Neural correlates of reward magnitude and delay during a probabilistic delay discounting task in alcohol use disorder
Alcohol-use disorder (AUD) is associated with the propensity to choose smaller sooner options on the delay discounting task. It is unclear, however, how inherent risk underlies delay discounting behavior. As impulsive choice is a hallmark feature in AUD, it is important to understand the neural response to reward and delay while accounting for risk in impulsive decision-making.
This study examined activation associated with delay and reward magnitude, while controlling for risk in a probabilistic delay discounting task in AUD and examined if differences in activation were associated with treatment outcomes.
Thirty-nine recently abstinent alcohol-dependent volunteers and 46 controls completed a probabilistic delay discounting task paired with functional magnetic resonance imaging. Alcohol use was collected using a self-report journal for 3 months following baseline scan.
During delay stimulus presentations, Controls exhibited greater activation compared to the Alcohol group notably in the anterior insula, middle/dorsal anterior cingulate cortex (ACC), dorsolateral prefrontal cortex (PFC), and inferior parietal lobule. For magnitude, the Alcohol group exhibited greater activation than Controls primarily in medial PFC, rostral ACC, left posterior parietal cortex, and right precuneus. Within the Alcohol group, alcohol craving severity negatively correlated with right lateral PFC activation during reward magnitude in individuals who completed the 3-month study without relapse, while non-completers showed the opposite relationship.
The results of this study extend previous findings that alcohol use disorder is associated with differences in activation during an immediate or delayed choice by delineating activation associated with the parameters of impulsive choice.
KeywordsAlcohol Impulsivity Delay discounting Probability discounting Craving Relapse
We thank the staff of the Veterans Affairs Portland Health Care System Substance Abuse Treatment Program, CODA Treatment Recovery, Hooper Detox Stabilization Center, Central City Concern, and Volunteers of America Residential Treatment Centers, Portland, OR, for their help and recruitment efforts and also Ethan Sawyer for his help with the manuscript.
MK conceptualized this approach, made significant contributions to the analysis and writing of this manuscript, and mentored LD in the interpretation of results and writing of this manuscript. LD, HM, BT, DS, and DL collected these data. DS, DL, WH, and SM each contributed significantly to designing the PDD task. BN was a Co-I on the grant and advised on imaging and design. LD performed initial data analyses with the neuroimages. WH was the PI on the project, supervised the collection and analysis of data, and contributed to the writing of the manuscript.
This work was supported in part by the National Institute on Alcohol Abuse and Alcoholism R21AA020039 (WFH); Department of Veterans Affairs Clinical Sciences Research and Development Merit Review Program, I01 CX001558-01A1 (WFH); Department of Justice 2010-DD-BX-0517 (WFH); National Institute on Drug Abuse P50DA018165 (WFH); and Oregon Clinical and Translational Research Institute, 1 UL1 RR024140 01 from the National Center for Research Resources, a component of the National Institutes of Health and National Institute of Health Roadmap for Medical Research. Dr. Kohno was supported by National Institute on Drug Abuse T32 DA007262, National Institute on Alcohol Abuse and Alcoholism T32 AA007468, Department of Veterans Affairs Clinical Sciences Research and Development Career Development Award CX17008-CDA2, Oregon Health & Science University Collins Medical Trust Award APSYC0249, and Medical Research Foundation of Oregon APSYC0250.
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Conflict of interest
The authors declare that they have no conflict of interest.
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