Early Change of Intracranial Pressure, Regional Cerebral Blood Flow and Cerebral Edema Depending on the Occlusion Site of the Superior Sagittal Sinus in Cats

Park, Sung Chan; Cho, Chung Kee; Park, Hae Kwan; Cho, Kyung Keun; Lee, Kyung Jin; Rha, Hyung Kyun; Kang, Joon Ki; Choi, Chang Rak

Abstract

OBJECTIVE
Although it is well known that cerebral sinus thrombosis or resection of large cerebral veins during surgery may cause venous hypertension, often leading to brain edema and intracerebral hemorrhage and the outcome is widely variable with symptoms from headache to coma, the pathophysiology of cerebral venous circulatory disturbance is poorly understood. The purpose of this study was to investigate the pathophysiological change of cerebral venous circulatory disturbance by measurement of intracranial pressure, regional cerebral blood flow and cerebral water content, and histological examination for extravasation of Evans blue dye and cerebral edema for 2 hours after occlusion of the superior sagittal sinus and diploic veins in cats.
METHODS
Thirty five cats were divided into 4 groups: (1) control group, 5 cats with sham operation, (2) experiment group I, 10 cats with occlusion at the anterior 1/3 of the superior sagittal sinus, (3) experiment group II, 10 cats with occlusion at the middle 1/3 of the superior sagittal sinus, (4) experiment group III, 10 cats with occlusion at the posterior 1/3 of the superior sagittal sinus.
RESULTS
The results were as follows: 1) After occlusion of the superior sagittal sinus, intracranial pressure was elevated with increased cerebral water content and regional cerebral blood flow was reduced in all experiment groups. The degree of their changes was the least in experiment group I, the most in experiment group III, and intermediate in experiment group II. 2) Extravasation of the Evans blue dye was not observed in any experiment groups 120 minutes after occlusion of the superior sagittal sinus. 3) On the histological examination, pericellular edematous change of the brain was observed in all experiment groups 120 minutes after occlusion of the superior sagittal sinus. The degree of edema also showed similar pattern in magnitude to that of changes of other parameters.
CONCLUSION
These results suggest that occlusion of the middle or posterior 1/3 of the superior sagittal sinus could bring a significant harmful effect to the cerebral hemodynamics, leading to secondary brain injury and the hydrostatic edema is responsible for the cerebral swelling in early stage after occlusion of the superior sagittal sinus.