Cerebral Venous Thrombosis Models

Cerebral venous thrombosis (CVT) is a relatively rare cause of stroke. The most common site for CVT is the superior sagittal sinus (SSS). It is characterized by an in situ thrombotic occlusion of one or more sinus, elevated brain parenchymal pressure caused by venous congestion (stasis), elevated cerebral blood volume and decreased regional CBF, blood-brain barrier disruption, and increased net capillary filtration that leads to progressive brain edema. CVT is frequently associated with venous infarctions with or without hemorrhagic transformation, intracerebral hemorrhage, and even subarachnoid hemorrhage. The severity of parenchymal damage is dependent on the degree of involvement of the venous drainage (114 ).

)n the first reported CVT model in 1836, both jugular veins of a rabbit were tied, and the animal died 7 days after the operation (115). Early models concentrated on injecting the SSS with sclerosing substances, such as lard oil, hot paraffin, sodium morhuate, ethanolamine, cyano-acrylate, etc., or on mechanical obstruction of the SSS by electrocoagulation or muscle and cotton tamponades (116). One group injected thrombin directly into the SSS of the dog to induce in situ thrombosis (117). In the rabbit, mechanical direct compression of the SSS led to local thrombus formation, which could subsequently be successfully treated with intravenous rtPA infusion (118). SSS could be successfully occluded by the retrograde insertion of a catheter-balloon system in the pig (119). In a rat model, mechanical obstruction of the SSS at 2 separate and distinct sites was combined with an injection of cephalin-caolin suspension into the SSS (116). Ligation of the SSS at a posterior part appears to be critically important for development of brain damage, and the findings are probably more severe with additional involvement of cortical veins. Similar models were developed for various species, including the gerbil (120) and the cat (121), with good success.

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