Venous thrombosis, intracranial

The clinical presentation varies from a sudden, abrupt onset with seizures, impaired consciousness and coma, to headache for many days, decreased mental status and progressive confusion.

Venous infarctions are often haemorrhagic and primarily affect the white matter rather than cortex.

Although cortical vein thrombosis and venous infarction can occur in isolation, most are associated with occlusion of a major dural sinus. The most commonly occluded is the superior sagittal sinus, followed by the transverse, sigmoid and cavernous sinuses.

Cortical veins are usually secondarily involved when thrombosis progresses from the sinus. Internal cerebral vein thrombosis, with possible extension to the vein of Galen and straight sinus, is a rare event that is accompanied by a fairly specific oedema of the basal ganglia and surrounding tissue that may be fatal but may also regress completely if recanalization occurs.

Imaging

CT scan shows tissue abnormalities with oedema in the infarcted area with petechial haemorrhages (Fig.1); oedema does not correspond to the classical distribution of arterial infarction. Hyperdense clot in the sinus may be seen as well as the so-called empty delta sign following contrast injection: the dura enhances around the affected sinus and the thrombus inside the sinus appears as a triangular structure which is comparatively hypodense.

When the internal cerebral veins are occluded, they appear hyperdense and the basal ganglia are markedly hypodense.

MR findings vary with clot age: acute thrombus is isointense with cortex while methaemoglobin is responsible for late T1 hyperintensity. MR angiography, with 2D TOF (time of flight) or 2D PC (phase contrast sequences) clearly show lack of flow within the occluded sinuses. Conventional angiography is not needed unless endovascular intravenous clot thrombolysis is suspected.

GS