Brain developmental venous anomaly thrombosis

Excerpt

A 62-year-old man was admitted for partial motor seizures and headaches. His medical history included arterial hypertension, obstructive sleep apnea syndrome and migraine. Because of his migraine, he had received an MRI 4 years earlier on which a right frontal developmental venous anomaly (DVA) had been fortuitously discovered. At admission, the patient presented with headaches since 2 weeks, different from his usual migraine headaches. The headache was permanent, more painful, and not relieved by usual analgesics. He had no focal neurological deficits. Brain MRI (Fig. 1a–d) revealed a filling defect in the collecting vein of the known right frontal DVA with limited perifocal edema on FLAIR and intravascular hypointensity on T2*, compatible with the diagnosis of DVA thrombosis. Brain MRI revealed no additional vascular malformations. Standard biological data were normal. Extensive laboratory investigations revealed isolated elevate d-dimer (730 ng/ml; N < 500). Protein C, protein S, antithrombin III, antiphospholipid and anticardiolipin β2-glycoprotein-1 complex antibodies were within the normal range. Factor V Leiden, prothrombin, and Janus Kinase 2 mutations were absent. Intravenous heparin infusion was rapidly introduced followed by daily oral vitamin K antagonists (fluindione 20 mg per day). Levetiracetam (500 mg twice per day) was also introduced. Three months later, repeated brain MRI (Fig. 1e–h) showed complete resolution of DVA thrombosis with complete recanalization of the DVA. Six months later, levetiracetam and fluindione were definitively stopped and the patient had no seizure or thrombosis recurrence.

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