Narcolepsy following COVID-19: A case report and review of potential mechanisms.

Key Clinical Message: The immune activation in COVID-19 may trigger narcolepsy in vulnerable patients. We suggest clinicians carefully evaluate patients with post-COVID fatigue and hypersomnia for primary sleep disorders, specifically narcolepsy. Abstract: The patient is a 33-year-old Iranian woman without a significant past medical history with the full range of narcolepsy symptoms that started within 2 weeks after her recovery from COVID-19. Sleep studies revealed increased sleep latency and three sleep-onset rapid eye movement events, compatible with a narcolepsy-cataplexy diagnosis.

Association between hypersomnolence and the COVID-19 pandemic: The International COVID-19 Sleep Study (ICOSS).

BACKGROUND: The COVID-19 pandemic and related restriction measures have affected our daily life, sleep, and circadian rhythms worldwide. Their effects on hypersomnolence and fatigue remain unclear. METHODS: The International COVID-19 Sleep Study questionnaire which included items on hypersomnolence such as excessive daytime sleepiness (EDS), and excessive quantity of sleep (EQS), as well as sociodemographic factors, sleep patterns, psychological symptoms, and quality of life was distributed in 15 countries across the world from May to September in 2020. RESULTS: Altogether responses from 18,785 survey participants (65% women, median age 39 years) were available for analysis. Only 2.8% reported having had COVID-19. Compared to before the pandemic, the prevalence of EDS, EQS, and fatigue increased from 17.9% to 25.5%, 1.6%-4.9%, and 19.4%-28.3% amid the pandemic, respectively. In univariate logistic regression models, reports of having a COVID-19 were associated with EQS (OR 5.3; 95%-CI 3.6-8.0), EDS (2.6; 2.0-3.4), and fatigue (2.8; 2.1-3.6). In adjusted multivariate logistic regression, sleep duration shorter than desired (3.9; 3.2-4.7), depressive symptoms (3.1; 2.7-3.5), use of hypnotics (2.3; 1.9-2.8), and having reported COVID-19 (1.9; 1.3-2.6) remained strong predictors of EDS. Similar associations emerged for fatigue. In the multivariate model, depressive symptoms (4.1; 3.6-4.6) and reports of having COVID-19 (2.0; 1.4-2.8) remained associated with EQS. CONCLUSIONS: A large increase in EDS, EQS, and fatigue occurred due to the COVID-19 pandemic, and especially in self-reported cases of COVID-19. These findings warrant a thorough understanding of their pathophysiology to target prevention and treatment strategies for long COVID condition.

Central hypersomnia and chronic insomnia: expanding the spectrum of sleep disorders in long COVID syndrome - a prospective cohort study.

INTRODUCTION: 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. This syndrome can affect up to 32% of affected individuals, with symptoms of fatigue, dyspnea, chest pain, cognitive disorders, insomnia, and psychiatric disorders. The present study aimed to characterize and evaluate the prevalence of sleep symptoms in patients with long COVID syndrome. METHODOLOGY: A 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. RESULTS: Among 189 patients included in the long COVID sample, 48 (25.3%) had sleep-related symptoms. Insomnia was reported by 42 patients (22.2%), and excessive sleepiness (ES) was reported by 6 patients (3.17%). Four patients with ES were evaluated with polysomnography and test, multiple sleep latencies test, and actigraphic data. Two patients had a diagnosis of central hypersomnia, and one had narcolepsy. A history of steroid use was related to sleep complaints (insomnia and excessive sleepiness), whereas depression was related to excessive sleepiness. We observed a high prevalence of cognitive complaints in these patients. CONCLUSION: Complaints 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.

