Cerebral venous sinus thrombosis pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:  Sharmi Biswas, M.B.B.S

## Overview

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Imbalance in prothrombotic and fibrinolysis processes are the main pathophysiologic mechanisms leading to cerebral venous sinus thrombosis.

## Pathophysiology

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There are two mechanisms for cerebral venous thrombosis. The first is thrombosis of cerebral veins causing local effects due to venous obstruction and the second cause is thrombosis of the cerebral sinuses leading to intracranial hypertension. Both of these processes occur in the majority of patients with CVT. Increased venous pressure due to the occlusion of the cerebral vein causes cytotoxic edema and venous infarction,blood brain barrier disruption associated vasogenic edema and parenchymal hemorrhage due to venous and capillary rupture.

Increased intracranial hypertension develops due to the occlusion of major cerebral venous sinuses.In normal condition, cerebrospinal fluid (CSF) is transported from the cerebral ventricles to subarachnoid spaces and arachnoid villi is responsible for the absorption of CSF and eventually drain to the superior sagittal sinus.Thrombosis of cerebral venous sinuses leads to increased venous pressure, decreased absorption of CSF and as a consequence intracranial pressure get increased along with parenchymal hemorrhage and cytotoxic and vasogenic edema.[1][2]

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.[2]

It is possible for the clot to break off and migrate (embolism) to the lungs, causing a pulmonary embolism.[2][3] An analysis of previous case reports concludes that this occurs in about 10% of cases, but has a very poor prognosis.[4]

## References

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1. ↑ Piazza, Gregory (2012). "Cerebral Venous Thrombosis". Circulation. 125 (13): 1704–1709. doi:10.1161/CIRCULATIONAHA.111.067835. ISSN 0009-7322.
2. ↑ 2.0 2.1 2.2 Stam, Jan (2005). "Thrombosis of the Cerebral Veins and Sinuses". New England Journal of Medicine. 352 (17): 1791–1798. doi:10.1056/NEJMra042354. ISSN 0028-4793.
3. ↑ 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.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
4. ↑ 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.CS1 maint: Multiple names: authors list (link)