Cerebral venous sinus thrombosis pathophysiology: Difference between revisions
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=Pathophysiology== | |||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology=
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 edema (both vasogenic and cytotoxic edema) through back pressure, and small petechial hemorrhages that may merge into large hematomas. 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 generalized, 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 Stam J (2005). "Thrombosis of the cerebral veins and sinuses". N. Engl. J. Med. 352 (17): 1791–8. doi:10.1056/NEJMra042354. PMID 15858188.
- ↑ Einhäupl K, Bousser MG, de Bruijn SF; et al. (2006). "EFNS guideline on the treatment of cerebral venous and sinus thrombosis". Eur. J. Neurol. 13 (6): 553–9. doi:10.1111/j.1468-1331.2006.01398.x. PMID 16796579.
- ↑ 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.