Different roles of arteriosclerosis in the rupture of intracranial dissecting aneurysms

Aims: Although intracranial dissecting aneurysm (IDA) is a newly described variant of the brain aneurysms that affects mainly the vertebrobasilar arte rial system, its pathogenesis remains obscure, We aimed to clarify the role of arteriosclerosis in the pathogenesis of IDA based on histopathological findings in seven autopsy cases of IDA. Methods and results: All cases exhibited systemic hypertension or left vent ricular hypertrophy. Macroscopically, all cases exhibited subarachnoid haem orrhage. Two types of dissection were recognized in the vertebral artery, S ix of seven IDA cases showed a widespread disruption of the entire thicknes s of the arterial wall with the formation of a dilated pseudoaneurysm, whic h consisted of thin adventitia (arterial wall disruption type), Medial disr uption of the arterial wall and subadventitial dissecting haemorrhage were also found, resulting in the formation of a false lumen and stenosis of the 'true' lumen of the artery. However, these lesions were connected to the s ite of rupture of the entire arterial wall. Within 1 day after onset of IDA , the autopsy cases showed formation of fibrin thrombus, marked leucocyte i nfiltration and necrosis of the arterial wall at the site of the lesion. Ca ses that survived more than 1 week showed smooth muscle cell proliferation, macrophage accumulation and lymphocytic infiltration in the lesions. These cases showed no atherosclerotic plaque, but non-atherosclerotic fibrocellu lar intima. The thickness of intima and media was significantly less in the vertebral artery of IDA patients than that of non-IDA patients with system ic hypertension. On the other hand, the remaining case showed severe athero sclerosis with haemorrhage into the lipid core without connection to the ar terial lumen (intra-atheromatous plaque haemorrhage type). However, unusual arterioles and neovascularization of the intra-and peri-arterial walls wer e observed. Conclusions: Our results suggest that disruption of the entire arterial wal l may be a critical event in the development of IDA and result in the media l disruption and subadventitial haemorrhage. Non-atheromatous intima might function as a protective factor in arterial wall disruption, On the other h and, atherosclerosis may predispose to intra-atheromatous plaque haemorrhag e type of IDA through intramural haemorrhage originating from the newly for med vessels.