The dimensions of the 10 triangles around the cavernous sinus were measured to define the anatomical characteristics of the triangles and to compare their consistency in shape and area. Twelve tissue blocks containing the bilateral cavernous sinuses and medial two-thirds of the middle cranial fossae were obtained from Japanese adults at autopsy, fixed to a stereotactic frame, and examined with an operative microscope. The dimensions of each triangle were measured with calipers and compared, based on the same point and border. The anteromedial triangle and the superolateral (Parkinson's) triangle were more consistent in shape than the paramedial and oculomotor triangles, but the oculomotor triangle was larger in area than these other triangles. The posteromedial (Kawase's) triangle was more consistent in shape and larger than the anterolateral, lateral, and the posterolateral (Glasscock's) triangles. The anteromedial and superolateral (Parkinson's) triangles are important for the combined epi- and subdural approach to cavernous sinus lesions. The posteromedial (Kawase's) triangle is important for gaining access to the posterior cranial fossa from the middle cranial fossa.

Chordomas are most commonly located in the extradural region. A 56-year-old man presented with a large chondroid chordoma located totally within the intradural retroclival region. The tumor was resected via the petrosal approach. Five years after subtotal removal, the residual tumor showed no sign of regrowth despite the fact that radiation therapy had not been used. The patient was free of symptoms except for moderate, conductive hearing loss in his right ear. The position of the intradural tumor could be preoperatively diagnosed by neuroimaging and, thus, the petrosal approach was selected. Primary intradural extraosseous chordomas are very rare and difficult to differentiate from ecchordoses physaliphorae on the basis of histological and radiological features; however, MIB-1 staining may be useful.

This 47-year-old man was admitted to the hospital with disturbance of consciousness due to subarachnoid hemorrhage caused by a ruptured dissecting aneurysm of the left anterior cerebral artery (ACA). Conservative treatment resulted in improvement in the patient's consciousness; however, repeated rupture occurred during the chronic stage. Endovascular coil embolization of the parent artery was successful. Serial angiography demonstrated all stages in the development of the aneurysm. Follow-up angiography demonstrated an incidental dissecting aneurysm of the right vertebral artery. This aneurysm was also treated by endovascular embolization. No new neurological deficit appeared during or after the treatment. Multiple dissecting aneurysms are rare, especially those involving both supra- and infratentorial regions. A ruptured dissecting aneurysm of the ACA is also an uncommon vascular disorder. This case shows that rebleeding may occur, even during the chronic stage, and thus appropriate treatment for the prevention of subsequent bleeding is essential. Incidental dissecting aneurysms can be treated using the endovascular technique, but further study is necessary.

Using electron microscopy, we investigated the small arteries and veins in ischemic lesions induced by occlusion of the ostium of the middle cerebral artery in 42 rats. We observed endothelial denudation In the small arteries of rats receiving occlusion for >6 hours. When the occluding cylinder was removed to allow for reperfusion, however, 2 hours of occlusion was sufficient for endothelial denudation to occur. Medial smooth muscle cells seemed to be more vulnerable to ischemia than endothelial cells because ultrastructural changes in the former cells preceded endothelial denudation. Moreover, endothelial denudation definitely exacerbated vascular changes so that medial necrosis appeared to be complete beneath the denuded areas, allowing erythrocytes, platelets, and exogenous tracers to penetrate into the cytoplasm of smooth muscle cells. These arterial lesions seemed to be repaired 10 days after removal of the occluding cylinder following 2 hours of occlusion. On the other hand, small veins in the ischemic lesion did not show endothelial denudation or medial necrosis. Our study suggests that arterial changes in ischemic lesions play a role in exacerbating the brain edema caused by recirculation after ischemia. (Stroke 1991^2:635-642)

In this study, some clinical and radiological factors were found to be associated with postoperative oculomotor nerve palsy.