What is the role of alcohol withdrawal in the pathogenesis of delirium tremens (DTs)?

Updated: Nov 06, 2020
  • Author: Michael James Burns, MD, FACEP, FACP, FIDSA; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, FAPS, MCCM  more...
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Answer

Chronic intake of alcohol affects several neurotransmitter systems in the brain. These effects include (1) increased release of endogenous opiates; (2) activation of the inhibitory gamma-aminobutyric acid-A (GABA-A) receptor producing increased GABA inhibition, with a resultant influx of chloride ions; (3) up-regulation of the postsynaptic N-methyl-D-aspartate (NMDA) type of glutamate receptor, which mediates the postsynaptic excitatory effects of glutamate; and (4) interactions with serotonin and dopamine receptors. During withdrawal from alcohol, the loss of GABA-A receptor stimulation causes a reduction in chloride flux and is associated with tremors, diaphoresis, tachycardia, anxiety, and seizures. In addition, the lack of inhibition of the NMDA receptors may lead to seizures and delirium. Excessive nervous system excitability during periods of abstinence from alcohol is related to the effect of alcohol on the number and function of brain receptors.


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