Imaging brain response to reward in addictive disorders

• Published in: Annals of the New York Academy of Sciences Vol. 1216; no. 1; pp. 50 - 61
• Main Authors: Hommer, Daniel W., Bjork, James M., Gilman, Jodi M.
• Format: Journal Article
• Language: English
• Published: Malden, USA Blackwell Publishing Inc 01.01.2011; Wiley Subscription Services, Inc
• Subjects: Addiction; Addictions; alcohol; Behavior, Addictive - diagnostic imaging; Behavior, Addictive - etiology; Behavior, Addictive - physiopathology; Brain - diagnostic imaging; Brain - physiopathology; Brain mapping; Dopamine; Dopamine receptors; Functional magnetic resonance imaging; Humans; Hypotheses; imaging; impulsive behavior; Impulsivity; Magnetic Resonance Imaging; Models, Neurological; Motivation; Neuroimaging; NMR; Nuclear magnetic resonance; Positron emission tomography; Receptor density; Reinforcement; Reward; Substance-Related Disorders - etiology; Substance-Related Disorders - psychology
• ISSN: 0077-8923; 1749-6632; 1749-6632
• DOI: 10.1111/j.1749-6632.2010.05898.x

We compare the evidence from human neuroimaging studies for and against two of the major hypotheses of how alterations in the brain's reward system underlie addiction. One of these, the impulsivity hypothesis, proposes that addiction is characterized by excessive sensitivity to reward combined with a failure of inhibition. The other, the reward‐deficiency hypothesis, proposes that addicted individuals have a reduced response to nondrug rewards that leads them to seek drugs in preference to more socially acceptable goals. Positron emission tomographic (PET) studies of dopamine receptor density and dopamine release strongly support the reward‐deficiency hypothesis, while the more recent and numerous functional magnetic resonance imaging (fMRI) studies of goal‐directed behavior provide both support and contradiction for each of the hypotheses. Differences in the time scale on which PET and fMRI make measurements probably account for differences in results, at least in part. It is likely that aspects of brain function described by both the impulsivity and reward‐deficiency hypotheses contribute to the pathophysiology of addiction.