Journal of Sleep Research最新文献

Excessive daytime sleepiness is a possible symptom of post-COVID syndrome and is also the cardinal symptom of narcolepsy, a rare life-long sleep disorder with a possible autoimmune background. Recent reports indicate that COVID-19 infection may trigger narcolepsy. However, it remains unclear how best to identify and treat such cases. A 25-year-old male developed daytime sleepiness after COVID-19 infection. A diagnosis of narcolepsy type II was made based on pathologically shortened sleep latencies in polysomnography and multiple sleep latency tests (MSLT) together with several sleep-onset REM-sleep periods (SOREMs). Pupillography and neuropsychological testing revealed reduced alertness levels. Hypocretin levels in the cerebrospinal fluid were borderline. Based on the postulated autoimmune background of narcolepsy, we performed an intravenous high-dose corticosteroid pulse therapy with methylprednisolone. Narcoleptic symptoms immediately and consistently remitted after the corticosteroid pulse. Follow-up after 4 months revealed normalisation of sleep latencies, no further SOREMs in the MSLT, and increased alertness in pupillography and neurocognitive testing. No further wakefulness promoting drug therapy was required. Narcolepsy should be considered in the differential diagnosis of post-COVID syndrome with leading symptoms of daytime sleepiness. Furthermore, immunosuppressive therapy may offer a treatment option in managing an otherwise lifelong disorder in select cases.

Central sleep apneas (CSA) can occur de novo at high-altitude in individuals without sleep-disordered breathing at low altitude. These apneas are usually brief, lasting only 5-15 s. This report presents the first documented case of a man experiencing extreme altitude-induced CSA lasting more than 100 s in the absence of any sleep breathing disorder in normoxia. A 23-year-old male with no pre-existing health conditions was recruited for a study examining the work of breathing during sleep at a simulated altitude of 3500 m (FiO₂:13%). A lowland polysomnography was first conducted to exclude moderate to severe sleep-disordered breathing and showed an apnea-hypopnea index (AHI) of 7.6/h, an oxygen desaturation index (ODI) of 4.8/h, and a mean pulse oximetry-based oxygen saturation (SpO₂) of 93.9%. During the recording in the hypoxic chamber, the participant experienced prolonged CSA lasting up to 1 min and 49 s. These apneas were associated with significant oxygen desaturations (nadir: 44%). To investigate the origin of these atypical CSA, the participant underwent a new low-altitude polysomnography with transcutaneous CO₂ measurement (mean PaCO₂:46 mmHg) and diurnal arterial blood gas analysis (pH: 7.42, pCO₂: 35.1 mmHg, pO₂: 79.9 mmHg, HCO₃ ^-: 22.4 mmol/L). These results indicated no signs of chronic hypercapnia or hypocapnia. A hypoxia tolerance test (FiO₂: 11.5%) demonstrated a good ventilatory response to hypoxia during exercise (1.004 L/min/kg). A rebreathing test according to the Read protocol in hyperoxia demonstrated an impaired ventilatory response to CO₂ (<0.6 L/min/mmHg). This report documents a rare form of extreme hypoxia-induced CSA, potentially caused by impaired CO₂ chemoreceptor sensitivity and an increased arousal threshold.

Polysomnography, the gold-standard for measuring sleep, is costly, intrusive and usually limited to 1 night. Actigraphy offers a more affordable, less intrusive method over multiple nights. However, little research validates ActiGraph accelerometers against polysomnography, especially in children. This study evaluated the validity of different algorithms and compared wrist versus ankle accelerometer placements for estimating sleep in children aged 1-12 years. Twenty-nine children undergoing overnight type 1 polysomnography wore ActiGraph accelerometers. Six algorithms were evaluated against polysomnography using Pearson correlations, intraclass correlation, paired t-tests and Bland-Altman plots. Agreement was classified as poor (intraclass correlation coefficient < 0.4), fair (0.4 < intraclass correlation coefficient < 0.6), good (0.6 < intraclass correlation coefficient < 0.75) or excellent (intraclass correlation coefficient > 0.75). Total sleep time was the primary outcome. For wrist-worn devices, the Sadeh (Actilife) and Cole-Kripke (Actilife and GGIR) algorithms showed excellent agreement with polysomnography (intraclass correlation coefficient = 0.80-0.85), while vanHees showed good agreement (intraclass correlation coefficient = 0.67) and Galland showed fair agreement (intraclass correlation coefficient = 0.46). The Cole-Kripke algorithm did not significantly differ from polysomnography total sleep time, whereas others underestimated total sleep time. For ankle-worn devices, Sadeh (Actilife), Cole-Kripke (Actilife) and vanHees algorithms demonstrated excellent agreement (intraclass correlation coefficient = 0.75-0.82). No significant differences were found between wrist and ankle placements for certain algorithms. The findings support accelerometry as a valid tool for sleep assessment in children, recommending that algorithm selection be tailored to specific study requirements.

