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Diabetes 55:1106-1113, 2006
DOI: 10.2337/diabetes.55.04.06.db05-1323
© 2006 by the American Diabetes Association
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Brain Magnetic Resonance Imaging Correlates of Impaired Cognition in Patients With Type 2 Diabetes

Sanne M. Manschot1, Augustina M.A. Brands2, Jeroen van der Grond3, Roy P.C. Kessels2, Ale Algra1,4, L. Jaap Kappelle1, Geert Jan Biessels1 on behalf of the Utrecht Diabetic Encephalopathy Study Group*

1 Department of Neurology, Rudolf Magnus Institute of Neuroscience, University Medical Center, Utrecht, the Netherlands
2 Helmholtz Research Institute, University Medical Center, Utrecht, the Netherlands
3 Department of Radiology, University Medical Center, Utrecht, the Netherlands
4 Julius Center for Health Sciences and Primary Care, University Medical Center, Utrecht, the Netherlands

Address correspondence and reprint requests to Sanne M. Manschot, Department of Neurology, G03.228, University Medical Center, P.O. Box 85500, 3508 GA Utrecht, Netherlands. E-mail address: s.m.manschot{at}umcutrecht.nl

Abbreviations: BCR, bicaudate ratio; BFR, bifrontal ratio; DWML, deep WML; FFR, frontal interhemispheric fissure ratio; FLAIR, fluid-attenuating inverse recovery; MRI, magnetic resonance imaging; PWML, periventricular WML; SFR, Sylvian fissure ratio; WML, white matter lesion

The structural correlates of impaired cognition in type 2 diabetes are unclear. The present study compared cognition and brain magnetic resonance imaging (MRI) between type 2 diabetic patients and nondiabetic control subjects and assessed the relationship between cognition and MRI findings and blood pressure and metabolic control. The study included 113 patients and 51 control subjects. Brain MRI scans were rated for white matter lesions (WMLs), cortical and subcortical atrophy, and infarcts. Neuropsychological test scores were divided into five cognitive domains and expressed as standardized Z values. Type 2 diabetes was associated with deep WMLs (P = 0.02), cortical (P < 0.001) and subcortical (P < 0.05) atrophy, (silent) infarcts (P = 0.06), and impaired cognitive performance (attention and executive function, information-processing speed, and memory, all P < 0.05). Adjustment for hypertension did not affect the results. Within the type 2 diabetic group, cognitive function was inversely related with WMLs, atrophy, and the presence of infarcts (adjusted for age, sex, and estimated IQ), and there was a modest association with HbA1c and diabetes duration. This association was strongest for age, even more so than in control subjects. We conclude that cognitive impairments in patients with type 2 diabetes are not only associated with subcortical ischemic changes in the brain, but also with increased brain atrophy.


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