Venous Thrombosis -Principles and Practice 130 Table 1. Most important causes of and risk factors associated with cerebral venous sinus thromobosis. Reproduced with the written permission from the paper by Stam (2005).In the prospective International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVST) cohort of 624 adults with CVST, women comprised 465 (75%) of the patients. Compared with men, women had significantly lower mean age (42 vs 34 years). Furthermore, a gender specific risk factor -oral contraceptives, pregnancy, puerperium, and hormone replacement therapy -was identified in 65% of the women. CVST is more common in neonates than it is in infants, children or adults. In adults, CVST affects patients who are younger on average than those with arterial types of stroke. In the ISCVST, the mean age of patients with CVST was 39 years, and only 8% of them were older than 65 years (Ferro & Canhao, 2011). Topographically, the most frequent occurrence of CVST has been observed in the superior sagitral sinus (62%) followed by the transverse (lateral) sinus (41-45%) (Figure 1).
www.intechopen.comCerebral Venous Sinus Thrombosis -Diagnostic Strategies and Prognostic Models: A Review Reproduced with the written permission from the paper by Saposnik et al. (2011) as derived from data on 624 patients in the International Study on Cerebral Venous and Dural Sinuses Thrombosis as reported by Manolidis & Kutz (2005).The pathogenesis of CVST remains incompletely understood because of the high variability in the anatomy of the venous system, and the paucity of experiments in animal models of CVST. However, there are at least two different mechanisms that may contribute to the clinical features of CVST: a) thrombosis of cerebral veins or dural sinus leading to cerebral parenchymal lesions or dysfunction; and b) occlusion of dural sinus resulting in decreased cerebrospinal fluid (CSF) absorption and elevated intracranial pressure. (Figure 2). Obstruction of the venous structures may result in increased venous pressure, decreased capillary perfusion pressure, and increased cerebral blood volume. Dilatation of cerebral veins and recruitment of collateral pathways play an important role in the early phases of CVST and may initially compensate for changes in pressure. The increase in venous and capillary pressure leads to blood-brain barrier disruption, causing vasogenic edema, with leakage of blood plasma into the interstitial space. As intravenous pressure continues to increase, mild parenchymal changes, severe cerebral edema, and venous hemorrhage may occur due to venous or capillary rupture. The increased intravenous pressure may lead to an increase in intravascular pressure and a lowering of cerebral perfusion pressure, resulting in decreased cerebral blood flow (CBF) and failure of energy metabolism. In turn, this allows intracellular entry of water from failure of the Na+/K+ ATPase pump, and consequent cytotoxic edema (Ferro & Canhao, 2011).www.intechopen.com Ferro & Canhao (2011).Advances in our understanding of ...