[Ventricular enlargement in experimental occlusion of superior sagittal sinus--in reference to histopathological findings (author's transl)].
An experimental occlusion of superior sagittal sinus was made in dogs according to ligation with thread at the posterior third portion of the sinus. Ventricular enlargement and histological changes in the cerebrum were studied in various stage after occulusion of the sinus. In the acute stage, no ventricular enlargement occured. However, in the chronic stage, nine dogs out of 12 dogs showed enlargement of the ventricle. Hitological examination revealed peeled ependymal layer from subependymal tissue, edematous findings in the periventricular tissue, perivascular gliofibrosis, perivascular hemorrhage, exanguination of plasm, and venous stasis in the ventricular wall and cerebral cortex in convexity. Extracellular space in the subependymal tissue, and the space between pial and glial membrane were widened remarkably. Two factors were raised by authors as the pathogenesis for ventricular enlargement. One factor was the hydrodynamic disturbance of CSF according to the CSF malabsorption into the superior sagittal sinus through arachnoid villi. The other one was the disturbance of venous circulation due to occlusion of the sinus.
D000818:Animals; D001253:Astrocytes / Q000648:ultrastructure; D001929:Brain Edema / Q000473:pathology; D002552:Cerebral Ventricles / Q000648:ultrastructure*; D002908:Chronic Disease; D003392:Cranial Sinuses / Q000473:pathology*; D004108:Dilatation, Pathologic; D004285:Dogs; D004805:Ependyma / Q000473:pathology; D008026:Ligation; D009457:Neuroglia / Q000648:ultrastructure; D012851:Sinus Thrombosis, Intracranial / Q000473:pathology; D013346:Subarachnoid Space / Q000648:ultrastructure; D013997:Time Factors