Department of Psychiatry, Massachusetts General Hospital, Charlestown MA, USA.
Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA.
Sleep. 2022 Mar 14;45(3). doi: 10.1093/sleep/zsab261.
Sleep disturbances increase risk of posttraumatic stress disorder (PTSD). Sleep effects on extinction may contribute to such risk. Neural activations to fear extinction were examined in trauma-exposed participants and associated with sleep variables.
Individuals trauma-exposed within the past 2 years (N = 126, 63 PTSD) completed 2 weeks actigraphy and sleep diaries, three nights ambulatory polysomnography and a 2-day fMRI protocol with Fear-Conditioning, Extinction-Learning and, 24 h later, Extinction-Recall phases. Activations within the anterior cerebrum and regions of interest (ROI) were examined within the total, PTSD-diagnosed and trauma-exposed control (TEC) groups. Sleep variables were used to predict activations within groups and among total participants. Family wise error was controlled at p < 0.05 using nonparametric analysis with 5,000 permutations.
Initially, Fear Conditioning activated broad subcortical and cortical anterior-cerebral regions. Within-group analyses showed: (1) by end of Fear Conditioning activations decreased in TEC but not PTSD; (2) across Extinction Learning, TEC activated medial prefrontal areas associated with emotion regulation whereas PTSD did not; (3) beginning Extinction Recall, PTSD activated this emotion-regulatory region whereas TEC did not. However, the only between-group contrast reaching significance was greater activation of a hippocampal ROI in TEC at Extinction Recall. A greater number of sleep variables were associated with cortical activations in separate groups versus the entire sample and in PTSD versus TEC.
PTSD nonsignificantly delayed extinction learning relative to TEC possibly increasing vulnerability to pathological anxiety. The influence of sleep integrity on brain responses to threat and extinction may be greater in more symptomatic individuals.
睡眠障碍会增加创伤后应激障碍(PTSD)的风险。睡眠对消退的影响可能导致这种风险。本研究在创伤后个体中检查了对恐惧消退的神经激活,并将其与睡眠变量相关联。
在过去 2 年内经历过创伤的个体(N=126,63 例 PTSD)完成了 2 周的活动记录仪和睡眠日记、3 个晚上的动态多导睡眠图和 2 天的 fMRI 方案,包括恐惧条件反射、消退学习,以及 24 小时后的消退回忆阶段。在总样本、PTSD 诊断和创伤暴露对照组(TEC)中,检查了前脑和感兴趣区域(ROI)的激活。使用睡眠变量来预测组内和总参与者的激活。使用非参数分析和 5000 次随机排列,控制家族误差在 p < 0.05 水平。
最初,恐惧条件反射激活了广泛的皮质下和皮质前脑区域。组内分析显示:(1)在恐惧条件反射结束时,TEC 的激活减少,但 PTSD 没有;(2)在整个消退学习过程中,TEC 激活了与情绪调节相关的内侧前额叶区域,而 PTSD 没有;(3)在开始消退回忆时,PTSD 激活了这个情绪调节区域,而 TEC 没有。然而,唯一达到显著差异的组间对比是 TEC 在消退回忆时,海马 ROI 的激活增加。在单独的组与整个样本以及 PTSD 与 TEC 中,更多的睡眠变量与皮质激活相关。
与 TEC 相比,PTSD 在消退学习方面存在非显著性延迟,可能增加了对病理性焦虑的易感性。睡眠完整性对大脑对威胁和消退的反应的影响在症状更明显的个体中可能更大。