Pathologic processes leading to cerebral hemorrhage in amyloid angiopathy

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This report concerns a study undertaken to eluidate the pathogenesis of arterial rupture related to amyloid deposition. For this purpose, histochemical and immunohistochemical analyses were carried out on brain tissue specimens of a case of cerebral amyloid angiopathy (CAA) with multiple cortical hemorrhages. A small amount of amyloid β‐protein was found in the tunica media vasorum in which the smooth muscle cells were well preserved. with increases in amyloiod deposition, the entire arteriolar wall became concenmtrically thick, with amyloid largely occupying the tunica media; the number of smooth muscle cells was decreased and these cells were located in the intimal side of the vessel wall. Under these conditions, the elastic fibers and endothhelial cells were relatively well preserved. In the advanced stage of amyloid deposition, the arterioles became devoid of smooth muscle cells and underwent wither fibrous luminal occlusionor aneurysmal dilatation with fibrinoid necrosis and loss of elastic fibers; the latterwould eventually rupture causing the hemorrhage. These findings suggest that amyloid β‐protein‐related loss of arteriolar smooth muscle cells could be the initial event, with the subsequent damage of the vascular wall leading to cerebral hemorrhages in CAA patients.