Objective:
To assess how COVID-19 impacts sleep architecture in a quantitative manner
Background:
Coronavirus disease 2019 (COVID-19) is an infection caused by Severe Acute Respiratory Syndrome – Coronavirus 2 (SARS-CoV2). In addition to its acute phase, there is interest in understanding the long-term neurologic consequences of COVID-19, as more patients report chronic sequelae of COVID-19 (termed Post-Acute Sequelae of COVID-19 [PASC]). Among the neurologic symptoms of PASC, sleep disturbance has been consistently endorsed in clinical settings and cohort studies, but these symptoms are largely based on subjective reports.
Design/Methods:
We performed a retrospective study of available polysomnography (PSG) data from adult patients within the University of Washington Medicine who had at least 2 sets of PSG studies done. COVID-19 participants (n = 9) had one PSG study at least 1 month after COVID-19 (verified with positive SARS-CoV2 PCR) and another PSG study at least 1 month prior to COVID-19. For controls (n = 24), PSG data were taken from studies performed before January 2020, in order to eliminate any possibility of prior SARS-CoV2 infection. All PSG tests in this study were obtained for the purposes of monitoring responses to sleep apnea treatment.
Results:
COVID-19 patients developed a significant decrease in percentage of N3 stage sleep in their post-COVID-19 study compared to their pre-COVID-19 study (p = 0.001) despite similar total sleep duration and latency. Furthermore, our COVID-19 PSG data were compared to pre-pandemic matched control data. This demonstrated that over a similar time period, the percentage of N3 stage sleep significantly decreased in COVID-19 patients (-80.6 ± 8.4%) in contrast to the controls who showed an increase (+62.9 ± 23.6 %; p = 0.0009).
Conclusions:
Given that reduced N3 stage sleep can contribute to the development of neurodegenerative diseases, these changes may have important implications for explaining the mechanisms underlying the neurologic symptoms of PASC.