Abstract
The current disease concept of alcohol dependence includes the psychosocial and neurobiological foundations and consequences of alcoholism. Relapse can be triggered by alcohol craving, which in turn can be elicited by conditioned urges for the rewarding properties of alcoholism or conditioned withdrawal. Neurobiological research points to the dispositional factor of monoaminergic dysfunction, which interacts with acute pleasant and unpleasant effects of alcohol intake. Alcohol consumption is maintained by neuroadaptation and withdrawal symptoms, which may also be elicited as a conditioned response by alcohol-associated cues and drinking situations. In the dopamine-opioidergic reward system, sensitization may contribute to reduced control of alcohol intake after exposure to alcohol cues or small amounts of alcohol. The rather high relapse risk can be reduced by psychosocial intervention and additive pharmacotherapy. Current pharmacological treatment options include medication that modulates excitatory and inhibitory neurotransmission via NMDA and GABA-A receptors such as acamprosate, blockade of mu-opiate receptors with naltrexone and modulation of ion channels with antiepileptic medication. We will review the evidence for the respective drugs and discuss the underlying mechanisms of relapse and relapse prevention.
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