NEUROTRANSMITTERS CHANGES IN DELIRIUM TREMENS
Diseases

Author: andrea scollo
Date: 30/03/2012

Description

Delirium tremens is a serious medical emergency which often occurs in heavy drinkers in case of prolonged abstinence from ethanol. It is characterized by confused state of mind and hallucinations, which cause agitation and hyperactivity, especially uncontrollable tremors. The massive activation of neurovegetative system is responsible for symptoms like fever, mydriasis, high heart rate and marked sweating. If not reated, delirium tremens may lead to death especially because of alcoholic myopathy 2012. Several studies have shown alterations in some brain neurotransmitters, although some results are still to be confirmed completely.

DELIRIUM AND NORADRENALINE
It seems clear that noradrenergic activity increases during the attacks. Elevated levels of norepinephrine are found in the cerebrospinal fluid of patients withdrawing from alcohol and are believed due to a decrease in the alpha-2 receptor-mediated inhibition of presynaptic norepinephrine release. The hyperactivity of noradrenaline and adrenaline is shown by sudden increasing of blood pressure, arrhythmias, mydriasis and seizures. The discover of this neurotransmitter as possible cause of hypomagnesemia and hyperactivity of other molecules in the brain has led and is leading right now to the develop of certain drugs to keep under control the clinical features just now described Delirium tremens.Recent neurophisiologic concepts and therapeutic outlook 1992. The importance of the whole adrenergic system is shown by high levels of AMPc in urine [Cyclic adenosine monophosphate (3'5' cAMP) in the alcohol withdrawal syndrome. Clinico-pathogenetic perspectives]. 1984

DELIRIUM AND SEROTONINE
The studies about the role of serotonine dont' agree one another. Serotonine is known to be an important slow-wave sleep mediator, which may be disturbed as in withdrawal syndrome as in drinking periods Alcohol's effects on sleep in alcoholics.2001. Serotonin levels are likely to increase, but why this happens is not known entirely. On the other hand, if serotonin levels diminished, at least in some areas of the brain, couldn't we explain the depression sometimes linked to post-attack periods in alcohol-witdrawal?
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5-HTP has been suggested as possible source of therapy in delirium, but this theory is still to be proved, as weel as its effectiveness in other brain illnesses The many uses of 5-HTP.2011.

DOPAMINE
Levels of dopamine are higher on chronic ethanol exposure, especially in ventral tegmental area and nucleus accumbens, little raising in nigrostriatal system. However, when chronic exposure is terminated and the person stops drinking alcohol for a while, as in delirium tremens, dopamine release is likely to be diminished, because of the inhibition of opioids on dopaminergic cells: the dopaminergic cells make GABA cells active and these inhibit the same cells responsible for their activation. Finally, though it's not fully confirmed, some polymorphisms in dopamine receptors, especially DRD2, were associated with at least some cases of delirium tremens Interaction of SLC6A4 and DRD2 polymorphisms is associated with a history of delirium tremens. 2010.

GABA
Gaba is the most important inhibiting neurotransmitter in the brain and ethanol amplifies his action. So, it isn't surprising GABA levels get low in withdrawal syndrome: this reduction can account for the extreme excitability typical of delirium tremens.

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