Neuroradiology (1998) 40: 15±18
Ó Springer-Verlag 1998

C. L. Merten
H. O. Knitelius
J.-P. Hedde
J. Assheuer
H. Bewermeyer

Received: 17 October 1996
Accepted: 14 May 1997

C. L. Merten × J. Assheuer ×
H. Bewermeyer ( )
Krankenhaus Merheim,
Department of Neurology,
Ostmerheimerstrasse 200,
D-51109 Cologne, Germany
Tel. 02 21/89 07-27 75; fax 02 21/89 07-27 72

)

H. O. Knitelius × J.-P. Hedde
Krankenhaus Merheim,
Department of Radiology,
Ostmerheimerstrasse 200,
D-51109 Cologne, Germany

D IA G N O S T I C NE URO R A D IO L OG Y

Intracerebral haemorrhage from a
venous angioma following thrombosis
of a draining vein

Abstract We report a case of putaminal haemorrhage from a venous
cerebral angioma following thrombosis in a draining vein. The patient
complained of numbness of the right
side, followed by headache and
aphasia. CT demonstrated an intracerebral haemorrhage due to
thrombotic occlusion of a draining
vein of the venous angioma. Carotid
angiography showed the venous angioma. MRI studies confirmed the
diagnosis and demonstrated recanalisation of the draining vein following therapy with phenprocoumon.

Introduction
In a series of autopsies, venous angiomas in the brain
were found in 0.25 %. These developmental anomalies
(DVA) make up 42 %±63 % of cerebral vascular malformations [1, 2]. Unlike arteriovenous malformations
and to a lesser extant cavernomas, DVA rarely produce
symptoms and in most cases are therefore diagnosed by
chance.

Case report
A 50-year-old woman suddenly developed a feeling of numbness in
her right foot that extended within minutes to the entire right side
of her body. The next day, she complained of headache and became
aphasic. On examination 3 days after the onset of symptoms she
was found to have hypoaesthesia of the right side and a Broca's
aphasia.
CT revealed a haematoma in the left putamen and dense, dilated transcerebral veins draining into an enlarged Sylvian vein
(Fig. 1 a, b). Alongside the cella media of the left lateral ventricle

Key words Venous cerebral
angioma × Intracerebral
haemorrhage

atypical vessels and dense vascular structures running through
the white matter and basal ganglia to the sylvian fissure were
identified. After contrast medium, these dilated medullary veins
appeared as a ªCaput Medusaeº (Fig. 1 c). At carotid angiography, the arterial phase revealed no abnormality. In the late
venous phase, dilated medullary veins were seen in the left
paraventricular region, draining into a large atypical vein. The
contrast medium had not drained away 30 s after injection
(Fig. 1 d).
MRI showed a draining vein which gave high signal on T1-,
proton density- and T2-weighted sequences, indicating a thrombosed vessel (Fig. 2). It was therefore concluded that the haematoma in the left putamen had been caused by haemorrhage from
the venous angioma following thrombosis in a large draining vein.
No associated cavernoma was found.
The patient's neurological disorder resolved within 4 weeks.
After initial treatment with intravenous heparin, she was given
anticoagulant therapy with phenprocoumon. CT showed complete
resorption of the haematoma.
MRI was repeated 8 months later. The dilated veins identified
in the earlier studies had significantly decreased in size. The
draining vein gave low signal on the T1-weighted spin-echo images,
demonstrating recanalisation (Fig. 3). Residual haemosiderin was
identified in the left putamen.

16

Fig. 1 a, b CT demonstrates a
small haematoma in the putamen (arrow) and dense, dilated
transcerebral veins draining
into an enlarged sylvian vein.
c Contrast-enhanced CT shows
dilated medullary veins in the
left cerebral hemisphere converging towards a subependymal vein. d Frontal
projection of late venous phase
of left carotid arteriography
demonstrates persistent filling
of dilated medullary, subependymal and transparenchymal veins with a typical
ªcaput Medusaeº appearance

a

c
Two years after the cerebral haemorrhage, the patient had recovered completely and treatment with phenprocoumon was discontinued.

Discussion
Cerebral venous angiomas differ from malformations
such as arteriovenous malformations and from cavernomas. They have a tuft- or featherlike structure
(ªCaput Medusaeº) and can be considered as a developmental variation of the normal cerebral venous system [3]. The main diagnostic criterion is large transparenchymal veins draining into large subependymal or
subarachnoid vessels.
DVA may be shown in patients being investigated for
epileptic seizures, and signs of cerebral ischaemia may be

b

d
shown on imaging [4±7]. It used to be assumed that cerebral haemorrhage was not infrequently caused by venous
angiomas [8, 9]. At the present there is controversy as to
whether DVA can in fact be incriminated for cerebral
haemorrhage. Cerebral haemorrhage is often ascribed to
be due to cerebral cavernomas, present in 33±48 % of
cases of DVA [4, 10]. Cerebral cavernomas are often not
seen on CT or angiography, but can be reliably detected
by MRI [4, 11]. Thus, attribution of cerebral haemorrhage to a DVA may have been mistaken if the diagnosis
had been made exclusively by angiography or CT [9].
In this case, no cavernoma was shown by MRI.
Therefore, the haemorrhage was probably due to haemorrhage from the DVA following thrombosis of its
principal vein and a resultant increase in pressure within
it. The progression of symptoms could be interpreted in
the light of a slowly developing thrombus in the draining

