This study developed a model of impaired inhibitory control in humans to test the efficacy of treatments for this deficit. Male social drinkers (N = 35) practiced a "go-stop" task that measured response inhibition. They then were assigned to 1 of 5 groups (n = 7) that performed the task under a different treatment. The model of impaired inhibitory control was provided by administering 0.62 g/kg alcohol to 1 group (A), whose response inhibition was compared with a placebo group (P). The other 3 groups received 0.62 g/kg alcohol plus a treatment designed to ameliorate alcohol impairment of inhibitory control: behavioral reinforcement (B), or 4.4 mg/kg caffeine (C), or a combination of both (B + C). Alcohol impaired inhibitory control, and all 3 treatments (B, C, and B + C) counteracted the impairment. The findings indicate that alcohol impairment of response inhibition may provide a useful human model to test conditions that may ameliorate or exacerbate deficits in behavioral control induced by drugs or other factors.
Much research on the effects of a dose of alcohol has shown that motor skills recover from impairment as blood alcohol concentrations (BACs) decline and that acute tolerance to alcohol impairment can develop during the course of the dose. Comparable alcohol research on cognitive performance is sparse but has increased with the development of computerized cognitive tasks. This article reviews the results of recent research using these tasks to test the development of acute tolerance in cognitive performance and recovery from impairment during declining BACs. Results show that speed and accuracy do not necessarily agree in detecting cognitive impairment, and this mismatch most frequently occurs during declining BACs. Speed of cognitive performance usually recovers from impairment to drug-free levels during declining BACs, whereas alcohol-increased errors fail to diminish. As a consequence, speed of cognitive processing tends to develop acute tolerance, but no such tendency is shown in accuracy. This "acute protracted error" phenomenon has not previously been documented. The findings pose a challenge to the theory of alcohol tolerance on the basis of physiological adaptation and raise new research questions concerning the independence of speed and accuracy of cognitive processes, as well as hemispheric lateralization of alcohol effects. The occurrence of alcohol-induced protracted cognitive errors long after speed returned to normal is identified as a potential threat to the safety of social drinkers that requires urgent investigation.
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