Sleep fragmentation reduces explorative behaviors and impairs motor coordination in male mice.

Sleep fragmentation (SF), which refers to discontinuous and fragmented sleep, induces cognitive impairment and anxiety-like behavior in mice. However, whether SF can affect motor capability in healthy young wild-type mice and the underlying mechanisms remain unknown. We performed seven days of sleep fragmentation (SF 7d) interventions in young wild-type male mice. While SF mice experienced regular sleep disruption between Zeitgeber time (ZT) 0-12, control mice were allowed to have natural sleep (NS) cycles. Homecage analysis and conventional behavioral tests were conducted to assess the behavioral alterations in behavioral patterns in general and motor-related behaviors. Sleep structures and the power spectrum of electroencephalograms (EEGs) were compared between SF 7d and NS groups. Neuronal activation was measured using c-Fos immunostaining and quantified in multiple brain regions. SF of 7 days significantly decreased bouts of rearing and sniffing and the duration of rearing and impaired motor coordination. An increase in the total sleep time and a decrease in wakefulness between ZT12-24 was found in SF 7d mice. In SF 7d mice, EEG beta1 power was increased in rapid eye movement (REM) sleep while theta power was decreased during wakefulness. SF 7d resulted in significant suppression in c-Fos (+) cell counts in the motor cortex and hippocampus but an increase in c-Fos (+) cell counts in the substantia nigra pars compacta (SNc). In summary, SF 7d suppressed explorative behaviors and impaired motor coordination as compared to NS. EEG power and altered neuronal activity detected by c-Fos staining might contribute to the behavioral changes.

Characteristics of obstructive sleep apnea related to insulin resistance.

BACKGROUND: Obstructive sleep apnea (OSA) is associated with multiple comorbidities, including diabetes. Its development is preceded by alterations in the initial phase of carbohydrate metabolism characterized by insulin resistance. This study aims to evaluate the role of intermittent hypoxia and sleep fragmentation characteristic of OSA on the risk of insulin resistance among apneic patients without diabetes. METHODOLOGY: 92 consecutive patients with OSA without evidence of diabetes were recruited. Overnight video polysomnography was performed and, the following morning, fasting blood glucose, insulin and glycosylated hemoglobin were determined. Insulin resistance was measured using the HOMA-IR index. RESULTS: Insulin resistance was present in 52.2% of OSA patients. In these subjects, insulin resistance was independently associated to the apnea index during REM sleep (adjusted odds ratio [aOR] 1.09; 95% CI, 1.03 to 1.16; p = 0.004), desaturation index (aOR 1.08; 95% CI: 1.04 to 1.13; p = 0.027), and sleep time with oxygen saturation below 90% (aOR 1.04; 95% CI 1.00 to 1.08; p = 0.049). Furthermore, the HOMA-IR level was also directly related to the desaturation index (standardized regression coefficient [B] = 0.514, p < 0.001) and to the apnea index during REM sleep (B = 0.344, p = 0.002). CONCLUSIONS: Intermittent hypoxia and disturbances in REM sleep emerge as main contributors to insulin resistance in OSA patients yet to experience diabetes onset.

Sleep-wake behavior, perceived fatigability, and cognitive reserve in older adults.

INTRODUCTION: The effects of sleep-wake behavior on perceived fatigability and cognitive abilities when performing daily activities have not been investigated across levels of cognitive reserve (CR). METHODS: CR Index Questionnaire (CRIq) data were collected and subjected to moderated mediation analysis. RESULTS: In amnestic mild cognitive impairment (aMCI; n = 41), CR moderated sleep-related impairments (SRIs), and fatigability at low CR (CRIq < 105.8, p = 0.004) and mean CR (CRIq = 126.9, p = 0.03) but not high CR (CRIq > 145.9, p = 0.65) levels. SRI affected cognitive abilities mediated by fatigability at low CR (p < 0.001) and mean CR (p = 0.003) levels. In healthy controls (n = 13), SRI in fatigability did not alter cognitive abilities across CR levels; controls had higher leisure scores than patients with aMCI (p = 0.003, effect size = 0.93). DISCUSSION: SRI can amplify impaired cognitive abilities through exacerbation of fatigability in patients with aMCI with below-mean CR. Therefore, improving sleep-wake regulation and leisure activities may protect against fatigability and cognitive decline. HIGHLIGHTS: Clinical fatigue and fatigability cannot be alleviated by rest. Clinical fatigability disrupts daily activities during preclinical Alzheimer's. High cognitive reserve mitigates sleep-wake disturbance effects. High cognitive reserve attenuates clinical fatigability effects on daily functioning. Untreated obstructive sleep apnea potentiates Alzheimer's pathology in the brain.