Distinguer la narcolepsie de type 2, l’hypersomnie idiopathique, la dépression et la somnolence dans le syndrome post-COVID-19

Résumé Les syndromes d’hypersomnolence d’origine centrale (c.-à-d. narcolepsie de type-1, narcolepsie de type-2 et hypersomnie idiopathique), la dépression ainsi qu’un sous-type du syndrome post-COVID-19 peuvent être confondus lors de l’établissement d’un diagnostic. Ce défi diagnostique s’explique par un symptôme clinique caractéristique retrouvé dans les quatre conditions, la somnolence diurne excessive, un chevauchement phénotypique considérable entre la narcolepsie de type-2 et l’hypersomnie idiopathique ainsi qu’une symptomatologie dysphorique pouvant être présente autant dans les hypersomnolences centrales que dans un sous-type du syndrome post-COVID-19. Considérant l’importance d’un diagnostic valide sur l’efficacité des traitements et des interventions futures, il est essentiel de définir précisément ces quatre conditions. Dans cette revue, nous reprendrons les critères diagnostiques, les présentations cliniques et les connaissances actuelles en ce qui a trait à la pathophysiologie de ces troubles en portant une attention particulière aux éléments distinctifs de la narcolepsie de type-2, de l’hypersomnie idiopathique, des épisodes dépressifs avec hypersomnolence et du syndrome post-COVID-19 avec somnolence. Bien que de nombreuses études se soient penchées sur les valeurs diagnostiques des différents outils employés dans l’identification des hypersomnolences centrales, très peu de marqueurs physiologiques ont été identifiés. Une meilleure compréhension de ces conditions cliniques pourrait permettre l’identification de marqueurs objectifs spécifiques à chaque condition réduisant ainsi la possibilité d’une erreur diagnostique et optimisant les plans de traitement. Summary Central disorders of hypersomnolence, including narcolepsy type-1 and type-2 as well as idiopathic hypersomnia, depression and a subtype of post-acute COVID-19 syndrome might be confused when establishing a diagnosis. This diagnostic challenge can be explained by the presence of excessive daytime sleepiness, a clinical symptom that is observed in all four conditions, an overlap in the phenotypic traits of narcolepsy type-2 and idiopathic hypersomnia, as well as the presence of depressive symptoms observed in central disorders of hypersomnolence and post-acute COVID-19 syndrome subtypes. Considering the importance of a valid diagnostic on treatment's efficacy and future interventions, it is essential to define those conditions with precision. In this review, we will discuss the diagnostic criteria, clinical presentation and current state of knowledge with regards to the pathophysiology of central disorders of hypersomnolence and post-acute COVID-19 syndrome. We will pay particular attention to the characteristics specific to narcolepsy type-2, idiopathic hypersomnia, depressive episodes with hypersomnolence, and post-acute COVID-19 syndrome with drowsiness. While many studies have assessed the ability of different tools used to diagnose central disorders of hypersomnolence, very few have focused on physiological markers. A better understanding and identification of biomarkers specific to narcolepsy type-1 and type-2, idiopathic hypersomnia and post-acute COVID-19 syndrome will reduce the possibility of misdiagnoses and allow the development of optimal treatment plans.

