Biological psychiatry · 2020
Alcohol and Neural Dynamics: A Meta-analysis of Acute Alcohol Effects on Event-Related Brain Potentials.
СтатьяМетаанализПоддержка NIH: внешняя программаНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Fairbairn Catharine E, Kang Dahyeon, Federmeier Kara D
Аннотация
BACKGROUND: An understanding of alcohol's acute neural effects could augment our knowledge of mechanisms underlying alcohol-related cognitive/motor impairment and inform interventions for addiction. Focusing on studies employing event-related brain potential methods, which offer a direct measurement of neural activity in functionally well-characterized brain networks, we present the first meta-analysis to explore acute effects of alcohol on the human brain.
METHODS: Databases were searched for randomized laboratory alcohol-administration trials assessing brain activity using event-related potentials. Hedges' g coefficients were pooled using 3-level random-effects meta-regression.
RESULTS: Sixty independent randomized controlled trials met inclusion (total N = 2149). Alcohol's effects varied significantly across neural systems, with alcohol leading to reductions in event-related potential components linked with attention (P3b), g = -0.40, 95% CI (-0.50, -0.29), automatic auditory processing (mismatch negativity), g = -0.44, 95% CI (-0.66, -0.22), and performance monitoring (error-related negativity), g = -0.56, 95% CI (-0.79, -0.33). These effects were moderated by alcohol dose, emerging as significant at doses as low as 0.026% blood alcohol concentration and increasing to moderate/large at 0.12%. In contrast, irrespective of dose, relatively small or nonsignificant alcohol effects emerged in other processing domains, including those linked to executive control (N2b responses) and stimulus classification (N2c responses).
CONCLUSIONS: Contrary to traditional conceptualizations of alcohol as a "dirty drug" with broad central nervous system depressant effects, results instead support accounts positing targeted alcohol effects in specific processing domains. By identifying alcohol effects on brain systems involved in performance monitoring and attention, results move toward the identification of mechanisms underlying alcohol-related impairment as well as factors reinforcing addiction.
METHODS: Databases were searched for randomized laboratory alcohol-administration trials assessing brain activity using event-related potentials. Hedges' g coefficients were pooled using 3-level random-effects meta-regression.
RESULTS: Sixty independent randomized controlled trials met inclusion (total N = 2149). Alcohol's effects varied significantly across neural systems, with alcohol leading to reductions in event-related potential components linked with attention (P3b), g = -0.40, 95% CI (-0.50, -0.29), automatic auditory processing (mismatch negativity), g = -0.44, 95% CI (-0.66, -0.22), and performance monitoring (error-related negativity), g = -0.56, 95% CI (-0.79, -0.33). These effects were moderated by alcohol dose, emerging as significant at doses as low as 0.026% blood alcohol concentration and increasing to moderate/large at 0.12%. In contrast, irrespective of dose, relatively small or nonsignificant alcohol effects emerged in other processing domains, including those linked to executive control (N2b responses) and stimulus classification (N2c responses).
CONCLUSIONS: Contrary to traditional conceptualizations of alcohol as a "dirty drug" with broad central nervous system depressant effects, results instead support accounts positing targeted alcohol effects in specific processing domains. By identifying alcohol effects on brain systems involved in performance monitoring and attention, results move toward the identification of mechanisms underlying alcohol-related impairment as well as factors reinforcing addiction.