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Original Article |
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Neuropsychopharmacology (2002) 26 376-386.www.accnp.org/citations/Npp091301175
Neural Systems and Cue-Induced Cocaine Craving
Katherine R Bonson1 Ph.D, Steven J Grant1 Ph.D, Carlo S Contoreggi1 MD, Jonathan M Links2 Ph.D, Janet Metcalfe3 Ph.D, H Lloyd Weyl1 CNMT, Varughese Kurian MS1, Monique Ernst1 MD, Ph.D and Edythe D London1 Ph.D |
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1Brain Imaging Center, National Institute on Drug Abuse, Baltimore, MD 21224 USA
2School of Public Health, Johns Hopkins University, Baltimore, MD 21205 USA
3Department of Psychology, Columbia University, New York, NY 10027 USA
Correspondence: Dr Katherine R Bonson, Controlled Substance Staff, HFD-009, Food and Drug Administration, 5600 Fishers Lane, Rockville, MD 20857. Tel.: 301-827-210; E-mail: bonsonk@cder.fda.gov
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ABSTRACT
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We have extended our previous work investigating the neural correlates of cue-induced cocaine craving through the use of positron emission tomography with greater spatial resolution (<4.6 mm), an evocative script, and a pixel-by-pixel analysis. Craving and cerebral glucose metabolism were measured after presentation of cocaine-related or neutral cues to 11 cocaine abusers. Cocaine cues elicited a higher degree of craving than has been previously reported and resulted in left hemispheric activation of lateral amygdala, lateral orbitofrontal cortex, and rhinal cortex and right hemispheric activation of dorsolateral prefrontal cortex and cerebellum. The intensity of activation in these areas (except cerebellum), as well as left insula, was also correlated with craving. Deactivation occurred in left ventral pole and left medial prefrontal cortex. The results suggest that induction of drug craving involves a neural network that assigns incentive motivational value to environmental stimuli through the coactivation of brain regions that process information about memories and emotions.
Keywords: Craving, Cocaine, Cognitive, Brain imaging, Positron emission tomography (PET), Cerebral glucose metabolism |
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