SLEEP-DISORDERED BREATHING AND LONG-HAUL COVID-19: A CASE REPORT

SESSION TITLE: Uncommon Presentations and Complications of Chest Infections SESSION TYPE: Rapid Fire Case Reports PRESENTED ON: 10/18/2022 10:15 am - 11:10 am INTRODUCTION: The correlation between long-haul Coronavirus 2019 (COVID-19) and sleep disorders remains poorly understood. In this report, we present a case of newly diagnosed central sleep apnea (CSA) and symptoms starting after a COVID-19 infection as part of a long-haul COVID-19 presentation. CASE PRESENTATION: A 69-year-old male presented to a sleep medicine clinic for evaluation of hypersomnia. He had a history of hypertension and pulmonary embolism. He contracted COVID-19 eight months prior to his presentation. He was not hospitalized, but received Remdesivir and prednisone. He complained of long-haul COVID-19 symptoms since his infection which included headaches, fatigue, cough, dyspnea, anosmia, poor appetite, dysgeusia, and memory impairment. He also started noticing nocturnal apneic episodes that frightened him and woke him up from sleep. His symptoms started after his infection and were not present prior. He went to the emergency department for evaluation and no etiology was identified. He was then referred to sleep medicine for further evaluation. A home sleep apnea test was done and showed severe sleep apnea with an Apnea-Hypopnea Index of 35.7 events per hour. His sleep apnea was predominantly central with a central apnea index of 15.3 events per hour. Cardiac testing showed no evidence of ischemia or cardiomyopathy with an ejection fraction of 52%. A CT angiogram showed no evidence of PE. Brain MRI showed no acute abnormalities. He was started on positive airway pressure therapy but could not tolerate it so he was sent for a phrenic nerve stimulator implantation. DISCUSSION: Long-term sequelae of COVID-19 infection have been increasingly recognized. However, the etiology and pathophysiology is poorly understood (1). Symptoms of long-haul COVID-19 include fatigue, dyspnea, cognitive manifestations, thrombosis and sleep disturbances (1). Sleep apnea was found in some studies to be a risk factor for severe COVID-19 illness and worse outcomes (2). The relationship between COVID-19 and sleep apnea in the post-viral syndrome remains unknown. Only few case reports have found obstructive sleep apnea as a new diagnosis and a possible cause of fatigue in post COVID-19 infection (3). There is no report of a relationship between CSA and COVID-19 in the literature. It is hypothesized that long-COVID can lead to brainstem dysfunction and dysautonomia, which can affect the ventilatory control mechanisms and lead to an unstable respiration (4–6). Our patient's nocturnal symptoms started after his infection as part of long-haul COVID-19. While we cannot determine if CSA was a result of COVID-19 infection or not, it is important to evaluate for sleep disordered breathing (SDB) in patients presenting with long-COVID symptoms to better understand the association. CONCLUSIONS: More research is need to better understand the correlation between SDB and long-haul COVID-19. Reference #1: 1. Mehandru S, Merad M. Pathological sequelae of long-haul COVID. Nat Immunol. 2022 Feb;23(2):194–202. 2. Miller MA, Cappuccio FP. A systematic review of COVID-19 and obstructive sleep apnoea. Sleep Medicine Reviews. 2021 Feb;55:101382. Reference #2: 3. Koczulla AR, Stegemann A, Gloeckl R, Winterkamp S, Sczepanski B, Boeselt T, et al. Newly detected rapid eye movement associated sleep apnea after coronavirus disease 2019 as a possible cause for chronic fatigue: two case reports. J Med Case Reports. 2021 Dec;15(1):211. 4. Barizien N, Le Guen M, Russel S, Touche P, Huang F, Vallée A. Clinical characterization of dysautonomia in long COVID-19 patients. Sci Rep. 2021 Dec;11(1):14042. Reference #3: 5. Yong SJ. Persistent Brainstem Dysfunction in Long-COVID: A Hypothesis. ACS Chem Neurosci. 2021 Feb 17;12(4):573–80. 6. White DP. Pathogenesis of Obstructive and Central Sleep Apnea. Am J Respir Crit Care Med. 2005 Dec;172(11):1363–70. DISCLOSURES: No relevant relationships by Amer Als ekh Mousa No relevant relationships by University of Arizona at Banne Institute No relevant relationships by Joyce Lee-Iannotti No relevant relationships by Anas Rihawi No relevant relationships by Amr Salem No relevant relationships by Mohanad Soliman No relevant relationships by Kristen Trimble

Donepezil Treatment of Hypersomnia After COVID-19

The long-term effects of coronavirus disease-2019 (COVID-19) are not yet fully understood and some are due to central nervous system involvement. COVID-19 was reported to cause fatigue in some people after a long-term viral illness, characterized by daytime wakefulness and disturbed sleep cycles. Herein, a 90-yearold patient is presented, who developed hypersomnia after COVID-19 and showed signs of cortical atrophy in the left chronic thalamic infarction area and bilateral temporal lobe anteromedial parts in cranial magnetic resonance imaging, as well as increased wakefulness with donepezil treatment. Donepezil is an acetylcholinesterase inhibitor that increases the level of acetylcholinesterase that inhibits gamma-aminobutyric acid release in the forebrain via the serotonin system, which increases dopamine levels in the nucleus accumbens. The serotonin system has been noted for its positive effect on excessive sleepiness and Epworth sleepiness scale score improvement. © 2021 by Turkish Neurological Society.

