Sleep (system call)

About: Sleep (system call) is a research topic. Over the lifetime, 2633 publications have been published within this topic receiving 27806 citations. The topic is also known as: Sleep() & sleep().

Method and system for non-contact sleep monitoring

Abstract: The invention provides a method and a system for non-contact sleep monitoring The method comprises the following steps: using an infrared monitoring camera to acquire video images of a head region and abdomen and thorax regions of a human body, and using a somatosensory device to acquire attitude information of the human body; acquiring sleep information of the human body; and comparing the sleep information of the human body with preset standard sleep information, and analyzing health degree of human body sleep quality The method is based on an image processing technology, and acquires sleep signals of a human body by a non-contact method The method maintains natural sleep state of a user to the greatest extent, and sleep state information with physiological significance is extracted through a video image processing technology The system is low in device cost, and provides convenience for daily use of a family

Predictors of sleep quality in medical students during COVID-19 confinement.

Abstract: Objectives We aimed to assess sleep quality of Tunisian medical students during home confinement due to the COVID-19 pandemic, and to analyze the relationship between sleep quality and sociodemographic, clinical, confinement-related and psychological variables. Methods A correlational cross-sectional study was conducted from April 11th to May 3rd 2020. Medical students who have been in home confinement and who accepted to participate in an online survey were targeted. Sociodemographic data, clinical variables, and data related to home confinement were collected. Participants also completed Pittsburgh Sleep Quality Index, Depression, Anxiety and Stress Scale and Beck Hopelessness Scale. Results Results showed a high prevalence of poor sleepers among medical students (72.5%) with poor subjective sleep quality, increased sleep latency, sleep disturbances and daytime dysfunction. Multiple regression analysis revealed that family history of suicide attempts, tobacco use, perception of home confinement and reduced physical activity during home confinement significantly contributed to poor sleep quality. Among the psychological variables, anxiety and hopelessness significantly contributed to poor sleep quality in medical students during home confinement. Conclusions Results revealed a high prevalence of poor sleep quality in medical students who have been in home confinement due to the COVID-19 pandemic. Except family history of suicide attempts, factors that significantly contributed to poor sleep quality were modifiable factors. Sleep quality and sleep parameters need to be assessed in this particular population and adequate measures aiming to promote quality of sleep need to be enhanced, given the crucial regenerative, homeostatic and psychological roles of sleep.

EEG signal features for computer-aided sleep stage detection

Abstract: Sleep apnea is a disorder in which individuals stop breathing during their sleep. Sleep apnea is categorized as obstructive, central or mixed. New techniques for sleep stage classification are being developed by bioengineers and clinicians for appropriate and timely detection of sleep disorders. The material presented in this work, includes a compendium of features extracted from the sleep studies of patients suffering from sleep apnea. Twenty-five subjects (21 males and 4 females) were selected (age: 50 ± 10 years, range 28–68 years, data was available online at the physionet database. Time and frequency domain algorithms were applied to polysomnographic signals such as EEG, EMG, and EOG signals. Results show that trends provided by this indicators could be used to automatically distinguish between sleep stages at a highly significant level (p ≪ 0.01.) This could prove very helpful in sleep apnea detection.

Disrupted nighttime sleep and sleep instability in narcolepsy

