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 .---- . Drinks per o E o� 0.0 I occasion 2.38 1.20 1-5 0 -I Drink Index* 9.62 9.19 1-40 co 0 105 140 * The Drink Index is the product of drinking days per month and 0 35 70 drinks per occasion. TIME (mIn)

Figure 1. Mean blood-alcohol levels (mg/IOO ml) as a func­ Experimental Design tion of time (minutes) under both the LD (black squares) and HD (white squares) conditions. Each subject was tested once under each of three con­ ditions: placebo (P), low-dose (LD) ethanol, or high­ Recording Methods and Parameters dose (HD) ethanol. Condition order was randomized The subject was seated comfortably in a dimly lighted, andthere was a minimum I-day interval between con­ temperature regulated, sound attenuated chamber (In­ ditions. In the LD and HD conditions, the subject re­ dustrial Acoustics Corp., Bronx, NY). He was told to ceived a volume (ml) of 100% ethanol equal to 0.5 and close his eyes and relax but not to fall asleep. Each sub­ 0.8 times his weight in kilograms, respectively, dis­ ject wore a &tted electrode cap (Electro-Cap Interna­ solved in a volume of ginger ale equal to three times tional, Inc., Eaton, OH) using all 21 electrodes of the that number (see Table 2). In the P condition, the sub­ 10/20 International System. The nasion served as ref­ ject drank a volume (ml) of ginger ale equal to twice erence and the forehead as ground. Both vertical and his weight in kilograms so that the total volume of liq­ horizontal eye movements were monitored. uid equalled that of the LD condition. Under each con­ Cortical activity was ampli&ed 20 k (bandpass 0.1 dition the subject ingested the drink over a lO-minute to 100 Hz) with a Grass Neurodata Acquisition System period. A specially designed container (Mendelson et (Quincy, MA). The data were sampled continuously al. 1984) was used to provide an equally strong ethanol at 128 Hz for a period of 120 seconds. Artifact rejection odor for both placebo and alcohol conditions. Within (EMG, EOG, and saturation artifact) was performed the container a small trap held 3 ml of a solution con­ blindly, off-line by a highly trained technician. sisting of three parts ethanol dissolved in seven parts gingerale; this ensured that under each condition, the subject's frrst taste was ethanol. However, the small Data Analysis amount of ethanol ingested did not produce a measur­ All 21 EEG channels were continuously displayed on able blood-alcohol level. Figure 1 presents mean blood­ a monitor. The &rst 12 artifact-free, 4-second frames alcohol level (mg/100 ml) at four postingestion inter­ were selected and then analyzed via the Fast Fourier vals for both the LD and HD conditions. Transform. The consequent power spectral densities Five EEG recordings were made under each of three were then summed and averaged. This procedure was conditions; the frrst, approximately 2 minutes before repeated for each of the &ve EEG recordings made un­ P, LD, or HD, and the second through fIfth at intervals der the P, LD, and HD conditions. Measures of rela­ of 35, 70, 105, and 140 minutes afterwards. A breath­ tive area under the power spectral curve at .25-Hz in­ alyzer (Alco-Sensor III; Intoximeters, Inc., St. Louis, MO) tervals were then obtained from the summed and was used to monitor the subject's blood-alcohol averaged power spectral densities. Determinations of level initially upon arrival at the laboratory and then relative area were made for each of the following fre­ immediately preceding each EEG recording. quency bands: slow alpha (SA, 7.5 to 10.0 Hz); fast al­ pha (FA, 10.5 to 13.0 Hz); slow beta (SB, 13.5 to 19.5 Table 2. Fluid Volume (ml) Consumed by Each Hz); and fast beta (FB, 20 to 26 Hz) at electrodes F3, Subject as a Function of Body Weight (kg) F4, C3, C4, P3, P4, 01, and 02. These measures were for Each Experimental Condition then normalized. Statistical analyses consisted of repeated-measures multivariate analysis of variance Vol. of Ethanol Vol. of Ginger Ale with Greenhouse-Geisser corrections conducted on Placebo (P) o 2.0 x kg normalized, relative area values for each frequency Low dose (L) 0.5 x kg + 3.0 (0.5 x kg) band at each electrode under the P, LD, and HD con­ High dose (H) 0.8 x kg + 3.0 (0.8 x kg) dition. 368 H.L. Cohen et al. NEUROPSYCHOPHARMACOLOGY 1993-VOL. 8, NO.4