Sleep Disturbances and Mental Health: A Transdiagnostic View of Sleep Disorders Symptoms in a Representative Canadian Sample

Introduction: Sleep problems can actively contribute to the onset, maintenance and worsening of mental disorders. Beyond insomnia, several other sleep pathologies may be associated with adverse mental health outcomes, and having multiple sleep disorders may be an aggravating factor. This study aimed to delineate the current landscape of sleep difficulties and symptoms of sleep disorders linked to poor mental health, investigate associations between the age at onset of sleep problems and subsequent mental health, and assess the perceived impacts of sleep problems. Materials and Methods: A representative sample of 1,200 Canadians (16 to 88 years old, 53% females) completed an online survey on sleep and mental health between 21 and 24 September 2021 (i.e. after the acute phase of the COVID-19 pandemic in Canada). The survey included questions inspired form the Sleep Disorders Questionnaire, Sleep Disorders Symptom Checklist-25, Pittsburgh Sleep Quality Index, STOP-Bang, and Insomnia Severity Index. The sample was stratified in two groups based on self-reported current mental disorder diagnosis: mental disorder diagnoses [219 (18.2%)] vs no diagnosis [960 (80.0%)]. Total scores on the General Anxiety Disorder-7 and Patient Health Questionnaire were used to determine anxiety and depression symptoms severity. Results: Of those with mental disorder diagnoses, 80.4% (176/219) endorsed symptoms of at least one sleep disorder, a proportion significantly higher compared to the 42.7% observed in the rest of the sample (p<.001, V=.29). The mental disorder diagnoses group included higher proportions of respondents endorsing symptoms of insomnia disorder, sleep apnea, bruxism, restless legs syndrome, nightmare disorder, hypersomnia and somnambulism. After adjusting for age, sex, income level and total sleep time, having a mental disorder diagnosis was associated with: insomnia (OR=3.52, p<.001), obstructive sleep apnea (OR=1.95, p=.006) and bruxism (OR=2.77, p<.001). Half of those with mental disorders diagnoses endorsed symptoms of multiple sleep disorders, a proportion significantly higher than what was observed in the rest of the sample (p<.001, V=.35). Endorsing symptoms of insomnia, sleep apnea, bruxism, restless legs syndrome, and hypersomnia were associated with more severe anxiety and depression symptoms after adjusting for age, sex, income level, total sleep time, and mental disorders diagnoses (B>.98, p<.012). Younger age at onset of sleep problems was a significant independent predictor for current self-reported diagnosis of mental disorders (OR=.96, p<.001). Compared to the rest of the sample, the mental disorder group reported significantly worse impacts of sleep problems on mental health, family relationships, physical health, cognitive functioning, productivity level, and global daily functioning. Conclusions: These results reinforce the transdiagnostic nature and cumulative impacts of the various profiles of sleep problems associated with mental health issues. These findings also suggest that the relationship between sleep and mental health is not solely driven by short sleep duration or insomnia. There is a need to enhance awareness about the diverse profiles of sleep issues linked to poor mental health and the relevance of early intervention, notably during youth. Should future longitudinal studies based on objective measures confirm these observations, this may inform further development of transdiagnostic sleep interventions for people with mental disorders.

