The neurophysiological and neurochemical effects of alcohol on the brain are inconsistent with current evidence based models of sleepwalking.

The DSM-5 and ICSD-3 have removed alcohol from the list of potential triggers for sleepwalking due to the lack of empirical evidence. Recent imaging and EEG based studies of sleepwalking and confusional arousals have provided a more data-based method of examining if alcohol is compatible with what is known about the neurophysiology and neurochemistry of sleepwalking. These studies have demonstrated a deactivation of the frontal areas of the brain, while the cingulate or motor cortex remains active and characterized activation in the form of beta EEG. This increase in activation is attributed to a decrease in the inhibitory activity the neurotransmitter GABAA. This cerebral excitability of the cingulate cortex of sleepwalkers is also present in the brains of sleepwalkers during wakefulness compared to normal controls. Alcohol is well established to have an inhibitory effect on the brain and specifically on the motor areas via the inhibitory effects of increased GABAA activity. Thus, the empirical data show sleepwalking is characterized by a decrease in the inhibitory activity of GABAA - permitting or facilitating motor activity while alcohol has the opposite effect of increasing GABAA and inhibiting motor activity. This is inconsistent with theories that alcohol is somehow a trigger or facilitator for sleepwalking.