of alcohol abuse (Smith and Fein, 2010). Our finding of negligible WM effects in non-treatment-seeking samples, in contrast to substantial WM atrophy in treatment-seeking samples, is consistent with these differences in cognitive functioning. Because healthy WM is critical to normal attention, executive function, memory, and spatial orienting (Filley, 2001), it is likely that WM atrophy accounts in part for the impairment observed in treatment-seeking samples. Further, the harmful effects of alcohol abuse on WM and cognition may be especially problematic in the context of psychosocial treatments for AUDs, which typically require effortful information processing and reevaluation of reward. Better understanding of the neurobiological risk factors associated with greater cognitive impairment and WM atrophy in treatment-seeking individuals is an important next step in research on AUDs.
