Neuropathological changes following occlusion of the superior sagittal sinus and cerebral veins in the cat

Superior sagittal sinuses (SSS) of 36 mongrel cats were occluded by polymer injection. Immediately prior to the occlusion, Evans–blue (EB) was administered intravenously. The cats were killed 1, 3, 6, 12, 24, 72 and 120 h after sinus occlusion. Two sham–operated cats were killed 6 h and two 120 h after the operation. In 16 cats in which the occlusion was limited to the SSS, as well as in the sham–operated cats, no EB extravasation was present. However, ultrastructurally in two animals, the extracellular spaces were moderately enlarged, corresponding to increased permeability for water without opening of the BBB for proteins. In 20 cats in which cortical veins were occluded, in addition to the SSS, EB was extravasated. In nine of these cats, which had moderate oedema, EB–staining was present only in the cortex. In 11 cats with severe oedema, massive EB extravasation was observed also in the white matter. The U–fibre layer was free of EB, suggesting that the extension of oedema was blocked by this zone. Cats with severe edema showed extensive haemorrhagic cerebral infarction widely, but not completely, overlapping with ischaemic necrosis, and corresponding to the differences in the territories of arterial supply and of venous drainage. Seven animals displayed haematomas in the parasagittal white matter. Electron microscopy (EM) showed damage to the endothelium of capillaries and venules with extravasation of platelets. In cats which survived longer than 24 h, the extracellular spaces were filled with proteinaceous transudate. Gliosis of the affected grey and white matter was observed in cats examined 24, 72 and 120 h after occlusion. Notwithstanding the differences between this model and human cerebral sinus and vein thrombosis, the procedure represents an experimental approach to understanding the variability of the clinical course in patients with thrombosis of SSS. The results stress the role of the occlusion of the cortical veins in the extension of brain damage.