Abstract: Free AccessReview ArticlesDisrupted nighttime sleep and sleep instability in narcolepsy Kiran Maski, MD, MPH, Emmanuel Mignot, MD, PhD, Giuseppe Plazzi, MD, Yves Dauvilliers, MD, PhD Kiran Maski, MD, MPH Address correspondence to: Kiran Maski, MD, MPH, Department of Neurology, Boston Children’s Hospital, 300 Longwood Avenue, Boston, MA 02130; Phone: +01 857-218-5536; Fax: +01 617-730-0282; Email: E-mail Address: [email protected] Department of Neurology, Boston Children’s Hospital, Boston, Massachusetts Search for more papers by this author , Emmanuel Mignot, MD, PhD Stanford Center for Sleep Sciences and Medicine, Redwood City, California Search for more papers by this author , Giuseppe Plazzi, MD Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio-Emilia, Modena, Italy IRCCS, Istituto delle Scienze Neurologiche, Bologna, Italy Search for more papers by this author , Yves Dauvilliers, MD, PhD National Reference Network for Narcolepsy, Sleep and Wake Disorders Centre, Department of Neurology, Gui de Chauliac Hospital, Montpellier, France University of Montpellier, INSERM Institute for Neurosciences Montpellier, Montpellier, France Search for more papers by this author Published Online:January 1, 2022https://doi.org/10.5664/jcsm.9638Cited by:1SectionsAbstractPDF ShareShare onFacebookTwitterLinkedInRedditEmail ToolsAdd to favoritesDownload CitationsTrack Citations AboutABSTRACTStudy Objectives:This review aimed to summarize current knowledge about disrupted nighttime sleep (DNS) and sleep instability in narcolepsy, including self-reported and objective assessments, potential causes of sleep instability, health consequences and functional burden, and management.Methods:One hundred two peer-reviewed publications from a PubMed search were included.Results:DNS is a key symptom of narcolepsy but has received less attention than excessive daytime sleepiness and cataplexy. There has been a lack of clarity regarding the definition of DNS, as many sleep-related symptoms and conditions disrupt sleep quality in narcolepsy (eg, hallucinations, sleep paralysis, rapid eye movement sleep behavior disorder, nightmares, restless legs syndrome/periodic leg movements, nocturnal eating, sleep apnea, depression, anxiety). In addition, the intrinsic sleep instability of narcolepsy results in frequent spontaneous wakings and sleep stage transitions, contributing to DNS. Sleep instability likely emerges in the setting of orexin insufficiency/deficiency, but its exact pathophysiology remains unknown. DNS impairs quality of life among people with narcolepsy, and more research is needed to determine its contributions to cardiovascular risk. Multimodal treatment is appropriate for DNS management, including behavioral therapies, counseling on sleep hygiene, and/or medication. There is strong evidence showing improvement in self-reported sleep quality and objective sleep stability measures with sodium oxybate, but rigorous clinical trials with other pharmacotherapies are needed. Treatment may be complicated by comorbidities, concomitant medications, and mood disorders.Conclusions:DNS is a common symptom of narcolepsy deserving consideration in clinical care and future research.Citation:Maski K, Mignot E, Plazzi G, Dauvilliers Y. Disrupted nighttime sleep and sleep instability in narcolepsy. J Clin Sleep Med. 2022;18(1):289–304.BRIEF SUMMARYCurrent Knowledge/Study Rationale: Narcolepsy is best known as a disorder of excessive daytime sleepiness, hence its categorization as a hypersomnolence condition. Disrupted nighttime sleep (DNS) is another key feature of narcolepsy that has received less attention; therefore, this manuscript reviews the definition of DNS, self-reported symptoms of DNS, objective markers of sleep instability, consequences of DNS/sleep instability on quality of life and health, and management of DNS.Study Impact: This review will alert clinical providers to the importance of DNS and prompt further discussion with patients about its symptoms and treatment. Gaps in the literature regarding the health consequences of DNS and pathophysiology of sleep instability are highlighted to encourage future research.INTRODUCTIONNarcolepsy is a disabling sleep disorder characterized by a pentad of symptoms: excessive daytime sleepiness (EDS), cataplexy, sleep-related hallucinations (hypnagogic and hypnopompic), sleep paralysis, and disrupted/disturbed nighttime sleep (DNS).1 Not all people with narcolepsy experience all 5 symptoms, but all experience EDS.1 Narcolepsy type 1 (NT1) is a lifelong disorder characterized by the presence of cataplexy and/or orexin deficiency (cerebrospinal