<unk>  is a component of alcohol withdrawal hypothesized to be the result of compensatory changes in response to chronic heavy alcohol use. Alcohol positively allosterically modulates the binding of GABA, enhancing its effect and resulting in inhibition of neurons projecting into the nucleus accumbens, as well as inhibiting NMDA receptors. This combined with desensitization of alpha-2 adrenergic receptors, results in a homeostatic upregulation of these systems in chronic alcohol use. When alcohol use ceases, the unregulated mechanisms result in hyperexcitability of neurons as natural GABAergic systems are down-regulated and excitatory glutamatergic systems are unregulated. This combined with increased noradrenergic activity results in the symptoms of<unk> .
Delirium tremens
Barbiturate
Ateliosis
Benzodiazepine withdrawal syndrome
Excited delirium
Hepatic encephalopathy
Bell's mania
Emergence delirium