Increased decision latency in alcohol use disorder (AUD) has been generally explained in terms of psychomotor slowing. Recent results suggest that AUD patients' slowed decision-making might rather reflect alterations in the neural circuitry underlying the engagement of controlled processing by salient stimuli. We addressed this hypothesis by testing a relationship between decision latency at the Cambridge Gambling Task (CGT) and intrinsic brain activity in 22 individuals with AUD and 19 matched controls. CGT deliberation time was related to two complementary facets of resting-state fMRI activity, i.e. coherence and intensity, representing early biomarkers of functional changes in the intrinsic brain architecture. For both metrics, we assessed a multiple regression (to test a relationship with deliberation time in the whole sample), and an interaction analysis (to test a significantly different relationship with decision latency across groups). AUD patients' slowed deliberation time (p < 0.025) reflected distinct facets of altered intrinsic activity in the cingulate node of the anterior salience network previously associated with the "output" motor stage of response selection. Its heightened activity in AUD patients compared with controls, tracking choice latency (p < 0.025 corrected), might represent a compensation mechanism counterbalancing the concurrent decrease of its internal coherent activity (p < 0.025 corrected). These findings provide novel insights into the intrinsic neural mechanisms underlying increased decision latency in AUD, involving decreased temporal synchronicity in networks promoting executive control by behaviourally relevant stimuli. These results pave the way to further studies assessing more subtle facets of decision-making in AUD, and their possible changes with rehabilitative treatment.
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