Clinical Radiology (1990) 42, 130-132

Case Report: Spontaneous Thrombosis of a Cerebral
Arteriovenous Malformation
C. S. BARKER and P. L. ANSLOW

Neuroradiology Section, Department of Radiology, RadcliffeInfirmary, Oxford
We report a patient who presented acutely to a neurosurgical unit with a mild left hemiparesis
following mild trauma and an episode of hypotension. Computed tomography of the brain
showed fresh partial thrombosis of a right parietal arteriovenous malformation. Subsequent
angiography confirmed partial obliteration of an arteriovenous malformation.
The malformation had completely thrombosed on follow up computed tomography, and
disappeared angiographically. Barker, C.S. & Anslow, P.L, (1990). ClinicalRadiology42, 130132. Case Report: Spontaneous Thrombosis of a Cerebral Arteriovenous Malformation

CASE REPORT
A 23-year-old right handed female cut her hand, and while washing
the hand in the bathroom she fell, striking her left temporal area. On
standing up she fainted, losing consciousness for about 15 seconds. She
was then well until 4 h later when she experienced sudden onset of severe
headache and vomiting. On admission to hospital she was found to have
a mild left hemiparesis.

(a)

Five days later computed tomography of the brain was performed.
The unenhanced scan (Fig. la) showed a 5 cm diameter mass in the right
parietal region, of mixed density, although predominantly hyperdense,
with a high density serpiginous structure arising from it and passing
along the wall of the lateral ventricle. There was surrounding oedema.
On other sections fresh thrombus was seen within the straight sinus (Fig.
lb). Following intravenous contrast medium an enlarged branch of the
right middle cerebral was seen passing towards the mass, but little

(b)

Fig. 1 - Day 6. Unenhanced CT. (a) Presumed older thrombus within the nidus of the arteriovenous malformation (black arrowhead) and fresh
thrombus within the draining vein (white arrow). (b) Fresh thrombus within the straight sinus (black arrow),

Correspondence to: Dr C. S. Barker, Department of Radiology,
Radcliffe Infirmary, Woodstock Road, Oxford OX2 6HE.

enhancement of the mass itself occurred. This was interpreted as
partially thrombosed arteriovenous malformation containing older
thrombus within the nidus and fresh thrombus in the draining vein.
A right carotid angiogram performed on day 8 (Fig. 2) showed a~

SPONTANEOUS THROMBOSIS OF A CEREBRAL ARTER1OVENOUS MALFORMATION

131

(a)

(a)

(b)
Fig. 2 - Day 8. Right carotid angiogram. (a) Arterial phase: enlarged
branch of middle cerebral artery (small black arrow) and apparently
small arteriovenous malformation (black arrow head) (b) Venous phase:
there is no filling o f deep veins.
enlarged branch of the middle cerebral artery with very low flow into a
small arteriovenous malformation in the parietal lobe, an appearance
consistent with a malformation into which the blood flow has recently
been markedly reduced. The venous phase showed drainage via
superficial veins with no filling of the deep veins.
Computed tomography was again performed on day 19 (Fig. 3),
before and after contrast enhancement. The unenhanced scan showed
mature isodense thrombus within the nidus and draining vein. Other
sections revealed fine calcification within the nidus o f the arteriovenous
malformation. The scan with contrast medium showed some marginal
enhancement o f the malformation. There was still moderate surrounding 0edema. Angiography on day 42 (Fig. 4) showed disappearance of
the malformation and reduction in the size of the middle cerebral artery.
Further computed tomography has shown progressive calcification o f
the nidus and reduction in the size o f the draining vein. The most recent
examination, 2½ years after the ictus, shows merely a small focus o f
calcification in the right parietal lobe (Fig. 5). There has been no
radiographic evidence of reopening o f the arteriovenous malformation
nor of haemorrhage from it. The patient's hemiparesis gradually
improved and she has remained well over 3 years apart from occasional
headaches.

