Overview
The Withdrawal Mechanism
Alcohol continuously enhances inhibitory GABA A signalling and suppresses excitatory NMDA glutamate activity.
NCLEX-RN
NCLEX-RN
Alcohol continuously enhances inhibitory GABA-A signalling and suppresses excitatory NMDA glutamate activity. With sustained heavy use, the brain compensates: GABA-A responsiveness is reduced, while NMDA activity is increased. When alcohol intake stops, those adaptations remain, but the alcohol-mediated inhibition is gone. The result is a hyperexcitable central nervous system. That mechanism explains the clinical pattern. Increased sympathetic activity produces tremor, sweating, anxiety, tachycardia, hypertension, and sometimes fever. Gastrointestinal upset, insomnia, agitation, and perceptual disturbances may appear early. As excitability rises, seizures and delirium tremens can develop. Symptoms often begin within 6 to 24 hours after the last drink. Hallucinosis may occur during the first 12 to 48 hours, withdrawal seizures commonly occur within 24 to 48 hours, and delirium tremens often appears later, around 48 to 96 hours. These time ranges are guides, not a schedule. A patient may seize without a long period of visibly worsening symptoms, and a positive blood alcohol level does not exclude withdrawal in a person who is physiologically dependent. Repeated withdrawal episodes can become progressively more severe through a process often called kindling. A...
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