Treatment with anticoagulants has been controversial due to the propensity of venous infarcts to bleed. In fact, approximately 40% of patients with CVT have a hemorrhagic infarct prior to any treatment (13). However, the risk of intracranial hemorrhage seems to be greater in CVT patients who do not receive anticoagulation (15). Currently, it is acceptable to administer hep-arin when radiologic evidence demonstrates a hemorrhagic lesion (7). The efficacy of heparin in CVT is based on case reports, retrospective series, and 3 randomized clinical trials, which compared the effect of intravenous heparin, high-dose subcutaneous nadroparin, and intravenous unfractionated heparin with placebo (29-31). The 3 trials demonstrated a nonsignificant benefit of anticoagulation treatment over placebo. These trials included patients who already had hemorrhagic infarcts prior to treatment and who, during the trial, did not demonstrate new ICH after treatment was initiated. Another argument for the use of heparin is the prevention of pulmonary embolism, a common complication seen in patients with CVT.

Animal models of CVT have also shown that rats that receive anticoagulation clinically do better than those that do not. Additionally, such treatments as inhibitors of platelet glyco-protein Ilb/IIIa appear to have benefit in rats and might eventually prove to be beneficial in humans as well.

No controlled data on the duration of oral anticoagulation post-CVT is established, but most treatment is given for 3 to 6 months (2). Recurrent CVT occurs in 2% of patients, and 4% have extracranial thrombotic events within 1 year (13). Longer or indefinite anticoagulation is recommended in patients with thrombophilia, recurrent CVT, inflammatory disease, malignancy, or immobilization (7). Arguments against the use of heparin include the risk of larger hemorrhage into a venous sinus that has resulted in infarction with hemorrhagic transformation, and the high incidence of spontaneous recovery seen in patients with CVT.

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