Once internalized, the virus replicates and matures, leading to a widespread inflammatory response with massive cytokine release. SARS-CoV-2 enters cells through interaction with angiotensin converting enzyme-2 (ACE2) receptors present in many cell types, including nasal mucosa, lungs, heart, liver, kidneys and brain, as well as arterial and venous endothelial cells. The new coronavirus SARS-CoV-2 rapidly spread around the world, turning into a pandemic. ConclusionĬomplaints related to sleep, such as insomnia and excessive sleepiness, seem to be part of the clinical post-acute syndrome (long COVID syndrome), composing part of its clinical spectrum, relating to some clinical data. We observed a high prevalence of cognitive complaints in these patients. A history of steroid use was related to sleep complaints (insomnia and excessive sleepiness), whereas depression was related to excessive sleepiness. Two patients had a diagnosis of central hypersomnia, and one had narcolepsy. Four patients with ES were evaluated with polysomnography and test, multiple sleep latencies test, and actigraphic data. Insomnia was reported by 42 patients (22.2%), and excessive sleepiness (ES) was reported by 6 patients (3.17%). ResultsĪmong 189 patients included in the long COVID sample, 48 (25.3%) had sleep-related symptoms. MethodologyĪ total of 207 patients with post-COVID symptoms were evaluated through clinical evaluation with a neurologist and specific exams in the subgroup complaining of excessive sleepiness. The present study aimed to characterize and evaluate the prevalence of sleep symptoms in patients with long COVID syndrome. This syndrome can affect up to 32% of affected individuals, with symptoms of fatigue, dyspnea, chest pain, cognitive disorders, insomnia, and psychiatric disorders. Long-onset COVID syndrome has been described in patients with COVID-19 infection with persistence of symptoms or development of sequelae beyond 4 weeks after the onset of acute symptoms, a medium- and long-term consequence of COVID-19.
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