Cerebral venous sinus thrombosis pathophysiology
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The veins of the brain, both the superficial veins and the deep venous system, empty into the dural venous sinuses, which carry blood back to the jugular vein. In cerebral venous sinus thrombosis, blood clots usually form both in the veins of the brain and the venous sinuses. The thrombosis of the veins themselves causes cerebral oedema (both vasogenic and cytotoxic oedema) through back pressure, and small petechial haemorrhages that may merge into large haematomas. Thrombosis of the sinuses is the main mechanism behind the increase in intracranial pressure due to decreased resorption of cerebrospinal fluid (CSF). Because this process is generalised, the condition does not lead to hydrocephalus.[1]
Any blood clot forms due to an imbalance between coagulation (the formation of the insoluble blood protein fibrin) and fibrinolysis. The three major mechanisms for such an imbalance are enumerated in Virchow's triad: alterations in normal blood flow, injury to the blood vessel wall, and alterations in the constitution of blood (hypercoagulability). Most cases of cerebral venous sinus thrombosis are due to hypercoagulability.[1]
It is possible for the clot to break off and migrate (embolism) to the lungs, causing a pulmonary embolism.[1][2] An analysis of previous case reports concludes that this occurs in about 10% of cases, but has a very poor prognosis.[3]
References
- ↑ 1.0 1.1 1.2 Invalid
<ref>tag; no text was provided for refs namedStam2005 - ↑ Invalid
<ref>tag; no text was provided for refs namedEFNS - ↑ Diaz JM, Schiffman JS, Urban ES, Maccario M (1992). "Superior sagittal sinus thrombosis and pulmonary embolism: a syndrome rediscovered". Acta Neurol. Scand. 86 (4): 390–6. PMID 1455986.