Ethanol-Induced Alterations in Electroencephalographic Activity in Adult Males Howard L
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NEUROPSYCHOPHARMACOLOGY 1993-VOL. 8, NO.4 365 Ethanol-Induced Alterations in Electroencephalographic Activity in Adult Males Howard L. Cohen, Ph.D., Bernice Porjesz, and Henri Begleiter The present investigation examined the effects of placebo following frequency bands: slow alpha (7.5 to 10 Hz); (P), low-dose (LD), and high-dose (HD) ethanol on fast alpha (10.5 to 13.0 Hz); slow beta (13.5 to 19.5 Hz); electroencephalographic (EEG) activity in 21 healthy, and fast beta (20 to 26 Hz) at electrodes F3, F4, C3, C4, adult males (X = 22.7 years). Only one condition (P, P3, P4, 01, and 02. Repeated-measures multivariate W, or HD) was presented per day and the condition analysis of variance performed on normalized relative area order was randomized. For each subject, blood-alcohol values revealed that ethanol had significant effects on levels measured via breathalyzer and EEG activity, using EEG activity at anterior sites: frontal (F3, F4) and the entire 10120 International System, were recorded both central (C3, C4) that presented as increased activity in prior to and at intervals of 35, 70, 105, and 140 minutes the slow alpha frequency band. These results suggest a after P, LD, or HD administration. The Fast Fourier differential responsivity of both cortical region and EEG Transform was used to calculate power spectral densities frequency band to the effects of ethanol ingestion. foreach EEG recording. Measures of the relative areas [Neuropsychopharmacology 8:365-370, 1993J under the power spectral curve were made for each of the KEY WORDS: Alpha; Beta; EEG; Power Spectra; Ethanol must be carefully determined. These include 1) elec Investigations into the effectsof acute ethanol adminis trode locations analyzed, 2) EEG frequency band(s) ex trationon adult, human electroencephalographic (EEG) amined, 3) ethanol concentration ingested, 4) mea activity have reported both decreases in the predomi sure(s) of EEG activity used, 5) predrug EEG activity nant baseline frequency and increases in power spec level, 6) time course over which EEG changes are ex tralenergy (Davis et al. 1941; Engel and Rosenbaum, amined, 7) individual's drinking history, and 8) family 1945; Holmberg and Martens, 1955; Begleiter and Platz history of alcoholism. Even after controlling for these 1972;Lehtinen et al. 1981; Lukas et al. 1986; Michel and variables, both EEG and subjective responses to acute Battig 1989). However, defIning the relationship be ethanol ingestion may be highly variable across indi tween ethanol ingestion and its effect on the EEG is viduals and within the same individual on differentoc complicated by numerous variables whose influence casions (Begleiter and Platz 1972; Lukas et al. 1986). The majority of studies have focused on the alpha frequency band, although investigators have not always From the Neurodynamics Laboratory, Department of Psychiatry, agreed upon its range or its composition. For example, State University of New York Health Science Center Brooklyn, although some have defInedalpha as a continuous band Brooklyn, New York. (Holmberg and Martens 1955; Lukas et al., 1986; Kaplan Address correspondence to: Dr. Howard1. Cohen, Neurodynamics Laboratory, Department of Psychiatry, Box 1203, S.U.N.Y. Health et al. 1988), others have divided alpha into both a slow Science Center Brooklyn, 450 Oarkson Avenue, Brooklyn, New York band and a fast band (Pollock et al. 1983; Volavka et 11203. al. 1985; Ehlers and Schuckit 1988, 1991; Ehlers et al. Received August 14, 1992; revised December 1, 1992; accepted December 8, 1992. 1989; Lukas et al. 1989). In general, those studies that © 1993 American College of Neuropsychopharmacology Published by Elsevier Science Publishing Co., Inc. 655 Avenue of the Americas, New York, NY 10010 0893-133X/93/$6.00 NEUROPSYCHOPHARMACOLOGY 1993-VOL. 8, 366 H.L. Cohen et al. No. 4 defIned alpha as a continuous band reported that etha after these levels had dropped considerably (Da Vis et nol ingestion increased alpha energy. In contrast, the al. 1941; Holmberg and Martens, 1955), or that no can. dichotomized band studies have typically reported in sistent correlations were detected between blOOd. creased slow alpha energy and either no change (Eh alcohol concentration and any measure of EEG actiVity lers and Schuckit 1988, 1991), a decrease (Ehlers et a1. (Ehlers et al. 1989). Lastly, Lehtinen et al. (1981) POinted 1989), or both increases and decreases (Pollock et a1. out that an important factor in the relationship between 1983; Volavka et a1. 1985; Lukas et a1. 1989) in fast al blood-alcohol level and changes in EEG activity is pha energy. whether the blood-alcohol level was measured directly The changes in alpha energy following ethanol in from the blood or indirectly from breathalyzer readings. gestion are frequently, but not always, accompanied Theirstudy measured both values, but found that When by a decrease in the predominant alpha frequency breathalyzer blood-alcohol values were kept constant (Davis et a1. 