El consumo de riesgo de alcohol y el riesgo de dependencia al alcohol presentan correlatos neurofisiológicos diferentes / Hazardous alcohol consumption and risk of alcohol dependence present different neurophysiological correlates

Introducción. El consumo de riesgo de alcohol (CRA) es un patrón de consumo que puede resultar dañino para el usuario o para los demás. Investigaciones previas sugieren que el CRA y la dependencia al alcohol comparten algunas características neurofisiológicas, pero difieren en otras. Objetivo. Determinar si el CRA y la dependencia al alcohol presentan correlatos neurofisiológicos diferentes. Sujetos y métodos. Doscientos sujetos realizaron la prueba de detección de CRA y riesgo de dependencia al alcohol (DEP). Se realizó un estudio de electroencefalografía cuantitativa para determinar la potencia absoluta, la potencia relativa y la frecuencia media de las bandas delta, theta, alfa y beta en sujetos con CRA, con DEP y controles. Resultados. Un total de 114 sujetos cumplió los criterios de inclusión. El grupo con CRA presentó mayor potencia absoluta, mayor potencia relativa y menor frecuencia media de la banda beta en comparación con los controles, mientras que el grupo con DEP presentó menor potencia absoluta de la banda delta que los controles. Conclusiones. El DEP y el CRA presentan diferentes correlatos neurofisiológicos. Hay un efecto importante de la gravedad de la dependencia al alcohol sobre sus correlatos neurofisiológicos. Nuestros resultados apoyan la existencia de dos tipos distintos de desinhibición conductual

Introduction. Hazardous alcohol consumption (HAC) is a pattern of alcohol use that may result in harm for the user and/or for those around them. Prior research has suggested that HAC and alcohol dependence share some neurophysiological features but differ in others. Aim. To determine whether HAC and alcohol dependence presented different neurophysiological correlates. Subjects and methods. Two hundred subjects were screened for HAC or alcohol dependence. A quantitative electroencephalographic analysis of delta, theta, alpha and beta absolute power, relative power and mean frequency in subjects with HAC but not alcohol dependence, subjects with risk of alcohol dependence and controls was performed. Results. One hundred and fourteen subjects met inclusion criteria. The HAC group presented with higher beta absolute power and relative power, as well as a lower beta mean frequency than the control group, while the group with risk of alcohol dependence presented lower delta absolute power than controls. Conclusions. HAC and risk of alcohol dependence present different neurophysiological correlates. There is an important effect of the severity of alcohol dependence on neurophysiological correlates of this condition. Our results support the existence of two different types of behavioral disinhibition

Quantitative electroencephalography analysis in university students with hazardous alcohol consumption, but not alcohol dependence.

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.