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(Stroke. 1999;30:481-483.)
© 1999 American Heart Association, Inc.
Editorial |
From Service de Neurologie, Hôpital Lariboisère, Paris, France.
Correspondence to Marie-Germaine Bousser, MD, Service de Neurologie, Hôpital Lariboisère 2, rue Ambroise Paré, 75475 Paris Cédex 10, France. E-mail bousser@ccr.jussieu.fr
Key Words: cerebral venous thrombosis heparin thrombolysis
Two articles in this issue of Stroke1 2 draw our attention to cerebral venous thrombosis (CVT), an infrequent but fascinating condition, remarkable for its extreme diversity, which still makes it a diagnostic and therapeutic challenge. Headache, focal deficits, seizures, disorders of consciousness, and papilledema, which can present in isolation or in association, are the most frequent signs.3 The mode of onset is highly variable, anything from sudden to progressive over weeks, so that CVT can mimic a host of conditions, such as ischemic or hemorrhagic stroke, abscess, tumor, encephalitis, metabolic encephalopathy, benign intracranial hypertension. . . .
Given this amazingly diverse clinical presentation, CVT should be considered in almost any brain syndrome, and appropriate neuroimaging investigations should be performed whenever suspicion is raised. A CT scan is usually the first investigation performed on an emergency basis. Although it can sometimes detect the spontaneously hyperdense thrombosed sinus, it usually shows nonspecific changes such as hypodensities, hyperdensities, and contrast enhancement, and in up to 30% of cases it is normal.3 4 The present "gold standard" for the diagnosis of CVT is no longer angiography but MRI, which visualizes the thrombosed sinus as an increased signal on both T1- and T2-weighted imaging. MR angiography or helical CT venography are nevertheless indicated at very early (before day 5) or late (after 6 weeks) stages when false-negatives may occur, or whenever MRI shows equivocal signs.
Once CVT is recognized, the next step is to find its etiology from
among the over 100 causes that have been identified,
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