The second factor that drove our prediction of at most very minimal P3b reduction in the TNAD group was that we examined P300 in an adolescent sample. Hence, the individuals investigated here were at an earlier stage of alcoholism and had comparatively lower lifetime alcohol exposure than more frequently examined adult samples. Alcohol exposure has a cumulative neurotoxic effect on the brain: electrophysiological abnormalities become more marked with increased consumption (Floyd et al., 1997; Polich and Bloom, 1986). If the degree of P3b amplitude reduction is moderated, at least partially, by amount of lifetime alcohol exposure, it is not surprising that this reduction was less marked in a younger sample with relatively low lifetime alcohol exposure.
