across DMN connections may be suggestive of neural hyperexcitability and disinhibition in AUD individuals [108,109,110,111,112], possibly modulated by GABAergic and glutamatergic mechanisms underlying neural excitability reflected in EEG and acute and chronic effects of alcohol in the brain [113,114,115,116,117]. While neural disinhibition in other electrophysiological measures (e.g., low P3 amplitude and suppressed delta and theta oscillations underlying P3 during cognitive processing, and increased resting state beta power) have been reported [108,118,119,120], resting state EEG source FC may serve as an important and novel index of neural disinhibition in AUD and other externalizing disorders, as it is a direct measure of neural communication and brain (dys)function [57]. Since there is only a single eLORETA study on AUD [59], and it is worth comparing our findings to it. Although both studies have examined resting state EEG source connectivity in AUD using eLORETA and showed similar finding of increased FC network multiple brain regions, Huang et al. [59] derived seed regions from fMRI activations during a cue-reactivity task and reported hyperconnectivity only in theta band across reward and executive network regions. Similar findings have also been reported in other addictive behaviors. For example, hyperconnectivity across long-range connections frontal-parietal regions in theta and alpha
