Alcohol use/abuse has been associated with working memory and attention deficits (Nixon and Glenn 1995; Ratti et al. 1999; Beatty et al. 2000; Schmidt et al. 2005), as well as with structural and functional neural adaptations in the brain as a result of chronic alcohol exposure (Nixon 2006). For example, animal and human studies have reported associations between chronic alcoholism and neurodegeneration in the hippocampus and superior frontal cortices (Walker et al. 1980; Agartz et al. 1999; Sullivan and Pfefferbaum 2005; Nixon 2006), areas involved in the working memory and attention deficits associated with alcoholism. These cognitive and brain deficits have been shown to recover, however, following periods of abstinence from alcohol (Nixon 2006; Fein and McGillivray 2007; Fein et al. 2010). Greater theta ERS in STAA and LTAA suggests that they are engaging working memory and attentional processes to a greater extent than are control participants in order to perform the target detection task successfully, a process that may be pronounced in STAA given that their larger theta ERS is concomitant with lower (relative to NAC and LTAA) prestimulus