0.5 FJ F4

0.4

.-­,A �___ 0.3 ��., .-­ ---.--

0.2

0.5 CJ C4

0.4

/.--. � ., . 0.3 �- .- . -- �.---. . �------. --- . . 0.2 ----- .�

0.5 PJ P4 3 . . o 0.4 �• . • • . . -- �• � ....J • • . Cf) . .-- .--. 0.3 . UJ > 0.2 ..... oc{ ....J UJ a: 0.5 01. . 02 - • Figure 2. Percent change in normal­ • � • • 0.4 . ized, relative SA area (a.u.) (7.5 to 10.0 . . �--. . -. ' . . · / Hz) at each electrode as a function of 0.3 /----.. . time (minutes) following P (black rec­ :-. .--- tangle), LD (white rectangle), and HD 0.2 (black diamond) ethanol ingestion. The EEG activity was amplifIed (20 k) ��I --+--+--�I--� and recorded over a bandpass of 0.1 140 to 100 Hz with a sampling rate of o 35 70 105 o J5 70 105 140 128 Hz. TIME (min) TIME (min)

RESULTS F4 (F = [13.58], df = [2,19], P < .0002), C3 (F = [6.05], df = [2,19], P < .009), and C4 (F = [4.70], df = 2,19], The results of this study indicate that ethanol ingestion P < .02), but not in the posterior electrodes P3, P4, and by healthy, adult males induces specifIcEEG changes 01,02. Lastly, laterality differenceswere examined by manifested as increased activity in the SA (7.5 to 10.0 comparing the activity between electrodes overlying ho­ Hz) frequency band. Initially, comparisons of EEG ac­ mologous cortical locations. The results indicated tivity were made among electrodes01, P3, C3, and F3, signifIcant differences at electrode pairs C3, C4 (F = and02, P4, C4, and F4 to determine whether there were [58.64], df = [1,20], p < .0001) and 01,02 (F = [28.28], signifIcantresponse differencesacross electrodes on the df = [1,20], P < .0001). This appears to reflect the fact same side. The main effectof IIelectrode" was signifIcant that at baseline, SA levels at C4 and 02 were 24.8% and in both the left hemisphere (F = [39.68], df = [3,18], 17.2% higher, respectively, than at C3 and 01. P < .0001) and in the right hemisphere (F = [11.68], df = Figure 2 presents, at each electrode, the changes [3,18], P < .0002). Then, MANOVA was performed on in normalized, relative SA (7.5 to 10.0 Hz) activity as the EEG activity at each electrode, separately. The a function of time (minutes) after P, LD, and HD etha­ results of these analyses indicated a signifIcantethanol­ nol ingestion. In general, increases in SA activity oc­ related increase in SA activity. These increases occurred curred after the changes in blood-alcohol level, which at frontal electrodes F3 (F = [4.17], df = [2,19], P < .03), tended to peak at between 35 and 70 minutes postin- NEUROPSYCHOPHARMACOLOGY 1993-VOL. 8, NO. 4 Ethanol-Induced Alterations in EEG Activity 369

