Abstract

Using a dipole tracing method based on the two-dipole model, the purpose of the present study was to investigate alcohol-induced changes in the alpha band of electroencephalogram (EEG) and its equivalent current dipoles (ECDs) in 12 healthy male volunteers, who were genetically typed for mitochondrial aldehyde dehydrogenase-2 (ALDH2). The alpha power and the mean interval dipolarity, which represents the goodness of fit of alpha EEG with the two-dipole model, increased at 30 min after 0.75 ml/kg of alcohol ingestion, when breath alcohol concentration showed its peak. However, the location of ECDs and distribution of alpha EEG did not change after alcohol ingestion. These findings indicate that alcohol enhances alpha EEG but does not change the location of its electrical sources. Interestingly, the time course of alcohol-induced EEG changes differed significantly according to the aversive flushing reaction after its intake. From 60 to 120 min, the non-flushing group which had homozygous ALDH2*1 (active type) displayed significant increase not only in the alpha power but also in the interval dipolarity compared to the baseline, whereas the flushing group with heterozygous ALDH2*1/2*2 (inactive type) did not exhibit this significant increase. The difference in the time course was discussed from the viewpoint of the protective effect of ALDH2*2 allele against the risk for alcoholism. These results suggest that the dipole tracing method could provide an alternative neurophysiological marker for the risk for alcoholism.

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