Description: Attention-deficit/hyperactivity disorder (ADHD) poses debilitating impairments in the neurobehavioral systems governing reward learning and processing—key components involved in the control of motivated behaviors. Specifically, individuals with ADHD may rely on a system that favors cue-driven habits—rooted in the posterior putamen—over caudate and prefrontal cortex-driven goal-directed behaviors. An impaired motivational control system may also accompany corticostriatal dysfunction in ADHD (e.g., altered connectivity and striatal recruitment). We examined the neural and behavioral correlates of motivational control in ADHD. Twenty-five adults with ADHD and 25 matched neurotypical adults underwent functional MRI while performing a free-operant reward-learning task with snack outcomes. Participants were moderately trained on two stimulus–response–outcome associations. A devaluation procedure followed, whereby they were selectively satiated on one of the two snack outcomes to decrease its value. A subsequent extinction test determined outcome-sensitivity (i.e., whether responses towards devalued snack diminished). We found that although both ADHD and neurotypical groups maintained outcome-sensitivity, the ADHD group displayed a distinct neural signature following moderate stimulus–response training. The ADHD group exhibited enhanced posterior putamen activation as a function of training. This region also displayed diminished functional connectivity with the dorsal anterior cingulate cortex/medial prefrontal cortex, regions closely associated with top-down control. Our whole brain analysis yielded ADHD-specific heightened posterior putamen and opercular/insular cortex activity over the course of moderate training—regions associated with stimulus-sensitivity and maladaptively rigid behaviors, respectively. Neural comparisons also identified hyper-recruitment of the hippocampus in the ADHD group during moderate training. These results highlight corticostriatal discrepancies in the ADHD brain, possibly serving as an endophenotype of the disorder. Understanding potential deficits in motivated behaviors and their neural underpinnings is imperative for enhancing diagnostic accuracy, treatment efficacy, and quality of life in this vulnerable population.
Related article: http://doi.org/10.1016/j.cortex.2020.02.009
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