阻塞性睡眠呼吸暂停与创伤后应激障碍共病的神经生物学机制

The prevalence of obstructive sleep apnea (OSA) in patients with posttraumatic stress disorder (PTSD) was 75%; hyperactivation of hypothalamic-pituitary-adrenal (HPA) axis is shared pathophysiology mechanism of the two illnesses. Continuous positive airway pressure (CPAP) can significantly reduce the scores of PTSD symptoms in patients with OSA and PTSD. The video analog trauma paradigm induces intrusive emotional memory which is a core symptom of PTSD and is often used for laboratorial research of PTSD. Previous studies utilizing this paradigm indicated that sufficient amount of sleep could facilitate the extinction of intrusive emotional memory and prevent the developments of PTSD. Therefore, we speculate that OSA patients with reduced quality of sleep may be vulnerable for the intrusive emotional memory, which may be pathophysiology of the comorbidity of OSA and PTSD. We plan to explore this hypothesis, through the evaluation of the relationships between the intrusive emotional memory induced by analog trauma paradigm vs. objective sleep, HPA activation and its related epigenetic features and the effects of CPAP therapy. This research would provide the basis and guidance of neurobiological mechanisms and intervention in the comorbidity of OSA and PTSD.

创伤后应激障碍（PTSD）合并阻塞性睡眠呼吸暂停（OSA）的机率约75%；持续气道正压通气治疗（CPAP）可显著改善共病患者PTSD症状；下丘脑-垂体-肾上腺（HPA）轴活性增高是二者共有的病理生理学机制。视频暴露创伤场景模拟创伤刺激，形成闯入性创伤情感记忆（PTSD核心症状），是研究PTSD常用的实验范式。采用这一范式的研究表明，创伤场景暴露后睡眠数量和质量的增加有助于创伤记忆的消退和预防PTSD的发生。据此，我们推测OSA患者客观存在的睡眠质量下降将不利于场景暴露后创伤记忆的消退，从而参与了OSA与PTSD共病的病理学成因。我们计划在OSA患者中采用视频暴露创伤场景的实验范式，通过对闯入性创伤情感记忆与客观睡眠质量、HPA轴活性及相关基因的表观遗传学之间关系的研究，结合CPAP治疗的反应，对此假说进行探讨。本研究将为OSA与PTSD共病的神经生物学机制和干预奠定理论基础并提供指导方向。

创伤后应激障碍（PTSD）与阻塞性睡眠呼吸暂停（OSA）临床共病率高。下丘脑-垂体-肾上腺（HPA）轴活性增高是二者共有的病理生理学机制。本研究围绕二者临床特征、睡眠电生理、HPA轴，并通过持续气道正压通气（CPAP）干预方式，探索了OSA与PTSD共病的神经生物学机制。明确了创伤后快速眼球运动期（REM）睡眠紊乱是创伤相关恐惧记忆形成的重要神经生物学基础，也是OSA患者经历创伤后其创伤相关恐惧更加严重的标志。CPAP治疗可有效减轻OSA与PTSD共病者的REM睡眠紊乱，有助于减轻创伤相关恐惧记忆的异常巩固与强化。本研究将为进一步理解OSA与PTSD共病的神经生物学机制奠定理论基础并提供指导方向。