Cerebral venous occlusion represents an often underdiagnosed cause for acute or slowly progressive neurological deterioration. The underlying pathophysiological basis is not well understood, but is different from those of arterial occlusion reflecting therefore different anatomical and physiological features of the cerebral venous system. Extensive collateral circulation within the cerebral venous system allows for a significant degree of compensation in the early stages of venous occlusion. Elevated cerebral venous pressure due to cerebral venous occlusion can result in a spectrum of phenomena including a dilated venous and capillary bed, development of interstitial edema, increased cerebrospinal fluid production, decreased cerebrospinal fluid absorption and rupture of venous structures (hematoma). All of these pathophysiological changes may explain the clinical observation that cerebral venous occlusion, if promptly diagnosed and adequately managed, contains reversible alterations and need not always lead to venous infarction. The present review outlines this different pathophysiological behavior of venous compared to arterial occlusion in the cerebral vasculature; special reference is given to the effect of these changes on the therapeutic impact.
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