Affiliations: Department of Neurology, Tohoku University School of Medicine, Sendai, Japan | Cyclotron and Radioisotope Center, Tohuku University, Sendai, Japan
Note: [] Correspondence to: H. Tanji, Department of Neurology, Tohoku University School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-77, Japan
Abstract: We studied the chronic effect of thyrotropin releasing hormone (TRH) in a patient with spinocerebellar degeneration by measuring cerebral metabolic rate for glucose (CMRG1c) using 2-[18F]fluoro-2-deoxy-D-glucose (18FDG) and positron emission tomography (PET). A 56-year-old female, who had suffered from progressive ataxia for 2 years, was treated by intravenous administration of 2 mg TRH for 3 weeks, and CMRG1c of the brain was measured before and after treatment. CMRG1c was markedly decreased in the cerebellum and there was no significant difference before and after the treatment, i.e. mean CMRG1c values were 4.92 and 4.90 mg/100 g/min, and the ratios of the cerebellum versus the frontal cortex were 0.50 and 0.51, respectively. The degree of disequilibrium of her body examined with stabilography became better by the 19th day and further improved by the 26th day after the start of TRH treatment. Based on the present study we conclude that long-term administration of TRH did not improve CMRG1c in the cerebellum, but evidently improved the sway of gravity center by stabilography. We speculate that the chronic effect of TRH was not necessarily due to an improvement of cerebellar function, because TRH receptors are widely distributed throughout the central nervous system.