Impact of sleep on educational outcome of Indigenous Australian children: A systematic review.

INTRODUCTION: The association between quality sleep and improved cognition is well reported in literature. However, very few studies have been undertaken to evaluate the impact of poor sleep on educational outcomes in Indigenous Australian children. OBJECTIVES: The objective of this review was to explore the association between sleep and educational outcomes of Indigenous children. METHODS: For this systematic review, a literature search covering research articles in academic databases and grey literature sources was conducted to retrieve studies published until March 2022. Eight online e-databases (PubMed, Ovid MEDLINE, CINAHL, SCOPUS, HealthinfoNet, PsycINFO, Cochrane and Google Scholar) were searched for data extraction and two appraisal tools (NIH and CREATE) were used for quality assessment. Studies that explored any aspect of sleep health in relation to educational/academic outcomes in school going Indigenous Australian children aged 5-18 were included in this study. All review articles and studies that focused on physical/ mental disabilities or parent perceptions of sleep and educational outcomes were excluded. A convergent integrated approach was used to collate and synthesize information. RESULTS: Only three studies (two cross-sectional and one longitudinal) met the eligibility criteria out of 574 articles. The sample size ranged from 21-50 of 6 to 13 year old children. A strong relationship was indicated between sleep quantity and educational outcomes, in two of the three studies. One study related the sleep fragmentation/shorter sleep schedules of short sleep class and early risers with poorer reading (B = -30.81 to -37.28, p = 0.006 to 0.023), grammar (B = -39.79 to -47.89, p = 0.012-0.013) and numeracy (B = -37.93 to -50.15, p = 0.003 to 0.022) skills compared with long sleep and normative sleep class whereas another reported no significant relation between sleep and educational outcomes. CONCLUSION: The review highlights the need for more research to provide evidence of potentially modifiable factors such as sleep and the impact these may have on academic performance.

Durative sleep fragmentation with or without hypertension suppress rapid eye movement sleep and generate cerebrovascular dysfunction.

Either hypertension or chronic insomnia is the risk factor of developing vascular dementia. Durative hypertension can induce vascular remodeling and is used for modeling small vessel disease in rodents. It remains undetermined if the combination of hypertension and sleep disturbance exacerbates vascular dysfunction or pathologies. Previously, we found chronic sleep fragmentation (SF) dampened cognition in young mice without disease predispositions. In the current study, we superimposed SF with hypertension modeling in young mice. Angiotensin II (AngII)-releasing osmotic mini pumps were subcutaneously implanted to generate persistent hypertension, while sham surgeries were performed as controls. Sleep fragmentation with repetitive arousals (10 s every 2 min) during light-on 12 h for consecutive 30 days, while mice undergoing normal sleep (NS) processes were set as controls. Sleep architectures, whisker-stimulated cerebral blood flow (CBF) changes, vascular responsiveness as well as vascular pathologies were compared among normal sleep plus sham (NS + sham), SF plus sham (SF + sham), normal sleep plus AngII (NS + AngII), and SF plus AngII (SF + AngII) groups. SF and hypertension both alter sleep structures, particularly suppressing REM sleep. SF no matter if combined with hypertension strongly suppressed whisker-stimulated CBF increase, suggesting the tight association with cognitive decline. Hypertension modeling sensitizes vascular responsiveness toward a vasoactive agent, Acetylcholine (ACh, 5 mg/ml, 10 µl) delivered via cisterna magna infusion, while SF exhibits a similar but much milder effect. None of the modeling above was sufficient to induce arterial or arteriole vascular remodeling, but SF or SF plus hypertension increased vascular network density constructed by all categories of cerebral vessels. The current study would potentially help understand the pathogenesis of vascular dementia, and the interconnection between sleep and vascular health.

Insomnia and REM sleep instability.

