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The former, indicated by reduced GABA and alpha-2-adrenoceptor activity, acts in conjunction with, and is exacerbated by, the latter, which itself may be due to the potentiation of NMDA activity by depletion of magnesium, and overactivity of catecholaminergic and CRF neurones. These dysfunctions produce immediate effects and may also contribute to the long-term changes in brain excitability by a kindling-like process. It is possible that early and active treatment may oppose this process. Present strategies for treatment of alcohol withdrawal enhance GABA and alpha-2 inhibitory, or reduce excitatory, mechanisms. 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