Hinostroza Fernando, Mahr Michele M
Centro de Investigación de Estudios Avanzados del Maule, Vicerrectoría de Investigación y Postgrado, Universidad Católica del Maule, Talca, Chile.
Centro de Investigación en Neuropsicología y Neurociencias Cognitivas, Facultad de Ciencias de la Salud, Universidad Católica del Maule, Talca, Chile.
Brain Behav. 2025 Jan;15(1):e70230. doi: 10.1002/brb3.70230.
This extensive literature review investigates the relationship between post-traumatic stress disorder (PTSD) and alcohol use disorder (AUD), focusing on the neurobiological changes associated with their co-occurrence. Given that these disorders frequently coexist, we analyze mechanisms through which alcohol serves as a coping strategy for PTSD symptoms, particularly highlighting the drinking-to-cope self-medication model, which suggests that alcohol use exacerbates PTSD symptoms and complicates recovery.
A systematic literature search was conducted across multiple databases, including PubMed and Google Scholar, to identify studies examining the intersection of the biopsychosocial model with PTSD, AUD, and associated neural alterations.
Findings demonstrate that chronic PTSD is associated with progressive dysfunction in the amygdala, hippocampus, prefrontal cortex, hypothalamic-pituitary-adrenal axis, and white matter pathways. Also, our findings underscore alterations within the reward system, prefrontal cortex, hippocampus, amygdala, basal ganglia, and hypothalamic-pituitary-adrenal axis that contribute to the pathophysiology of AUD. Our results support the notion that a biopsychosocial framework is essential for contemporary addiction treatment, particularly in the context of alcohol addiction and PTSD.
PTSD frequently leads individuals to use alcohol as a maladaptive coping strategy, ultimately resulting in neuroadaptive alterations across critical brain regions. These neurobiological changes contribute to the development and maintenance of AUD. The findings reiterate the necessity of employing a biopsychosocial model in treating individuals grappling with both PTSD and AUD. This model allows for a comprehensive understanding of the unique challenges faced by this population, integrating biological, psychological, and social factors that influence recovery.
本广泛的文献综述调查了创伤后应激障碍(PTSD)与酒精使用障碍(AUD)之间的关系,重点关注与它们共病相关的神经生物学变化。鉴于这些障碍经常共存,我们分析了酒精作为PTSD症状应对策略的机制,特别强调了饮酒应对自我药物治疗模型,该模型表明饮酒会加剧PTSD症状并使康复复杂化。
在多个数据库(包括PubMed和谷歌学术)中进行了系统的文献检索,以识别研究生物心理社会模型与PTSD、AUD及相关神经改变交叉点的研究。
研究结果表明,慢性PTSD与杏仁核、海马体、前额叶皮质、下丘脑 - 垂体 - 肾上腺轴和白质通路的渐进性功能障碍有关。此外,我们的研究结果强调了奖赏系统、前额叶皮质、海马体、杏仁核、基底神经节和下丘脑 - 垂体 - 肾上腺轴内的改变,这些改变促成了AUD的病理生理学。我们的结果支持这样一种观点,即生物心理社会框架对于当代成瘾治疗至关重要,特别是在酒精成瘾和PTSD的背景下。
PTSD经常导致个体将酒精作为一种适应不良的应对策略,最终导致关键脑区的神经适应性改变。这些神经生物学变化促成了AUD的发展和维持。研究结果重申了在治疗同时患有PTSD和AUD的个体时采用生物心理社会模型的必要性。该模型有助于全面理解这一人群面临的独特挑战,整合影响康复的生物、心理和社会因素。