Kelmendi Benjamin, Adams Thomas G, Yarnell Stephanie, Southwick Steven, Abdallah Chadi G, Krystal John H
Department of Psychiatry, Yale University School of Medicine, New Haven, CT.
Clinical Neuroscience Division, Department of Veterans Affairs, National Center for Posttraumatic Stress Disorder, Veterans Affairs Connecticut Healthcare System, West Haven, CT;
Eur J Psychotraumatol. 2016 Nov 8;7:31858. doi: 10.3402/ejpt.v7.31858. eCollection 2016.
Posttraumatic stress disorder (PTSD) is a chronic debilitating psychiatric disorder characterized by symptoms of re-experience, avoidance, and hyperarousal that can arise immediately or many years after exposure to a traumatic event and injury. Although extensive research has been done over the past 30 years, the etiology of PTSD remains largely unknown. Several neurobiological systems have been implicated in the pathophysiology and vulnerability for developing PTSD; however, first-line pharmacotherapies are limited. Less than 30% achieve full remission, and even then, approved pharmacological treatments often take weeks for therapeutic effect. This article aims to review the pathophysiology of PTSD within multiple neurobiological systems and how these mechanisms are used as pharmacologic targets of treatment, as well as their potential for future targets of intervention.
创伤后应激障碍(PTSD)是一种慢性致残性精神障碍,其特征为反复体验、回避和过度警觉等症状,这些症状可在接触创伤事件和损伤后立即出现或多年后出现。尽管在过去30年里进行了广泛研究,但PTSD的病因在很大程度上仍不清楚。几个神经生物学系统与PTSD的病理生理学和易感性有关;然而,一线药物治疗有限。不到30%的患者能完全缓解,即便如此,获批的药物治疗通常需要数周才能产生治疗效果。本文旨在综述多个神经生物学系统中PTSD的病理生理学,以及这些机制如何用作治疗的药理学靶点,以及它们作为未来干预靶点的潜力。