Sleep disturbances in craniopharyngioma: a challenging diagnosis

Introduction: The hypothalamus plays a crucial role in regulating vital functions and circadian rhythms. Both the tumor involving the hypothalamic area and its treatment can lead to hypothalamic dysfunction, resulting in disturbances in sleep-wake patterns, sleep fragmentation, and increased daytime sleepiness. We describe two patients with craniopharyngioma who came to our attention due to the occurrence of episodes characterized by psychomotor slowing and afinalistic limb movements, temporal and spatial disorientation, psychomotor agitation, and oneiric stupor like episodes diagnosed as severe sleep disturbances. Case reports: Patient 1 is a 19-year-old male diagnosed with surgically treated craniopharyngioma. Subsequently, episodes of psychomotor slowing, afinalistic movements of the upper limbs diagnosed as seizures in another neurological center appeared;antiepileptic treatment was started without improvement. At the first examination in our center, excessive daytime sleepiness (EDS), fragmented nighttime sleep, episodes characterized by bimanual automatic gestures occurring during drowsy state, hypnagogic hallucinations, and sudden loss of muscle tone while awake were recognized. Actigraphy demonstrated irregular bedtimes, frequent nocturnal activity, and inappropriate daytime rest episodes. The Epworth Sleepiness Scale (ESS) showed subjective EDS (ESS=19). At PSG, hypersomnolence, severe sleep-related breathing disorder (SRBD), and no interictal and ictal seizure abnormalities were found. A BiPAP NIV was started, and antiepileptic therapy was discontinued. In the following months, PSG revealed marked improvement in SRBD and 1 SOREMP, and the MSLT a mean SOL of 6 min and 10 sec and 3 SOREMPs. These data allowed the diagnosis of secondary narcolepsy, and treatment with pitolisant was initiated with clinical improvement and reduced daytime sleepiness (ESS=9). Patient 2 is a 12-year-old male, surgically treated for craniopharyngioma at the age of 4 years, who developed episodes of myoclonic jerks, temporal and spatial disorientation, and psychomotor agitation during the lockdown period for COVID-19 emergency. Surmising paroxysmal epileptic episodes, the patient was hospitalized. The anamnestic data collection revealed a sleep-wake rhythm dysregulation, fragmented nighttime sleep, EDS, oneiric stupor-like episodes during which the patient performed simple automatic gestures mimicking daily-life activity, and severe impairment of alertness. The Long-term video-EEG, including polygraphic measurements, showed destruction of the wake-NREM sleep-REM sleep boundaries, episodes of undetermined state of vigilance, and concurrence of elements typical of different sleep stages. Moreover, a severe SRBD (AHI 19/h) has been observed. The MRI showed a volumetric increase in the post-surgical interpeduncular fossa and right paramedian cysts. Therefore, a multifactorial therapeutic plan including sleep hygiene and slow-release melatonin was started with improvement in nighttime sleep, but EDS persisted. Surgical treatment of cyst fenestration improved sleep-wake rhythm and behavior;BiPAP NIV was initiated with very poor adherence. Discussion: We aim to focus on sleep disorders as a possible complication of tumors involving the hypothalamic region. Our cases highlight that the clinical manifestation of these dysfunctions can be challenging to diagnose and can lead to misdiagnosis and inappropriate treatment that can harm patients' health and the quality of life of patients and their families. Conclusion: These findings support the need to incorporate comprehensive sleep assessment in survivors from childhood brain tumors involving the suprasellar/hypothalamic region.

COVID-19 and Central Nervous System Hypersomnias.

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.

Clinically mild encephalitis/encephalopathy with a reversible splenial lesion of the corpus callosum in childhood: a single-center experience

Background/aim: Mild encephalitis/encephalopathy with a reversible splenial lesion (MERS) is a rare clinicoradiological syndrome that typically presents with central nervous system symptoms such as loss of consciousness, seizure, headache, and ophthalmoparesis. Materials and methods: Here, we highlight the characteristics of this syndrome together with the clinical and MRI findings of 6 pediatric patients with MERS. Results: Between January 2017 and October 2020, 6 patients with MERS (3 boys and 3 girls) presented to our center. The mean age was 122 ± 54.6 (min-max: 44-180) months. None of the patients had a chronic disease. In our study, infectious agents were detected in 4 patients (66.6%), while noninfectious causes (one seizure and the other hyponatremia) were detected in two patients. All of our cases were discharged without any sequelae after an average of 12.1 ± 7 (min–max: 4–20) days of hospitalization. In 1 patient (case 6), control MRI could not be performed, and the radiological recovery of our other patients was shown to be between 14 days and 2 months. Conclusion: MERS is an acute encephalopathy with good prognosis and should be considered by neurologists in differential diagnosis due to its variable clinical presentation and specific MRI findings.

COVID-19 Vaccine Could Trigger the Relapse of Secondary Hypersomnia.

The coronavirus disease (COVID-19) has brought significant social and economic disruptions and devastating impacts on public health, and vaccines are being developed to combat the disease. Timely vaccination may prevent complications and morbidity but may also potentially result in unforeseen outcomes in some special clinical populations. We report on a case of hypersomnia relapse after the COVID-19 vaccination, with the aim of informing the development of the guideline on vaccination in specific groups. A 19-year old female presented with persistent daytime sleepiness after receiving the COVID-19 vaccine. She had a known history of hypersomnia secondary to infectious mononucleosis but has fully recovered for 8 months. A series of examinations were performed on this patient. Neurologic and psychiatric examinations were unremarkable. Despite normal nocturnal subjective sleep quality (Pittsburgh Sleep Quality Index score = 5, Insomnia Severity Index score = 7), her Epworth sleepiness scale score (15) suggested an abnormal level of subjective sleepiness. Consistent with the subjective report, the objective assessment by Multiple Sleep Latency Test found mean sleep latency was 1.3 min with no sleep onset rapid-eye-movement (REM) period. We speculate that COVID-19 vaccine may potentially trigger the relapse of hypersomnia. The immune memory could be an explanation for the increased response to vaccine in patients with secondary hypersomnia. Caution should be warranted when administering COVID-19 vaccine in patients with hypersomnia secondary to infections.