fluid [CSF] orexin-A, also called hypocretin-1: ≤ 110 pg/mL).1 In narcolepsy type 2 (NT2), cataplexy is absent and CSF orexin levels are typically normal or mildly reduced.1 NT2 may sometimes be challenging to distinguish from other hypersomnolence disorders.2 Symptoms of narcolepsy mainly begin in adolescence, but diagnosis is often delayed.3DNS has historically been an underrecognized symptom of narcolepsy,4 as the clinical focus has been EDS and cataplexy management. Narcolepsy was previously described as a dyssomnia due to the severity of sleep disturbances, but is now considered a disorder of hypersomnolence.5 Due to variability in definition, assessment methods, and exclusion of comorbid sleep disorders, the estimated prevalence of DNS in narcolepsy ranges widely, from 30% to 95%.6 Fifty-three percent to 78% of pediatric patients with NT1 and their caregivers report DNS.7 In a study using the Narcolepsy Severity Scale (NSS)8 to assess individual symptoms of narcolepsy, 60.8% of untreated patients and 40.3% of treated patients reported experiencing nighttime sleep disturbance.9In 2013, an expert panel reviewed the literature and detailed the evidence that DNS is a common feature of narcolepsy that differs in certain key respects from sleep disruption in other disorders.6 Subsequently, the American Academy of Sleep Medicine (AASM) added DNS as an associated feature of narcolepsy in the International Classification of Sleep Disorders, third edition (ICSD-3), diagnostic criteria.1 Since the publication of the consensus characterization and the update to the classification, which focused additional attention on DNS in narcolepsy, there have been advancements in understanding of this condition.The aim of this review is to summarize the current state of knowledge about DNS and, more specifically, the intrinsic sleep instability unique to narcolepsy. Topics covered include assessment of self-reported DNS, objective assessment of sleep instability, potential causes of sleep instability in narcolepsy, health consequences and the functional burden of DNS, and available evidence regarding DNS management. The newer literature since the publication of the 2013 Roth et al6 review will be emphasized. No new data were generated or analyzed in support of this research.METHODSLiterature searchTo identify peer-reviewed publications on nighttime sleep, sleep instability, and DNS in narcolepsy, PubMed was searched (June 23, 2020), without limits on date or language, for articles on narcolepsy that also included the terms disrupted/disturbed nighttime sleep, sleep stability, sleep instability, insomnia, nighttime sleep, polysomnography (PSG), REM, fragmentation, fragmented, disrupted, sleep transitions, transitional sleep, sleep architecture, arousals, actigraphy, actigraphic, hypocretin, orexin, cardiovascular, obesity, puberty, or mood, and were not about studies in rats, mice, or dogs (canines). A total of 894 items were returned (Figure 1). Additional literature was identified from the bibliographies of articles from the initial search, further targeted searching, and the collections of the authors. After reviewing for relevance, a total of 102 articles were included in this report. Characteristics of clinical studies that assessed nighttime sleep in participants with narcolepsy are summarized in Table 1 and Table 2. The term(s) used to describe the patient population in the original article were used to describe the patient population in the current report (ie, “NT1” or “narcolepsy with cataplexy” [NwC], “NT2” or “narcolepsy without cataplexy” [NwoC]). If the narcolepsy subtype was not defined in the original article or the population consisted of a mix of the subtypes, then “narcolepsy (mixed population)” was used in the current report.Figure 1: Literature search results.Download FigureTable 1 Summary of studies involving PSG assessment of nocturnal sleep architecture in narcolepsy.ReferenceComparisonAdult or Pediatric PopulationGroup SizesTSTWASOAwakeningsArousalsN1N2N3 (S3/S4; SWS)REM SleepSleep EfficiencyNarcolepsy vs controls Narcolepsy (mixed population) Jiménez-Correa 200922N vs HCAdultN: 23 HC: 23nsns (“wakefulness”)↑ (< 3 min)↑↑ (%) (S1)↑ (%) (S2)↓ (%) (SWS)↓ (%)ns (index) Narcolepsy with cataplexy/NT1 Mukai 200325NwC vs HCAdultNwC: 8 HC: 8ns↑––↑ (%)ns (%) (↓P = .06)↓ (%) (S3+S4)ns (%)ns (%) Dauvilliers 200726NwC