Abubaker Ibrahim, Matteo Cesari, Qi Tang, Merve Aktan Süzgün, Elisabeth Brandauer, Evi Holzknecht, Alexander Wachter, Victoria Anselmi, Anna Heidbreder, Ambra Stefani, Birgit Högl
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引用次数: 0
Abstract
Study objectives: Insomnia associated with COVID-19 infection is a common complaint in long-COVID. Studies to date have predominantly examined post-COVID-19 sleep disturbances with questionnaires. We aimed to investigate whether there are distinctive polysomnographic findings in post-COVID-19 insomnia compared to non-COVID-related chronic insomnia.
Methods: We included 150 patients with chronic insomnia, stratified into three groups: post-COVID-19 insomnia (n = 50), chronic insomnia during the pandemic without a history of COVID-19 infection (n = 50), and pre-pandemic chronic insomnia (n = 50). All patients underwent one-night video-polysomnography (v-PSG). The sleep architecture, respiratory variables and REM sleep without atonia (RWA) were compared across the groups.
Results: Classical polysomnographic variables showed no significant differences across groups with regard to total sleep time, sleep efficiency, sleep stage percentages, and the apnea-hypopnea index. Post-COVID-19 insomnia patients had significantly increased RWA at both the chin and the flexor digitorum superficialis (FDS) (p=.020 for both), and higher nocturnal heart rates (p=.046). Sleep-bout analysis indicated shorter sustained N3-sleep periods (p=.001) and longer onset to stable REM-sleep (p=.016) in the post-COVID-19 insomnia group. Although sleep transitions did not withstand multiple comparison corrections, they revealed a trend towards decreased N3-sleep continuity and increased probabilities of transitioning to lighter stages (N3 → N3: unadjusted-p=.012; REM → N1: unadjusted-p=.027) in the post-COVID-19 insomnia.
Conclusions: Classical PSG profile of post-COVID-19 insomnia does not differ from non-COVID-related chronic insomnia. However, subtle differences in RWA and sleep integrity suggest that post-COVID-19 insomnia is driven not merely by pandemic-related stress factors but by additional physiological alterations linked to viral CNS involvement.
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