Clergue-Duval Virgile, Coulbault Laurent, Questel Frank, Cabé Nicolas, Laniepce Alice, Delage Clément, Boudehent Céline, Bloch Vanessa, Segobin Shailendra, Naassila Mickael, Pitel Anne-Lise, Vorspan Florence
Département de Psychiatrie et de Médecine Addictologique, Site Lariboisière Fernand-Widal, GHU APHP Nord-Université Paris Cité, APHP, F-75010 Paris, France.
Inserm UMRS-1144 Optimisation Thérapeutique en Neuropsychopharmacologie, Université Paris Cité, F-75006 Paris, France.
Antioxidants (Basel). 2022 Oct 21;11(10):2078. doi: 10.3390/antiox11102078.
Alcohol use is a leading cause of mortality, brain morbidity, neurological complications and minor to major neurocognitive disorders. Alcohol-related neurocognitive disorders are consecutive to the direct effect of chronic and excessive alcohol use, but not only. Indeed, patients with severe alcohol use disorders (AUD) associated with pharmacological dependence suffer from repetitive events of alcohol withdrawal (AW). If those AW are not managed by adequate medical and pharmacological treatment, they may evolve into severe AW, or be complicated by epileptic seizure or (DT). In addition, we suggest that AW favors the occurrence of Wernicke's encephalopathy (WE) in patients with known or unknown thiamine depletion. We reviewed the literature on oxidative stress as a core mechanism in brain suffering linked with those conditions: AW, epileptic seizure, DT and WE. Thus, we propose perspectives to further develop research projects aiming at better identifying oxidative stress brain damage related to AW, assessing the effect of repetitive episodes of AW, and their long-term cognitive consequences. This research field should develop neuroprotective strategies during AW itself or during the periwithdrawal period. This could contribute to the prevention of severe alcohol-related brain damage and cognitive impairments.
饮酒是导致死亡、脑部疾病、神经并发症以及从轻度到重度神经认知障碍的主要原因。酒精相关神经认知障碍不仅是长期过量饮酒直接作用的结果。实际上,患有与药物依赖相关的严重酒精使用障碍(AUD)的患者会经历反复的酒精戒断(AW)。如果这些酒精戒断情况没有得到适当的医学和药物治疗,可能会发展为严重的酒精戒断,或并发癫痫发作或震颤谵妄(DT)。此外,我们认为酒精戒断会促使已知或未知硫胺素缺乏的患者发生韦尼克脑病(WE)。我们回顾了关于氧化应激作为与这些情况(酒精戒断、癫痫发作、震颤谵妄和韦尼克脑病)相关的脑部损伤核心机制的文献。因此,我们提出了进一步开展研究项目的前景,旨在更好地识别与酒精戒断相关的氧化应激脑损伤,评估反复酒精戒断发作的影响及其长期认知后果。该研究领域应在酒精戒断期间或戒断期周围制定神经保护策略。这可能有助于预防严重的酒精相关脑损伤和认知障碍。