![]() For this reason, there have been many attempts to classify symptoms of AWS either by severity or time of onset to facilitate prediction and outcome. The alcohol withdrawal syndrome is a dynamic and complex process. ![]() In withdrawal, excitotoxicity is induced by further raise in homocysteine via rebound activation of glutamatergic neurotransmission. During active drinking, there is an increase in homocysteine through stimulation of the NMDA receptors. 9 Another excitotoxic compound that is increased in AUD is homocysteine. 12 In combination with increased glutamate and norepinephrine, it may also cause the elongation of the QT interval in people who have active epilepsy this can increase the risk of sudden unexpected death in epilepsy (SUDEP). 10, 11 Moreover, polymorphisms in the dopamine receptor 2 gene seem to influence not only AUD but also the clinical manifestation of alcohol withdrawal symptoms. In withdrawal, increase in dopamine levels contributes to the clinical manifestations of autonomic hyperarousal and hallucinations. During alcohol use, increase in dopamine positively influences the reward system thereby maintaining abuse. Dopamine is another neurotransmitter involved in alcohol withdrawal states. 8 As upregulation of NMDA receptors as well as reduced GABA‐A receptor inhibition largely explain the clinical symptoms, the therapeutic approach to AWS mainly targets these mechanisms. 8 Therefore, the trigger zone of these seizures is distinct from that believed to be responsible for seizures in the context of epilepsy, and this may explain why epileptiform activity is rarely observed in the EEG after alcohol withdrawal seizures. 10 The latter are usually of generalized tonic–clonic type and are mediated largely in the brainstem by abrogation of the tonic inhibitory effect of the GABAergic delta subunits. 7Ībrupt cessation of chronic alcohol consumption unmasks these changes with a glutamate‐mediated CNS excitation resulting in autonomic overactivity and neuropsychiatric complications such as delirium and seizures. 9 Prolonged alcohol use leads to the development of tolerance and physical dependence, which may result from compensatory functional changes by downregulation of GABA receptors and increased expression of NMDA receptors with production of more glutamate to maintain central nervous system (CNS) transmitter homeostasis. 7, 8 The local distribution of these subunits explains why the cerebellum, cortical areas, thalamic relay circuitry, and brainstem are the main networks that mediate the intoxicating effects of alcohol. The purpose of this review is to increase the awareness of the early clinical manifestations of AWS and the appropriate identification and management of this important condition in a neurological setting.Įthanol is a central nervous system depressant that produces euphoria and behavioral excitation at low blood concentrations due to increased glutamate binding to N‐methyl‐D‐aspartate (NMDA) receptors at higher concentrations, it leads to acute intoxication by potentiation of the gamma‐aminobutyric acid (GABA) effects, 7 particularly in receptors with delta subunits. ![]() Nonetheless, diagnosis and treatment are often delayed until dramatic symptoms occur. 6ĪUDs are common in patients referred to neurological departments, admitted for coma, epileptic seizures, dementia, polyneuropathy, and gait disturbances. However, with early detection and appropriate treatment, the expected mortality is in the range of 1% or less. ![]() 4, 5 Delirious patients show high rates of comorbidities, and their mortality rate is comparable to patients having severe malignant diseases. A complicated AWS includes epileptic seizures and/or delirium tremens (DT), the occurrence of which may be as high as 15% in AUD patients. 3 Severe AWS more than doubles the length of stay and frequently requires treatment at the ICU. 2 Alcohol withdrawal syndrome (AWS) is a well‐known condition occurring after intentional or unintentional abrupt cessation of heavy/constant drinking, and it occurs in about 8% of hospitalized AUD inpatients. 1 It is estimated that up to 42% of patients admitted to general hospitals, and one‐third of patients admitted to hospital intensive care units (ICU) have AUD. 1. Introduction ‐ Medical Burden of Alcohol AbuseĪn estimated 76.3 million people worldwide have alcohol use disorders (AUDs), and these account for 1.8 million deaths each year.
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