NORMENT, KG Jebsen Centre for Psychosis Research, TOP Study Group, Division of Mental Health and Addiction, Institute of Clinical Medicine, University of Oslo, Bygg 49, Ullevål Sykehus, Nydalen, PO Box 4956, 0424, Oslo, Norway.
Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway.
Int J Bipolar Disord. 2016 Dec;4(1):2. doi: 10.1186/s40345-015-0042-0. Epub 2016 Jan 13.
This review will discuss the role of childhood trauma in bipolar disorders. Relevant studies were identified via Medline (PubMed) and PsycINFO databases published up to and including July 2015. This review contributes to a new understanding of the negative consequences of early life stress, as well as setting childhood trauma in a biological context of susceptibility and discussing novel long-term pathophysiological consequences in bipolar disorders. Childhood traumatic events are risk factors for developing bipolar disorders, in addition to a more severe clinical presentation over time (primarily an earlier age at onset and an increased risk of suicide attempt and substance misuse). Childhood trauma leads to alterations of affect regulation, impulse control, and cognitive functioning that might decrease the ability to cope with later stressors. Childhood trauma interacts with several genes belonging to several different biological pathways [Hypothalamic-pituitary-adrenal (HPA) axis, serotonergic transmission, neuroplasticity, immunity, calcium signaling, and circadian rhythms] to decrease the age at the onset of the disorder or increase the risk of suicide. Epigenetic factors may also be involved in the neurobiological consequences of childhood trauma in bipolar disorder. Biological sequelae such as chronic inflammation, sleep disturbance, or telomere shortening are potential mediators of the negative effects of childhood trauma in bipolar disorders, in particular with regard to physical health. The main clinical implication is to systematically assess childhood trauma in patients with bipolar disorders, or at least in those with a severe or instable course. The challenge for the next years will be to fill the gap between clinical and fundamental research and routine practice, since recommendations for managing this specific population are lacking. In particular, little is known on which psychotherapies should be provided or which targets therapists should focus on, as well as how childhood trauma could explain the resistance to mood stabilizers.
这篇综述讨论了童年创伤在双相情感障碍中的作用。通过 Medline(PubMed)和 PsycINFO 数据库检索截至 2015 年 7 月发表的相关研究。这篇综述有助于人们更好地理解早期生活压力的负面影响,将童年创伤置于易感性的生物学背景下,并探讨双相情感障碍中新颖的长期病理生理后果。童年创伤是发生双相情感障碍的危险因素,此外,随着时间的推移,还会导致更严重的临床表现(主要是发病年龄更早,自杀企图和物质滥用的风险增加)。童年创伤会导致情绪调节、冲动控制和认知功能的改变,从而降低应对后续压力源的能力。童年创伤与属于多个不同生物学途径(下丘脑-垂体-肾上腺 (HPA) 轴、5-羟色胺传递、神经可塑性、免疫、钙信号和昼夜节律)的几个基因相互作用,降低疾病发病年龄或增加自杀风险。表观遗传因素也可能参与双相情感障碍中童年创伤的神经生物学后果。生物学后果,如慢性炎症、睡眠障碍或端粒缩短,可能是童年创伤对双相情感障碍负面影响的潜在介质,尤其是在身体健康方面。主要的临床意义是系统地评估双相情感障碍患者的童年创伤,或者至少在那些病情严重或不稳定的患者中进行评估。未来几年的挑战是填补临床和基础研究与常规实践之间的差距,因为缺乏针对这一特定人群的管理建议。特别是,对于应该提供哪种心理治疗或治疗师应该关注哪些目标,以及童年创伤如何解释对情绪稳定剂的抵抗,人们知之甚少。