Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Case Reports
. 2004 Mar;24(1):21-9.
doi: 10.1111/j.1440-1789.2003.00534.x.

Pathology of the cerebral artery in Binswanger's disease in the aged: observation by serial sections and morphometry of the cerebral arteries

Affiliations
Case Reports

Pathology of the cerebral artery in Binswanger's disease in the aged: observation by serial sections and morphometry of the cerebral arteries

Riki Okeda et al. Neuropathology. 2004 Mar.

Abstract

Binswanger's disease (BD) is not rare in the aged. The aim of the present study was to compare the etiopathogenesis of BD of the aged (aged-BD) with that of classic-BD, with the aid of morphometry of the arterial medial thickness and reconstruction of the cerebral medullary arteries using serial sections from five autopsy cases. The age range of the aged-BD cases was 73-89 years. The mean heart weight of these cases was 296 g, in contrast to 391 g of the five age-matched cases of hypertension without diffuse myelin loss and atrophy of the cerebral white matter (HT). Although significant medial hypertrophy of the subarachnoid and medullary arteries was not found in all aged-BD cases, differently from classic-BD, all five cases of aged-BD commonly presented significantly widespread loss of the medial smooth muscle cells (SMC) of the medullary arteries as compared with HT, similar to the case in classic-BD. The etiopathogenesis of aged-BD is common to that of classic-BD; stiffening caused by hypertensive changes of the medullary artery, especially SMC loss, is responsible for the diffuse myelin loss and atrophy of the cerebral white matter of BD, rather than grade of hypertension itself or hypertensive medial hypertrophy. As the mechanism of such an especially severe involvement of the cerebral medullary artery in BD, some genetic abnormality in the functional response or vulnerability to hypertension of the artery should be considered.

PubMed Disclaimer

Similar articles

Cited by