Abstract

A new experimental model of cerebral sinus occlusion was devised, using 16 mongrel dogs to study the regional cerebral blood flow (r-CBF) change in intracranial venous hypertension. A mixture of α-cyanoacrylate monomer and pantopaque was injected through a catheter introduced into the superior sagittal sinus (SSS). According to the extent of the sinus occlusion, the animals were divided into three groups: group A, SSS occlusion only; group B, SSS occlusion+ transverse sinus (TS) occlusion; group C, SSS occlusion+TS occlusion+cortical vein occlusion. To make a model of the dural arteriovenous malformation, normal saline was infused under constant pressure through a catheter introduced into the SSS and the sinus pressure was elevated from 10 mmHg to 60 mmHg in group D. Changes in intracranial pressure (ICP), SSS pressure (SSSP), and r-CBF and histological changes were evaluated in these groups. Before sinus occlusion, ICP and SSSP were 9±3.2 mmHg and 4±2.5 mmHg, respectively. After sinus occlusion, ICP and SSSP were 20±5.5 mmHg and 27±4.5 mmHg in group A, 30±5.4 mmHg and 38± 5.1 mmHg in group B, and 65±7.9 mmHg and 74±6.1 mmHg in group C. No ICP change was noted in group D. r-CBF showed no change in group A or D, and minimal reduction for a short period in group B. In group C, r-CBF decreased to 20-30% of the value prior to sinus occlusion due to marked venous congestion, which was complicated by subarachnoid hemorrhage and intracerebral hematoma. From the above results, it may be concluded that cortical veins play an important role as a collateral channel in sinus occlusion.

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