COVID-19 and Central Nervous System Hypersomnias

Abstract

Purpose of review Central nervous system (CNS) hypersomnias can be triggered by external factors, such as infection or as a response to vaccination. The 2019 coronavirus disease (COVID-19) pandemic, which was caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), led to a worldwide effort to quickly develop a vaccine to contain the pandemic and reduce morbidity and mortality. This narrative review is focused on the literature published in the past 2 years and provides an update on current knowledge in respect of the triggering of CNS hypersomnias by infection per se , vaccination, and circadian rhythm alterations caused by social isolation, lockdown, and quarantine. Recent findings At present, there is no consensus on the association between hypersomnias and COVID-19 vaccination or infection per se ; however, the data suggest that there has been an increase in excessive daytime sleepiness due to vaccination, but only for a short duration. Kleine Levin syndrome, hypersomnia, excessive daytime sleepiness, and narcolepsy were aggravated and exacerbated in some case reports in the literature. Both increased and decreased sleep duration and improved and worsened sleep quality were described. In all age groups, delayed sleep time was frequent in studies of patients with hypersomnolence. Summary The hypothesis that there is a pathophysiological mechanism by which the virus, vaccination, and the effects of quarantine aggravate hypersomnias is discussed in this review.

Neurological Adverse Reactions to SARS-CoV-2 Vaccines

“…SC2V-related cerebrovascular diseases include VST, ischemic stroke, ICH, SAB, pituitary apoplexy, RCVS, cerebral vasculitis, and Susac syndrome ( Table 2 ) [ 4 , 6 …”

“…The patient did not carry human leukocyte antigen alleles associated with narcolepsy [ 94 ]. There are also case reports documenting aggravation or exacer-bation of Kleine Levin syndrome, hypersomnia, excessive daytime sleepiness, and narcolepsy after SC2V [ 95 ].…”

Associations between changes in habitual sleep duration and lower self-rated health among COVID-19 survivors: findings from a survey across 16 countries/regions

“…The prolonged fatigue, together with abnormal immune responses may be similar to those observed during the development of idiopathic hypersomnia [ 21 , 63 ], which has been suggested to be triggered by Epstein-Barr infection [ 64 , 65 ]. Although the evidence is insufficient, SARS-CoV-2 infection itself and/or Epstein-Barr virus reactivation due to SARS-CoV-2 infection may trigger the onset of central nervous system hypersomnias [ 66 , 67 ]. Meanwhile, shortness of breath and diarrhea/nausea/vomiting might reduce individuals’ habitual sleep duration and lower SRH through their bodily effect.…”

Impact of Taiwan’s 2021 COVID-19 lockdown on the symptom severity and quality of life of patients with narcolepsy

“…An online survey study revealed that patients with hypersomnia disorder had delayed schedules, longer nighttime sleep, less daytime sleepiness, less fatigue, fewer sleep attacks, and better attention during the pandemic [ 12 , 33 ]; however, COVID-somnia can still occur in such patients. Autoimmune reactions related to the virus can also trigger hypersomnia symptoms [ 34 ] and even aggravate previous hypersomnia disorder, as indicated in case reports [ 35 , 36 ]. One study revealed that during lockdowns, those with NT1 and NT2 exhibited a disturbed circadian rhythm, more fragmented sleep, increased daytime sleepiness and napping, and poorer quality of life; however, other narcoleptic symptoms such as cataplexy, sleep paralysis, and hypnagogic and hypnopompic hallucinations remained unchanged [ 37 ].…”