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Microvascular Disease in Type 1 Diabetes Alters Brain Activation

A Functional Magnetic Resonance Imaging Study

¹ Department of Medical Psychology, Vrije University (VU) Medical Center, Amsterdam, the Netherlands
² Department of Physics and Medical Technology, VU Medical Center, Amsterdam, the Netherlands
³ Department of Endocrinology/Diabetes Center, VU Medical Center, Amsterdam, the Netherlands
⁴ Department of Clinical Epidemiology and Biostatistics, VU Medical Center, Amsterdam, the Netherlands
⁵ Department of Radiology, VU Medical Center, Amsterdam, the Netherlands
⁶ Department of Neurology, VU Medical Center, Amsterdam, the Netherlands

Address correspondence and reprint requests to Alette M. Wessels, VU Medical Center, Department of Medical Psychology, Van der Boechorststraat 7, 1081 BT Amsterdam, Netherlands. E-mail: am.wessels{at}vumc.nl

Key Words: BOLD, blood oxygenation level dependent • CBF, cerebral blood flow • fMRI, functional magnetic resonance imaging • NART, National Adult Reading Test • WAIS, Wechsler Adult Intelligence Scale

Individuals with type 1 diabetes have mild performance deficits on a range of neuropsychological tests compared with nondiabetic control subjects. The mechanisms underlying this cognitive deterioration are still poorly understood, but chronic hyperglycemia is now emerging as a potential determinant, possibly through microvascular changes in the brain. In 24 type 1 diabetic patients, we tested at euglycemia and at acute hypoglycemia whether the presence of proliferative diabetic retinopathy, as a marker of microvascular disease, adversely affects the ability of the brain to respond to standardized hypoglycemia, using functional magnetic resonance imaging with a cognitive task. Patients with retinopathy, compared with patients without, showed less deactivation (hence, an increased response) in the anterior cingulate and the orbital frontal gyrus during hypoglycemia compared with euglycemia (P < 0.05). Task performance and reaction time were not significantly different for either group. We conclude that microvascular damage in the brain of patients with retinopathy caused this increased brain response to compensate for functional loss.

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