vs HCAdultNwC: 16 HC: 16ns–––ns (%)↓ (%)ns (%) (SWS)ns (%)↓ Khatami 200723NwC vs HCAdultNwC: 11 HC: 11↓↑––↑ (min)↓ (min)ns (min) (SWS)ns (min)↓ (%) Khatami 200824NwC vs HCAdultNwC: 6 HC: 6↓↑––↑ (min)↓ (min)ns (min) (SWS)ns (min)↓ (%) Frauscher 201127NwC vs CMixedNwC: 6 Con: 6nsns––ns (%)↓ (%)ns (%) (S3/S4)ns (%)ns (%) Antelmi 201728NT1 vs HCPediatricNT1: 40 HC: 22ns↑––↑ (%)↓ (%)ns (%) (N3)ns (%)ns (%) Walacik-Ufnal 201729NT1 vs HCAdultNT1: 15 HC: 15ns↑––↑ (%)↓ (%)↓ (%) (S3+S4)ns (%)ns (%) Vandi 201930NT1 vs CPediatricNT1: 27 C: 19ns↑––↑ (%)ns (%)ns (%) (↓P = .07)ns (%)ns (%) Pizza 201531NT1 vs sHSAdultNT1: 79 sHS: 52ns↑↑–↑ (%) ↑ (min)↓ (%) ↓ (min)↓ (%) ns (min)ns (%) ns (min)↓ (%) Maski 202132NT1 vs SSSPediatricNT1: 46 SSS: 48ns↑–↑ (index)↑ (%)↓ (%)ns (%)ns (%)↑ (%) Narcolepsy without cataplexy/NT2 Pizza 201531NT2 vs sHSAdultNT2: 22 sHS: 52nsnsns–ns (%)ns (%)ns (%)ns (%)ns (%) Maski 202132NT2 vs SSSPediatricNT2: 12 SSS: 48nsns–ns (index)ns (%)ns (%)ns (%)↑ (%)↑ (%)Narcolepsy with cataplexy/NT1 vs narcolepsy without cataplexy/NT2 Harsh 200015NwC vs NwoCAdultNwC: 430 NwoC: 100↓–↑ (index)↑ (index)↑ (%)↓ (%)ns (%) (SWS)ns (%)↓ Takei 201234NwC vs NwoCAdultNwC: 52 NwoC: 62ns↑–↑ (index)↑ (%)↓ (%)ns (%) (3/4)ns (%)↓ (%) DelRosso 201335NwC vs NwoCAdultNwC: 4 NwoC: 4ns↑––ns (%)ns (%)ns (%)ns (%)ns Sorensen 201336NwC vs NwoCAdultNwC: 43 NwoC: 20ns–––↑ (%)ns (%)ns (%)ns (%)ns (%) Pizza 201531NT1 vs NT2AdultNT1: 79 NT2: 22ns↑↑–↑ (%) ↑ (min)↓ (%) ↓ (min)ns (%) ns (min)ns (%) ns (min)↓ (%) Maski 202132NT1 vs NT2PediatricNT1: 46 NT2: 12ns↑–↑ (index)ns (%)ns (%)ns (%)ns (%)ns (%) Presence vs absence of DQB1*0602 allele in patients with NwC or NwoC Hong 200038NwC/ DQB1*0602 positive vs NwC/DQB1*0602 negativeAdultNwC/ DQB1*0602 positive: 312 NwC/DQB1*0602 negative: 114ns↑ (%)––↑ (%)↓ (%)ns (%) (S3, S4)↓ (%)↓ (%) Hong 200038NwoC/ DQB1*0602 positive vs NwoC/DQB1*0602 negativeAdultNwoC/ DQB1*0602 positive: 52 NwoC/DQB1*0602 negative: 36ns↑ (%)––↑ (%)ns (%)ns (%)ns (%)ns (%)Narcolepsy vs other disorders of hypersomnolence Narcolepsy (mixed population) DelRosso 201335N vs IHAdultN: 8 IH: 8↓ns––ns (%)ns (%)ns (%)↑ (%)ns Narcolepsy with cataplexy/NT1 Takei 201234NwC vs IH w/o LSTAdultNwC: 52 IH w/o LST: 50ns↑–↑ (index)↑ (%)↓ (%)ns (%) (3/4)ns (%)ns (%) DelRosso 201335NT1 vs IHAdultNT1: 4 IH: 8ns (P = .06)ns––ns (%)ns (%)ns (%)ns (%)ns (%) Pizza 201531NT1 vs IHAdultNT1: 79 IH: 22ns↑↑–↑ (%) ↑ (min)↓ (%) ↓ (min)ns (%) ns (min)ns (%) ns (min)↓ (%) Walacik-Ufnal 201729NT1 vs PsychAdultNT1: 15 Psych: 14ns↑––↑ (%)↓ (%)↓ (%) (3/4)ns (%)ns (%) Maski 202132NT1 vs IHPediatricNT1: 46 IH: 18↓↑–↑ (index)↑ (%)↓ (%)↑ (%)ns (%)ns Narcolepsy without cataplexy/NT2 DelRosso 201335NT2 vs IHAdultNT2: 4 IH: 8nsns––ns (%)ns (%)ns (%)↑ (%)ns Pizza 201531NT2 vs IHAdultNT2: 22 IH: 22nsnsns–ns (%) ns (min)ns (%) ns (min)ns (%) ns (min)ns (%) ns (min)ns (%) Maski 202132NT2 vs IHPediatricNT2: 12 IH: 18nsns–nsns (%)↓ (%)ns (%)ns (%)nsC = control, HC = healthy control, IH = idiopathic hypersomnia, LST = long sleep time, N = narcolepsy (mixed population), N1/2/3 = stage 1/2/3 non-REM sleep, ns = not significant, NT1 = narcolepsy type 1, NT2 = narcolepsy type 2, NwC = narcolepsy with cataplexy, NwoC = narcolepsy without cataplexy, PSG = polysomnography, psych = psychiatric disorder, REM = rapid eye movement, sHS = subjective hypersomnolence, SSS = subjectively sleepy subjects, SWS = slow-wave sleep, TST = total sleep time, w/o = without, WASO = wake after sleep onset.Table 2 Summary of studies involving PSG assessment of wake-sleep stages (duration, number, or transitions) during nocturnal sleep in narcolepsy.Narcolepsy vs ControlsNwC/NT1 vs NwoC/NT2Narcolepsy vs Other Disorders of HypersomnolenceCSF hcrt-1 LevelsAntelmi 201728Vandi 201930Pizza 201531Pizza 201531Maski 202132Maski 202132Sorensen 201336Pizza 201531Maski 202132Pizza 201531Pizza 201531Maski 202039Maski 202132Maski 202132Barateau 202060Sorensen 201336ComparisonNT1 vs HCNT1 vs CNT1 vs sHSNT2 vs sHSNT1 vs SSSNT2 vs SSSNwC vs NwoCNT1 vs NT2NT1 vs NT2NT1 vs IHNT2 vs IHNT1 vs NT2/ IH/ SSSNT1 vs IHNT2 vs IHCSF hcrt-1 ≤ 110 pg/mL vs CSF hcrt-1 > 110 pg/mLCSF hcrt-1 < 129 pg/mL vs CSF hcrt-1 ≥ 129 pg/mLPopulationPedPedAdultAdultPrimarily ped (5–21 y)Primarily ped (5–21 y)AdultAdultPrimarily ped (5–21 y)AdultAdultPedPrimarily ped (5–21 y)Primarily ped (5–21 y)Adult (n = 229) and ped (n = 71)AdultGroup sizesNT1: 40 HC: 