Vascular cell components of the medullary arteries in Binswanger's diseasebrains - A morphometric and immunoelectron microscopic study

Background and Purpose-It has been hypothesized that fibrohyalinosis of the medullary arteries may cause white matter lesions in Binswanger's disease (BD). However, previous reports have been inconsistent on the pathological alterations of the cellular components, which may vary in terms of vessel s izes. We therefore quantitatively examined vasculopathy in the medullary ar teries of a defined caliber in ED brains with a quantitative technique. Methods-A total of 20 brains were examined: 10 from patients with ED and 10 from age-matched nonneurological control patients. The alterations in the vascular cell components were examined with quantitative immunohistochemist ry and immunoelectron microscopy for collagen and smooth muscle actin. Results-The nonneurological control patients showed no white matter lesions . In contrast, the patients with ED invariably had marked white matter lesi ons, as well as fibrohyalinosis of the medullary arteries. The ratio of the area immunolabeled for collagen type I and type IV to the cross-sectional area was 2-fold higher in the ED patients than in the control patients, reg ardless of the vessel caliber (P<0.005). Although the ratio for smooth musc le actin in the ED brains was increased in arteries of <100 mu m (P<0.0001) , there was no corresponding increase in the arteries of >100 mu m However, in the ultrastructure of these vessels, the cell bodies immunolabeled for smooth muscle actin were hypertrophic and segregated from each other by pro liferated fibrils. The basal lamina appeared multilayered, and the endothel ial cells were swollen. Collagen type I and type IV immunoreactive fibrils also proliferated in the pericapillary space of the ED brains. Conclusions-The proliferation of collagen fibrils in the media and adventit ia of the blood vessels in ED brains was not specific to small arteries and arterioles but also occurred in the pericapillary spaces. Pericapillary sc lerosis, smooth muscle cell proliferation in the terminal arterioles, and t heir morphological transformation in the proximal arteries may alter the sh ear rates and thus cause profound microcirculatory disturbances in ED brain s.