Abstract
Substance use disorders (SUDs) are a major public health problem—with over 200 million people reporting drug use in 2016. Electroencephalography (EEG) is a powerful tool that can provide insights into the impact of SUDs on cognition. Specifically, modulated gamma activity may provide an index of the pathophysiology of SUDs. Thus, the purpose of this review was to investigate the impact of alcohol, tobacco, cannabis, cocaine, and amphetamine on gamma activity, among pre-clinical and clinical populations during acute and chronic exposure and withdrawal states. We searched multiple databases for key terms related to SUDs, EEG, and gamma and ensured rigorous methods by using a standardized review reporting tool. We included 30 studies in this review and found that all substances were associated with modulation of gamma activity, across states and in both preclinical and clinical populations. Gamma oscillations appeared to be differentially modulated in clinical versus preclinical populations and had the most complex relationship with alcohol, indicating that it may act differently than other substances. The findings of this review offer insights into the pathophysiology of SUDs, providing a potential window into novel treatments for SUDs via modulation of gamma activity.
Highlights
Substance abuse represents a rapidly growing global public health concern
The goal of this paper is to provide a comprehensive review of the existing body of literature on the effects of alcohol, tobacco, cannabis, cocaine, and amphetamine use on gamma oscillatory activity, among preclinical and clinical populations during acute, chronic, and withdrawal states
Tsurugizawa and colleagues investigated the effects of alcohol on local field potential (LFP) oscillations in the nucleus accumbens of 34 male Wistar rats [51]
Summary
Substance abuse represents a rapidly growing global public health concern. According to the United Nations Office on Drugs and Crime, 271 million people used at least one illicit drug in 2016 [1], of which 35 million have developed substance use disorders (SUDs) [1]. Cognition has been shown to be modulated with acute and chronic substance use. Studies have found that working memory, the ability to maintain and manipulate information over short periods of time [4], has been impaired with alcohol and cannabis use disorders (AUDs and CUDs) [5,6]. Cognitive deficits have been reported in individuals following acute alcohol intoxication, including disruptions in memory [10], divided attention [11], and information processing [12]. Cognition has been shown to rebound with discontinuing substance use (e.g., cannabis [20]), thereby furthering support for the association between cognition and SUDs, possibly through shared pathophysiology [21]. Investigating different states (e.g., acute, chronic, and withdrawal) of substance use on such pathophysiology may help to optimize the treatment for SUDs and associated cognitive deficits
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