RT Journal Article SR Electronic T1 Regional Cerebral Glucose Metabolic Abnormality in Prader–Willi Syndrome: A 18F-FDG PET Study Under Sedation JF Journal of Nuclear Medicine JO J Nucl Med FD Society of Nuclear Medicine SP 1088 OP 1092 VO 47 IS 7 A1 Kim, Sang Eun A1 Jin, Dong-Kyu A1 Cho, Sang Soo A1 Kim, Ji-Hae A1 Hong, Sungdo David A1 Paik, Kyung Hoon A1 Oh, Yoo Joung A1 Kim, An Hee A1 Kwon, Eun Kyung A1 Choe, Yon Ho YR 2006 UL http://jnm.snmjournals.org/content/47/7/1088.abstract AB Prader–Willi syndrome (PWS) is a genetic disorder caused by the nonexpression of paternal genes in the PWS region of chromosome 15q11-13 and is the most common cause of human syndromic obesity. Methods: We investigated regional brain metabolic impairment in children with PWS by 18F-FDG PET. Sixteen children with PWS (9 males, 7 females; mean age ± SD, 4.2 ± 1.1 y) and 7 healthy children (4 males, 3 females; mean age ± SD, 4.0 ± 1.7 y) underwent brain 18F-FDG PET in the resting state. The images of PWS children were compared using statistical parametric mapping analysis with those of healthy children in a voxelwise manner. Results: Group comparison showed that children with PWS had decreased glucose metabolism in the right superior temporal gyrus and left cerebellar vermis, regions that are associated with taste perception/food reward and cognitive and emotional function, respectively. Metabolism was increased in the right orbitofrontal, bilateral middle frontal, right inferior frontal, left superior frontal, and bilateral anterior cingulate gyri, right temporal pole, and left uncus, regions that are involved in cognitive functions related to eating or obsessive–compulsive behavior. Interestingly, no significant metabolic abnormality was found in the hypothalamus, the brain region believed to be most involved in energy intake and expenditure. Conclusion: This study describes the neural substrate underlying the abnormal eating behavior and psychobehavioral problems of PWS.