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Am J Psychiatry 1997; 154:50-55
Copyright © 1997 by American Psychiatric Association
Effects of methylphenidate on regional brain glucose metabolism in humans: relationship to dopamine D2 receptors
ND Volkow, GJ Wang, JS Fowler, J Logan, B Angrist, R Hitzemann, J Lieberman and N Pappas
Medical and Chemistry Departments, Brookhaven National Laboratory, Upton, N.Y. 11973, USA. volkow@brain.med.bnl.gov
OBJECTIVE: The authors' goals were to determine whether baseline dopamine
activity contributes to response to methylphenidate and to assess the
pattern of metabolic responses associated with enhanced dopamine activity.
METHOD: They used positron emission tomography with
2-deoxy-2[18F]fluoro-D-glucose to evaluate the effects of two sequential
doses of methylphenidate on brain metabolism in 15 healthy subjects.
Dopamine D2 receptor availability was measured with [11C]raclopride to
evaluate its relation to methylphenidate-induced metabolic changes.
RESULTS: Methylphenidate increased brain metabolism in six subjects,
decreased it in two, and did not change it in seven; however, it
consistently increased cerebellar metabolism. Methylphenidate significantly
increased "relative" (region relative to the whole brain) metabolism in the
cerebellum and decreased it in the basal ganglia. Regional metabolic
changes in the cerebellum and the frontal and temporal cortices were
significantly correlated with D2 availability. Frontal and temporal
metabolism were increased in subjects with high D2 receptors and decreased
in subjects with low D2 receptors. CONCLUSIONS: Methylphenidate induced
variable changes in brain metabolism, but it consistently increased
cerebellar metabolism. It also induced a significant reduction in relative
metabolism in the basal ganglia. The significant association between
metabolic changes in the frontal and temporal cortices and in the
cerebellum and D2 receptors suggests that methylphenidate's metabolic
effects in these brain regions are due in part to dopamine changes and that
differences in D2 receptors may be one of the mechanisms accounting for the
variability in response to methylphenidate.
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