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Alcohol Withdrawal Seizures: Neurobiological Mechanisms, Clinical Predictors, and Evidence- Based Management
Valentin Skryabin1, Alexandra Malygina2, Svetlana Sokolova2
1Books Committee, Royal College of Psychiatrists, London, UK.
Alcohol withdrawal seizures stem from brain chemical imbalances during alcohol cessation. Early recognition and tailored treatments are crucial for managing these seizures and preventing long-term cognitive issues.
Area of Science:
- Neuroscience
- Clinical Neurology
- Pharmacology
Background:
- Alcohol withdrawal (AW) seizures are acute symptomatic seizures linked to alcohol cessation in dependent individuals.
- These seizures increase risks of delirium tremens, prolonged hospitalization, and neurocognitive decline.
- This review synthesizes current knowledge on AW seizures' neurobiology, clinical aspects, genetics, and treatments.
Purpose of the Study:
- To review recent findings on the neurobiological underpinnings of alcohol withdrawal seizures.
- To explore clinical features, genetic risk factors, and treatment strategies for AW seizures.
Main Methods:
- Focused narrative review of PubMed and Scopus (2000-2024).
- Keywords included alcohol withdrawal seizures, pathophysiology, GABA, NMDA receptors, kindling, carbamazepine, hippocampal neurogenesis, and genetic susceptibility.
- Emphasis on clinical trials, animal models, and integrated reviews.
Main Results:
- AW seizures result from GABAergic and glutamatergic imbalance, worsened by abrupt alcohol cessation.
- Hippocampal neurogenesis and dentate gyrus dysfunction contribute to seizure susceptibility.
- Genetic polymorphisms (e.g., SLC6A3, APOE) influence vulnerability; carbamazepine shows efficacy as an adjunct treatment.
Conclusions:
- AW seizures are a key clinical and neurobiological marker in alcohol use disorders.
- Understanding pathophysiology and prognosis aids stratified treatment.
- Integrated approaches for acute symptom control and long-term relapse prevention are supported.
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