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| It is most common in people who have a history of alcohol withdrawal, especially in those who drink the equivalent of 7 - 8 pints of beer (or 1 pint of "hard" alcohol) every day for several months. Delirium tremens also commonly affects those with a history of habitual alcohol use or alcoholism that has existed for more than 10 years. | | It is most common in people who have a history of alcohol withdrawal, especially in those who drink the equivalent of 7 - 8 pints of beer (or 1 pint of "hard" alcohol) every day for several months. Delirium tremens also commonly affects those with a history of habitual alcohol use or alcoholism that has existed for more than 10 years. |
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| The exact pharmacology of ethanol is not fully understood: however, it is theorized that delirium tremens is caused by the effect of alcohol on the benzodiazepine-GABA<sub>A</sub>-chloride receptor complex for the inhibitory neurotransmitter [[Gamma-aminobutyric acid|GABA]]. Constant consumption of [[alcoholic beverage]]s (and the consequent chronic sedation) causes a counterregulatory response in the brain in attempt to regain [[homeostasis]].
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| This causes [[downregulation]] of these [[Receptor (biochemistry)|receptor]]s, as well as an up-regulation in the production of excitatory [[neurotransmitters]] such as norepinephrine, dopamine, epinephrine, and serotonin - all of which further the drinker's tolerance to alcohol and may intensify [[tonic-clonic seizure]]s. When alcohol is no longer consumed, these down-regulated GABA<sub>A</sub> receptor complexes are so insensitive to GABA that the typical amount of GABA produced has little effect; compounded with the fact that GABA normally inhibits [[action potential]] formation, there are not as many receptors for GABA to bind to - meaning that [[sympathetic nervous system|sympathetic]] activation is unopposed. This is also known as an "[[adrenergic]] storm". Effects of this "[[adrenergic]] storm" can include (but are not limited to) [[tachycardia]], [[hypertension]], [[hyperthermia]], [[hyperreflexia]], [[diaphoresis]], [[myocardial infarction|heart attack]], [[cardiac arrhythmia]], [[stroke]], [[anxiety]], [[panic attacks]], [[paranoia]], and [[agitation]].
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| This is all made worse by excitatory neurotransmitter upregulation, so not only is sympathetic nervous system over-activity unopposed by GABA, there is also more of the [[serotonin]], [[norepinephrine]], [[dopamine]], [[epinephrine]], and particularly [[glutamate]]. Excitory [[NMDA receptor]]s are also upregulated, contributing to the delirium and neurotoxicity (by [[excitotoxicity]]) of withdrawal. Direct measurements of central norepinephrine and its metabolites is in direct correlation to the severity of the alcohol withdrawal syndrome.[http://findarticles.com/p/articles/mi_m0847/is_n4_v13/ai_8276920]
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| It is possible that [[Psychology|psychological]] (''i.e.'', non-physical) factors also play a role, especially those of [[infection]]s, [[malnutrition]], or other underlying medical disorders - often related to [[alcoholism]].
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| ==References== | | ==References== |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Vishnu Vardhan Serla M.B.B.S. [2]
Causes
Causes of delirium tremens include
Delirium tremens can occur after a period of heavy alcohol drinking, especially when the person does not eat enough food.
It may also be triggered by head injury, infection, or illness in people with a history of heavy use of alcohol.
It is most common in people who have a history of alcohol withdrawal, especially in those who drink the equivalent of 7 - 8 pints of beer (or 1 pint of "hard" alcohol) every day for several months. Delirium tremens also commonly affects those with a history of habitual alcohol use or alcoholism that has existed for more than 10 years.
References
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