Alcohol, alcoholism, and the neural correlates of emotion

The relationship between alcohol and emotion is extremely complex. Prolonged heavy alcohol consumption and acute alcohol administration both have impacts on emotional processing in the brain. In this thesis, we use functional magnetic resonance imaging to explore differences in emotional processing between alcoholic patients and healthy controls, and administer intravenous alcohol in order to investigate how alcohol affects the neural correlates of emotion.;Consistent with several theories of addiction, we find that alcoholic patients relative to healthy controls demonstrate an increased neural response to negative, fear-inducing visual stimuli, and a decreased response to positive stimuli. This difference can be reduced through the presentation of visual alcohol cues, which may have become conditioned anxiolytic cues to alcoholic patients. Deficits in emotional processing can also be modulated by treatment with the anxiolytic drug LY686017, which appears to decrease the response to negative and increase response to positive cues in patients on active drug relative to those on a placebo treatment. We then show that alcoholic patients activate frontal brain structures more so than controls when engaged in cognitive or emotional decision-making tasks, perhaps suggesting inefficiency of frontal brain systems involved in emotional processing.;We suggest that alcoholic patients use alcohol to neutralize this increased negative/decreased positive emotional response. In an intravenous alcohol challenge with social drinkers, we show that alcohol enhances positive affect via its activity in the mesocorticolimbic brain circuit, and decreases negative affect via its modulation of visual-emotional brain circuits. These experiments together suggest that alcoholism may devolve into a reinforcing cycle of emotional disregulation and increased alcohol consumption, which may contribute to the maintenance of alcoholism. We argue that emphasis must be placed on treating mood dysregulation when developing new alcoholism therapies.