Journal
BIOLOGICAL PSYCHIATRY
Volume 48, Issue 4, Pages 276-286Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S0006-3223(00)00236-5
Keywords
P300; P3a; P3b; alcoholics; auditory event-related potential; Current Source Density; frontal cortex; cortical disinhibition
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Funding
- NIAAA NIH HHS [U10AA08402, U10AA08401, U10AA08403] Funding Source: Medline
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Background: P3a amplitude differences between alcoholic and control groups have not been well defined. Because event-related potential (ERP) differences between these groups appear to be influenced by task difficulty, the present study employed a new auditory ERP paradigm, in which target/standard tone discriminability was difficult, with infrequent nontarget stimuli used to elicit the P3a. Methods: A total of n = 27 male alcoholics and n = 25 male controls were assessed using a three-tone discrimination paradigm, in which the discriminability between the target and standard was difficult, with easily discriminable infrequent nontarget tones also presented. A P3a component with a centro-frontal maximum to the rare nontargets and a P3b with a parietal maximum amplitude to the target stimulus were obtained Current Source Density (CSD) maps were derived from the potential data and employed to assay topographical differences between subject groups. Results: Alcoholics produced smaller P3a amplitudes than control subjects to the rare nontargets with no peak latency differences observed The most prominent current sources are apparent more anteriorly for the nontarget compared to the target stimulus in both groups. There were more sources and sinks in the alcoholics than in the control subjects for P3a. A bootstrap analysis method showed that P3a CSD maps evinced distinct topographic distributions between alcoholics and control subjects in all brain regions. Conclusions: The lower P3a amplitude and weaker sources in alcoholics coupled with less topographic specificity in their CSD maps, suggests disorganized inefficient brain functioning. This global electrophysiological pattern suggests cortical disinhibition perhaps reflecting underlying CNS hyperexcitability in alcoholics. (C) 2000 Society of Biological Psychiatry.
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