## 1 Introduction  
Executive functioning refers to cognitive processes underlying the self-regulation of goal-directed actions, and thus the ability to avoid maladaptive behaviors, via top-down inhibitory control on bottom-up repetitive drives [1; 2]. Defective executive skills are indeed considered a core facet of cognitive alterations in addictions, including alcohol use disorder (AUD) [2; 3; 4]. The chronic compulsive drinking behavior inherent in AUD, leading to over 3 million deaths per year (WHO), is indeed associated with negative emotional states during abstinence and, therefore, loss of control over alcohol intake. As for other addictions, maladaptive behavioral learning might promote the establishment of drinking habits [5; 6], which are reinforced by the reward inherent in consumption (positive reinforcement) and/or in avoiding the punishing experience associated with abstinence (negative reinforcement) [7]. The latter, in particular, might drive the progression from impulsivity to compulsivity by potentiating the avoidance of craving-related aversive states. At the neural level, this process seems to involve a progressive imbalance between reward-related \"reflexive\" drives generated by the limbic subcortical structure and \"reflective\" skills of executive control associated with fronto-striatal networks, mediating the shift from goal-directed to habitual behaviors [8]. Increasing evidence indeed shows prominent executive deficits in AUD [2; 9], reflecting structural and/or functional alterations in fronto-striatal networks underlying executive control [10]. The presence of such impairments in AUD has several consequences. First, these changes might promote a vicious circle in which altered decision-making mediates the effect of decreased executive skills on relapses, thus further impairing inhibitory skills and perpetuating addictive behaviors. Cognitive remediation procedures increase the likelihood of breaking this circle, with cognitive enhancements being transferred to functional improvements [11], but again treatment efficacy depends on \"baseline\" executive skills [12]. Moreover, despite the promising effects of neuromodulation techniques on craving [13; 14] and cognitive control [15] in alcoholic patients, this approach requires the preliminary identification of \"target\" regions. This multifaceted evidence highlights the need for a detailed characterization of executive impairments, and their neural bases, in AUD. By coupling an extensive neuro-cognitive assessment with magnetic resonance imaging (MRI) metrics of brain structure and function, we have recently addressed this issue via voxel based morphometry (VBM) [16; 17; 18], diffusion tensor imaging (DTI) [19; 20], and resting-state functional magnetic resonance imaging (rs-fMRI) [21; 22; 23]. The latter approach is becoming increasingly valuable in clinical neuroscience, based on the spatial overlap between patterns of brain activity underlying task performance and the networks showing low-frequency and temporally coherent fluctuations of the Blood Oxygen Level Dependent (BOLD) signal at rest [24]. Variations of performance across several domains have been related to distinct metrics of such a resting state, i.e., \"intrinsic\" brain activity, both in normal subjects [25] and pathological populations [26]. In AUD, a prominent impairment of basic executive functions such as working memory, attention and visuomotor speed reflects grey matter (GM) loss [16; 17], as well as abnormal intrinsic connectivity [19; 20; 21; 22; 23], in fronto-striatal and fronto-insulin regions mediating the recruitment of controlled processes by salient stimuli. We aimed to complement these findings by focusing on an inherent property of intrinsic brain activity such as the degree of resting-state _synchrony_.