CEREBRAL GLUCOSE-METABOLISM IN TYPE-1 DIABETIC-PATIENTS

To evaluate whether cerebral glucose metabolism is impaired in diabete s the [F-18]-2-deoxy-2-fluoro-D-glucose method and positron emission t omography were used to determine the regional cerebral metabolic rate of glucose in 12 healthy subjects, 8 newly diagnosed Type 1 diabetic p atients, 6 Type 1 diabetic subjects without peripheral neuropathy, and 7 Type 1 diabetic patients with symptomatic peripheral neuropathy, al l of whom were men. In addition, multimodal evoked potentials were ass essed. Cerebral glucose consumption was significantly reduced in the g roup with neuropathy as compared with the newly diagnosed diabetic pat ients and the healthy subjects (26.9 +/- 1.0 vs 33.9 +/- 1.9 and 32.5 +/- 1.1 mumol 100 g-1 min-1; p < 0.05), while in the patients without neuropathy it was 30.2 +/- 2.5 mumol 100 g-1 min-1 (NS vs the remainin g groups). There were no significant differences between the groups re garding brainstem auditory and visual evoked potentials. No relationsh ip was noted between cerebral glucose metabolism and P300 latency of e vent-related potentials as an index of cognitive function, but there w as an inverse correlation with age (r = -0.42; p < 0.05) and duration of diabetes (r = -0.67; p < 0.05). These results suggest that cerebral glucose metabolism is normal at the time of diagnosis of Type 1 diabe tes, but may become altered with both increasing duration of diabetes and age in the absence of central conduction deficits or cognitive dys function. Diabetic neuropathy may constitute a possible additional cor relate of reduced cerebral glucose consumption.