In this narrative review, we give an overview of the concept of rapid eye movement sleep instability and its reported implications in the context of insomnia. The term rapid eye movement sleep instability was coined to describe the observation of a modified rapid eye movement quality in insomnia, characterized by an increased tendency of perceiving rapid eye movement sleep as wake, a small but consistent rapid eye movement sleep reduction and an increased rapid eye movement sleep arousal index. Current research highlights relationships that are transdiagnostic in nature, corresponding to the known interaction of insomnia with many psychiatric disorders, and showing relationships to chronic stress and anxiety disorders.

Associations of environmental and lifestyle factors with spatial navigation in younger and older adults.

OBJECTIVE: Advanced age is associated with prominent impairment in allocentric navigation dependent on the hippocampus. This study examined whether age-related impairment in allocentric navigation and strategy selection was associated with sleep disruption or circadian rest-activity fragmentation. Further, we examined whether associations with navigation were moderated by perceived stress and physical activity. METHOD: Sleep fragmentation and total sleep time over the course of 1 week were assayed in younger (n = 42) and older (n = 37) adults via wrist actigraphy. Subsequently, participants completed cognitive mapping and route learning tasks, as well a measure of spontaneous navigation strategy selection. Measurements of perceived stress and an actigraphy-based index of physical activity were also obtained. Circadian rest-activity fragmentation was estimated via actigraphy post-hoc. RESULTS: Age was associated with reduced cognitive mapping, route learning, allocentric strategy use, and total sleep time (ps < .01), replicating prior findings. Novel findings included that sleep fragmentation increased with advancing age (p = .009) and was associated with lower cognitive mapping (p = .022) within the older adult cohort. Total sleep time was not linearly associated with the navigation tasks (ps > .087). Post-hoc analyses revealed that circadian rest-activity fragmentation increased with advancing age within the older adults (p = .026) and was associated with lower cognitive mapping across the lifespan (p = .001) and within older adults (p = .005). Neither stress nor physical activity were robust moderators of sleep fragmentation associations with the navigation tasks (ps > .113). CONCLUSION: Sleep fragmentation and circadian rest-activity fragmentation are potential contributing factors to age effects on cognitive mapping within older adults.

Fine motor deficits exhibited in rat string-pulling behavior following exposure to sleep fragmentation and deep space radiation.

Deep space flight missions will expose astronauts to multiple stressors, including sleep fragmentation and space radiation. There is debate over whether sleep disruptions are an issue in deep space. While these stressors independently impair sensorimotor function, the combined effects on performance are currently unknown. String-pulling behavior involves highly organized bimanual reach-to-grasp and withdraw movements. This behavior was examined under rested wakeful conditions and immediately following one session of sleep fragmentation in Sham and irradiated rats 3 months after exposure (10 cGy 4Helium or 5-ion simulated Galactic Cosmic Radiation). Sleep fragmentation disrupted several aspects of string-pulling behavior, such that rats' ability to grasp the string was reduced, reach endpoint concentration was more variable, and distance traveled by the nose increased in the Y-range compared to rested wakeful performance. Overall, irradiated rats missed the string more than Sham rats 3 months post-exposure. Irradiated rats also exhibited differential impairments at 3 months, with additional deficits unveiled after sleep fragmentation. 4Helium-exposed rats took longer to approach the string after sleep fragmentation. Further, rats exposed to 4Helium traveled shorter withdraw distances 3 months after irradiation, while this only emerged in the other irradiated group after sleep fragmentation. These findings identify sleep fragmentation as a risk for fine motor dysfunction in Sham and irradiated conditions, in addition to radiation exposure. There may be complex temporal alterations in performance that are stressor- and ion-dependent. Thus, it is critical to implement appropriate models of multi-flight stressors and performance assessments in preparation for future deep space flight missions.

Self-reported sleep fragmentation and sleep duration and their association with cognitive function in PROTECT, a large digital community-based cohort of people over 50.

