COMPLEMENTARY VALUES OF STATIC AND DYNAMIC SCINTIGRAPHY, COMPUTERIZED TOMOGRAPHY AND ANGIOGRAPHY IN
THE DIAGNOSIS OF A PARTIALLY THROMBOSED GIANT INTRACRANIAL ANEURYSM
J. T. Wilrnink* and L. M. Vencken

SUMMARY
The case history is presented of a 17 year-old male admitted with right hemiplegia and motor aphasia.
Static and dynamic scintigraphy allowed prediction of a giant aneurysm in the deep left frontotemporal
region, and this supposition was confirmed by CT and carotid angiography. CT also revealed the
aneurysm to extend farther medially than the other two examinations had indicated, the medial portion of
the aneurysm being thrombosed.
Evaluation of the diagnostic information obtained from the three procedures, combined with the
clinical data, makes possible a reconstruction of the probable course of events. The presenting signs were
probably caused by a newly formed thrombus within the aneurysm. Death, which occurred after five days,
was apparently due to subarachnoid hemorrhage.

CASE HISTORY

A 17 year-old male without a history of previous neurological disease was discovered
on a holiday-cruise lying next to his bed, unable to speak or to move his right arm or
leg. On the previous evening he had complained of a vague headache, for which he
had taken a salicylate.
The patient was first admitted to a regional hospital, where neurologic
examination revealed motor aphasia, right hemiparesis and a slight echo-shift to the
right. On the basis of these findings the patient was transferred to the Neurological
Department of the University Hospital of Groningen, The Netherlands.
On arrival the patient was found to be mildly obtunded. There was a complete
motor aphasia, questions and instructions, however, being readily understood.
There was a right facial palsy of the central type, and a near-total flaccid paresi s of
fight arm and leg, with abolished superficial reflexes and an extensor plantar
response. The various modalities of sensation could not be extensively tested due to
the aphasic disorder, but did not appear grossly disturbed.
The remaining neurological and general physical examination was normal.
Echo-encephalography confirmed the slight displacement of the median structures
to the right, earlier reported.
Laboratory screening revealed no significant abnormalities.
* Department of Neuroradiology, University Hospital, Groningen, The Netherlands.
Clin. Neurol. Neurosurg., 1979, Vol. 81-2

88

a
b
Fig. 1.
Technetium brain scintisram with area of increased uptake in deep left frontotemporal region, planeconvex in anterior view (a) and round in left lateral view (b). Round appearance of lesion is unusual for
arteriovenous malformation.

The technetium brain scintigram performed approximately 24 hours after onset
of symptoms demonstrated a rounded area of abnormal uptake deep in the left
frontotemporal region (Fig. 1). Serial scintigraphy showed rapid visualization of the
lesion, consistent with intravascular blood pooling (Fig. 2).
CT (EMI 5005) performed on the same day confirmed the scintigraphic findings
of a lesion deep in the left frontotemporal region. The lesion on CT was hyperdense
but inhomogenous in the unenhanced CT study, the lateral portion being less dense
than the medial part (Fig. 3a). After injection of contrast medium, however, the
lesion became homogenous (Fig. 3b). These features are illustrated in a density
analysis performed on the computer print-out of the lesion before and after contrast
injection (Figs. 3c and 3d). These findings were interpreted as representing a giant
aneurysm containing a thrombus (not influenced by contrast injection) in its medial
portion, and circulating blood (increasing in CT attenuation values after contrast
injection) in the lateral part. There was minimal displacement of the third ventricle
to the right. In addition there was a lucent zone visible medial to and above the
supposed aneurysm (not visible on CT sections in Fig. 3). This hypodense area was
not influenced by contrast injection, and was thought to indicate either edema or
infarction.

12"-15"

15~18"

18~21"

21%24"

27~30"

33%36 .

