Department of Psychiatry, College of Medicine, Korea University, Seoul, Republic of Korea.
Department of Neuroscience, Fasa University of Medical Sciences, Fasa, Iran.
Prog Neuropsychopharmacol Biol Psychiatry. 2019 Apr 20;91:103-112. doi: 10.1016/j.pnpbp.2018.06.008. Epub 2018 Jun 19.
The heterogeneity of post-traumatic stress disorder (PTSD) symptoms indicates that multiple neurobiological mechanisms underlie the pathophysiology of the condition. However, no generally accepted PTSD biomarkers in clinical practice currently exist. The sequential responses to recurrent and chronic stress by the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system (ANS) system are considered to play a significant role in the onset and progression of PTSD. Decreased activity of the HPA axis and parasympathetic nervous system, along with increased activity of the sympathetic nervous system, have been observed in PTSD, which may lead to increased levels of proinflammatory cytokines. Such heightened activity of the immune system may cause alterations in the structure and function of brain regions-for example, the amygdala, hippocampus, medial prefrontal cortex, anterior cingulate cortex, and insula-through changes in levels of serotonin and kynurenine pathway metabolites, and direct neurotoxic effects of cytokines. Although chronic inflammation-induced alterations in brain regions critical in controlling emotional behavior and fear regulation may represent a strong candidate biomarker of PTSD, future studies are necessary to further elucidate inflammation-associated neural biomarkers of PTSD. Continued research on therapeutic methods that involve the normalization of the HPA axis, ANS, and immune system is expected to contribute to the development of novel ways to treat PTSD.
创伤后应激障碍（PTSD）症状的异质性表明，多种神经生物学机制是该病症病理生理学的基础。然而，目前临床上尚未存在被普遍接受的 PTSD 生物标志物。下丘脑-垂体-肾上腺（HPA）轴和自主神经系统（ANS）系统对反复和慢性应激的序贯反应被认为在 PTSD 的发病和进展中起重要作用。在 PTSD 中观察到 HPA 轴和副交感神经系统的活性降低，而交感神经系统的活性增加，这可能导致促炎细胞因子水平升高。免疫系统的这种高度活跃可能导致大脑区域的结构和功能发生改变，例如杏仁核、海马体、内侧前额叶皮层、前扣带皮层和脑岛，这是通过改变 5-羟色胺和犬尿氨酸途径代谢物的水平以及细胞因子的直接神经毒性作用来实现的。尽管慢性炎症引起的对控制情绪行为和恐惧调节至关重要的大脑区域的改变可能代表 PTSD 的一个强有力的候选生物标志物，但仍需要进一步的研究来阐明与 PTSD 相关的炎症相关的神经生物标志物。对涉及 HPA 轴、ANS 和免疫系统正常化的治疗方法的持续研究，有望为治疗 PTSD 的新方法的发展做出贡献。
