Abstract
Impairments in emotional regulation and mood symptoms are interrelated and associated with alcohol use disorder (AUD) risk, but the underlying aberrant neural circuitry involved is poorly understood. In the present study, we examined alterations in effective (directional) connectivity (EC) during emotional face processing in individuals with and without AUD. We utilized functional MRI data from the Human Connectome Project obtained during an emotional face processing task in 70 participants with AUD and 70 controls (CON). Focusing on ventromedial prefrontal cortex (VMPFC), bilateral ventrolateral prefrontal cortex (VLPFC), amygdala (AMY), and fusiform gyrus (FG), and right (R) hypothalamus (HTN) nodes, we performed dynamic causal modeling analysis to test group-level differences in EC. Linear regressions characterized EC relationships with measures of cumulative alcohol exposure and depression and anxiety. Compared to CON participants, AUD participants had lower ECs from VMPFC → bilateral VLPFC, left (L)-VLPFC → L-VLPFC and VMPFC, R-VLPFC → L-FG, R-FG → HTN, and R-AMY → L-VLPFC; and greater ECs from VMPFC → VMPFC, L-VLPFC → R-VLPFC and bilateral FG, L-FG → R-AMY and HTN, R-AMY → VMPFC and L-FG, and L-AMY → HTN connectivities. In regression analyses, these cortical-to-cortical and cortical-to-subcortical ECs were associated with cumulative alcohol exposure. EC from R-VLPFC to L-FG was negatively associated with depression. Individuals with AUD have disrupted EC in cortical-to-cortical and cortical-to-subcortical circuits during emotional face processing in brain regions purported to govern emotion control, which may explain linkages between cumulative alcohol exposure and depression.