背景:为了评估Omicron感染引起的神经系统改变,比较Omicron患者慢性失眠与慢性失眠加剧的大脑变化,并检查没有失眠的人以及新发失眠的人。
方法:在本研究中,在2023年1月11日至5月4日期间共招募了135名参与者,其中包括26名没有恶化的慢性失眠患者,24例慢性失眠患者加重,40例无睡眠障碍患者,以及30例感染Omicron后出现新发失眠的患者(共120例患者感染后睡眠状态不同),以及15名从未感染过Omicron的健康对照。神经精神病学数据,临床症状,并收集了多模态磁共振成像数据。灰质厚度与T1、T2、质子密度、和血管周围空间值进行分析。通过相关性分析评估了多模态磁共振成像结果的变化与神经精神病学数据之间的关联。
结果:与健康对照组相比,感染后有和没有慢性失眠史的患者的灰质厚度变化相似,包括顶叶附近皮质厚度的增加和额叶皮质厚度的减少,枕骨,和内侧大脑区域。分析表明,与Omicron感染后慢性失眠加重的患者相比,慢性失眠患者的灰质厚度降低,并且在右侧内侧眶额叶区域发现了减少(平均值[SD],2.38[0.17]vs.2.67[0.29]mm;P<0.001)。在Omicron患者睡眠恶化的亚组中,有慢性失眠病史的患者,在感染后失眠症状恶化,表现为内侧眶额皮质厚度增加,不同脑区的质子密度值增加。相反,睡眠质量良好的患者在感染后出现了新的失眠,其表现为钙皮区域的皮质厚度减少,质子密度值降低。在Omicron感染后的新发失眠患者中,右侧果皮厚度与焦虑自评量表(r=-0.538,P=0.002,PFDR=0.004)和抑郁自评量表(r=-0.406,P=0.026,PFDR=0.026)评分呈负相关。
结论:这些发现有助于我们理解Omicron侵入神经系统并在感染后诱发各种形式的失眠所涉及的病理生理机制。在未来,我们将继续关注与Omicron感染引起的失眠相关的大脑动态变化。
BACKGROUND: To evaluate the neurological alterations induced by Omicron infection, to compare brain changes in chronic insomnia with those in exacerbated chronic insomnia in Omicron patients, and to examine individuals without insomnia alongside those with new-onset insomnia.
METHODS: In this study, a total of 135 participants were recruited between January 11 and May 4, 2023, including 26 patients with chronic insomnia without exacerbation, 24 patients with chronic insomnia with exacerbation, 40 patients with no sleep disorder, and 30 patients with new-onset insomnia after infection with Omicron (a total of 120 participants with different sleep statuses after infection), as well as 15 healthy controls who were never infected with Omicron. Neuropsychiatric data, clinical symptoms, and multimodal magnetic resonance imaging data were collected. The gray matter thickness and T1, T2, proton density, and perivascular space values were analyzed. Associations between changes in multimodal magnetic resonance imaging findings and neuropsychiatric data were evaluated with correlation analyses.
RESULTS: Compared with healthy controls, gray matter thickness changes were similar in the patients who have and do not have a history of chronic insomnia groups after infection, including an increase in cortical thickness near the parietal lobe and a reduction in cortical thickness in the frontal, occipital, and medial brain regions. Analyses showed a reduced gray matter thickness in patients with chronic insomnia compared with those with an aggravation of chronic insomnia post-Omicron infection, and a reduction was found in the right medial orbitofrontal region (mean [SD], 2.38 [0.17] vs. 2.67 [0.29] mm; P < 0.001). In the subgroups of Omicron patients experiencing sleep deterioration, patients with a history of chronic insomnia whose insomnia symptoms worsened after infection displayed heightened medial orbitofrontal cortical thickness and increased proton density values in various brain regions. Conversely, patients with good sleep quality who experienced a new onset of insomnia after infection exhibited reduced cortical thickness in pericalcarine regions and decreased proton density values. In new-onset insomnia patients post-Omicron infection, the thickness in the right pericalcarine was negatively correlated with the Self-rating Anxiety Scale (r = - 0.538, P = 0.002, PFDR = 0.004) and Self-rating Depression Scale (r = - 0.406, P = 0.026, PFDR = 0.026) scores.
CONCLUSIONS: These findings help us understand the pathophysiological mechanisms involved when Omicron invades the nervous system and induces various forms of insomnia after infection. In the future, we will continue to pay attention to the dynamic changes in the brain related to insomnia caused by Omicron infection.