Disrupted Brain Network Efficiency and Decreased Functional Connectivity in Multi-sensory Modality Regions in Male Patients With Alcohol Use Disorder.

: Recent studies have reported altered efficiency in selective brain regions and functional networks in patients with alcohol use disorder (AUD). Inefficient processing can reflect or arise from the disorganization of information being conveyed from place to place. However, it remains unknown whether the efficiency and functional connectivity are altered in large-scale topological organization of patients with AUD. : Resting-state functional magnetic resonance imaging (rsfMRI) data were experimentally collected from 21 right-handed males with AUD and 21 right-handed, age-, gender- and education-matched healthy controls (HCs). Graph theory was used to investigate inter-group differences in the topological parameters (global and nodal) of networks and inter-regional functional connectivity. Correlations between group differences in network properties and clinical variables were also investigated in the AUD group. : The brain networks of the AUD group showed decreased global efficiency when compared with the HC group. Besides, increased nodal efficiency was found in the left orbitofrontal cortex (OFC), while reduced nodal efficiency was observed in the right OFC, right fusiform gyrus (FFG), right superior temporal gyrus, right inferior occipital gyrus (IOG), and left insula. Moreover, hypo-connectivity was detected between the right dorsolateral prefrontal cortex (DLPFC) and right superior occipital gyrus (SOG) in the AUD group when compared with the HC group. The nodal efficiency of the left OFC was associated with cognitive performance in the AUD group. : AUD patients exhibited alterations in brain network efficiency and functional connectivity, particularly in regions linked to multi-sensory modalities. These disrupted topological properties may help to obtain a more comprehensive understanding of large-scale brain network activity. Furthermore, these data provide a potential neural mechanism of impaired cognition in individuals with AUD.