22NT1: 27 C: 19NT1: 79 sHS: 52NT2: 22 sHS: 52NT1: 46 SSS: 48NT2: 12 SSS: 48NwC: 43 NwoC: 20NT1: 79 NT2: 22NT1: 46 NT2: 12NT1: 79 IH: 22NT2: 22 IH: 22NT1: 150 NT2: 22 IH: 27 SSS: 117NT1: 46 IH: 18NT2: 12 IH: 18CSF hcrt-1 ≤ 110 pg/mL: 164 CSF hcrt-1 > 110 pg/mL: 136CSF hcrt-1 < 129 pg/mL: 37 CSF hcrt-1 ≥ 129 pg/mL: 20Transitions between/among wake, sleep, sleep stages (bidirectional) Wake, sleep↑a–↑ansa––↑b↑a–↑ansa––––↑b Wake, NREM sleep, REM sleep↑a–↑ansa–––↑a–↑ansa––––– Wake, N1, N2/N3, REM sleep↑a–↑ansa–––↑a–↑ansa––––– REM sleep, NREM sleep––––––nsb––––––––nsb N1, N2, N3––––––nsb––––––––nsb N1, N2, N3, REM––––––nsb––––––––nsb Wake, N1, N2, N3, REM sleep–ns (↑ P = .07)c–––––––––––––Transitions from sleep to wake (directional) Sleep to wake–––––––––––↑d––↑– REM sleep to wake––––––––––––––↑– REM sleep to N1/wake–––––––––––↑d–––– NREM sleep to wake––––––––––––––↑– N1 to wake–––––––––––––↑– N2 to wake––––––––––––––↑– N3 to wake––––––––––––––↑– N2/N3 to N1/wake–––––↑d–––N2/N3/REM sleep to N1/wake–––––––––––↑d–––– Sleep to wake and N2/N3/REM sleep to N1–––––––––––↑d––––Transitions from wake to sleep (directional) Wake to sleep––––––––––––––↑– Wake to REM sleep––––––––––––––↑– Wake to NREM sleep––––––––––––––↑–Wake bouts Wake bouts, total number––––↑ns––↑–––↑ns↑– Wake bouts/h of wake time, index––––––––––––––↓– Wake bouts of 30 s, %––––––––––––––↑– Wake bouts of 1 min 30 s, %––––––––––––––↑–Sleep bouts Sleep bouts, total number––––––––––––––↑– Sleep bouts/h of sleep time, index––––––––––––––↑– Sleep bouts of ≤14 min (2–5 min), %––––––––––––––↑– Sleep bouts of >32 min 30 s, number––––––––––––––↓–N1 bouts, number↑ns↑↑nsN2 bouts, number↑ns↑nsnsN3 bouts, numbernsnsnsnsnsREM sleep bouts, number↑nsns↑nsaNumber of transitions between states divided by time in bed (in hours). bNumber of transitions per hour of sleep of the investigated sleep stage. cNumber of transitions per hour between the start and the end of nocturnal sleep. dNumber of transitions per hour of total sleep time. C = control, CSF = cerebrospinal fluid, HC = healthy control, hcrt-1 = hypocretin-1, IH = idiopathic hypersomnia, N1/2/3 = stage 1/2/3 non-REM sleep, NREM = nonrapid eye movement, ns = not significant, NT1 = narcolepsy type 1, NT2 = narcolepsy type 2, NwC = narcolepsy with cataplexy, NwoC = narcolepsy without cataplexy, ped = pediatric, PSG = polysomnography, REM = rapid eye movement, sHS = subjective hypersomnolence, SSS = subjectively sleepy subjects.RESULTSDNS terminologyThere is still no single agreed-upon definition of DNS in narcolepsy. The AASM ICSD-3 guidelines describe DNS as “an inability to maintain continuous sleep.”1 However, there are many nocturnal symptoms of narcolepsy that may disrupt sleep continuity, and thus the term DNS could be conceptualized in a broad sense to encompass underlying narcolepsy-related sleep symptoms and disorders. Hypnagogic/hypnopompic hallucinations and/or sleep paralysis are found in 33%–80% of patients with NT11 and may lead to sleep disturbances if they cause distress and difficulty initiating sleep or maintaining sleep when they occur in the middle of the night. Narcolepsy (mixed population) is associated with sleep-related movement disorders, including rapid eye movement (REM) sleep behavior disorder (RBD), restless legs syndrome, and periodic limb movements of sleep (PLMS).10 RBD presents as REM sleep without atonia and abnormal movements during REM sleep related to acting out dreams, and is reported in up to 61% of people with NwC.11 Such REM sleep abnormalities have been less studied in NT2. In a small pediatric cohort, patients with NT2 had numerically higher REM sleep without atonia density than subjectively sleepy controls, and 2 of the 6 NT2 patients demonstrated vocalizations and/or movements consistent with RBD.12 PLMS involves repetitive movements of the legs that occur during REM and non-REM (NREM) sleep13 and is reported in up to 75% of people with narcolepsy (mixed population).14 These abnormal movements during sleep may be associated with sleep disruption through frequent awakenings or arousals (narcolepsy [mixed population]),15 but the degree of sleep disturbance they cause is unknown. Patients with narcolepsy (mixed population) report problematic nightmares and nocturnal eating that may also contribute to sleep disruption.16 Furthermore, obesity is more common among patients with narcolepsy (mixed