of Fried et al. (1992): There
was severe neuronal loss and signs of old bleeding
characterized by the presence of numerous macrophages with hemosiderin in the mesiotemporal lobe.
Recurrent slight bleeding without clinical manifestations of subarachnoid hemorrhage as reported by
Sengupta et al. (1978) also may have provoked localized brain damage acting as an epileptogenic focus.
Willmore et al. (1978) demonstrated that injection
of ferrous or ferric chloride into rat or cat sensorimotor cortex resulted in recurrent focal paroxysmal
EEG discharges as well as behavioral convulsions
and electrical seizures. The pathologic findings included iron-filled macrophages, ferruginated neurons, and astroglial cells. Willmore et al., (1978)
postulated that neurochemical alterations induced
by the main metallic ions in whole blood could be
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E . M . T . YACUBIAN ET AL.

1320

responsible for development of human posttraumatic epilepsy. Although Lange et al. (1980) could
not confirm this model of chronic epilepsy in cats,
our case suggests that bleeding may have elicited an
epileptogenic focus. Compression of the giant aneurysm against the hippocampus is another possible
mechanism (Stewart et al., 1980), associated or not
with the previous mechanism. Whatever the mechanism, giant intracranial aneurysms, although constituting only a few of the possible etiologic agents,
might be considered in temporal lobe epilepsy.

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