OBJECTIVE: Sleep is vital for normal cognitive function in daily life, but is commonly disrupted in older adults. Poor sleep can be detrimental to mental and physical health, including cognitive function. This study assessed the association between self-reported short (<6 h) and long (>9 h) sleep duration and sleep fragmentation (3≥ nightly awakenings) in cognitive function. METHODS: Cross-sectional data from 8508 individuals enroled in the PROTECT study aged 50 and above formed the basis of the univariate linear regression analysis conducted on four cognitive outcomes assessing visuospatial episodic memory (VSEM), spatial working memory, verbal working memory (VWM), and verbal reasoning (VR). RESULTS: Short (ß = -0.153, 95% CI [-0.258, -0.048], p = 0.004) and long sleep duration (ß = -0.459, 95% CI [-0.826, -0.091], p = 0.014) were significantly associated with poorer cognitive performance in VWM. Long sleep duration (ß = -2.986, 95% CI [-5.453, -0.518], p = 0.018) was associated with impaired VR. Short sleep (ß = -0.133, 95% CI [-0.196, -0.069], p = <0.001) and sleep fragmentation (ß = -0.043, 95% CI [-0.085, -0.001], p = 0.043) were associated with reduced VSEM. These associations remained significant when including other established risk factors for dementia and cognitive decline (e.g., depression, hypertension). CONCLUSIONS: Our findings suggest that short and long sleep durations and fragmented sleep, may be risk factors for a decline in cognitive processes such as working memory, VR and episodic memory thus might be potential targets for interventions to maintain cognitive health in ageing.

The effect of fragmented sleep on emotion regulation ability and usage.

Sleep has a profound effect on our mood, but insight in the mechanisms underlying this association is still lacking. We tested whether emotion regulation is a mediator in the relationship between fragmented sleep and mood disturbance. The effect of fragmented sleep on the emotion regulation strategies, including cognitive reappraisal, distraction, acceptance and suppression ability, was assessed. We further tested whether the use of these strategies, as well as rumination and self-criticism, mediated the association between fragmented sleep and negative and positive affect. Participants (N = 69) wore an actiwatch and filled in a sleep diary for 12 consecutive nights. They had one control night and one sleep fragmentation night. Emotion regulation ability was assessed with an experimental task. Usage of emotion regulation strategies and negative and positive affect were assessed four times during the day with a survey after the control and sleep fragmentation night. Cognitive reappraisal, distraction, acceptance and suppression ability did not differ between the sleep fragmentation and control condition. However, participants reported higher usage of rumination and distraction after the sleep fragmentation night and rumination significantly mediated the negative association between fragmented sleep and negative affect.

Fragmentation of rest periods, astrocyte activation, and cognitive decline in older adults with and without Alzheimer's disease.

INTRODUCTION: Sleep disruption is associated with astrocyte activation and impaired cognition in model organisms. However, the relationship among sleep, astrocyte activation, and cognition in humans is uncertain. METHODS: We used RNA-seq to quantify the prefrontal cortex expression of a panel of human activated astrocyte marker genes in 1076 older adults in the Religious Orders Study and Rush Memory and Aging Project, 411 of whom had multi-day actigraphy prior to death. We related this to rest fragmentation, a proxy for sleep fragmentation, and to longitudinal cognitive function. RESULTS: Fragmentation of rest periods was associated with higher expression of activated astrocyte marker genes, which was associated with a lower level and faster decline of cognitive function. DISCUSSION: Astrocyte activation and fragmented rest are associated with each other and with accelerated cognitive decline. If experimental studies confirm a causal relationship, targeting sleep fragmentation and astrocyte activation may benefit cognition in older adults. HIGHLIGHTS: Greater fragmentation of rest periods, a proxy for sleep fragmentation, is associated with higher composite expression of a panel of genes characteristic of activated astrocytes. Increased expression of genes characteristic of activated astrocytes was associated with a lower level and more rapid decline of cognitive function, beyond that accounted for by the burden of amyloid and neurofibrillary tangle pathology. Longitudinal and experimental studies are needed to delineate the causal relationships among sleep, astrocyte activation, and cognition.

Sleep Fragmentation Accelerates Carcinogenesis in a Chemical-Induced Colon Cancer Model.

Aims of this study were to test whether sleep fragmentation (SF) increased carcinogenesis and to investigate the possible mechanisms of carcinogenesis in a chemical-induced colon cancer model. In this study, eight-week-old C57BL/6 mice were divided into Home cage (HC) and SF groups. After the azoxymethane (AOM) injection, the mice in the SF group were subjected to SF for 77 days. SF was accomplished in a sleep fragmentation chamber. In the second protocol, mice were divided into 2% dextran sodium sulfate (DSS)-treated, HC, and SF groups and were exposed to the HC or SF procedures. Immunohistochemical and immunofluorescent stainings were conducted to determine the level of 8-OHdG and reactive oxygen species (ROS), respectively. Quantitative real-time polymerase chain reaction was used to assess the relative expression of inflammatory and ROS-generating genes. The number of tumors and average tumor size were significantly higher in the SF group than in the HC group. The intensity (%) of the 8-OHdG stained area was significantly higher in the SF group than in the HC group. The fluorescence intensity of ROS was significantly higher in the SF group than the HC group. SF accelerated cancer development in a murine AOM/DSS-induced model of colon cancer, and the increased carcinogenesis was associated with ROS- and oxidative stress-induced DNA damage.