EEG spectral analysis provides a more sensitive measure of sleep disruption than conventional sleep macro-architecture. We aimed to examine the use of this technique applied to overnight polysomnography in distinguishing children with narcolepsy and idiopathic hypersomnia (IH) from subjectively sleepy children with a non-diagnostic multiple sleep latency test. The relative power was calculated for delta (0.5-3.9 Hz), theta (4-7.9 Hz), alpha (8-11.9 Hz), sigma (12-13.9 Hz), and beta power (14-30 Hz). A mean value for each frequency was calculated for each 30 s epoch then averaged for each sleep stage within each child. Data are presented as median and interquartile range. Twenty-eight children with narcolepsy, 11 with IH, and 26 with subjective sleepiness were included and individually matched for age and sex with a control child. In N2, the F4 beta power was lower in the narcolepsy compared with the IH group (p < 0.05). The F4 theta power was higher in the narcolepsy compared with the subjectively sleepy group during wake (p < 0.001), N2 (p < 0.01), N3 (p < 0.05), and total sleep (p < 0.01). During total sleep the F4 delta power was lower in both the narcolepsy and IH groups compared with the subjectively sleepy group (p < 0.05 for both). Our study identified specific EEG frequencies which differed between groups of children referred for assessment of EDS. In particular, differences in theta and delta power in children with narcolepsy and IH compared with others with subjective sleepiness may provide insights into the pathophysiology associated these conditions.

This study aimed to test for an association between hair cortisol, as an indicator of chronic stress, and possible sleep bruxism among children participating in the 2015 Pelotas Birth Cohort Study. Data from 3229 children were analysed. Possible sleep bruxism was identified based on caregivers' reports when the child was 4 years old. Trained fieldworkers collected hair samples from children, and a standardized protocol was used for hormone extraction and cortisol quantification from the hair. Information on socioeconomic, demographic, psychological and behavioural characteristics was gathered through questionnaires. Poisson regression with robust variance was used to evaluate the impact of hair cortisol concentration on the occurrence of possible sleep bruxism, guided by a directed acyclic graph. The prevalence of possible sleep bruxism was 21.46% (n = 693); median hair cortisol concentration was 7.8 pg mg^-1. Hair cortisol concentration was not found to be associated with the occurrence of sleep bruxism. However, the presence of sleep bruxism was linked to higher maternal education (p = 0.027), maternal stress level (p = 0.032), excessive use of electronic devices (p = 0.007), and child emotional and behavioural problems (p = 0.003). Furthermore, female sex was associated with a lower frequency of possible sleep bruxism (p = 0.003). There was no association between chronic stress, as measured by hair cortisol concentration, and the occurrence of possible sleep bruxism. This study underscores the role of sociodemographic factors and children's mental health in the occurrence of sleep bruxism among children in this population.

Poor sleep quality is well recognised in both post-traumatic stress disorder (PTSD) and pain conditions. Comorbid chronic pain is prevalent in populations with PTSD and is believed to maintain symptoms of PTSD and increase the complexity of the condition. Ongoing diminished sleep quality may serve to maintain pain and PTSD symptoms, and thus affect the efficacy of first-line PTSD treatment. This study examined the mechanisms underlying the PTSD-pain relationship over time by investigating if perceived sleep quality mediates the relationship between PTSD symptom severity and levels of pain interference. Furthermore, we considered whether the interrelation between these three variables could in fact be linked in an alternative model where the causality was reversed, with pain interference mediating the relation between PTSD severity and perceived sleep quality. Relationships among our variables were assessed within a path analysis framework, conducted and controlled for covariates using structural equation modelling and mediation analysis. The analysis of our hypothesised model revealed that improvement in perceived sleep quality was a significant partial mediator of the association between reduction in PTSD severity and pain interference. Approximately 28% of the effect of PTSD severity on pain interference was mediated by improvement in perceived sleep quality. Evaluation of our alternative model revealed a non-significant mediation effect. Sleep thus represents a modifiable mechanism that contributes to the mutual maintenance of PTSD and pain. The study is the first to investigate these relationships in trauma-affected refugees and thus contributes new knowledge and clinical implications for the treatment of poor sleep quality and pain symptomatology in trauma-affected refugees.

