Nutt D J
School of Medical Sciences, University of Bristol, United Kingdom.
J Clin Psychiatry. 2000;61 Suppl 5:24-9; discussion 30-2.
Posttraumatic stress disorder (PTSD) develops after exposure to events that are threatening and/or intensely distressing. Accumulating evidence suggests that intense psychological trauma can cause long-standing alterations in the neurobiological response to stress. These alterations translate into a number of symptoms commonly experienced by patients with PTSD. Current treatments for this disorder are only partially effective in managing the disease, and patients have to endure unpleasant symptoms associated with hyperarousal. As a result, they often withdraw from social interaction and increase the use of central nervous system depressants. Data suggest that biological dysregulation of the glutamatergic, amine neurotransmitter (noradrenergic and serotonergic), and neuroendocrine pathways plays a fundamental part in the pathology of PTSD and may cause brain structural as well as functional abnormalities. Knowledge of these pathologic changes in PTSD provides direction for the development of new treatments that will offer more comprehensive management of PTSD and enable patients to enjoy a much improved quality of life. This article reviews current knowledge regarding the psychobiology of PTSD and considers specific agents that are emerging as key modulators of this pathological process.
创伤后应激障碍（PTSD）在接触到具有威胁性和/或极度痛苦的事件后发生。越来越多的证据表明，强烈的心理创伤会导致对应激的神经生物学反应长期改变。这些改变转化为PTSD患者常见的一些症状。目前针对这种疾病的治疗在控制病情方面仅部分有效，患者不得不忍受与过度觉醒相关的不适症状。结果，他们常常退出社交互动，并增加中枢神经系统抑制剂的使用。数据表明，谷氨酸能、胺类神经递质（去甲肾上腺素能和5-羟色胺能）以及神经内分泌途径的生物调节异常在PTSD的病理过程中起重要作用，可能导致大脑结构和功能异常。了解PTSD中的这些病理变化为开发新的治疗方法提供了方向，这些新疗法将对PTSD进行更全面的管理，并使患者的生活质量得到显著改善。本文综述了关于PTSD心理生物学的当前知识，并考虑了作为这一病理过程关键调节因子出现的特定药物。