Cognitive Impairments, Neuroinflammation and Blood-Brain Barrier Permeability in Mice Exposed to Chronic Sleep Fragmentation during the Daylight Period.

Obstructive sleep apnea (OSA) is a chronic condition characterized by intermittent hypoxia (IH) and sleep fragmentation (SF). In murine models, chronic SF can impair endothelial function and induce cognitive declines. These deficits are likely mediated, at least in part, by alterations in Blood-brain barrier (BBB) integrity. Male C57Bl/6J mice were randomly assigned to SF or sleep control (SC) conditions for 4 or 9 weeks and in a subset 2 or 6 weeks of normal sleep recovery. The presence of inflammation and microglia activation were evaluated. Explicit memory function was assessed with the novel object recognition (NOR) test, while BBB permeability was determined by systemic dextran-4kDA-FITC injection and Claudin 5 expression. SF exposures resulted in decreased NOR performance and in increased inflammatory markers and microglial activation, as well as enhanced BBB permeability. Explicit memory and BBB permeability were significantly associated. BBB permeability remained elevated after 2 weeks of sleep recovery (p < 0.01) and returned to baseline values only after 6 weeks. Chronic SF exposures mimicking the fragmentation of sleep that characterizes patients with OSA elicits evidence of inflammation in brain regions and explicit memory impairments in mice. Similarly, SF is also associated with increased BBB permeability, the magnitude of which is closely associated with cognitive functional losses. Despite the normalization of sleep patterns, BBB functional recovery is a protracted process that merits further investigation.

Glutamatergic Neurons in the Preoptic Hypothalamus Promote Wakefulness, Destabilize NREM Sleep, Suppress REM Sleep, and Regulate Cortical Dynamics.

Clinical and experimental data from the last nine decades indicate that the preoptic area of the hypothalamus is a critical node in a brain network that controls sleep onset and homeostasis. By contrast, we recently reported that a group of glutamatergic neurons in the lateral and medial preoptic area increases wakefulness, challenging the long-standing notion in sleep neurobiology that the preoptic area is exclusively somnogenic. However, the precise role of these subcortical neurons in the control of behavioral state transitions and cortical dynamics remains unknown. Therefore, in this study, we used conditional expression of excitatory hM3Dq receptors in these preoptic glutamatergic (Vglut2+) neurons and show that their activation initiates wakefulness, decreases non-rapid eye movement (NREM) sleep, and causes a persistent suppression of rapid eye movement (REM) sleep. We also demonstrate, for the first time, that activation of these preoptic glutamatergic neurons causes a high degree of NREM sleep fragmentation, promotes state instability with frequent arousals from sleep, decreases body temperature, and shifts cortical dynamics (including oscillations, connectivity, and complexity) to a more wake-like state. We conclude that a subset of preoptic glutamatergic neurons can initiate, but not maintain, arousals from sleep, and their inactivation may be required for NREM stability and REM sleep generation. Further, these data provide novel empirical evidence supporting the hypothesis that the preoptic area causally contributes to the regulation of both sleep and wakefulness.SIGNIFICANCE STATEMENT Historically, the preoptic area of the hypothalamus has been considered a key site for sleep generation. However, emerging modeling and empirical data suggest that this region might play a dual role in sleep-wake control. We demonstrate that chemogenetic stimulation of preoptic glutamatergic neurons produces brief arousals that fragment sleep, persistently suppresses REM sleep, causes hypothermia, and shifts EEG patterns toward a "lighter" NREM sleep state. We propose that preoptic glutamatergic neurons can initiate, but not maintain, arousal from sleep and gate REM sleep generation, possibly to block REM-like intrusions during NREM-to-wake transitions. In contrast to the long-standing notion in sleep neurobiology that the preoptic area is exclusively somnogenic, we provide further evidence that preoptic neurons also generate wakefulness.

