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ALCOHOL, WITHDRAWAL SYNDROME AND MEDIATORS IN THE CENTRAL NERVOUS SYSTEM /
ALKOHOL, APSTINENTSKI SINDROM I MEDIJATORI U CENTRALNOM NERVNOM SISTEMU

Authors

 

Neykova - Vasileva Lyudmila1

1 Clinic of Emergency Toxicology, Military Medical Academy, Sofia

 

UDK: 616-074-056.85:613.81


The paper recieved/ Rad primljen: 10.04.2018.

Accepted / Rad prihvaćen: 05.05.2018.

 


Correspondent to


Assist. prof. Neykova - Vasileva Lyudmila, MD,PhD
Clinic of Emergency Toxicology, Military Medical Academy
Georgi Sofiiski 3, Sofia 1606, Bulgaria
e-mail: laneykova@abv.bg

 

 

Abstract

 

The Alcohol withdrawal syndrome (AWS) reflects the neuro-biochemical adaptation of the organism to recurrent alcohol consumption and the symptoms are opposite of those caused by the substance. The core of the multiple abstinence pathology consists of changes in neuro-mediators. Ethanol rapidly crosses the blood-brain barrier and affects membranes, ion channels, enzymes and central nervous system (CNS) neurons.The material aims to analyze the data in the literature about the influence of the chronic alcohol use on the catecholamine levels, which are the basis for the intensity and duration of the alcohol withdrawal syndrome.To conclude: the catecholamine neurotransmission is the basis for the various symptoms of ethanol withdrawal. All patients with alcohol addiction develop AWS. Their pathogenesis is the plasma levels of adrenaline and noradrenaline. AWS is often of a short duration, but can quickly enter into a pre-delirium or delirium. In the pre-crisis period, the somatic manifestations are discrete – light tremor, tendency to tachycardia, minor increase in blood pressure (BP), skin moistening. It is during this period that an active observation is needed to capture these prodromal signs. In the meantime, the onset of treatment often prevents the onset of delirium tremens.

 

 

Key words:

alcohol, withdrawal syndrome, mediators in the central nervous system, catecholamine’s

 

 

Sažetak

 

Alkoholni apstinentski sindrom je odraz neurobiohemijske adaptacije organizma na ponovljenu konzumaciju alkohola, a simptomi koji se javljaju su suprotni onima koji su uzrokovani supstancom. Razlog apstinentske pojave nalazi se u promenama u neuromedijatorima. Etanol brzo prelazi krvno-moždanu barijeru i utiče na membrane, jonske kanale, enzime i neurone centralnog nervnog sistema (CNS). Cilj rada je analiza podataka u literaturi o uticaju hroničnog korišćenja alkohola na nivoe kateholamina, koji su osnova intenziteta i trajanja alkoholnog apstinentskog sindroma. Da zaključimo: neurotransmisija kateholamina je osnova za razne simptome alkoholne apstinencije. Svi pacijenti sa zavisnošću od alkohola razvijaju alkohlni apstinentski sindrom. Za patogenezu ovog oboljenja su odgovorni nivoi adrenalina i noradrenalina u plazmi. Apstinentski sindrom je često kratkog trajanja, ali može brzo ući u pre-delirium ili delirijum. U periodu pre krize, somatske manifestacije su diskretne - blagi tremor, tendencija ka tahikardiji, blago povećanje krvnog pritiska, vlaženje kože. Tokom ovog perioda potrebno je aktivno posmatranje kako bi se uhvatili ovi prodromalni znaci. U međuvremenu, početak lečenja često sprečava pojavu delirium tremensa.

 

 

Ključne reči:

alkohol, apstinentski sindrom, medijatori u centralnom nervnom sistemu, kateholamini

 

 

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PDF Neykova Vasileva L. • MD-Medical Data 2018;10(2): 077-080

 

 

 

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