1941; Engel and Rosenbaum 1945; Lehti by upward and downward adjustments of an intrave. nen et a1. 1981; Pollock et a1. 1983; Lukas et a1. 1986) nous ethanol infusion, EEG changes followed directly and, as in the studies of changes in alpha energy, measured blood-alcohol levels. dichotomized alpha band studies report differential Many previous studies of the effects of ethanol on effects (Ehlers et a1. 1989). Additionally, there is evi human adult EEG have typically focused on a limited dence that both the probability and the magnitude of portion of the frequency spectrum, have sampled EEG the decrease may be influenced by the individual's base activity at a small number of electrodes, and have of. line EEG activity (Engel and Rosenbaum 1945; Begleiter ten yielded inconsistent results. It is the intent of the and Platz 1972; Lukas et a1. 1986). present investigation to sample ethanol-induced changes Reports of ethanol-induced changes in faster activ in EEG activity in both the alpha and beta frequency ity (beta) have also been contradictory. There have been bands over a larger number of cortical regions than have observations of decreased beta power with subsequent typically been examined, in a carefully defIned popu replacement by alpha activity (Engel and Rosenbaum lation of healthy, adult males. Additionally, most pr evi. 1945; Murphree et al. 1970; Ehlers et al. 1989), increased ous investigations have typically used a placebo and beta activity (Holmberg and Martens 1955; Murphree a single ethanol dose. In contrast, the subjects in this et a1. 1970), both increases and decreases in mean fre investigation received placebo, low-dose, and high quency in the beta range (Lehtinen et a1. 1978), and no dose ethanol in a randomized order using a repeated ethanol-induced effects on beta (Lolli et al. 1964; Eh measures design. lers and Schuckit 1988, 1990; Lukas et al. 1989). Addi tionally, there is evidence (Ehlers et al. 1989; Ehlers and Schuckit 1990) that ethanol-induced changes in beta ac METHODS tivity may be influenced by an individual's drinking his Subjects tory. "Moderate" drinkers, in contrast to '1ow" drinkers, had more beta energy and a higher peak frequency both The participants in this study were 21 males ranging at baseline and at 90 minutes postethanol ingestion. from 19 to 39 years of age (mean 22.7 years). These in The rise and fall in blood-alcohol level following eth dividuals had responded to either newspaper ads or anol ingestion is influenced by factors such as the vol to notices for subjects posted in the Health Science Cen ume and concentration of alcohol ingested and the time ter. An irlitial screening procedure required the prospec period over which ingestion occurs. Attempts to corre tive subject to hIl out a questionnaire detailing his med late the temporal pattern of EEG changes with the dy ical and psychiatric history, his drug and alcohol use namic phases of the blood-alcohol curve have yielded and those of his relatives. A candidate for the study was inconsistent results. For example, there are reports that rejected ifhe had any fIrst or second degree relative who during the ascending phase, increases in alpha energy was alcoholic. Additional criteria for exclusion included were greater than during the descending phase (Beg major medical problems, use of medication that affected leiter and Platz 1972; Lukas et al. 1986), maximal alpha the central nervous system, or a history of psychiatric activity coincided with peak blood-alcohol levels problems and/or drug or alcohol abuse. Furthermore, (Kaplan et a1. 1988), and slowing of the predominant a potential subject was excluded ifhe had a fIrst or sec frequency was generally proportional to the blood ond degree relative with drug abuse or psychiatric prob alcohol level (Newman 1959). In contrast, there are lems. Table 1 summarizes the demographiC data for observations that EEG changes were greater when these subjects. It includes a "Drink Index," which was blood- and breath-alcohol levels were falling than at cor obtained by multiplying the number of days per month responding concentrations when the alcohol concen that the subject drank by the number of drinks peroc tration was rising (Lehtinen et a1. 1981), that decreased casion. Eighteen of the subjects had a "Drink Indet frequency and increased power occurred only after peak of less than 20, indicating that the subjects comprised blood-alcohol levels were attained, and continued even a homogeneous population of light drinkers. NWROPSYCHOPHARMACOLOGY 1993-VOL. 8, NO.4 Ethanol-Induced Alterations in EEG Activity 367 Table 1. Summary of 21 Subjects' Characteristics -I 0.06 w HD > Mean SO Range w 0,05 -I � -I - 0.04 Age (yrs) 22.7 4.51 19-39 o E Education (yrs) 15.8 2.43 12-20 IO 00 0.03 ----. Drinking days u- . LD -I ...... ---- per month 4.05 3.32 1-14 ..:( 0> 0.02 .---- .