Citation

Núñez-Jaramillo L, Vega-Perera P, Ramírez-Lugo L, Reyes-López JV, Santiago-Rodríguez E, Herrera-Morales WV. Neuroreport 2015; 26(10): 555-560.

Affiliation

aHealth Sciences Division, University of Quintana Roo, Colonia Magisterial, Chetumal, Quintana Roo bNeurosciences Division, Cellular Physiology Institute, National and Autonomous University of Mexico, Delegación Coyoacán cCentral Nervous System Clinic, Biomedical Research Department, Medicine School, Autonomous University of Queretaro, Santiago de Querétaro dNeurologic Diagnosis, Treatment and Research, Querétaro, Querétaro, México.

Copyright

(Copyright © 2015, Lippincott Williams and Wilkins)

DOI

10.1097/WNR.0000000000000384

PMID

26035281

Abstract

Hazardous alcohol consumption is a pattern of consumption that leads to a higher risk of harmful consequences either for the user or for others. This pattern of alcohol consumption has been linked to risky behaviors, accidents, and injuries. Individuals with hazardous alcohol consumption do not necessarily present alcohol dependence; thus, a study of particular neurophysiological correlates of this alcohol consumption pattern needs to be carried out in nondependent individuals. Here, we carried out a quantitative electroencephalography analysis in health sciences university students with hazardous alcohol consumption, but not alcohol dependence (HAC), and control participants without hazardous alcohol consumption or alcohol dependence (NHAC). We analyzed Absolute Power (AP), Relative Power (RP), and Mean Frequency (MF) for beta and theta frequency bands under both eyes closed and eyes open conditions. We found that participants in the HAC group presented higher beta AP at centroparietal region, as well as lower beta MF at frontal and centroparietal regions in the eyes closed condition. Interestingly, participants did not present any change in theta activity (AP, RP, or MF), whereas previous reports indicate an increase in theta AP in alcohol-dependent individuals. Our results partially resemble those found in alcohol-dependent individuals, although are not completely identical, suggesting a possible difference in the underlying neuronal mechanism behind alcohol dependence and hazardous alcohol consumption. Similarities could be explained considering that both hazardous alcohol consumption and alcohol dependence are manifestations of behavioral disinhibition.

Language: en