Understanding the Impact of the COVID-19 Pandemic, Lockdowns and Social Isolation on Sleep Quality.

The uncertain, ever-changing and an ongoing nature of the COVID-19 pandemic means that it may take some time before we can fully appreciate the negative effect of the pandemic and lockdown on our sleep and mental health. It is increasingly recognised that in the aftermath of pandemic, several persistent sleep, neuropsychiatric and physical sequelae may continue long after the pandemic is over. A body of evidence to date also highlights a significant disparity in sleep and mental health difficulties in specific vulnerable groups in the community, with different temporal profiles and sleep issues that are reported. In this perspective, we argue for a possible mechanistic impact of the COVID-19 pandemic, with its imposed restrictions and social isolation on sleep quality. We similarly discuss some of the potential international differences, as well as similarities, behind reported idiosyncratic biological vulnerabilities that may have contributed to the genesis of sleep issues. Lastly, we propose some possible implementations and innovations that may be needed in restructuring of sleep disorders services in order to benefit recovering COVID-19 patients.

SARS-CoV-2 Infection Causes Relapse of Kleine-Levin Syndrome: Case Report and Review of Literature.

Recurrent episodes of hypersomnia, hypersexuality, compulsive eating, behavioral and cognitive disturbances, are the basic clinical features of Kleine-Levin syndrome (KLS). Our case report describes a patient who was diagnosed with KLS at the age of 20. With appropriate therapy, the disease had a satisfactory course until patient had a moderate form of SARS-CoV-2 infection, which led to a significant exacerbation of all symptoms. SARS-CoV-2 virus can cause almost any neurological disease, and relapse of KLS is another evidence of neurotropicity of the virus.

Sleeping through a pandemic: impact of COVID-19-related restrictions on narcolepsy and idiopathic hypersomnia.

STUDY OBJECTIVES: To assess the impact of coronavirus disease 2019 (COVID-19)-related restrictions on narcolepsy type 1 (NT2), narcolepsy type 2 (NT2), and idiopathic hypersomnia (IH). METHODS: Participants with NT1, NT2, and IH followed in a university hospital completed an online 78-question survey assessing demographic, clinical, and occupational features of the population during the first COVID-19-related lockdown. RESULTS: A total of 219 of 851 (25.7%) respondents of the survey reported a mean increase of 1.2 ± 1.9 hours (P < .001) in night sleep time and a mean decrease of 1.0 ± 3.4 points (P < .001) on the Epworth Sleepiness Scale during lockdown. Bedtime was delayed by 46.1% of participants and wakeup time was delayed by 59.6%, driven primarily by participants with IH. Teleworkers (but not in-person workers) reported a mean increase of 0.9 ± 1.2 hours in night sleep (P < .001) and a mean decrease in sleepiness score of 1.6 ± 3.1 (P < .001). Cataplexy improved in 54.1% of participants with NT1. Sleepiness correlated with psychological wellness (r = .3, P < .001). As many as 42.5% enjoyed the lockdown, thanks to reallocation of time usually spent commuting toward longer sleep time, hobbies, and family time, and appreciated a freer napping schedule. Conversely, 13.2% disliked the lockdown, feeling isolation and psychological distress. CONCLUSIONS: Extended sleep time, circadian delay (in patients with IH), and teleworking resulted in decreased symptoms of central hypersomnias. These findings suggest that people with IH, NT1, and NT2 may benefit from a decrease in social and professional constraints on sleep-wake habits, and support advocacy efforts aimed at facilitating workplace and schedule accommodations for this population. CITATION: Nigam M, Hippolyte A, Dodet P, et al. Sleeping through a pandemic: impact of COVID-19-related restrictions on narcolepsy and idiopathic hypersomnia. J Clin Sleep Med. 2022;18(1):255-263.