~erlal sclnugrapny in lelt Lateral projection. ~ote early visualization Ol lesion, simultaneous with carotid
arteries at 12"-15" after injection. Lesion does not decrease in intensity after arterial phase, early filling
veins are not seen. This is unusual for arteriovenous malformation.

a

b

Fig. 3.
CT sections demonstrating lesion without (a) and with contrast enhancement (b). Note faint difference m
attenuation between medial and lateral portions of lesion in a, abolished in b.
These features are high-lighted in density analysis of computer print-outs of the lesion without (c) and with
enhancement (d). Num[~ers indicate EMI values. Thin line is drawn around areas having EMI values of 15
or higher. Heavy line surrounds areas with EMI values of 21 or higher.
Vertical columns of EMI values within shaded area have been averaged to construct graphs.

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90
At angiography the presence of a giant aneurysm was confirmed (Fig. 4). The
aneurysm appeared to originate from the most distal portion of the supraclinoidal
(C1) segment of the left internal carotid artery, and via the malformation delayed
filling of the middle cerebral branches was seen. The precommunicating (A1)
segment of the left anterior cerebral artery was not demonstrated; an injection into
the right carotid artery demonstrated overflow via the anterior communicating
artery into the distal portion of the left anterior cerebral artery, but no filling of the
aneurysm. There was no significant displacement from the midline of the anterior
cerebral arteries, and possibly slight displacement of the deep veins to the right.
Neurosurgical intervention was not considered advisable at this stage, and appropriate conservative measures were instituted.
On the third day there was a short period of restlessness with heavy perspiration,
arterial hypertension and bradycardia, without other changes in the neurological
status. The following morning the patient displayed slight cervical rigidity and it was
assumed that there had been some leakage from the aneurysm.
On the fifth day there was a sudden deterioration of the level of consciousness,
with dilation of the right pupil and arterial hypertension, but with a normal pulse
rate. Some minutes later the patient became unresponsive to stimuli and apnoea set
in. Artificial ventilation was initiated, but after five more minutes the left pupil also
dilated and became fixed. By this time no reflexes could be elicited. Attempts at
resuscitation failed and the patient died shortly afterwards. Post-mortem suboccipital puncture revealed xanthochromic spinal fluid containing many erythrocytes.
Permission to perform autopsy was refused.
DISCUSSION

Although it was not possible to obtain verification by autopsy, we nevertheless feel
that the three neuroradiological procedures employed permit a reliable diagnosis of
the lesion under investigation. Rapid filling of a lesion in the arterial phase of the
serial scintigram, as seen in our patient, is consistent with intravascular pooling of
blood such as in arteriovenous malformation (AVM) or giant aneurysm. An AVM,
however, rapidly decreases in scintigraphic intensity after the arterial phase (PENNING and FRONT, 1975) while the lesion in question does not exhibit this characteristic (Fig. 2), thus suggesting rapid filling, but slow emptying. This is unusual for an
AVM. The absence of signs of early filling of the venous sinuses points in the same
direction. Moreover, the rounded configuration of the lesion in the lateral
projection is not typical of an AVM, as these malformations usually present a more
irregular appearance. These features make the existence of a giant aneurysm more
likely. The diagnosis of meningeoma was considered, but thought less likely because
of the intense early visualization of the lesion. Angiography confirms the presence
of a giant aneurysm arising from the most distal portion of the left internal carotid
artery. The circulation within the aneurysm is slow (contrast medium is still visible
within the aneurysm 12 seconds after injection) thus explaining the findings at serial
scintigraphy, nUBER and RIVOIR (1971) have mentioned similar angiographic findings.

91

~.

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_Ja.

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f

Fig. 4.
Left carotid anglogram in AP and
lateral projection at 2,2 sec. (a, b)
and at 3,3 sec. (c, d). Configuration of aneurysm did not
change after 3,3 sec. Aneurysm
was still faintly visible at 11,5 sec.
Aneurysm arises from supraclinoid portion of internal carotid
artery (arrow head), branches of
middle cerebral artery seem to
arise from lateral portion of
aneurysm (arrow).
Note smooth lateral surface of
contrast image but blurred medial
surface, probably representing
lateral edge of thrombus,

92
The CT scan demonstrates that the lesion extends farther medially than the
scintigram or the angiogram indicate. As Fig. 5 illustrates, on CT the lateral portion
of the lesion corresponds with the picture at angiography and scintigraphy. The
medial, denser portion of the lesion on CT is not visualized with the other two
techniques.
We believe that the medial portion of the aneurysm contains a thrombus having
higher attenuation values than unenhanced blood, a difference which is abolished
when the attenuation values of the circulating blood are elevated by contrast
injection.

