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Morphometric characterization of Binswanger's disease: comparison with Alzheimer's disease

Akihiko Shiino1, Ichiro Akiguchi, Toshiyuki Watanabe

  • 1Biomedical MR Science Center, Shiga University of Medical Science, Seta, Ohtsu, Shiga 520-2192, Japan. shiino@belle.shiga-med.ac.jpc.jp

European Journal of Radiology
|June 29, 2011
PubMed

Insights

Binswanger's disease (BD) causes anterior cortical atrophy, unlike Alzheimer's disease (AD). This pattern suggests BD results from hypertensive vascular disease impacting white matter and frontal-subcortical circuits.

Area of Science:

  • Neurology
  • Neuroimaging
  • Vascular Dementia Research

Background:

  • Hypertensive vascular disease can lead to dementia, with Binswanger's disease (BD) being a poorly understood subcortical vascular dementia.
  • Understanding BD's specific brain atrophy patterns is crucial for early intervention.

Purpose of the Study:

  • To investigate the topographic distribution of brain atrophy in Binswanger's disease (BD) using morphometric analysis.
  • To differentiate BD from Alzheimer's disease (AD) based on distinct patterns of gray matter atrophy.

Main Methods:

  • Magnetic resonance imaging (MRI) was used to compare gray matter atrophy in 20 BD patients, 50 AD patients, and 80 elderly controls.
  • Voxel-based morphometry with DARTEL (diffeomorphic anatomical registration through exponential Lie algebra) was employed to analyze brain atrophy patterns.

Main Results:

  • Alzheimer's disease (AD) showed predominant posterior cortical atrophy, while Binswanger's disease (BD) exhibited significant anterior cortical atrophy.
  • Atrophy in the amygdala and hippocampus was comparable between BD and AD.
  • BD patients displayed significantly greater atrophy in the thalamus, caudate nucleus, insula, anterior cingulate cortex, and frontal cortices compared to AD patients.

Conclusions:

  • Distinct topographic patterns of brain atrophy were identified in Binswanger's disease (BD).
  • The observed atrophy in BD aligns with the anatomical connections of frontal-subcortical circuits.
  • These findings support the hypothesis that BD pathology originates from hypertensive vascular disease and subsequent white matter damage.
Abstract

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