Cerebral Venous Thrombosis

Two articles in this issue of Stroke 1,2 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 T1and 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, which schematically encompass all causes of deep-vein leg thrombosis and numerous local causes such as traumas, tumors, or infections.3 However, despite an extensive initial work-up, the proportion of cases of unknown etiology remains between 20% and 25%.3,4 This stresses the need, when no cause is found, for a prolonged follow-up with repeated investigations. One of the most puzzling aspects of CVT is its diversity in outcome. Recognized as early as 150 years ago, CVT has for a century been diagnosed almost exclusively at autopsy and therefore thought to be always lethal. In early angiographic series, mortality still ranged between 30% and 50%, but in a See articles on page 484 and page 489