Zhang Yuyi, Guo Yunxiao, Wang Xiaoqin, Liu Yinong, Liu Sijun, Zhao Junrong, Liu Lianzhong, Yu Ping, Ren Zhihong
Key Laboratory of Adolescent Cyberpsychology and Behavior (Ministry of Education), School of Psychology, Central China Normal University, Wuhan, Hubei, 430012, China; Key Laboratory of Human Development and Mental Health of Hubei Province, National Intelligent Society Governance Experiment Base (Education), School of Psychology, Central China Normal University, Wuhan, Hubei, 430012, China.
Department of Psychology, Zhejiang Normal University, Jinhua, 321004, China; Key Laboratory of Intelligent Education Technology and Application of Zhejiang Province, Zhejiang Normal University, Jinhua, Zhejiang, 321004, China.
J Psychiatr Res. 2025 Sep;189:125-137. doi: 10.1016/j.jpsychires.2025.06.002. Epub 2025 Jun 4.
Sleep disturbances and difficulties in emotion regulation are core symptoms of post-traumatic stress disorder (PTSD) and are closely related. However, the neural mechanisms underlying this relationship remain underexplored. To address this gap, we used task-based functional magnetic resonance imaging (fMRI) to examine brain mechanisms related to emotional processing and regulation in PTSD patients with and without insomnia.
Forty-six PTSD patients (23 with insomnia, 23 without insomnia) and 28 controls reported clinical symptoms (including PTSD, insomnia, and anxiety/depression) and completed the Shifted Attention Emotion Appraisal Task (SEAT) during fMRI. We compared the neural differences in implicit emotion regulation-related regions between PTSD patients with and without insomnia based on both whole-brain and ROI analyses.
Compared to PTSD patients without insomnia, those with comorbid insomnia exhibited significant deactivation in the left dorsolateral prefrontal cortex (BA46) and the left inferior frontal gyrus (triangular part, BA47) during implicit emotion processing. Additionally, during appraisal-based implicit emotion regulation, the left inferior temporal gyrus (BA37) showed significant deactivation. Furthermore, in the PTSD-insomnia group, insomnia severity was significantly correlated with activation in the left fusiform gyrus (BA37).
These findings highlight potential neural mechanisms underlying the differences between PTSD patients with and without insomnia. The observed alterations in these regions may serve as neural biomarkers for PTSD with comorbid insomnia and could be potential targets for developing novel therapeutic interventions.
睡眠障碍和情绪调节困难是创伤后应激障碍(PTSD)的核心症状,且密切相关。然而,这种关系背后的神经机制仍未得到充分探索。为填补这一空白,我们使用基于任务的功能磁共振成像(fMRI)来研究伴有和不伴有失眠的PTSD患者中与情绪加工和调节相关的脑机制。
46名PTSD患者(23名伴有失眠,23名不伴有失眠)和28名对照者报告了临床症状(包括PTSD、失眠和焦虑/抑郁),并在fMRI期间完成了注意力转移情绪评估任务(SEAT)。我们基于全脑和感兴趣区(ROI)分析,比较了伴有和不伴有失眠的PTSD患者在与内隐情绪调节相关区域的神经差异。
与不伴有失眠的PTSD患者相比,伴有共病失眠的患者在内隐情绪加工期间,左侧背外侧前额叶皮质(BA46)和左侧额下回(三角部,BA47)表现出显著失活。此外,在基于评估的内隐情绪调节期间,左侧颞下回(BA37)表现出显著失活。此外,在PTSD-失眠组中,失眠严重程度与左侧梭状回(BA37)的激活显著相关。
这些发现突出了伴有和不伴有失眠的PTSD患者之间差异潜在的神经机制。这些区域观察到的改变可能作为共病失眠的PTSD的神经生物标志物,并且可能是开发新型治疗干预措施的潜在靶点。