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at higher concentrations, it leads to acute intoxication by potentiation of the gamma‐aminobutyric acid (GABA) effects,7 particularly in receptors with delta subunits.7, 8 The local distribution of these subunits explains why the cerebellum, cortical areas, thalamic relay circuitry, and brainstem are the main networks that mediate the intoxicating effects of alcohol.9 Prolonged alcohol use leads to the development of tolerance and physical dependence, which may result from compensatory functional changes by downregulation of GABA receptors and increased expression of NMDA receptors with production of more glutamate to maintain central nervous system (CNS) transmitter homeostasis.7 Abrupt cessation of chronic alcohol consumption unmasks these changes with a glutamate‐mediated CNS excitation resulting in autonomic overactivity and neuropsychiatric complications such as delirium and seizures.10 The latter are usually of generalized tonic–clonic type and are mediated largely in the brainstem by abrogation of the tonic inhibitory effect of the GABAergic delta subunits.8 Therefore, the trigger zone of these seizures is distinct from that believed to be responsible for seizures in the context of epilepsy, and this may explain why epileptiform activity is rarely observed in the EEG after alcohol withdrawal seizures.8 As upregulation of NMDA receptors as well as reduced GABA‐A receptor inhibition largely explain the clinical symptoms, the therapeutic approach to AWS mainly targets these mechanisms
