Dissociable neural processes during risky decision-making in individuals with Internet-gaming disorder.
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ABSTRACT: Risk-taking is purported to be central to addictive behaviors. However, for Internet gaming disorder (IGD), a condition conceptualized as a behavioral addiction, the neural processes underlying impaired decision-making (risk evaluation and outcome processing) related to gains and losses have not been systematically investigated. Forty-one males with IGD and 27 healthy comparison (HC) male participants were recruited, and the cups task was used to identify neural processes associated with gain- and loss-related risk- and outcome-processing in IGD. During risk evaluation, the IGD group, compared to the HC participants, showed weaker modulation for experienced risk within the bilateral dorsolateral prefrontal cortex (DLPFC) (t = - 4.07; t = - 3.94; PFWE < 0.05) and inferior parietal lobule (IPL) (t = - 4.08; t = - 4.08; PFWE < 0.05) for potential losses. The modulation of the left DLPFC and bilateral IPL activation were negatively related to addiction severity within the IGD group (r = - 0.55; r = - 0.61; r = - 0.51; PFWE < 0.05). During outcome processing, the IGD group presented greater responses for the experienced reward within the ventral striatum, ventromedial prefrontal cortex, and orbitofrontal cortex (OFC) (t = 5.04, PFWE < 0.05) for potential gains, as compared to HC participants. Within the IGD group, the increased reward-related activity in the right OFC was positively associated with severity of IGD (r = 0.51, PFWE < 0.05). These results provide a neurobiological foundation for decision-making deficits in individuals with IGD and suggest an imbalance between hypersensitivity for reward and weaker risk experience and self-control for loss. The findings suggest a biological mechanism for why individuals with IGD may persist in game-seeking behavior despite negative consequences, and treatment development strategies may focus on targeting these neural pathways in this population.
SUBMITTER: Liu L
PROVIDER: S-EPMC5385591 | biostudies-literature | 2017
REPOSITORIES: biostudies-literature
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