Third-Trimester Maternal Dietary Patterns Are Associated with Sleep Health among Adolescent Offspring in a Mexico City Cohort.

BACKGROUND: Maternal diet during gestation has been linked to infant sleep; whether associations persist through adolescence is unknown. OBJECTIVES: We explored associations between trimester-specific maternal diet patterns and measures of sleep health among adolescent offspring in a Mexico City birth cohort. METHODS: Data from 310 mother-adolescent dyads were analyzed. Maternal diet patterns were identified by principal component analysis derived from FFQs collected during each trimester of pregnancy. Sleep duration, midpoint, and fragmentation were obtained from 7-d actigraphy data when adolescents were between 12 and 20 y old. Unstratified and sex-stratified association analyses were conducted using linear regression models, adjusted for potential confounders. RESULTS: Mean ± SD age of offspring was 15.1 ± 1.9 y, and 52.3% of the sample was female. Three diet patterns were identified during each trimester of pregnancy: the Prudent Diet (PD), high in lean proteins and vegetables; the Transitioning Mexican Diet (TMD), high in westernized foods; and the High Meat & Fat Diet (HMFD), high in meats and fat products. Mean ± SD sleep duration was 8.5 ± 1.5 h/night. Most associations were found in the third trimester. Specifically, PD maternal adherence was associated with shorter sleep duration among offspring (-0.57 h; 95% CI: -0.98, -0.16 h, in the highest tertile compared with the lowest) and earlier sleep midpoint among females (-0.77 h; 95% CI: -1.3, -0.26 h). Adherence to the HMFD and TMD was nonlinearly associated with less fragmented sleep, with the latter only evident among females. CONCLUSIONS: Findings indicate that maternal dietary patterns, especially during the third trimester of pregnancy, may have long-term impacts on offspring sleep.

The effects of napping on night-time sleep in healthy young adults.

The discrepancies in the effects of napping on sleep quality may be due to differences in methodologies, napping behaviours, and daytime activity levels across studies. We determined whether napping behaviours and daytime activity levels are associated with night-time sleep fragmentation and sleep quality in young adults. A total of 62 healthy adults (mean [SD] age 23.5 [4.2] years) completed screening questionnaires for sleep habits, physical activity, medical and psychological history. Actigraphy was used to record sleep including naps. The fragmentation algorithm (KRA ) was applied to the actigraphic data to measure night-time sleep fragmentation. We classified participants' nap frequency as "non-nappers" (0 naps/8 days), "moderate nappers" (1-2 naps/8 days) or "frequent nappers" (≥3 naps/8 days) naps. Nap duration was defined as "short" (≤60 min) or "long" (>60 min). Naps' proximity to the night sleep episode was defined as "early" (≥7 h) and "late" (<7 h) naps. Outcome variables were night-time KRA and actigraphic sleep variables. Frequent nappers had a significantly higher KRA than moderate nappers (p < 0.01) and non-nappers (p < 0.02). Late naps were associated with poorer measures of night sleep quality versus early naps (all p ≤ 0.02). Nap duration and daytime activity were not associated with significant differences in the outcome variables (all p > 0.05). KRA correlated with sleep duration, sleep efficiency, and awakenings (r = -0.32, -0.32, and 0.53, respectively; all p < 0.05). Frequent napping and late naps may be associated with increased sleep fragmentation and poorer sleep quality, reflected in longer sleep onsets and increased awakenings. These findings have implications for public health sleep hygiene recommendations.

Pediatric Obstructive Sleep Apnea: What's in a Name?

Obstructive sleep apnea is a highly prevalent disease across the lifespan and imposes substantial morbidities, some of which may become irreversible if the condition is not diagnosed and treated in a timely fashion. Here, we focus on the clinical and epidemiological characteristics of pediatric obstructive sleep apnea, describe some of the elements that by virtue of their presence facilitate the emergence of disrupted sleep and breathing and its downstream consequences, and also discuss the potential approaches to diagnosis in at-risk children.

Potential Role of Obstructive Sleep Apnea on Pain Sensitization and Jaw Function in Temporomandibular Disorder Patients.

