BACKGROUND AND METHODS: The cause of childhood hyperactivity (attention deficit-hyperactivity disorder) is unknown. We investigated the hypothesis that cerebral glucose metabolism might differ between normal adults (controls) and adults with histories of hyperactivity in childhood who continued to have symptoms. Each patient was also the biologic parent of a hyperactive child. None of the adults had ever been treated with stimulant medication. To measure cerebral glucose metabolism, we administered 148 to 185 MBq (4 to 5 mCi) of [18F]fluoro-2-deoxy-D-glucose intravenously to 50 normal adults and 25 hyperactive adults while they performed an auditory-attention task. Images were obtained for 30 minutes with a Scanditronix positron-emission tomograph with a resolution of 5 to 6 mm. Whole-brain and regional rates of glucose metabolism were measured with computer assistance by two trained research assistants, working independently, who were blinded to the subjects' status (control or hyperactive). RESULTS: Global cerebral glucose metabolism was 8.1 percent lower in the adults with hyperactivity than in the normal controls (mean +/- SD, 9.05 +/- 1.20 mg per minute per 100 g vs. 9.85 +/- 1.68 mg per minute per 100 g; P = 0.034). In the adults with hyperactivity, glucose metabolism was significantly reduced, as compared with the values for the controls, in 30 of 60 specific regions of the brain (P less than 0.05). Among the regions of the brain with the greatest reductions in glucose metabolism were the premotor cortex and the superior prefrontal cortex. When the seven women with hyperactivity or the six patients with learning disabilities were omitted from the analysis, the results were similar. CONCLUSIONS: Glucose metabolism, both global and regional, was reduced in adults who had been hyperactive since childhood. The largest reductions were in the premotor cortex and the superior prefrontal cortex--areas earlier shown to be involved in the control of attention and motor activity.
BACKGROUND AND METHODS: The cause of childhood hyperactivity (attention deficit-hyperactivity disorder) is unknown. We investigated the hypothesis that cerebral glucose metabolism might differ between normal adults (controls) and adults with histories of hyperactivity in childhood who continued to have symptoms. Each patient was also the biologic parent of a hyperactive child. None of the adults had ever been treated with stimulant medication. To measure cerebral glucose metabolism, we administered 148 to 185 MBq (4 to 5 mCi) of [18F]fluoro-2-deoxy-D-glucose intravenously to 50 normal adults and 25 hyperactive adults while they performed an auditory-attention task. Images were obtained for 30 minutes with a Scanditronix positron-emission tomograph with a resolution of 5 to 6 mm. Whole-brain and regional rates of glucose metabolism were measured with computer assistance by two trained research assistants, working independently, who were blinded to the subjects' status (control or hyperactive). RESULTS:Global cerebral glucose metabolism was 8.1 percent lower in the adults with hyperactivity than in the normal controls (mean +/- SD, 9.05 +/- 1.20 mg per minute per 100 g vs. 9.85 +/- 1.68 mg per minute per 100 g; P = 0.034). In the adults with hyperactivity, glucose metabolism was significantly reduced, as compared with the values for the controls, in 30 of 60 specific regions of the brain (P less than 0.05). Among the regions of the brain with the greatest reductions in glucose metabolism were the premotor cortex and the superior prefrontal cortex. When the seven women with hyperactivity or the six patients with learning disabilities were omitted from the analysis, the results were similar. CONCLUSIONS:Glucose metabolism, both global and regional, was reduced in adults who had been hyperactive since childhood. The largest reductions were in the premotor cortex and the superior prefrontal cortex--areas earlier shown to be involved in the control of attention and motor activity.
Authors: Michael Michaelides; Javier Pascau; Juan-Domingo Gispert; Foteini Delis; David K Grandy; Gene-Jack Wang; Manuel Desco; Marcelo Rubinstein; Nora D Volkow; Panayotis K Thanos Journal: Eur J Neurosci Date: 2010-07-16 Impact factor: 3.386
Authors: Marc Schneider; Wolfgang Retz; Andrew Coogan; Johannes Thome; Michael Rösler Journal: Eur Arch Psychiatry Clin Neurosci Date: 2006-09 Impact factor: 5.270
Authors: Nikos Makris; Larry J Seidman; Eve M Valera; Joseph Biederman; Michael C Monuteaux; David N Kennedy; Verne S Caviness; George Bush; Katherine Crum; Ariel B Brown; Stephen V Faraone Journal: J Atten Disord Date: 2010-01 Impact factor: 3.256
Authors: T Sigi Hale; Susan L Smalley; Jeff Dang; Grant Hanada; James Macion; James T McCracken; James J McGough; Sandra K Loo Journal: J Psychiatr Res Date: 2009-12-16 Impact factor: 4.791
Authors: C J Vaidya; G Austin; G Kirkorian; H W Ridlehuber; J E Desmond; G H Glover; J D Gabrieli Journal: Proc Natl Acad Sci U S A Date: 1998-11-24 Impact factor: 11.205