The majority of EEG investigations of alcohol drinkers have focused on alcoholics or individuals with a family history of alcoholism. These results also are difficult to extend to binge drinking populations as the related variables confound alcohol consumption effects for EEG measures. However, EEG studies of alcoholics have demonstrated decreased alpha band (8–12 Hz) power [8,9], increased beta band (12–30 Hz) power [10,11], and the presence of low-voltage fast (<20 μV, 14–30 Hz) EEG patterns [12,13]. These low-voltage fast desynchronized patterns have been interpreted as reflecting hyperarousal of the central nervous system (CNS) [10]. Hyperarousal of the CNS in alcoholics has been substantiated by the discovery of a corresponding elevation in cardiac output, which suggests that these individuals require greater sedation to achieve a “normal” arousal level [14]. Increasing the amount of alcohol consumption is associated with greater amounts of alpha activity and slowing of the predominant alpha frequency [15,16]. CNS hyperarousal is indexed by high-frequency beta (19.5–39.8 Hz) activity, which has been used to predict relapse rates among abstinent alcoholics [14,17] and differentiate between abstinent and non-abstinent alcoholics [10].