17

Fig. 2 a Unenhanced
T1-weighted coronal spin-echo
MRI confirms thrombosis of
the superficial draining vein.
b Gadolinium-enhanced coronal MRI demonstrates the
entire DVA

Fig. 3 MRI 8 months after
Fig. 2. a Coronal T1-weighted
image: there has been a decrease in signal intensity in
the draining vein, indicating
recanalisation. b Contrastenhanced image demonstrates reduction in size of the
lumina of all the atypical
veins, compatible with recanalisation of the draining
vein

vein and haemorrhage from the DVA when this vein was
almost totally occluded; the patient did not suffer from a
coagulopathy which could have induced venous thrombosis. DVA consist of thickened, hyalinised veins whose
walls contain hardly any smooth muscle cells or elastic
connective tissue [12]. This abnormal structure and the
slow drainage of blood are perhaps the reasons for an
increased risk of thrombosis, even in the absence of a
coagulopathy.
There is no formally established therapy for DVA. It
is generally acknowledged that asymptomatic DVA

need not be treated. Some workers recommend surgical
removal if haemorrhage has occurred [9], but extirpation of a DVA will interfere with the draining of blood
from the adjacent cerebral parenchyma. We therefore
consider surgical treatment dangerous, as fatal postoperative cerebral infarction has been reported [13, 14].
Our patient's clinical progress was satisfactory. CT and
MRI showed resorption of the intracerebral haematoma, and MRI showed recanalisation of the draining
veins.

References
1. Jellinger K (1986) Vascular malformations of the central nervous system: a
morphological overview. Neurosurg
Rev 9: 177±216
2. Sarwar M, McCormick WF (1978) Intracerebral venous angioma. Case report and review. Arch Neurol 35: 323±
325

3. Lasjaunias P, Burrows P, Planet C
(1986) Developmental venous anomalies (D. V. A): the so-called venous angioma. Neurosurg Rev 9: 233±244
4. Huber G, Piepgras U, Henkens H, Faubert C (1991) Venenanomalien des Gehirns. Radiologe 31: 274±282

5. Bouchacourt E, Carpena JP, Bories J,
Koussa A, Chiras J (1986) Accident
ischeÂmique par thrombose d'un angiome veineux. A propos d' un cas.
J Radiol 67: 631±635
6. Burke L, Berenberg RA, Kim KS
(1984) Choreoballismus: a nonhemorrhagic complication of venous anomalies. Surg Neurol 21: 245±248

18

7. Pelz DM, VinÄuela F, Fox AJ (1983)
Unusual radiologic and clinical presentations of posterior fossa venous angiomas. AJNR 4: 81±84
8. Handa H, Morikake K (1985) Venous
angiomas of the brain. In: Fein JM,
Flamm ES (eds) Cerebrovascular surgery, vol 4 Springer, New York,
pp 1139±1149
9. Malik GM, Morgan JK, Boulos RS
(1988) Venous angiomas: an underestimated cause of intracranial hemorrhage. Surg Neurol 30: 350±358

B O O K R E V I EW
Stroke: A practical guide to management. Eds:
C. P. Warlow, M. S. Dennis, J. van Gijn, et al.
1996, Blackwell Science, ISBN 0-86542874-3 HB, £ 99.50
It was a pleasure for me to read and review
this book. This is a very important book.
The editors state that the purpose was to
write a problem-orientated book about
stroke. As pointed out in the foreword by
HJM Barnett, the authors (all innovative in
the stroke field) have written this book to
assist us at the bedside or in the clinic ªin

10. Ostertun B, Solymosi L (1993) Magnetic resonance angiography of cerebral
developmental venous anomalies: its
role in differential diagnosis. Neuroradiology 35: 97±104
11. Lasaunias P, Terbrugge K, Rodesch G,
Willinsk R, Burrows P, Pruvost PH,
Piske R (1989) Vrais et fausses leÂsions
veineuses ceÂreÂbrales: pseudoangiomes
veineux et heÂmangiomes caverneux.
Neurochirurgie 53: 132±139
12. McCormick WF (1966) The pathology
of vascular (ªarteriovenousº) malformations. J Neurosurg 24: 807±816

13. Biller J, Toffol GJ, Shea JF, Fine M,
Behrooz AK (1985) Cerebellar venous
angiomas: a continuing controversy.
Arch Neurol 42: 367±370
14. Senegor M, Dohrmann GJ, Wollmann
RL (1983) Venous angiomas of the
posterior fossa should be considered
anomalous venous drainage. Surg Neurol 19: 26±32

sorting out what is truly valuable, to point
out what is likely to become valuable and
to caution about therapeutic strategies
which remain in the realm of speculationº.
I am convinced that the authors have succeeded in this goal.
Instead in the typical manner of a multiauthor book with the common custom of
collecting a series of chapters written in
many different individual styles the authors
have together written a book in such a way,
that each chapter is influenced by the
knowledge and ideas of every author.
In order to enabled the reader to manage stroke patients at different stages of
their disease this book covers every facet of
care in stroke patients. The text is written

well formulated and succinet. It is very
useful, that the contents are listed at the
beginning of every chapter. The bibliography offers a broad selection of current references. CT and MR-images are well integrated in the text, the image-quality is good
to excellent. Most of the sketches are very
helpful to make images understandable.
The authors deserve congratulations for
their impressive achievement. I am convinced that this will be a standard textbook
for neurologists, neuroradiologists, neurosurgeons and for anyone else who wants
practical guidance about all and any of the
problems to do with stroke.
H. BruÈckmann, Munich