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阐明创伤后应激障碍(PTSD)与物质使用障碍共病的神经生物学病因。

Elucidating the Neurobiologic Etiology of Comorbid PTSD and Substance Use Disorders.

作者信息

Hinckley Jesse D, Danielson Carla Kmett

机构信息

Division of Addiction Science, Treatment & Prevention, Department of Psychiatry, University of Colorado School of Medicine, 1890 N Revere Court, MS-F570, Aurora, CO 80045, USA.

National Crime Victims Research & Treatment Center, Department of Psychiatry & Behavioral Sciences, Medical University of South Carolina, 67 President Street, MSC 861, Charleston, SC 29425, USA.

出版信息

Brain Sci. 2022 Aug 31;12(9):1166. doi: 10.3390/brainsci12091166.

Abstract

Early childhood maltreatment and other traumatic event experiences ("trauma") are common among youth, including those with substance use problems including substance use disorders (SUD). Particularly, interpersonal violence is associated with high rates of comorbidity between posttraumatic stress disorder (PTSD) and SUD, and these comorbid disorders exhibit high levels of overlapping symptomatology. Theoretical models proposed to explain the bidirectional relationship between PTSD and SUD include the self-medication hypothesis and susceptibility hypothesis. In this article, we explore neurobiologic changes associated with trauma, PTSD, and SUD that underly dysregulated stress response. Examining lessons learned from recent translational and clinical research, we propose that further elucidating the neurobiologic etiology of comorbid PTSD and SUD will require a collaborative, interdisciplinary approach, including the integration of preclinical and clinical studies, exploration of biologic markers in clinical studies, and accumulation of larger studies and longitudinal studies with the power to study PTSD and SUD. Such research can transform the field and ultimately reduce high rates and costly impairment of co-occurring PTSD and SUD across the lifespan.

摘要

儿童期受虐及其他创伤性事件经历(“创伤”)在青少年中很常见,包括那些有物质使用问题(包括物质使用障碍,SUD)的青少年。特别是,人际暴力与创伤后应激障碍(PTSD)和SUD之间的高共病率相关,并且这些共病障碍表现出高度重叠的症状。为解释PTSD与SUD之间的双向关系而提出的理论模型包括自我药物治疗假说和易感性假说。在本文中,我们探讨了与创伤、PTSD和SUD相关的神经生物学变化,这些变化是应激反应失调的基础。通过研究近期转化研究和临床研究的经验教训,我们提出,要进一步阐明PTSD和SUD共病的神经生物学病因,需要一种协作性的跨学科方法,包括整合临床前研究和临床研究、在临床研究中探索生物标志物,以及开展更大型的研究和有能力研究PTSD和SUD的纵向研究。此类研究能够变革该领域,并最终降低一生中PTSD和SUD共病的高发生率及高昂的损害代价。

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