BACKGROUND: The relationships between obstructive sleep apnea (OSA) and diverse types of pain disorders have been reported. However, the interaction between OSA and pain-related temporomandibular disorder (TMD) remains obscure. METHODS: A total of 60 adults (male/female, 48/12; mean age, 41.7 ± 13.2 years) with pain-related TMD were enrolled. All participants underwent overnight full-channel polysomnography and had assessment of size and position of the tongue, tonsillar size, height, and weight. Diagnostic Criteria/TMD criteria was applied to diagnose TMD. Myofascial trigger points (TrPs) were bilaterally evaluated in the two masticatory and four cervical muscles including the temporalis, masseter, trapezius, sternocleidomastoid, occipitalis, and splenius capitis muscles. Participants were divided into three groups in accordance with their levels of OSA. RESULTS: The significantly higher number of active TrPs were detected in participants with severe OSA. The number of active TrPs in the masticatory muscles significantly interacted with diverse types of apneic and arousal indices. CONCLUSION: The myofascial pain modulating mechanisms and jaw function could have interactions with nocturnal hypoxia and sleep fragmentation in chronic pain-related TMD patients.

Sleep arousal burden is associated with long-term all-cause and cardiovascular mortality in 8001 community-dwelling older men and women.

AIMS: To quantify the arousal burden (AB) across large cohort studies and determine its association with long-term cardiovascular (CV) and overall mortality in men and women. METHODS AND RESULTS: We measured the AB on overnight polysomnograms of 2782 men in the Osteoporotic Fractures in Men Study (MrOS) Sleep study, 424 women in the Study of Osteoporotic Fractures (SOF) and 2221 men and 2574 women in the Sleep Heart Health Study (SHHS). During 11.2 ± 2.1 years of follow-up in MrOS, 665 men died, including 236 CV deaths. During 6.4 ± 1.6 years of follow-up in SOF, 105 women died, including 47 CV deaths. During 10.7 ± 3.1 years of follow-up in SHHS, 987 participants died, including 344 CV deaths. In women, multivariable Cox proportional hazard analysis adjusted for common confounders demonstrated that AB is associated with all-cause mortality [SOF: hazard ratio (HR) 1.58 (1.01-2.42), P = 0.038; SHHS-women: HR 1.21 (1.06-1.42), P = 0.012] and CV mortality [SOF: HR 2.17 (1.04-4.50), P = 0.037; SHHS-women: HR 1.60 (1.12-2.28), P = 0.009]. In men, the association between AB and all-cause mortality [MrOS: HR 1.11 (0.94-1.32), P = 0.261; SHHS-men: HR 1.31 (1.06-1.62), P = 0.011] and CV mortality [MrOS: HR 1.35 (1.02-1.79), P = 0.034; SHHS-men: HR 1.24 (0.86-1.79), P = 0.271] was less clear. CONCLUSIONS: Nocturnal AB is associated with long-term CV and all-cause mortality in women and to a lesser extent in men.

Influence of sleep fragmentation and fatigue on turnover of female nurses working rotating shifts.

AIMS AND OBJECTIVES: To investigate whether the sleep quality and fatigue of female nurses working rotating shifts could be used to predict future turnover status. BACKGROUND: Female nurses working rotating shifts often suffer from sleep problems and fatigue, and the turnover rates of nurses are generally higher than those of other hospital personnel. DESIGN: A prospective study. METHODS: We recruited a total of 198 female nurses working rotating shifts from December 2017 to March 2019. The nurses completed the Checklist Individual Strength (CIS) scale and wore an actigraph for seven consecutive days in order to collect their sleep parameters. Their turnover status was tracked until 31 May 2021 at which time 55 participants (27.8%) had resigned. The Cox proportional hazard model was used to analyse the factors influencing turnover. In addition, the study adhered to the STROBE checklist. RESULTS: The results revealed significant differences between the nurses in the still-working group and the resigned group in terms of the sleep quality parameters sleep efficiency (SE) and wake after sleep onset (WASO) as well as CIS scores. WASO was significantly correlated with intensity of fatigue, and fatigue was common among all of the nurses working rotating shifts. As time progressed, the sleep quality parameter WASO and CIS scores could be used to predict turnover status after 2.4 years. CONCLUSION: The results of this study indicated more sleep fragmentation and poor sleep efficiency in the resigned group. Sleep fragmentation was highly correlated with fatigue, and sleep fragmentation and fatigue could be used to predict turnover status. RELEVANCE TO CLINICAL PRACTICE: We suggest that relevant hospital management pay more attention to the sleep conditions and fatigue of female nurses working rotating shifts when arranging personnel and schedules and offer them more understanding.