Electroencephalographic Changes and Vigilance Behavior During Experimentally Induced Intoxication with Alcoholic Subjects

Docter, Richard F.; Naitoh, Paul; Smith, James C.

doi:10.1097/00006842-196607000-00036

Cited by 74 publications

(12 citation statements)

References 16 publications

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“…The increase in alpha 1 (or slow alpha) has been described as the primary EEG response to ethanol ingestion during the descending phase of alcohol absorption (Begleiter & Platz, 1972;Davis et al, 1941;Doctor et al, 1966;Lukas, et al, 1986). The other common change in EEG reported during the descending phase is the increase in alpha activity accompanied by increases in theta activity (Ehlers et al, 1989;13 Lukas et al, 1989;Schwarz et al, 1981).…”

Section: Discussionmentioning

confidence: 99%

Time Course and Regional Distribution of Cortical Changes During Acute Alcohol Ingestion

Tran

Craig

Bartrop

et al. 2004

International Journal of Neuroscience

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Behavioral effects of alcohol are known to be greater when the blood alcohol is rising, known as the Mellanby effect, however, research investigating the cortical changes during this period is scarce. The objective of this study was to investigate the effects of consumption of alcohol on cortical activity measured by the electroencephalogram (EEG) during the absorption or rising phase of alcohol. EEG signals were recorded using the entire 10/20 montage system. The experimental design consisted of a repeated measures randomized crossover design in which subjects acted as their own control. This involved recording two EEG baseline measures, each of which was followed by a placebo or alcohol condition, delivered over two days for ten subjects. All subjects had a 50% chance of receiving the alcohol first. All subjects were shown to have mean peak blood alcohol concentration (BAC) levels of around 0.03%. No significant differences were found between the two baselines. Significant increases in EEG magnitude occurred in the theta (4-7.75Hz), alpha 1 (8-9.75Hz) and beta 1 (13.25-19.75Hz) spectrum in the frontal EEG regions, and alpha 1 (8-9.75Hz) in the central and posterior regions. No significant changes were found in the theta (4-7.75Hz) or beta (13.5-30Hz) spectrums in the central and posterior regions. There were also no significant results for alpha 2 (10-13Hz) in any of the regions. These results suggest that rapid cortical changes occur within the first 35 minutes after alcohol consumption.

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Section: Discussionmentioning

confidence: 99%

Time Course and Regional Distribution of Cortical Changes During Acute Alcohol Ingestion

Tran

Craig

Bartrop

et al. 2004

International Journal of Neuroscience

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“…It is well established that intoxicating doses of alcohol increase heart rate (Docter et al 1966;Iwase et al 1995 McCaul et al 1989;Sellers et al 1972;Turkkan et al 1988;van de Borne et al 1997). These heart rate increases are hypothesized to be positively associated with the reinforcing or appetitive motivational effects of alcohol (Peterson et al 1996) .…”

Section: Alcohol Ingestion Activates the Autonomic Nervous System Andmentioning

confidence: 99%

“…It is well established that intoxicating doses of alcohol increase heart rate (Docter et al 1966;Iwase et al 1995;N EUROPSYCHOPHARMACOLOGY 2001 -VOL . 25 , NO .…”

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confidence: 99%

Naltrexone Dampens Ethanol-Induced Cardiovascular and Hypothalamic- Pituitary-Adrenal Axis Activation

