Cerebral venous thrombosis (CVT) is rare and involves thrombosis of the veins and sinuses of the brain, most commonly the superior sagittal sinus. Approximately 5 CVT cases occur per 1 million persons in western countries. CVT causes 0.5% of strokes. Early diagnosis is crucial to prevent such outcomes as hydrocephalus, intracranial hypertension, and further seizures. Standard medical treatment of CVT consists of low-molecular-weight heparin and endovascular thrombolysis. Small case reports have found that the newer oral anticoagulants can be used for CVT treatment; however, they are associated with increased risk of bleeding and other adverse effects.
CVT can be triggered by an imbalance of the body’s homeostasis or reduced action of the intrinsic antithrombotic mechanism. Factors influencing this change include infection, brain tumor, inflammatory conditions, genetic thrombophilias, head trauma that causes intracranial bleeding, and certain medications. CVT may cause brain infarction and increased intracranial pressure. Sometimes, idiopathic intracranial hypertension presents as the only clinical manifestation. Confirmation of the diagnosis typically is through neuroimaging. Current CVT treatment depends on disease extent and severity.
CVT is a rare neurological disease with potentially serious implications and high neurological morbidity and mortality rates. Understanding the role of risk factors—such as genetic or acquired thrombophilia, pregnancy, use of oral contraceptives, and hyperhomocysteinemia—in CVT development is important. Although heparin and warfarin have been used for more than 50 years, newer oral anticoagulants (eg, dabigatran, rivaroxaban, apixaban) might offer an alternative to traditional therapy.