Ir
Fig. 5.
Composite illustration of, from top to bottom,
coronal reconstruction of CT, CT slice in canthomeatal plane, angiogram and scintigram in
anterior view. Lateral, less dense portion of CT
lesion corresponding with circulating blood, is well
demonstrated on angiogram and scintigram while
denser medial portion, corresponding with
thrombus mass, is not visible with the other two
techniques.

An alternative explanation is that the lateral portion of the CT lesion represents
the whole aneurysm, that there is no thrombosis and that the hyperdense medial
portion represents an intracerebral hemorrhage adjacent to the medial wall of the
aneurysm. We consider this unlikely, mainly because of the shape of the lesion on
CT. Although intracerebral hemorrhages with a smooth outline have been described (SCOTXet aL, 1974), in our patient the medial and the lateral portion of the lesion
form one smooth globoid mass. This is a highly unlikely configuration for a vascular
malformation with an adjacent hemorrhage. The medial surface of the lesion at
angiography also presents an irregular appearance. This seems more likely to
correspond with the surface of a thrombus than the aneurysm wall. Finally, an
intracerebral hemorrhage might be expected to have caused a greater displacement
of intracerebral structures.

93
With regard to the sequence of events in this patient, a number of speculations
can be made.
1. The presenting symptoms (rapid outset of motor aphasia and hemiparesis, with
a relatively well-preserved level of consciousness and without cervical rigidity) are
unusual for a giant aneurysm. There is considerable disagreement concerning the
risk of rupture of giant aneurysms. MORLEYand BARR(1968) review the literature in
this respect, and in their own 28 cases point to hemorrhage as the presenting
symptom in 6 out of the 17 cases with intracranial (extracavernous) aneurysms, with
two other patients bleeding at a later date. The other patients presented symptoms
of a mass lesion due to the giant aneurysm, the nature of the neurological deficit
being determined by the localisation of the aneurysm. The three patients with
aneurysms of the middle cerebral artery all had epilepsy as a presenting symptom;
in none of the other patients was this found. Other authors reporting on nonbleeding giant middle cerebral aneurysms (SADIKet al., 1965; CANTU and LEMAY,
1966; rIUBER and RIVOIR, 1971; LUKIN et al., 1975; SEGAL and MCLAURIN, 1977)
usually describe histories of often vague complaints, with findings such as
hemiparesis, disorders of speech and papilledema. In none of these patients was the
neurological deficit as severe and as rapid in outset as in our patient. In other words,
while the clinical findings in the patients mentioned above are compatible with a
supratentorial mass lesion, the evolution of the symptoms in our patient appears to
indicate a cerebrovascular etiology. The findings at CT and angiography which
demonstrate only minimal displacement ofmidline cerebral structures, also indicate
that the aneurysm in our patient had. no significant mass effect. Many of the authors
mentioned above describe marked displacement of cerebral vessels in their patients.
It seems very unlikely that the presenting symptoms were caused by subarachnoid
hemorrhage (SAH). The clinical picture affords no evidence for SAH, and CT failed
to demonstrate blood in the subarachnoid space, scoTrI et al. (1977) consider that
CT may be 100% reliable in demonstrating extravasated blood if performed within a
week of the bleeding episode.
For reasons mentioned above, we do not consider intracerebral hemorrhage a
likely explanation for the symptoms at admission.
An interesting possibility is that of cerebral ischemia in the area supplied by the
left middle cerebral artery. This could account for the clinical picture, and
angiography demonstrated delayed filling of middle cerebral branches. Possibly
there was spasm of these arteries, but it seems more likely that the thrombus within
the aneurysm was at fault, either by direct compromise of circulation within the
aneurysm, or by release of emboli into the middle cerebral branches. SCOXT and
BALLANTINE(1972), reporting on a left middle cerebral giant aneurysm, describe an
episode of transient speech disorder, ascribed to embolus from the aneurysm. At a
repeat angiogram performed several years later, the aneurysm was not demonstrated, and was thought to have spontaneously thrombosed.
The CT and scintigraphic characteristics of the lesion in our patient differ from
those mentioned in the literature. Authors reporting on CT findings in partially
thrombosed giant aneurysms (PRESSMANet al., 1975; DAVISet al., 1977; JONES and