population) and likely contributes to frequent reporting of obstructive sleep apnea (OSA), which may further fragment sleep.10,17–19 Last, the degree to which comorbidities such as anxiety and depression or use of wake-promoting medications such as traditional stimulants may contribute to problems of sleep continuity is unclear (narcolepsy [mixed population]).20The expert panel convened in 2011 to refine the definition of DNS that may exist independently of comorbid conditions such as OSA, RBD, and PLMS; review the literature; and formulate a consensus characterization of DNS in narcolepsy based on self-reported and objective data.6 The panel concluded that patients with narcolepsy (mixed population) typically describe frequent, usually brief, nocturnal awakenings and generally poor sleep quality, and that objective measures of their sleep problems included increased arousals, increased wake after sleep onset (WASO) time, frequent shifts to wake or increased N1 sleep with reduction of N3/N4, and overall decreased sleep efficiency. The authors proposed that DNS in narcolepsy (mixed population) is “a stand-alone and specific symptom that is not associated with other sleep disorders,”6 but this claim has not yet been substantiated against other disorders such as primary OSA.While this panel highlighted important nocturnal sleep continuity impairment in narcolepsy, the term DNS continues to be used inconsistently in the subsequent literature. Most important, when patients with narcolepsy are queried about DNS or sleep disruptions, they may be reporting the effects of the broad range of sleep disorders that commonly occur in narcolepsy. In this review, we favor using DNS as an umbrella term for all sleep symptoms/conditions common to narcolepsy as well as the intrinsic sleep instability that produces spontaneous wakings, arousals, and excessive sleep stage transitions.Characteristics of DNS in narcolepsyResearchers have described DNS in narcolepsy using objective tools such as PSG and actigraphy, as well as self-reported measures obtained by clinical interviews, sleep diaries, and questionnaires. Patients with common narcolepsy-related sleep disorders/conditions such as PLMS and RBD have not typically been excluded from clinical studies; thus, it is not possible to say whether findings are a reflection of sleep instability intrinsic to narcolepsy.Objective DNS measures reported in the literature include standard (static) measures of sleep continuity, such as time spent asleep (total sleep time [TST]), time awake after sleep onset (WASO), number of awakenings, arousal index, time spent (or percentage of TST spent) in sleep stages (NREM sleep, NREM sleep stages [N1, N2, N3], slow-wave sleep [SWS], and REM sleep), and sleep efficiency, as well as dynamic measures of sleep architecture and stability, which relate to the frequency and nature of transitions among sleep states and between wake and sleep states. Transitions have been quantified in terms of raw numbers (counts), by transitional indices (eg, number of transitions per hour of sleep), sleep and wake bout numbers, or sleep and wake bout median durations. Techniques including sophisticated statistical analyses and computer scoring algorithms have been used to examine the diagnostic utility of sleep stage dynamics.21Although an extensive body of research in this field is lacking, trends in objective and self-reported measures of sleep instability are observable in comparisons of narcolepsy (including NT1 or NwC, NT2 or NwoC, and mixed populations of both narcolepsy groups) with controls (including healthy controls [HCs], subjectively sleepy controls [people with self-reported daytime sleepiness but normal PSG and Multiple Sleep Latency Test results], and people with other central nervous system disorders of hypersomnolence), and comparisons between narcolepsy subtypes (NT1/NwC and NT2/NwoC).Objective assessment of sleep instability: PSGNarcolepsy vs healthy controls or subjectively sleepy controlsStatic measures:Findings related to static measures of sleep architecture in people with narcolepsy vs HCs or subjectively sleepy controls (subjectively sleepy subjects [SSS] or subjective hypersomnolence [sHS], defined here as people with self-reported daytime sleepiness but who do not meet the clinical criteria for NT1, NT2, or a different disorder1) are summarized in Table 