gestion. Elevated SA activity levels were maintained roanatomy alone cannot adequately explain our results. even after blood-alcohol level began to decrease. Al­ For example, although ethanol had a signifIcanteffect thoughthe increases in SA activity did not correspond on SA activity at electrodes F3 and F4, which overlie to changes in blood-alcohol level, a statistically sig­ association cortex in the middle frontal gyrus, it had nificant dose effect was observed at electrodes F3, F4 no effect on SA activity at P3 and P4, which overlie andC3, C4, but not at aI, 02 and P3, P4. However, posterior association cortex in the superior parietal lob­ theethanol-induced increases in SA activity, although ule (Homan et al. 1987). It is important to recognize that signiflcantlygreater than those occurring during the P cortical recordings at a specifIclocus do not necessarily condition, were not signifIcantlydifferent from one an­ reflect localized activity, but, in fact, may represent other, as demonstrated by the overlying LD and HD afferent volleysoriginating at distant cortical or subcor­ functions. tical sites. Furthermore, it is not clear that the same mechanisms by which ethanol reduces ERP amplitude and increases component latencies underlies the ob­ served increases in SA activity, which may reflect ei­ DISCUSSION ther excitatory or inhibitory processes. Lastly, it is un­ likely that the SA increases, particularly at C3 and C4, This study demonstrates that ethanol ingestion by reflectedchanges in motor activity, as the subjects were healthy, adult males induces an increase in SA activity relaxed, with eyes closed, and were not required to thatocc urs at frontal sites (F3, F4 and C3, C4). In con­ make any responses. trast, almost no ethanol-induced changes in EEG ac­ Although Figures 1 and 2 demonstrate the effects tivitywere observed in the posterior locations exam­ of increased blood-alcohol levels on SA activity at each ined.The ethanol-induced increases in SA activity did electrode, signifIcant dose effects were observed only not correspond to changing blood-alcohol levels and at electrodes F3, F4 and C3, C4. In general, ethanol in­ typicallypeaked after the blood-alcohol level began to gestion signifIcantlyincreased the magnitude of SA ac­ fall. Further, although ethanol produced signifIcantly tivity compared with the effects of P, although there largerincreases in SA activity than did the P, there were was no difference between HD and LD as evidenced no differences between the effects of the two doses. by the overlapping functions. Interestingly, to our In general, the increase in spectral magnitude in knowledge, there are almost no other studies that have the SA frequency band has been described as the pri­ examined the effects of multiple doses of ethanol on maryEEG response to ethanol ingestion (Davis et al. human EEG activity in the same subject population. 1941; Engel and Rosenbaum 1945; Holmberg and Mar­ Other studies administering multiple ethanol doses tens 1955; Begleiter and Platz 1972; Lehtinen et al. 1978; have either used each dose on separate groups of sub­ 1981; Lukas et al. 1986; Michel and Battig 1989), al­ jects (Lukas et al. 1986), did not record EEG activity un­ thoughsome studies reported that the changes in SA der each condition (Ehlers and Schuckit 1988, 1990, were accompanied by altered activity in theta (Lukas 1991), or used differentforms of ethanol, such as, bour­ etal. 1986; Ehlers et al. 1989) and Fast Alama (Volavka bon and vodka (Murphree et al. 1970) and red wine and et al. 1985; Lukas et al. 1989, 1990) frequency bands. Martini (Lolli et al. 1964). The fact that Figure 2 shows Additionally, although we recorded signiftcantchanges no signifIcantdifference between the HD and LD func­ inEEGactivity over frontal cortical regions, in contrast, tions suggests that a greater differencebetween doses other studies have often reported more widespread may be necessary to elicit a signifIcantdose-dependent ethanol-inducedEEG changes (Davis et al. 1941; Holm­ difference. However, even a greater differencebetween berg and Marten 1955; Lehtinen et al. 1978, 1981; ethanol doses may not induce these effects as there is Volavka et al. 1985; Ehlers and Schuckit 1988; Ehlers a high degree of inter- and intrasubject variability in etal. 1989; Lukas et al. 1989, 1990). both the blood-alcohol and EEG response to ethanol Regional differences in the electrophysiologic (Lehtinen et al. 1981; Lukas et al. 1986; Porjesz and effectsof ethanol have also been obtained from studies Begleiter 1983). of event-related potentials (ERP). These studies demon­ Figures 1 and 2 also demonstrate that increases in stratedthat ethanol both reduced some ERP amplitudes SA activity lagged behind increases in blood-alcohol andinc reased latencies of long latency (>100 msec) com­ level under both the LD and HD conditions, and that ponents (Salamy and Williams 1973; Porjesz and increased SA activity typically persisted even after Begleiter 1975, 1983, 1985); the magnitude of these blood-alcohol level decreased. A similar functional rela­ effects is typically greater in association cortex than in tionship, wherein increases in alpha activity peaked and primarysensory cortex (Salamy and Williams 1973; Por­ remained elevated during decreasing blood-alcohol jesz and Begleiter 1975, 1983, 1985). It has been sug­ level, has been observed by several investigators (Davis gested that this sensitivity may reflect the complex, et al. 1941; Holmberg and Martens 1955; Lehtinen et polysynapticstructure of association cortex (Himwich al. 1981). andCallison 1972; Kalant 1975). However, cortical neu- The results of the current investigation indicate that 370 H. L. Cohen et al. NEUROPSYCHOPHARMACOLOGY 1993- VOL. 8, NO.4

the response of the central nervous system to ethanol, Kalant H (1975): Direct effects of ethanol on the nervous sys· as reflected in the analysis of EEG activity, is not uni­ tern. Fed Proc 34:1930-1941 form. Rather, it appears that ethanol has differentlocal Kaplan RF, Hesselbrock VM, O'Connor S, de Palma N (1988): cortical effects and/or may differentiallyinfluence sub­ Behavioral and EEG responses to alcohol in nonalcoholic men with a family history of alcoholism. Prog Neuro· cortical structures whose ascending cortical projections psychopharmacol BioI Psychiatry 12:873-885 terminate in the cortical loci examined. To investigate Lehtinen I, lang AH, Keskinen E (1978): Acute effects of small these possibilities, our laboratory is currently engaged doses of alcohol on the NSD parameters (Normalized in ongoing research using both topographic analyses Slope Descriptors) of human EEG. Psychopharmacology and dipole localization techniques to defIne sources of 60:87-92

EEG activity. Comparisons of ethanol-induced EEG re­ Lehtinen I, lang AH,Jantii V, Pakkanen A, Keskinen E, Nyrke sponse will then be made between both normal indi­ T, lempiainen M (1981): Ethanol-induced disturbance viduals and those at high risk for the development of in human arousal mechanism. Psychopharmacology alcoholism. 73:223-229 lolli G, Nencini R, Misti R (1964): Effects of two alcoholic beverages on the electroencephalographic and elec· tromyographic tracings of healthy men. Q J Stud Alco· ACKNOWLEDGMENTS hoI 25:451-458

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