Cerebral venous thrombosis (CVT) is less frequent than arterial thrombosis, however, it is still frequently overlooked. Pathophysiologically it is characterized by a disturbance of the equilibrium between endogenous thrombogenic and fibrinolytic factors. In addition, the time course depends on the presence or absence of efficient venous collaterals. A wide variety of clinical symptoms do occur, however, they may be grouped into at least four relatively typical syndromes: a) the pseudotumor cerebri syndrome, b) the combination of headache and focal neurologic deficit, c) the combination of focal epileptic seizure (with or without Todd's paresis) and headache, and d) deep CVT characterized by headache, nausea, bilateral long-tract symptoms and usually a rapidly progressing decline in the level of consciousness. Two diagnostic routes are generally accepted, the one consisting of cranial computed tomography plus radiographic angiography, the other one consisting of magnetic resonance imaging and magnetic resonance angiography. The mainstay of therapy is partial thromboplastin time-effective anticoagulation (PTT at least doubled, target PTT between 80 and 100 secs). Anticoagulation should be performed even if intracranial hemorrhage is present. In cases where deterioration occurs despite effective heparin treatment and in subjects presenting with stupor or coma, more aggressive therapy, e.g., local fibrinolysis during venous angiography, may be considered.