BACKGROUND AND PURPOSE: Occlusion of the anterior third of superior sagittal sinus (SSS) is generally well tolerated because of sufficient collateral venous blood flow. In contrast, the pathophysiologic effects of occlusion of the SSS posterior to the rolandic vein remain controversial. We aimed to identify the specific hemodynamic effects of this subtype of SSS occlusion. METHODS: We ligated the SSS just behind rolandic vein and in the posterior part near the confluens sinus in three anesthetized cats. Regional cerebral blood flow (rCBF) was measured before and at 2 and 24 hours after the SSS occlusion. At around 48 hours, experimental settings were terminated with perfusion fixation with 4% paraformaldehyde solution. Hematoxylin-eosin histologic evaluation was performed. RESULTS: In all three cats with SSS occlusion, rCBF was reduced over the time period of measurement; this finding was observed in areas covering 5-20% of the brain in planes affected by the occlusion. The degree of rCBF reduction and the extension and severity of histologically proved venous infarction were correlated. CONCLUSION: To our knowledge, this is the first demonstration that occlusion of the SSS posterior to the rolandic vein is associated with a significant rCBF reduction to still-viable tissue in the related vascular territory at 24 hours after occlusion. We describe subacute venous infarction in an experimental occlusion of the SSS. Analogous to clinical conditions, occlusion of SSS alone without additional occlusion of bridging veins is adequate for producing a venous circulatory disturbance.
BACKGROUND AND PURPOSE: Occlusion of the anterior third of superior sagittal sinus (SSS) is generally well tolerated because of sufficient collateral venous blood flow. In contrast, the pathophysiologic effects of occlusion of the SSS posterior to the rolandic vein remain controversial. We aimed to identify the specific hemodynamic effects of this subtype of SSS occlusion. METHODS: We ligated the SSS just behind rolandic vein and in the posterior part near the confluens sinus in three anesthetized cats. Regional cerebral blood flow (rCBF) was measured before and at 2 and 24 hours after the SSS occlusion. At around 48 hours, experimental settings were terminated with perfusion fixation with 4% paraformaldehyde solution. Hematoxylin-eosin histologic evaluation was performed. RESULTS: In all three cats with SSS occlusion, rCBF was reduced over the time period of measurement; this finding was observed in areas covering 5-20% of the brain in planes affected by the occlusion. The degree of rCBF reduction and the extension and severity of histologically proved venous infarction were correlated. CONCLUSION: To our knowledge, this is the first demonstration that occlusion of the SSS posterior to the rolandic vein is associated with a significant rCBF reduction to still-viable tissue in the related vascular territory at 24 hours after occlusion. We describe subacute venous infarction in an experimental occlusion of the SSS. Analogous to clinical conditions, occlusion of SSS alone without additional occlusion of bridging veins is adequate for producing a venous circulatory disturbance.
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