Substrati anatomo-patologici degli aneurismi cerebrali

Abstract

Atherosclerosis and fibromuscular dysplasia are the two most common causes of cerebral aneurysms. Saccular aneurysms are mainly congential and located in the bifurcations. Fusiform aneurysms are caused by atherosclerosis and involve the posterior portion, mainly the vertebral and basilar arteries and may develop into giant aneurysms. Cerebral atherosclerosis causes two types of lesions: stenosis with the formation of atheromatous plaque jutting into the lumen, and aneurysms leading to vascular remodelling with erosion of the internal elastic membrane, atrophy of the media and thickening and hyalinization of the intima. Atheromatous plaque is characterised by a fibromuscular intimal cap and a necrotic lipid core with atrophy of the underlying media. Plaque may thicken to occlude the vessel by intraplaque haemorrhage and superimposed occlusive thrombosis due to ulceration, or rupture of the fibrous cap caused by inflammation. It remains unsettled whether atherosclerotic cerebral aneurysms are malformations, with congenital abnormalities of the internal elastic membrane and elastic fibres constituting the media, or whether atheromatous changes are secondary to impaired blood flow. Thinning of the wall could also be caused by flow changes with parietal stress resulting from the turbulence caused by atherosclerotic stenotic lesions or the outcome of dissection of the arterial wall. Fibromuscular dysplasia is a multifocal vascular disease of unknown origin, not atherosclerotic or inflammatory, mainly affecting the brain media with lesions characterized by areas of concentric fibromuscular tissue jutting into the vessel lumen alternating with areas of thinning to almost disappearance of the tunica media and discontinuity of the internal elastic membrane in areas of thinning with the formation of aneurysms. Vessel calibre varies with areas of luminal stenosis alternating with areas of aneurysmal dilatation. The origin of this disease remains unknown and it is thought to be multifactorial possibly associated with saccular aneurysms, fusiform giant aneurysms, dissection of the intracranial arteries, cavernous fistulae and stenosis or occlusion associated with dysplasia. Aneurysms in the brain may share the same underlying mechanisms as aneurysms elsewhere involving atherosclerosis and fibromuscular dyspasia, i.e. remodelling of the extracellular matrix. A recent hypothesis suggested that cerebral aneurysms were caused by an active mechanisms in the arterial wall rather than a passive process linked to genetically determined structural defects or purely haemodynamic events. Apoptosis has also been implicated in the remodelling of the extracelular matrix in the wall of cerebral aneurysms.