Journalof

J Neurol (1990) 237 : 4%50

Neurology

© Springer-Verlag 1990

Giant aneurysm causing frontal lobe syndrome
C. Bokemeyer i, B. Frank I, A. Brandis 2, and W. Weinrich 1
Departrnents of 1Neurology and 2Pathology, Städtisches Krankenhaus Nordstadt, Haltenhoffstrasse 41, D-3000 Hannover 1,
Federal Republik of Germany

Summary. A 67-year-old patient with a completely thrombosed giant aneurysm of the anterior communicating artery is
described. The only neurological findings were a disturbance
of stance and gait and slight bilateral grasp reflexes. He had
had the features of a frontal lobe psychotic syndrome for more
than 12 years. Computed tomography demonstrated a primarily hyperdense calcified suprasellar space-occupying lesion.
Magnetic resonance imaging proved valuable in establishing
the correct diagnosis, which was confirmed post mortem.
Key words: Giant aneurysm - Frontal lobe syndrome - Cranial computed tomography - Magnetic resonance imaging

Introduction
Intracranial giant aneurysms (GIAs) are defined as aneurysms
measuring more than 2.5 cm in diameter [8]. Their overall frequency has been cited as approximately 5-13% of all intracranial aneurysms [10]. They constitute a special group which do
not usually cause subarachnoid haemorrhage (SAH). Instead,
they are commonly detected as slow-growing, space-occupying mass lesions [4]. Although cranial computed tomography
(CT) facilitates early diagnosis, there may still be confusion
with other cerebral mass lesions, such as meningioma, craniopharyngioma or pituitary adenoma [5]. Angiography will usually establish the correct diagnosis, but it can fall when there
is complete thrombosis in the aneurysm, which occurs in 1320% of cases [12]. The introduction of magnetic resonance imaging (MRI), which uses signal differences resulting from
blood flow within the lesion, has proven to be more specific in
detecting a G I A [2, 3, 11].
We present here a case of an unusually large completely
thrombosed giant aneurysm of the anterior communicating
artery (ACoA). For more than 12 years the 67-year-old patient suffered from a progressive frontal lobe syndrome without any focal neurological defects. The clinical presentation
and radiological features of this unusual case, including angiography, CT and MRI and post-mortem findings, are discussed with reference to the current literature.

Case report
A 67-year-old Caucasian male was transferred to the hospital
for surveillance after acute head trauma. The history was
Offprint requests to: W. Weinrich

mainly contributed by his wife: She had noticed a personality
change in her husband throughout the last 12 years with increasing deteriorating in the last 3 years. Furthermore, her
husband had developed a progressive loss of memory involving especially short-term memory. Spontaneous movements
and speech had been markedly reduced and he had recently
lost control of bowel and bladder function. On higher mental
function examination the patient was alert, but responded
slowly to questioning and simple commands, occasionally incorrectly. He appeared disoriented, particularly with respect
to time and place. Naming, spelling and repetition were all intact, but verbal communication was markedly reduced. He
was unable to remember three test objects after 5 min. The patient displayed little spontaneous behaviour and had to be
strongly prompted to produce a reaction to our commands.
He showed no change in affect, but also no disinhibition of behavior.
Examination of the skull revealed tenderness over the
right temporal region. The patient had a right-sided periorbital heamatoma. No nuchal rigidity was present. Pupillary responses and extraocular movements were intact, without nystagmus. The optic disks were flat with sharply defined margins; the fundi appeared to be pale. The other cranial nerves
were normal. Tendon reflexes were symmetrical; no pathological reflexes were present. There was no abnormality of muscle bulk, torte of power, and sensation was normal to light
touch, pinprick and vibration. Slight grasp reflexes of both
hands were present. The patient was unable to stand upright
without help. His steps were shortened to a shuffle, and he
was not capable of walking.
The electroencephalogram showed a normal alpha rhythm
without focal slow activity or epileptic discharges. On the
plain skull radiographs the sharply defined line of a right temporal fracture and in addition, a paramedial curvilinear calcification in the suprasellar region were seen. There were no
signs of raised intracranial pressure.
The unenhanced CT scan showed a hyperdense calcified
suprasellar mass of 7.5 cm in diameter in the anterior fossa.
There was minimal surrounding brain oedema and compression of the anterior horns of the lateral ventricles. Intravenous
contrast medium gave no further enhancement. Intra-arterial
cerebral angiography revealed a normal pattern of internal
and external carotid arteries. Both anterior cerebral arteries
were depressed and displaced to either side. Anteriorly the
pericallosal artery curved laterally and appeared semicircular
before returning to the midline at its junction with the posterior internal frontal artery (posteromedial frontal artery)(lateral view not shown). A small deposit of contrast medium