1.Narcolepsy (mixed population): In a single study in people with narcolepsy (mixed population) vs HCs, there was no significant between-group difference in TST, WASO (“wakefulness”), or sleep efficiency; however, the patient population had increased awakenings and arousals, increased N1 and N2 percentage, and decreased SWS and REM sleep percentage.22NwC/NT1: In 10 studies comparing people with NwC or NT1 vs controls (HC or sHS), TST was reduced significantly in people with NwC/NT1 in 2 studies23,24 but did not differ between groups in the remaining 8 studies.25–32 WASO was increased significantly in people with NwC/NT1 in 8 of 9 studies examining WASO.23–25,28,29,31,32 One study reported no significant difference in WASO between NwC and controls, although the study only included a total of 12 participants and thus may have been underpowered to detect differences.27 Of 10 studies, 8 reported that participants with NwC/NT1 had significant increases in N1 sleep (N1 percentage or total duration of N1)23–25,28–32 and decreases in N2 sleep (N2 percentage or total duration of N2) compared with controls;23,24,26–29,31,32 however, N3 sleep and REM sleep were generally similar between groups, with only 3 of 10 studies reporting a significant decrease in N3 percentage25,29,31 and no studies reporting a significant group difference in REM sleep percentage or duration.23–32 Four of the 10 studies reported significantly decreased sleep efficiency in NT1/NwC vs controls23,24,26,31 and 1 reported significantly increased sleep efficiency in NT1 vs subjectively sleepy controls.32NwoC/NT2: In 2 studies comparing participants with NT2 vs sHS or SSS, there were no group differences in TST, WASO, awakenings, N1, N2, or N3.31,32 In one of these studies, in pediatric participants, REM sleep and sleep efficiency were increased in NT2 compared with subjectively sleepy controls,32 but in the other, in adults, there were no differences in these parameters.31Dynamic measures:Three studies examined wake and sleep stage transitions in NT1 vs HC or sHS (Table 2).28,30,31 In a study by Antelmi et al28 involving drug-naïve children and adolescents with NT1 vs HC, transitions between wake and sleep or sleep stages (calculated as sleep transitional indexes, or frequency of transitions between combinations of sleep stages) were significantly increased in NT1, including transitions between wake and sleep; transitions among wake, NREM sleep, and REM sleep; and transitions among wake, N1, N2/N3, and REM sleep. Vandi et al30 compared nocturnal sleep stage transitions using a frameshift index (calculated as number of transitions between states [wake, N1, N2, N3, REM sleep]) in children and adolescents with NT1 vs subjectively sleepy controls. The NT1 frameshift index was numerically higher in the NT1 group; however, results neared but did not meet statistical significance. The results of the 2 studies are not necessarily conflicting, as they assessed transitions with different measures and differed in comparator groups (HCs vs subjectively sleepy people). Pizza, Vandi, et al31 examined adults with NT1 or NT2 vs sHS in terms of transitions between sleep and wake; among wake, NREM sleep, and REM sleep; and among wake, N1, N2/N3, and REM sleep and found increases in all 3 types of transitions in people with NT1 vs sHS but no significant group differences between NT2 and sHS.Maski, Colclasure, and colleagues32 compared young people (5–21 years of age) with NT1, NT2, idiopathic hypersomnia (IH), or SSS in terms of nocturnal wake and sleep stage (N1, N2, N3, and REM sleep), bout duration, bout number, and survival of bouts using nocturnal PSG. Findings suggested different sleep phenotypes for each group. Compared with SSS, the NT1 group showed evidence of sleep fragmentation with unstable REM sleep and N2 sleep, the NT2 group showed comparable sleep with the exception of longer N1 bouts, and the IH group showed increased N2 sleep stability and shorter N3 bout duration.A detailed examination of nocturnal sleep stage sequences and transitions (due to complexity of analyses, not included in Table 2) was conducted by Ferri and colleagues,33 who found that the sleep stage transition pattern was significantly different between people with NT1 vs sHS, NT2, and IH. Comparisons of between-stage transition probabilities (derived from standardized sleep stage transition