Multiple disease processes can cause cerebral venous thrombosis, including local processes such as mastoiditis, trauma, sinusitis, and tumor as well as systemic disorders such as infection, hypercoagulability (OCP’s), pregnancy, malignancy, inflammatory bowel disease, collagen vascular disease, and other hypercoagulable states. In up to 25% of patients, the cause is unknown. Thrombosis transitions to infarction in 50% of patients, with infarctions frequently resulting in seizures, headaches, papilledema, and focal neurologic deficits. Subcortical hemorrhage, bilateral hemorrhages, and gyriform hemorrhages are suspicious for venous infarction.

The superior sagital sinus (SSS), followed by the transverse, sigmoid, and cavernous sinuses are the most commonly occluded sinuses, and the superficial cortical veins that drain into the SSS also commonly occlude. Internal cerebral vein thrombosis is rare, but devastating due to resultant infarcts in the deep grey matter nuclei and upper midbrain.

MR findings vary with clot age – acute thrombus is isointense on T1WI, with late acute clots hyperintense on T1 and hypointense on T2WI. Subacute thrombi will be hyperintense on all pulse sequences. Signal void will be seen on gradient-refocused scans instead of the typical high signal intensity. Chronically thrombosed sinuses often undergo fibrosis and develop prominent collaterals.