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could be seen at the base of the aneurysm, there marking the
former connection with the parent vessel. The capillary and
the venous phase showed a central avascular zone and posterior displacement of the venous angle.
O n T l - w e i g h t e d M R images m e d i u m signal intensity was
found throughout the whole area representing the thrombosed aneurysm without demonstrating a patent lumen. In
contrast to these, T2-weighted images displayed hypointensities inside the capsule of the aneurysm representing deposits
of haemosiderin and thrombus calcification.
The patient died of intercurrent pneumonia before a planned neurosurgical operation could be performed. Important
post-mortem findings included a giant aneurysm of the A C o A
with a maximum diameter of 7 . 5 c m and a total volume of
more than 169ml. It contained multiple layers of calcified
thrombotic material without any residual lumen. No further
neuropathological findings were made.

Discussion
G I A s are rare. They are found more commonly in the posterior cerebral circulation [4]. In one large series only 3 of 21
G I A s were located on the A C o A [14]. The most c o m m o n presentation is that of an intracranial space-occupying lesion:
headache, ocular pain and focal neurological signs involving
the cranial nerves, particularly nerve VIII, followed by V, VI
and IX in order of frequency [9]. G I A s of the anterior cerebral artery ( A C A ) and A C o A usually cause visual problems,
especially bilateral hemianopia. A patient presenting with decreased intelligence as the only neurological abnormality has
been d o c u m e n t e d [14]. In about 70% of cases, the duration of
illnes spans more than a year [13] with gradual progression of
symptoms. A history of more than 12 years, as in the case discussed here, can be regarded as the upper end of the scale.
The patient's characteristical disturbance of stance and galt
has been described with bilateral frontal lesions [1, 6]. A n innervatory apraxia for walking may be related to the magnetic
syndrome seen in patients with frontal lobe affections [1]. The
term deseribes a fixation on objects, which prevents the patient from shifting his centre of attention or activity. The patient's feet remain fixed to the ground when he tries to walk.
The prognosis of G l A s remains poor. The incidence of
S A H for G I A s is usually around 30% [14]. Furthermore, ischaemic cerebral complications can result from compression
due to the G I A itself or due to emboli emanating from the aneurysm. Therefore, surgical treatment or embolization are
preferable e r e n though the success rates are low ( 2 0 - 4 0 % )

[13].
Three different C T patterns have been documented in
G I A s after the injection of contrast medium: (1) a well-defined hyerpdense mass which enhances strongly and homogeneously and can possibly mimic a meningioma [9]; (2) a
' target sign" which consists of an outer hyperdense zone corresponding to dense fibrous tissue layers surrounding an isodense area with central enhancement produced by a partly
t h r o m b o s e d aneurysm; (3) a primarily hyperdense calcified lesion without contrast c n h a n c e m e n t resulting from complete
thrombosis of the aneurysm as found in the case presented
here (Fig. 1).
lntra-arterial angiography will only show the non-thrombosed areas of the aneurysm; the full size taust be estimated

