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Amyloid angiopathies comprise a group of systemic vessel diseases that may also be organ specific, e.g.,to the cerebrum. The vessel walls possess extracellular deposition of amyloid, which can be demonstrated histologically by its binding affinity to Congo Red(polarized light: green birefringence), to thioflavine
S or T, and to periodic acid Schiff (PAS). Deposition of amorphous material leads to thickening of the vessel walls, which become increasingly more rigid and fragile. The vessels are also conspicuous in H&E stain as being abnormally round and thick-walled,especially in the cortex.The most common type of amyloid angiopathy is recognizable by deposition of β-amyloid peptide(βA4) affecting medium-sized and small arteries and arterioles (see Fig. 31.4d). Topographically, the sites most often affected are the cerebral cortex and meninges of the parietal and occipital lobes. Bleeding due to vessel rupture occurs in the frontal or
frontoparietal regions. Amyloid angiopathy is the cause of 5−12% of all primary intracerebral hemorrhages
that are not mechanically induced (Gilbert
and Vinters 1983).