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 sizes. We therefore quantitatively examined vasculopathy in the medullary arteries of a defined caliber in BD brains with a quantitative technique. METHODS: A total of 20 brains were examined: 10 from patients with BD and 10 from age-matched nonneurological control patients. The alterations in the vascular cell components were examined with quantitative immunohistochemistry and immunoelectron microscopy for collagen and smooth muscle actin. RESULTS: The nonneurological control patients showed no white matter lesions. In contrast, the patients with BD invariably had marked white matter lesions, 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 BD patients than in the control patients, regardless of the vessel caliber (P<0.005). Although the ratio for smooth muscle actin in the BD brains was increased in arteries of <100 microm (P<0.0001), there was no corresponding increase in the arteries of >100 microm. However, in the ultrastructure of these vessels, the cell bodies immunolabeled for smooth muscle actin were hypertrophic and segregated from each other by proliferated fibrils. The basal lamina appeared multilayered, and the endothelial cells were swollen. Collagen type I and type IV immunoreactive fibrils also proliferated in the pericapillary space of the BD brains. CONCLUSIONS: The proliferation of collagen fibrils in the media and adventitia of the blood vessels in BD brains was not specific to small arteries and arterioles but also occurred in the pericapillary spaces. Pericapillary sclerosis, smooth muscle cell proliferation in the terminal arterioles, and their morphological transformation in the proximal arteries may alter the shear rates and thus cause profound microcirculatory disturbances in BD brains.
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 sizes. We therefore quantitatively examined vasculopathy in the medullary arteries of a defined caliber in BD brains with a quantitative technique. METHODS: A total of 20 brains were examined: 10 from patients with BD and 10 from age-matched nonneurological control patients. The alterations in the vascular cell components were examined with quantitative immunohistochemistry and immunoelectron microscopy for collagen and smooth muscle actin. RESULTS: The nonneurological control patients showed no white matter lesions. In contrast, the patients with BD invariably had marked white matter lesions, 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 BD patients than in the control patients, regardless of the vessel caliber (P<0.005). Although the ratio for smooth muscle actin in the BD brains was increased in arteries of <100 microm (P<0.0001), there was no corresponding increase in the arteries of >100 microm. However, in the ultrastructure of these vessels, the cell bodies immunolabeled for smooth muscle actin were hypertrophic and segregated from each other by proliferated fibrils. The basal lamina appeared multilayered, and the endothelial cells were swollen. Collagen type I and type IV immunoreactive fibrils also proliferated in the pericapillary space of the BD brains. CONCLUSIONS: The proliferation of collagen fibrils in the media and adventitia of the blood vessels in BD brains was not specific to small arteries and arterioles but also occurred in the pericapillary spaces. Pericapillary sclerosis, smooth muscle cell proliferation in the terminal arterioles, and their morphological transformation in the proximal arteries may alter the shear rates and thus cause profound microcirculatory disturbances in BD brains.
Authors: Aleksandra Pikula; Rainer H Böger; Alexa S Beiser; Renke Maas; Charles DeCarli; Edzard Schwedhelm; Jayandra J Himali; Friedrich Schulze; Rhoda Au; Margaret Kelly-Hayes; Carlos S Kase; Ramachandran S Vasan; Philip A Wolf; Sudha Seshadri Journal: Stroke Date: 2009-07-30 Impact factor: 7.914
Authors: Karin M E Forsberg; Yingshuang Zhang; Johanna Reiners; Martina Ander; Alexandra Niedermayer; Lubin Fang; Hermann Neugebauer; Jan Kassubek; Istvan Katona; Joachim Weis; Albert C Ludolph; Kelly Del Tredici; Heiko Braak; Deniz Yilmazer-Hanke Journal: Acta Neuropathol Commun Date: 2018-11-23 Impact factor: 7.801
Authors: Whitney C McFadden; Hadley Walsh; Felix Richter; Céline Soudant; Clare H Bryce; Patrick R Hof; Mary Fowkes; John F Crary; Andrew T McKenzie Journal: Acta Neuropathol Commun Date: 2019-09-05 Impact factor: 7.801