from the extent of displacement of surrounding vessels. It has
also been suggested that local vasospasm and haemodynamic
disturbances can prevent contrast filling of a residual aneurysmal lumen [7]. As shown in Fig. 2 there is no contrast enhancement inside the aneurysm, hut contrast m e d i u m protrudes from the A C o A towards the base of the aneurysm. The
A C A s are seen to be pushed widely apart. The absence of
pathological vascularization combined with the considerable
size of the mass lesion renders the diagnosis of a malignant tumour less probable.
C T and M R I studies of G I A s have demonstrated a similar
mechanism of growth as that of encapsulated chronic subdural
haematomas. Recurrent haemorrhage occurs from the vessels
of the highly vascularized membranous wall of a giant aneurysm. The blood dissects between old thrombotic material and
the surrounding membranous capsule, which leads to the expansion of the aneurysm by newly added layers of thrombus
[8]. The cross - section shows the multiple layers of thrombotic material inside the fibrous capsule.
The characteristics of G I A S in M R I scans are multilaminated intensity patterns in the area of the thrombus and a signal void from the residual channel and from the parent vessel
of the aneurysm [3]. Signal void is seen on T l - and T2-weighted images in areas of rapidly flowing blood, since the excited
protons are r e m o v e d from a particular section too rapidly to
create a spin echo [11]. This p h e n o m e n o n was also seen in the
neck of the G I A in the case described here (Fig. 3). Echo rephasing represents a further M R I feature in the differentiation
of vascularized brain lesions [2], but it was not used in the case
presented hefe. These "functional capacities" of M R I in combination with its excellent morphological resolution may add
to the higher diagnostic specificity compared with CT.

Fig.1. Completely thrombosed ACoA aneurysm. Non-contrast axial
CT scan demonstrating a hyperdense suprasellar midline tumour of
the anterior fossa extending into left and right anterior horns of the
lateral ventricles. The corresponding contrast scan revealed no enhancement of the aneurysm (picture not shown)
Fig.2a, b. Intraarterial internal carotid angiogram (subtraction technique) of a thrombosed giant anterior communicating artery (ACoA)
aneurysm. In the anteroposterior view the aneurysm is located between the two anterior cerebral arteries, which are laterally displaced
to either side. Apart from a smalt deposite at the base there is no
contrast enhancement inside the aneurysm
Fig. 3. Giant ACoA aneurysm. Tl-weighted (TR = 600 ms/TE = 32 ms)
coronal (a) and T2-weighted (TR = 2000msFFE = 90ms) axial (b)
MR images. Medium signal intensity persisting on all Tl-weighted images represents thrombus filling the whole aneurysm. The hypointense area adjacent to the aneurysm represents signal void from blood
flow in the former heck of the aneurysm on the ACoA. On the T2weighted image (b) the thrombosed area appears hypointense, since
the thrombotic material contains large deposits of haemeosiderin and
partially calcified areas. The pictures demonstrate the extension of
the aneurysm into the third ventricle and the anterior corpus callosum, thereby pushing the septum pellucidum to the left. Only minimal perianeurysmal brain oedema is seen
Fig. 4. a The basal view of the brain demonstrates the giant aneurysm
in situ. It is located between the frontal lobes and compression of the
surrounding brain parenchyma, which contains multiple minute perianeurysmal haemorrhages, can be seen. b The circle of Willis, displaying the large size of the giant aneurysm, which covers the vessels
between both middle cerebral arteries. The aneurysm is completely
filled with multiple layers of calcified thrombotic material

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50
This case describes the unsual o c c u r r e n c e of a giant A C o A
a n e u r y s m p r e s e n t i n g with a n organic b r a i n s y n d r o m e w i t h o u t
focal n e u r o l o g i c a l defects.

Acknowledgements. We thank Drs. M.Fricke and W. Proett (Radiologische Gemeinschaftspraxis, Am Raschplatz 5, D-3000 Hannover 1)
for the MRI examinations and kind supply of MR images.

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Received March 20, 1989 / Received in revised form October 5, 1989 !
Accepted October 12, 1989