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Cocaine-Induced Redoppuction of Glucose Utilization in Human BrainA Study Using Positron Emission Tomography and [Fluorine 18]-Fluorodeoxyglucose
Edythe D. London, PhD;
Nicola G. Cascella, MD;
Dean F. Wong, MD;
Robert L. Phillips, PhD;
Robert F. Dannals, PhD;
Jonathan M. Links, PhD;
Ronald Herning, PhD;
Roger Grayson, MD;
Jerome H. Jaffe, MD;
Henry N. Wagner, Jr, MD
Arch Gen Psychiatry. 1990;47(6):567-574.
Abstract
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• We examined the effects of cocaine hydrochloride (40 mg intravenously) on regional cerebral metabolic rates for glucose and on subjective self-reports of eight polydrug abusers in a double-blind, placebo-controlled, crossover study. The regional cerebral metabolic rate for glucose was measured by the [fluorine 18]-fluorodeoxyglucose method, using positron emission tomography. With eyes covered, subjects listened to a tape that presented white noise, "beep" prompts, and questions about subjective effects of cocaine or saline. Cocaine produced euphoria and reduced glucose utilization globally (mean reduction, 14%). Twenty-six of 29 brain regions (all neocortical areas, basal ganglia, portions of the hippocampal formation, thalamus, and midbrain) showed significant decrements (5% to 26%) in the regional cerebral metabolic rate for glucose. No significant effects of cocaine were observed in the pons, the cerebellar cortex, or the vermis. Right-greater-than-left hemispheric asymmetry of regional cerebral metabolic rates for glucose occurred in the lateral thalamus. The findings demonstrate that reduced cerebral metabolism is associated with cocaine-induced euphoria.
Author Affiliations
From the Addiction Research Center, National Institute on Drug Abuse (Drs London, Cascella, Phillips, Herning, and Jaffe); and Division of Nuclear Medicine, Department of Radiology (Drs Wong, Dannals, Links, and Wagner), and Department of Anesthesiology (Dr Grayson), The Johns Hopkins Medical Institutions, Baltimore, Md.
Footnotes
Accepted for publication October 18, 1989.
Presented in part as an abstract at the following annual meetings: Society for Neuroscience, New Orleans, La, November 19, 1987, and Toronto, Canada, November 17, 1988; American Psychiatric Association, Chicago, Ill, May 11, 1987, and San Francisco, Calif, May 10, 1989; Society of Nuclear Medicine, San Francisco, June 17, 1988; and American College of Neuropsychopharmacology, San Juan, Puerto Rico, December 14, 1988.
Reprint requests to National Institute on Drug Abuse Addiction Research Center, PO Box 5180, Baltimore, MD 21224 (Dr London).
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