Cognitive Control of Drug Craving Inhibits Brain Reward Regions in Cocaine Abusers
By Nora D. Volkow, J. S. Fowler, Gene-Jack Wang, Frank Telang, Jean Logan, Millard Jayne, Yeming Ma, K. Pradhan, Christopher T. Wong, James M. Swanson. NeuroImage, 2009
297 citations recorded by the source corpus.
Loss of control over drug taking is considered a hallmark of addiction and is critical in relapse. Dysfunction of frontal brain regions involved with inhibitory control may underlie this behavior. We evaluated whether addicted subjects when instructed to purposefully control their craving responses to drug-conditioned stimuli can inhibit limbic brain regions implicated in drug craving. We used PET and 2-deoxy-2[18F]fluoro-d-glucose to measure brain glucose metabolism (marker of brain function) in 24 cocaine abusers who watched a cocaine-cue video and compared brain activation with and without instructions to cognitively inhibit craving. A third scan was obtained at baseline (without video). Statistical parametric mapping was used for analysis and corroborated with regions of interest. The cocaine-cue video increased craving during the no-inhibition condition (pre 3+/-3, post 6+/-3; p<0.001) but not when subjects were instructed to inhibit craving (pre 3+/-2, post 3+/-3). Comparisons with baseline showed visual activation for both cocaine-cue conditions and limbic inhibition (accumbens, orbitofrontal, insula, cingulate) when subjects purposefully inhibited craving (p<0.001). Comparison between cocaine-cue conditions showed lower metabolism with cognitive inhibition in right orbitofrontal cortex and right accumbens (p<0.005), which was associated with right inferior frontal activation (r=-0.62, p<0.005). Decreases in metabolism in brain regions that process the predictive (nucleus accumbens) and motivational value (orbitofrontal cortex) of drug-conditioned stimuli were elicited by instruction to inhibit cue-induced craving. This suggests that cocaine abusers may retain some ability to inhibit craving and that strengthening fronto-accumbal regulation may be therapeutically beneficial in addiction.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience
View Paper: https://www.semanticscholar.org/paper/efd8b17fd0edc25055fda7b7f649a930ba2f780a
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Citations in the corpus
- Food cue reactivity and craving predict eating and weight gain: a meta-analytic review (2015, unknown): “Cognitive strategies include the regulation of craving through cognitive reappraisal, which reduces neural reactivity and self-reported craving for highcalorie foods (116,151,152,195), cigarettes (116,151), alcohol (196), cocaine (197) and methamphetamine (198).”
- The Brain on Drugs: From Reward to Addiction. (2015, background): “, 2004), was associated with the deactivation of the NAc and ventral PFC upon successful control of cocaine craving (Volkow et al., 2010).”
- Prefrontal–striatal pathway underlies cognitive regulation of craving (2010, background): “stimuli (34, 35) that did not observe significant reductions in craving.”
- Pro v Con Reviews: Is Food Addictive? (2012, background): “In addition, a study that prompted cocaine-addicted subjects to purposefully inhibit craving when exposed to drug cues showed that those subjects who were successful at inhibiting craving displayed decreased metabolism in medial OFC (which processes the motivational value of a reinforcer) and NAc (w”
- Addiction: Beyond dopamine reward circuitry (2011, background): “Moreover, in a subsequent study in which we prompted cocaine-addicted subjects to inhibit craving purposefully when exposed to drug cues, we showed that subjects who were successful in inhibiting craving decreased metabolism in medial OFC (processes motivational value of reinforcer) and NAc (predict”