The effects of ethanol on EEG activity in males at risk for alcoholism

Abstract

The present investigation examined the effects of placebo (P), low dose (LD) and high dose (HD) ethanol on EEG activity in two groups of males. One group consisted of individuals at high risk for the development of alcoholism (HR, N = 21) while the other consisted of matched, low risk (LR, N = 21) controls. Only one condition (P, LD or HD) was presented each day and condition order was randomized. For each subject, both blood alcohol level(s) (BAL) measured via breathalyzer and EEG activity, using the entire 10/20 international system, were recorded priot to and at intervals of 35, 70, 105 and 140 min after P, LD or HD administration. The Fast Fourier Transform (FFT) was used to calculate power spectral densities (PSD). Measures of relative area under the power spectral curve were obtained for each of the following frequency bands; slow alpha (SA, 7.5–10 Hz), fast alpha (FA, 10.5–13.0 Hz), slow beta (SB, 13.5–19.5 Hz) and fast beta (FB, 20–26 Hz) at electrodes: F3, F4, C3, C4, P3, P4, O1 and O2. The results of repeated measures MANOVA conducted on the normalized values of relative areas revealed that at each electrode F3, F4 adn P4. These differences were the consequences of differential ethanol effects rather than differences i observed only at electrodes F3, F4 and P4. These differences were the consequence of differential ethanol effects rather than differences in baseline SA levels. Further analyses indicated that across all 8 electrodes there were significant risk group differences in the magnitude of change in SA activity as a function of thhe ascending and descending phases of the blood alcohol curve (BAC). HR individuals manifested significantly greater increases in SA activity on the ascending curve (acute sensitization) and significantly faster recovery to baseline SA levels during the descending phase (acute tolerance). Evidence is also presented that genetic factors, rather than differences in drinking history, may account for risk group differences in the ethanol-induced EEG response.