This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lin, J.-X. Articles by Budka, H. Search for Related Content PubMed PubMed Citation Articles by Lin, J.-X. Articles by Budka, H. Pubmed/NCBI databases Substance via MeSH Related Collections Pathophysiology Smooth muscle proliferation and differentiation Cerebral Lacunes Pathology of Stroke Other Vascular biology

(Stroke. 2000;31:1838.)
© 2000 American Heart Association, Inc.

Original Contributions

Vascular Cell Components of the Medullary Arteries in Binswanger’s Disease Brains

A Morphometric and Immunoelectron Microscopic Study

Jin-Xi Lin, MD; Hidekazu Tomimoto, MD; Ichiro Akiguchi, MD; Akinori Matsuo, MD; Hideaki Wakita, MD; Hiroshi Shibasaki, MD Herbert Budka, MD

From the Department of Neurology (J.-X.L., H.T., I.A., A.M., H.W., H.S.), Faculty of Medicine, Kyoto University, Kyoto, Japan; and Institute of Neurology (H.B.), University of Vienna, Wien, Austria.

Correspondence to Jin-Xi Lin, MD, Department of Neurology, Faculty of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8507, Japan.

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 µm (P<0.0001), there was no corresponding increase in the arteries of >100 µm. 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.

Key Words: Binswanger’s disease • dementia • leukoencephalopathy • white matter

This article has been cited by other articles:

				A. Pikula, R. H. Boger, A. S. Beiser, R. Maas, C. DeCarli, E. Schwedhelm, J. J. Himali, F. Schulze, R. Au, M. Kelly-Hayes, et al. Association of Plasma ADMA Levels With MRI Markers of Vascular Brain Injury: Framingham Offspring Study Stroke, September 1, 2009; 40(9): 2959 - 2964. [Abstract] [Full Text] [PDF]

				X.-K. Tong, N. Nicolakakis, A. Kocharyan, and E. Hamel Vascular Remodeling versus Amyloid {beta}-Induced Oxidative Stress in the Cerebrovascular Dysfunctions Associated with Alzheimer's Disease J. Neurosci., November 30, 2005; 25(48): 11165 - 11174. [Abstract] [Full Text] [PDF]

				A. Hassan, K. Gormley, M. O'Sullivan, J. Knight, P. Sham, P. Vallance, J. Bamford, and H. Markus Endothelial Nitric Oxide Gene Haplotypes and Risk of Cerebral Small-Vessel Disease Stroke, March 1, 2004; 35(3): 654 - 659. [Abstract] [Full Text] [PDF]

				A. Hassan, B. J. Hunt, M. O'Sullivan, R. Bell, R. D'Souza, S. Jeffery, J. M. Bamford, and H. S. Markus Homocysteine is a risk factor for cerebral small vessel disease, acting via endothelial dysfunction Brain, January 1, 2004; 127(1): 212 - 219. [Abstract] [Full Text] [PDF]

				A. Hassan, B. J. Hunt, M. O'Sullivan, K. Parmar, J. M. Bamford, D. Briley, M. M. Brown, D. J. Thomas, and H. S. Markus Markers of endothelial dysfunction in lacunar infarction and ischaemic leukoaraiosis Brain, February 1, 2003; 126(2): 424 - 432. [Abstract] [Full Text] [PDF]

				H. Tomimoto, I. Akiguchi, R. Ohtani, H. Yagi, M. Kanda, H. Shibasaki, and Y. Yamamoto The Coagulation-Fibrinolysis System in Patients With Leukoaraiosis and Binswanger Disease Arch Neurol, October 1, 2001; 58(10): 1620 - 1625. [Abstract] [Full Text] [PDF]