Alcoholism and Human Electrophysiology : Part 5

by National Institute of Health

(Page 5 of 5)

Summary

One of the most consistent electrophysiological measures that characterize male alcoholics is the low amplitude of their P3 components; female alcoholics also manifest reduced visual and auditory P3 amplitudes, although to a lesser extent than male alcoholics. Recent findings indicate that not only are P3 components at low amplitude in alcoholics, but the neural oscillations underlying P3 are deficient in alcoholics as well. The findings that both evoked delta and evoked theta oscillations underlying P3 are deficient in alcoholics imply dysfunction in both the cognitive processes and neural correlates that mediate these oscillations. Event-related delta oscillations are related to signal detection (stimulus discrimination of one object from all other objects) and decisionmaking, whereas theta oscillations are associated with cognitive processes such as attention, alertness, and memory. Alcoholics are also deficient in the production of evoked gamma oscillations during the processing of target stimuli. As these oscillations are related to selective attention processes and working memory, these findings indicate that alcoholics manifest deficits in cognitive functions associated with these oscillatory processes.

Alcoholics are deficient not only in their response to task-relevant target stimuli but also in response to task-irrelevant rare stimuli, as revealed by ERP findings. Recent ERO findings indicate that alcoholics manifest decreased theta and delta oscillations to both Go and No-Go stimuli in a Go/No-Go task. As increased theta power indicates inhibition of responding to irrelevant information during selective information processing tasks, decreased theta oscillations in alcoholics may reflect deficient inhibitory control.

During oddball tasks, control subjects manifest enhanced P3 components and evoked theta, delta, and gamma oscillations when processing the target stimulus but not when processing a nontarget or novel stimulus. Alcoholics, however, manifest less electrophysiological differentiation among the three stimulus categories. Topographic maps of P3s and these EROs during target processing indicate that not only do alcoholics manifest weaker sources, they have less topographically distinct spatial-temporal patterns. This less differentiated mode of responding during various tasks indicates that alcoholics are less proficient at processes which involve comparing a new stimulus to a template, suggesting alcoholics have attention and memory deficits. Alcoholics seem less able to efficiently use available information (a template in working memory) to respond differentially to incoming stimuli (targets, nontargets); hence each incoming stimulus must be evaluated anew. This more global mode of responding in alcoholics regardless of stimulus and task requirements indicates a basic diminution of differential inhibition. In healthy people, familiar stimuli are processed with less neuronal activity than unfamiliar stimuli. Evidence from monkey studies indicates that repeated stimuli elicit less neuronal firing than novel stimuli, suggesting inhibition of masses of neurons, which leads to increased synaptic efficiency. Differential inhibition allows the animal to efficiently process a given stimulus (target). Thus, reduced differential neuronal inhibition of relevant and irrelevant stimuli in alcoholics may account for the electrophysiological aberrations observed in alcoholics.

For many years it was assumed that the P3 deficit observed in alcoholics was the consequence of the deleterious effects of alcohol on the brain. However, after a sufficient period of abstinence, many of the clinical abnormalities characteristic of alcohol dependence, as well as electrophysiological measures of hearing deficits, return to normal, but the P3 amplitude abnormality persists. This protracted deficit in long-term abstinent alcoholics suggests the possibility that P3 deficits may precede alcohol use and dependence. Indeed, a number of studies have reported low P3 amplitudes in young people at high risk for developing alcoholism, such as young sons of alcoholic fathers.

Recent findings indicate that in addition to P3, many of the aberrations in resting and event-related oscillations reported in alcoholics already are apparent in high-risk offspring of alcoholics before alcohol exposure. The increased resting beta power observed in alcoholics also is present in both male and female offspring of alcoholics. The frontal theta deficits observed in alcoholics during a mental calculation task also are apparent in offspring of alcoholics. Similar to their alcoholic parents, the offspring manifest increased resting theta and decreased active frontal theta, suggesting that cognitive processing may be inefficient in these people before the development of alcoholism. As the electrophysiological differences are not related to length of abstinence and are apparent in people at risk before they have been exposed to alcohol, these neural oscillations could be considered markers of risk. The electrophysiological imbalances in excitation-inhibition observed in the offspring of alcoholics may be involved in the predisposition to develop alcoholism. Long-term studies of childhood and adolescent precursors of adult alcohol abuse consistently identify a cluster of behavioral traits described as disinhibited, undercontrolled, impulsive, or aggressive, which significantly predict high levels of alcohol consumption or abuse.

Taken together, the electrophysiological findings suggest that an imbalance between excitation and inhibition may be involved in a predisposition to develop alcoholism. Alcoholics and people at risk for alcoholism manifest increased resting oscillations and decreased "active" oscillations in the same frequency bands during cognitive tasks. Not only does this underlying CNS disinhibition appear to be involved in the predisposition toward alcoholism, but it also is hypothesized that neuroelectric features related to CNS disinhibition may provide insights into the neurobiology of craving and relapse. The relationship between this underlying CNS hyperexcitability and the induction of alcohol abuse leading to alcohol dependence remains to be explained.

About the Author

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