94
SCHWARZ, 1977; SCOTTI et al., 1977; HANDA et al., 1978) describe, as we do, two
'compartments' within the aneurysm, with the portion which contains circulating
blood demonstrating increased enhancement upon contrast injection, while the
portion made up of thrombus material is not influenced. However, the lesion is
usually described as being more or less isodense before contrast injection, with the
portion containing circulating blood becoming relatively hyperdense after the enhancement procedure. This is the opposite to our findings. In other words, the
attenuation values of the thrombus in our patient appear to be higher than in
patients reported in the literature.
It is our opinion that these variations in attenuation values are dependent on the
age of the thrombus. In a recent literature report FODSTADet al. (1978) describe the
evolution of the CT picture of thrombosis of a giant aneurysm after carotid ligation.
Two days after ligation the attenuation values of the lesion had increased markedly,
and these values were not significantly influenced by contrast injection. Two
months later CT showed that a vascular channel had developed in the aneurysm,
but the attenuation values of the thrombosed portion had decreased drastically, and
appeared isodense or possibly slightly hypodense with relation to normal brain
tissue. The aneurysm was then excised and was found to be largely thrombosed,
with signs of organization in the peripheral portions of the thrombus, and small
endothelium-lined blood vessels in the remainder.
Thus it appears that attenuation values of a fresh thrombus increase markedly,
decreasing as the process of organization sets in. Probably in a later stage the
attenuation values will rise again if and when calcium is deposited in the lesion. This
is the most likely explanation for the single case with a partially thrombosed
aneurysm with high attenuation values reported by SCOTT1et al. (1977).
Another argument for a thrombus of recent origin in our patient can be derived
from the scintigraphic findings. Two of the authors mentioned above (JONESand
SCHWARZ, 1977; SEGALet al., 1977) present scintigraphic findings in two of their four
patient with partially thrombosed giant aneurysms. In both cases the lesion at
scintigraphy is considerably larger than at angiography, and probably represents
the thrombosed as well as the unthrombosed portion of the aneurysm. In our case,
however, the scintigraphic lesion is approximately equal in size to the angiographic
lesion, and the thrombosed portion of the aneurysm is not visualized by scintigraphy (Fig. 5).
It is known that intracerebral hemorrhages as a rule are not visualized scintigraphically within the first few days, as scintigraphic visualization probably
depends on development of newly-formed capillaries which do not yet possess a
blood-brain barrier (SUGITANI et al., 1973). If the same applies to intravascular
blood clots, this would confirm that the thrombus within the aneurysm in our
patient, being invisible at scintigraphy, was of recent origin.
It thus seems probable that the formation of the thrombus in our patient
coincided with the appearance of neurological symptoms, and was possibly
responsible for the appearance of these symptoms.

95
2. The precipitate demise of the patient and the post-mortem findings of hemorrhagic cerebrospinal fluid indicate subarachnoid hemorrhage as the cause of death.
This case reiterates the value of CT studies with and without contrast enhancement in patients with intracranial aneurysms in order to ascertain the true size and
composition of the lesion. This is not always possible by means of angiography.
Others have pointed out this fact, and in addition the value of CT in the follow-up of
patients submitted to procedures such as carotid ligation for giant aneurysm is
stressed (DAVIS e l aL, 1977; HANDAet aL, 1978). Undoubtedly more information will
become available in the near future on the CT characteristics ofintravascular blood
clots in various stages of organization. At the present time we were only able to trace
one case in the literature in which serial follow-up CT studies were made of a
thrombosed aneurysm.
ACKNOWLEDGEMENTS

We are grateful to Dr. L. Nederveen, neurologist of the Delfzicht Hospital, Delfzijl,
to Prof. Dr. J. M. Minderhoud, head of the Department of Neurology and to Prof.
Dr. M. G. Woldring, head of the Isotope Laboratory of the University Hospital in
Groningen, The Netherlands, to H. v.d. Zwaag and D. Buiter for the illustrations,
and to Yolande Kool who typed the manuscript.

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