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a Service de
Neuroradiologie, Hôpital Purpan, Toulouse, b Service de Neuroradiologie, Herman Fishgold,
Hôpital Salpétrière, Paris, c Neuroradiology Department, Karolinska Hospital,
Stockolm, Sweden, d Service
de Neuroradiologie, René Djindjian, Hôpital Lariboisière, Paris, e Service de
Neuroradiologie, Charcot, Hôpital Salpétrière, Paris
Correspondence to: Dr C Cognard, Service de Neuroradiologie, Hopital Purpan, Place du Dr Baylac, 31059 Toulouse Cedex, France. Telephone 0033 5 61 77 23 39; fax 0033 5 61 77 76 51.
Received 27 June 1997 and in revised form 5 December 1997;
Accepted 15 January 1998
OBJECTIVES
A
retrospective study was carried out on 13 patients with intracranial
dural arteriovenous fistulas (DAVFs) who presented with isolated or
associated signs of intracranial hypertension.
METHODSNine patients
presented with symptoms of intracranial hypertension at the time of
diagnosis. Ocular fundoscopy available in 12 patients showed bilateral
papilloedema in eight and optic disk atrophy in four. Clinical
evolution was particularly noticeable in five patients because of
chronic (two patients) or acute (after lumbar shunting or puncture:
three patients, one death) tonsillar herniation.
RESULTSTwo patients
had a type I fistula (drainage into a sinus, with a normal antegrade
flow direction). The remaining 11 had type II fistulas (drainage into a
sinus, with abnormal retrograde venous drainage into sinuses or
cortical veins). Stenosis or thrombosis of the sinus(es) distal to the
fistula was present in five patients. The cerebral venous drainage was
abnormal in all patients.
CONCLUSIONType II
(and some type I) DAVFs may present as isolated intracranial
hypertension mimicking benign intracranial hypertension. Normal
cerebral angiography should be added as a fifth criterion of benign
intracranial hypertension. The cerebral venous drainage pattern must be
carefully studied by contralateral carotid and vertebral artery
injections to correctly evaluate the impairment of the cerebral venous
outflow. Lumbar CSF diversion (puncture or shunting) may induce acute
tonsillar herniation and should be avoided absolutely. DAVF may induce
intracranial hypertension, which has a poor long term prognosis and may
lead to an important loss of visual acuity and chronic tonsillar
herniation. Consequently, patients with intracranial hypertension must
be treated, even agressively, to obliterate the fistula or at least to
reduce the arterial flow and to restore a normal cerebral venous
drainage. The endovascular treatment may associate arterial or
transvenous embolisation and /or surgery. Patients in whom the fistula
is not obliterated after an endovascular therapeutic procedure, need continous clinical and angiographical follow up.
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