Pathological mechanism and three-dimensional structure of cerebral dissecting aneurysms

Object. The goal of this study was to investigate the pathological mechanis m and precise three-dimensional (3D) structure of cerebral dissecting aneur ysms in association with their clinical course. Methods. Nine aneurysm specimens were excised from eight patients. Of the n ine aneurysms, seven arose from the vertebral artery, one from the anterior cerebral artery, and one from the superior cerebellar artery. Eight aneury sms were accompanied with subarachnoid hemorrhage (SAH) and one with infarc tion. Seven aneurysms were obtained at autopsy and two were obtained during surgery (trapping and bypass). All nine aneurysms were sectioned into seri al axial slices measuring 5 to 10 mum in thickness. Taking each slice as an element, we reconstructed the 3D structure of the aneurysm. The true lumen communicated with a pseudolumen through the disrupted portio n of the internal elastic lamina (IEL) in all nine aneurysms. The ruptured portion was located just above the disrupted IEL. Two aneurysms had an exit back into the true lumen, but the other seven had no such exit. Conclusions. The primary mechanism by which a cerebral dissecting aneurysm is created is by the sudden disruption of the IEL. The plane of dissection extends through the media. The majority of aneurysms have one entrance into the pseudolumen (entry-only type). This type is associated with an unstabl e clinical course. Some cerebral dissecting aneurysms have both an entrance and exit (entry-exit type). This type of aneurysm occasionally contains a constant flow of blood through the pseudolumen and is clinically more stabl e than entry-only aneurysms.