Purpose: Head CT and MRI show characteristic changes in the syndrome of acute bilateral basal ganglia lesions in patients with diabetic uremia. However, they do not provide further insight into the underlying pathophysiology. To further clarify the biologic mechanism of the syndrome, F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) was used in 2 patients.
Methods: PET studies were performed in 2 diabetic uremic patients with acute movement disorders. The cerebral glucose metabolic rates in these 2 patients were compared with 11 normal age-matched controls. The images were further analyzed with statistical parametric mapping to identify regions of significant metabolic abnormality.
Results: The cases showed markedly reduced glucose metabolism in the bilateral basal ganglia, especially in the bilateral putamens, where the glucose uptake was nearly absent.
Conclusions: FDG-PET correlates better with the clinical conditions and provides more pathophysiological information than head CT or MRI scans in bilateral basal ganglia lesions in patients with diabetic uremia. We propose that acute exacerbation of a long-term glucose utilization failure in the basal ganglia cells produced these lesions.