For many years it was assumed that the P3 deficit observed in alcoholics was the consequence of the deleterious effects of alcohol on the brain. However, after a sufficient period of abstinence, many of the clinical abnormalities characteristic of alcohol dependence, as well as electrophysiological measures of hearing deficits, return to normal, but the P3 amplitude abnormality persists (Porjesz and Begleiter 1985). This protracted deficit in long-term abstinent alcoholics suggests the possibility that P3 deficits may precede alcohol use and dependence. Indeed, a number of studies have reported low P3 amplitudes in young people at high risk for developing alcoholism, such as young sons of alcoholic fathers (Begleiter et al. 1984; Polich et al. 1994).
