Cognitive dysfunction associates with white matter hyperintensities and subcortical atrophy on magnetic resonance imaging of the elderly diabetes mellitus Japanese elderly diabetes intervention trial (J-EDIT)

Background Type 2 diabetes is associated with cognitive dysfunction and increases the risk of dementia in the elderly. The aim of this study was to explore, by means of magnetic resonance (MR) imaging, possible relationships among clinical profiles of diabetes, cognitive function, white matter hyperintensities (WMHs) and subcortical brain atrophy. Methods Data were obtained from 95 nondemented type 2 diabetic participants aged 65 years or over, enrolled in an intervention trial for Japanese elderly diabetic patients. Cognitive function was measured with neuropsychiatric tests, including mini-mental state examination (MMSE), verbal memory, digit symbol substitution and Stroop tests. Hyperintensity was classified into periventricular, deep white matter, thalamic and basal ganglia. Four ventricle-to-brain ratios were used to measure subcortical atrophy. To identify clinical features of diabetes, indices of glycemic control, lipid metabolism, blood pressure and complications were examined. Canonical correlation analysis and regression analysis were used to assess correlation. Results Scores for digit symbol substitution and MMSE negatively correlated with WMHs in the parietal lobe and hyperintensities in the thalamus, respectively. Lower scores for memory and digit symbol substitution showed positive association with enlarged subcortical atrophy adjacent to lateral ventricles. There was no association between clinical pictures of diabetic patients with cognitive dysfunction and of those with morphological changes in the brain. Conclusions Impaired cognitive domains of the speed of mental processes and memory were associated with WMHs and subcortical atrophy. Degenerative changes in the cerebral small vessels may constitute predictive factors for the rate of cognitive dysfunction in elderly diabetic patients. (c) Copyright 2006 John Wiley & Sons, Ltd.