DISCUSSION
There have been about 50 reported cases of spontaneous
thrombosis of cerebral and dural arteriovenous malfor,

(b)
Fig. 3 - Day 19. (a) Unenhanced CT: mature thrombus throughout the
malformation. (b) Enhanced scan at same level shows a little marginal
enhancement (black arrowheads).

132

CLINICALRADIOLOGY

Fig. 4 - Day 42. Carotid angiogram: no evidence of arteriovenous
malformation.

The mechanisms of spontaneous thrombosis are not
certain, but in the majority of cases it is associated with an
episode of intracranial bleeding, either intracerebral or
subarachnoid (Wakai et aL, 1983; Yasargil, 1987). Acute
thrombosis is thought to occur due to compression frona
haematoma or oedema, or to reduced flow secondary to
vasospasm. Less commonly thrombosis may occur sub.
acutely due to increased blood coagulability or altera.
tions in general cerebral perfusion. Other postulated
mechanisms include occlusion of feeding vessels by
atheroma or embolism (Sukoff et al., 1972).
In our patient there was no radiographic evidence of
intracranial haemorrhage. However, she did have a short
period ofhypotension after cutting her hand and this may
have initiated subacute thrombosis within the nidus of the
arteriovenous malformation.
In an assessment of future risk o f haemorrhage from a
thrombosed arteriovenous malformation it is important
to know whether the occlusion is partial or complete.
Angiography may be misleading in this respect: Norl6n
(1949) showed that partial thrombosis may so diminish
the flow within the malformation that the abnormal
vessels do not fill with sufficient contrast medium to
appear radio-opaque. The greater contrast resolution of
computed tomography should allow this small flow to be
detected on a contrast enhanced scan but extravasation
into damaged tissues also contributes to the enhancement
shown by some of these malformations (Golden and
Kramer, 1978). Magnetic resonance imaging has demonstrated persistence of an arteriovenous malformation in
angiographically complete occlusion (Yasargil, 1987).
However, magnetic resonance imaging may not always
demonstrate patent vessels within such a lesion, particularly if flow is slow or there is local haemosiderin
deposition from past haemorrhage (Needell and Maravilla, 1988).
We suggest that the marginal enhancement demonstrated in our patient (Fig. 3b) was due to extravasation of
contrast medium and that thrombosis was complete at
that time. The patient has remained well, but should
recanalization and bleeding occur, reassessment as
regards the suitability of the lesion for Surgery, endovascular embolization, or radiosurgery would be required.
Aeknowledge'ments:We would like to thank Mrs Jean Cox for typing
the manuscript and Mr P. J. Teddy for permission to report the case.
REFERENCES

Fig. 5- Computed tomography two and a half years after initial
presentation shows a small focus of calcification in the right cerebral
hemisphere.
mations over the past 40 years (Yasargil, 1987). Regression has been documented by angiography, radionuclide
studies, computed tomography, or a combination of these.
Most reports have been of isolated cases, and many have
shown only partial thrombosis. However, several authors
have collated the data from these case reports in order to
draw general conclusions (Wakai et al., 1983).
Patients in whom thrombosis is demonstrated are
usually young or middle aged adults. Spontaneous
thrombosis is more likely in a small arteriovenous
malformation drained by a single vein (Conforti, 1971;
Pasqualin et al., 1985). In most cases regression has
occurred acutely.

Conforti, P (1971). Spontaneous disappearance of cerebral arteriove"
nous angioma: Case report. Journal of Neurosurgery, 34, 432-434.
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Needell, WM & Maravilla, KR (1988). MR flow imaging in vascular
malformationsusinggradient recalledacquisition. American Journal
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Norl6n, G (1949). Arteriovenousaneurysms of the brain: report of ten
cases of total removalof the lesion. Journal of Neurosurgery, 6, 475494.
Pasqualin, A, Vivenza,C, Rosta, L, Screnza,R, De Pren, R & Colangeli,
M (1985). Spontaneousdisappearance ofintracranial arteriovenous
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