Elevated nucleus accumbens structural connectivity associated with proneness to hypomania: a reward hypersensitivity perspective.

Abstract

The Reward Hypersensitivity Model of bipolar disorder argues that hypersensitivity to reward-relevant cues characterizes risk for hypo/mania. This hypersensitivity leads to increased goal-directed motivation during reward-relevant life events that, in the extreme, is reflected in hypo/manic symptoms. In line with this perspective, individuals with bipolar disorder display elevated activation in a cortico-striatal reward circuit including the nucleus accumbens (NAcc) and medial orbitofrontal cortex (mOFC). To date, however, research on reward-related neural circuitry underlying bipolar symptoms focuses on syndromal bipolar disorder (bipolar I, bipolar II), and typically examines neural regions in isolation of each other. Accordingly, this study examines the relationship between subsyndromal hypo/mania proneness and structural connectivity between the NAcc and both the mOFC and amygdala in a medication-free sample. Fifty-four community participants completed diffusion-weighted imaging and a self-report measure of bipolar risk (hypo/mania proneness). As predicted, elevated structural connectivity between the NAcc and both the mOFC and amygdala were associated with elevated hypo/mania proneness. This relationship was specific to NAcc-centered reward connectivity, as there was no relationship between hypo/mania proneness and either whole-brain or cortico-amygdala connectivity. Results suggest that reward-relevant tractography from cortical (mOFC) and subcortical (amygdala) regions amplify NAcc-centered reward processing in bipolar risk.