matrices containing the probability of stage transitions, rather than the absolute number of transitions, and confirmed using Markovian analysis of group matrices) indicated a higher probability of transitions from REM sleep to wake, wake to N1, N1 to N2, and wake to REM sleep and a lower probability of transitions from N2 to N1, N3 to N2, REM sleep to N2, and N2 to REM sleep in people with NT1 vs sHS, NT2, or IH.33 The lower probability of the REM sleep to N2 transition was the most reliably observed of these, leading the authors to propose that frequent alternation between REM and NREM sleep may represent a PSG fingerprint of orexin-deficient hypersomnia, and thus may be useful as a diagnostic tool.33NT1 vs NT2Static measures:Relatively little information is available regarding sleep instability in NT1 vs NT2 because both are rare disorders and thus small sample sizes are typically reported in existing studies. Based on the evidence that does exist, the overall impression is one of greater sleep instability in NT1 compared with NT2.Findings relating to static measures of sleep architecture are summarized in Table 1. Six studies compared participants with NwC/NT1 vs NwoC/NT2. In 5 of these studies, no group difference was noted in TST,31,32,34–36 but Harsh et al15 reported decreased TST in participants with NwC vs NwoC. All 4 studies that examined WASO showed increased WASO among participants with NwC/NT1 vs NwoC/NT2.31,32,34,35 Participants with NwC/NT1 had increased N1 sleep in 4 of 6 studies15,31,34,36 and decreased N2 sleep in 3 of 6 studies vs NwoC/NT2.15,31,34 No significant group differences were detected in N3 or REM sleep.15,31,32,34,35,37 Sleep efficiency was decreased significantly in NwC/NT1 vs NwoC/NT2 in 3 of 6 studies.15,31,34Hong et al38 compared participants with NwC or NwoC categorized by the presence or absence of the human leukocyte antigen (HLA) DQB1*06:02 allele (Table 1). They found that the presence of the allele in participants with NwC was associated with increased WASO and N1 sleep percentage and decreased N2 sleep and REM sleep percentage and sleep efficiency, but no group differences in TST or N3 sleep, compared with the absence of the allele. In participants with NwoC, the presence of the allele was associated with increased WASO and N1 sleep percentage but no significant difference (compared with the absence of the allele) in TST; N1, N2, N3, or REM sleep percentage; or sleep efficiency.38Dynamic measures:Two studies, both in adults, examined wake and sleep stage transitions in NT1 vs NT2 (Table 2). Sorensen, Knudsen, and Jennum36 reported that transitions (quantified as “number of transitions per hour of sleep of the investigated sleep stage”) between wake and sleep were significantly increased in participants with NT1 vs NT2, but transitions between REM and NREM sleep; transitions to/from N1, N2, and N3; and transitions between all sleep stages were not significantly different between groups. Pizza, Vandi, et al31 reported that transitions between wake and sleep; transitions among wake, REM sleep, and NREM sleep; and transitions among wake, N1, N2/N3, and REM sleep (calculated as sleep transitional indexes per hour of sleep) were significantly higher in drug-naïve adults with NT1 vs N

Apparatus for displaying or printing used to evaluate quality of sleep, method, computer program, breathing assistance device, breathing assistance device for chronic cardiac disease patient, sleep introduction device, massage device, inspection device

Abstract: PROBLEM TO BE SOLVED: To provide an apparatus for displaying or printing used to evaluate quality of sleep to enable a sleep inspection at home without requiring measurement of brain waves, a method, a computer program, a breathing assistance device, a breathing assistance device for a chronic cardiac disease patient, a sleep introduction device, a massage device, and an inspection device SOLUTION: A waveform in which a high frequency component of a heartbeat variation waveform varying with time is processed by wavelet conversion Temporal transition of power of the frequency corresponding to the sleep period (ultradian rhythm) is displayed or printed The apparatus is configured so that a medical person can evaluate the quality of sleep from clarity, number, and position of the peak in the temporal transition graph COPYRIGHT: (C)2009,JPO&INPIT