McCaul

2001

Neuropsychopharmacology

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Alcohol ingestion activates the autonomic nervous system and the hypothalamic-pituitary-adrenal axis. This study examined naltrexone effects on alcohol-induced increases in physiological responses and their association with alcohol liking. Using a within-subjects design, heavy drinking men (N ϭ 19) were maintained on each of three naltrexone doses (0, 50, and 100 mg, p.o.) over an 8-day inpatient stay. Within each naltrexone dose, subjects had three alcohol challenge sessions (none, moderate, high) The brain opioid system has been proposed to be part of the neurocircuitry involved in alcohol reward and heavy alcohol drinking (Froehlich and Wand 1997;Gianoulakis and deWaele 1994;Reid et al. 1991). Pharmacological studies indicate that opioid receptor antagonists, such as naloxone hydrochloride and naltrexone, decrease alcohol self-administration in animal models (Altshuler et al. 1980;Froehlich et al. 1990;Hubbell et al. 1986Hubbell et al. , 1991Marfaing-Jallat et al. 1983;Samson and Doyle 1985;Weiss et al. 1990). Clinical trials demonstrated that naltrexone reduces alcohol drinking and self-reported "high," alcohol craving, as well as relapse rates in recently abstinent outpatient alcohol-dependent patients (O'Malley et al. 1992;Volpicelli et al. 1992Volpicelli et al. , 1995 . These findings led to naltrexone's approval by the Food and Drug Administration as a pharmacotherapeutic agent for the treatment of alcohol dependence. Naltrexone is thought to reduce alcohol-induced high and relapse by binding to opioid receptors in discrete brain regions associated with reward and craving, and to prevent receptor activation by alcohol-induced release of endogenous opioid peptides.Alcohol induces a variety of acute physiological responses when consumed in moderate-to-high doses. It is well established that intoxicating doses of alcohol increase heart rate (Docter et al. 1966;Iwase et al. 1995 McCaul et al. 1989;Sellers et al. 1972;Turkkan et al. 1988;van de Borne et al. 1997). These heart rate increases are hypothesized to be positively associated with the reinforcing or appetitive motivational effects of alcohol (Peterson et al. 1996) . Alcohol has less predictable effects on blood pressure, with reports of blood pressure increases (Iwase et al. 1995;Sellers et al. 1972) and no effects following alcohol ingestion (Turkkan et al. 1988;van de Borne et al. 1997). Finally, alcoholinduced peripheral vasodilation and associated skin temperature increases have been consistently reported (Iwase et al. 1995;Turkkan et al. 1988) and is thought to be one explanation for the lack of a consistent rise in blood pressure after alcohol consumption.Acute administration of intoxicating doses of alcohol also activates the hypothalamic-pituitary-adrenal (HPA) axis thereby increasing ACTH and glucocorticoid levels (Inder et al. 1995;Rivier et al. 1984;Waltman et al. 1993). It remains unclear whether alcohol-induced activation of the HPA axis has any relationship to its reinforcing properties. Rodent studies show that alcohol increases pla...

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“…Using a simple continuous visuomotor performance task, Cohen et al (1983) found that alcoholics made more correct responses when intoxicated than when tested 3 weeks post-detoxification. Docter et al (1966) reported that relative to detoxified alcoholics, experimentally intoxicated alcoholics displayed heightened and prolonged attentional behavior on a visuomotor task. Based on these findings, and earlier studies of psychophysiological response patterning in alcoholics by Docter and colleagues (Docter and Perkins 1960;Docter and Bernal 1964), Naitoh and Docter (1968) suggested that alcoholics drink to achieve a calm, alert, and mildly stimulated psychological state facilitative to information processing.…”

mentioning

confidence: 99%

Event-related brain potentials in intoxicated and detoxified alcoholics during visuospatial learning

Schandler

Cohen

McArthur³

1988

Psychopharmacology

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Event-related potentials and visuospatial learning performance were examined to understand the effects of chronic alcohol use on complex information processing. A total of 18 alcoholic male in-patients in an alcohol treatment program served as participants. Nine persons were seen at time of admission to the program while intoxicated (mean BAC = 18.0 mg/dl). The second group of nine persons was seen detoxified after 4 weeks in the treatment program. Learning consisted of a paired-associate paradigm requiring participants to learn the distinct spatial positions of six, randomly presented "nonsense" shapes. The visuospatial learning performance of the intoxicated alcoholics was superior to that of the detoxified alcoholics. Evaluation of event-related potentials during the visuospatial learning task indicated that while both groups displayed greater right hemisphere amplitudes of P3, P2, N1, and N2-P3 components, the amplitudes of the latter three components were significantly greater in the intoxicated alcoholics. The overall results suggest that compared to the intoxicated alcoholic, the detoxified alcoholic may suffer a disruption in attentional mechanisms related to visuospatial information processing, providing support for a theory that alcohol ingestion serves to balance information processing in the chronic alcoholic.

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Electroencephalographic Changes and Vigilance Behavior During Experimentally Induced Intoxication with Alcoholic Subjects

Cited by 74 publications

References 16 publications

Time Course and Regional Distribution of Cortical Changes During Acute Alcohol Ingestion

Time Course and Regional Distribution of Cortical Changes During Acute Alcohol Ingestion

Naltrexone Dampens Ethanol-Induced Cardiovascular and Hypothalamic- Pituitary-Adrenal Axis Activation

Event-related brain potentials in intoxicated and detoxified alcoholics during visuospatial learning

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