It is unclear to what extent posture shifts during sleep are associated with prior arousal and full awakening, and if supine-avoidance alarms to discourage supine sleep promote more extended wake following supine alarms. Thus, this study sought to examine relationships between posture shifts, arousals and awakenings, and to establish if a vibro-tactile supine-avoidance alarm delays the return to sleep following supine posture shifts. Detailed posture shift and sleep data from a chest-worn device with an inactive or active supine-avoidance alarm, and in-home sleep study data were from 37 participants who completed a randomised controlled trial of supine-avoidance device treatment for supine-predominant obstructive sleep apnea. Posture shifts, sleep, arousal and awakening responses, and sleep onset latency following posture shifts were compared between baseline and supine-avoidance treatment nights. Compared to baseline, there was a marked reduction in overnight supine time with active supine-avoidance treatment. Around 90% of posture shifts were preceded by either wake, arousal or full awakening. Sleep onset latency was longer for posture shifts occurring from prior wake compared to those from prior sleep but was not different between baseline or supine-avoidance treatment nights or between shifts from non-supine to supine or vice-versa. Most overnight posture shifts are associated with either prior wake or brief arousal, which likely facilitates co-ordinated body movements needed for effective posture shifts. Thus, sleep is typically already interrupted around the time that supine-avoidance alarms are activated, and the alarm itself does not significantly delay the return to sleep.

In analogical problem solving, the solution to a previously experienced problem (source) is used to solve a new but structurally similar problem (target). Yet, analogical transfer is seldom successful, as structural commonalities between source and target problems can be difficult to recognise. Theoretically, memory consolidation processes during REM sleep may help to identify and strengthen connections between weakly related memories, improving the ability to use analogical transfer. In the current experiment, participants attempted to solve source problems, were told the solutions, and then attempted to solve new but structurally similar target problems. After a 2-h break including a nap (n = 28) or wakefulness (n = 30), participants attempted to solve target problems they were unable to solve before the break. Measures of source problem memory and perceived similarity between source and target problems were also obtained. The nap group solved a greater proportion of target problems after the break than the wake group, despite no group differences in solution rates before the break or source problem memory. The nap group also perceived greater similarity between source and target problems after the break than the wake group, and the time spent in REM sleep predicted the proportion of post-break target problems solved. These results indicate that sleep improves the ability to solve target problems that could not be initially solved and suggest that REM sleep improves the use of analogical transfer by highlighting commonalities between source and target problems that were unnoticed before a nap.

This study prospectively analysed the difference in the blood flow of the optic nerve head (ONH) between patients with obstructive sleep apnea/hypopnea syndrome (OSA) and control subjects by laser speckle flowgraphy (LSFG), and determined the correlations between LSFG variables and the severity of OSA. A total of 100 participants consecutively underwent full-night polysomnography, ophthalmologic examinations, and LSFG measurements. The LSFG parameters were summarised as the mean blur rate in all areas of the ONH (MA), in the big vessel area of ONH (MV), and in the tissue area of ONH (MT). When the control (17 subjects) and patients with mild/moderate OSA (42 patients) were grouped together and compared with patients with severe OSA (41 patients), the MA, MV, and MT were decreased significantly in patients with severe OSA compared with control subjects and patients with mild/moderate OSA (p < 0.0001, p = 0.0001, and p = 0.0034, respectively). Negative correlations were identified between the apnea-hypopnea index and MA (ρ = -0.244, p = 0.0016), between AHI and MV (ρ = -0.263, p = 0.0006), and between AHI and MT (ρ = -0.198, p = 0.0105). Positive correlations were identified between the lowest saturation of oxygen (LSaO₂) and MA (ρ = 0.332, p < 0.0001), between LSaO₂ and MV (ρ = 0.354, p < 0.0001), and between LSaO₂ and MT (ρ = 0.227, p = 0.0035). Our study demonstrated that OSA could have a negative impact on the microcirculation of the optic nerve head, including MA, MV, and MT measurements. Furthermore, the decreased blood flow of the optic nerve head obviously correlated with the severity of OSA.