Venous Thrombosis

When a cerebral vein is unable to return blood, normally due to thrombosis, the tissue pressure can increase due to continued normal arterial flow. The brain then swells, as do the neighboring venous structures (compensatory), with a tendency for tissue ischemia and hemorrhage (hemorrhagic infarction or confluent petechial hemorrhages that can appear as a large parenchymal hematoma). Autopsy studies reveal dilated veins, tissue edema, ischemic neurons, and hemorrhagic changes (of varying sizes and degrees). The final pathology depends on the site and completeness of thrombosis and the timing of thrombosis to death.

As with other venous clots, fibrin and erythrocytes with a paucity of platelets comprise the majority of fresh thromboses, and fibrous tissue is seen within older clots. Thrombus formation generally originates from venous stasis, procoagulant states, and changes in the vessel wall. As many patients with CVT survive and are left without clinical or imaging evidence of permanent tissue damage (infarction), the pathophysiologic process is mostly consistent with temporary ischemia and edema.

The International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT) (13) studied the frequency of thrombosis. The transverse sinus was the most commonly thrombosed structure (86%), followed by the SSS (62%), straight sinus (18%), cortical veins (17%), jugular veins (12%), and vein of Galen/internal cerebral veins (11%). With adequate collateral circulation, the level of tissue ischemia might be insufficient to cause permanent tissue damage or infarction.

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