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Bonnet MH, Arand DL. Clinical effects of sleep fragmentation versus sleep deprivation. Sleep Med Rev 7: 297-310
Abstract
Common symptoms associated with sleep fragmentation and sleep deprivation include increased objective sleepiness (as measured by the Multiple Sleep Latency Test); decreased psychomotor performance on a number of tasks including tasks involving short term memory, reaction time, or vigilance; and degraded mood. Differences in degree of sleepiness are more related to the degree of sleep loss or fragmentation rather than to the type of sleep disturbance. Both sleep fragmentation and sleep deprivation can exacerbate sleep pathology by increasing the length and pathophysiology of sleep apnea. The incidence of both fragmenting sleep disorders and chronic partial sleep deprivation is very high in our society, and clinicians must be able to recognize and treat Insufficient Sleep Syndrome even when present with other sleep disorders.
... While acute increases in cortisol are part of the short-term stress response, promoting alertness and delaying sleep onset (Chapotot et al., 1998;Katsu & Baker, 2021), chronically (long-term) high levels of cortisol are associated with greater physiological costs, such as immunosuppression and cardiovascular disease (James et al., 2023), and often reduced survival (Koren, Nakagawa, et al., 2012), and they indicate chronic stress (Russell et al., 2012). Alongside this, increases in chronic stress interfere with the homeostatic regulation of sleep (Christensen et al., 2022), reduce sleep quantity and quality (Lo Martire et al., 2020), and increase sleep fragmentation, ultimately leading to the detrimental effects of sleep loss on health and cognition similar to those observed in sleep deprived individuals (Bonnet & Arand, 2003). We therefore predict that neonates with higher levels of chronic cortisol levels at birth should sleep less daily and in more bouts of lower quality. ...
... More fragmented sleep is known to inversely correlate with sleep depth and arousal threshold (Smeltzer et al., 2022), triggers sleep homeostasis increasing sleep pressure (the drive to sleep, Baud et al., 2015) and is associated with health costs similar to those due to sleep loss (Bonnet, 2004). The duration of the longest sleep bout (hours) in a day reflects sleep quality since a longer bout offers the best opportunity to accrue the benefits of deep sleep (Bonnet & Arand, 2003), and sleep depth increases with longer bout duration (in humans and other animals; Carskadon & Dement, 2005, Joyce et al., 2024, Ruckebusch, 1972. Sleep depth and duration in neonates is also particularly important for brain development (Lokhandwala & Spencer, 2022). ...
... We find that fawns differed since close to birth in all sleep measures and retained such differences throughout the first few weeks of life (Mortlock, English, et al., 2024). Individuals with lower sleep quantity (TST), quality (duration of the longest bout), or efficiency (higher fragmentation) should gain fewer benefits of sleep and so pay a cost in the short or long term, as evidenced in humans (Bonnet & Arand, 2003;Bryant et al., 2004;Knutson et al., 2007;Liew & Aung, 2021;Lim & Dinges, 2010) and other animals (Johnsson et al., 2022;Kayser & Biron, 2016;Rechtschaffen et al., 1989;Samson et al., 2019 In addition to our earlier findings that sleep time rapidly declines to likely adult durations and becomes consolidated into fewer bouts over the first few weeks of life in fallow deer neonates (Mortlock, English, et al., 2024), here we also find that the proportion of daily sleep during the daytime is progressively reduced as fawns age. Thus, we suggest that sleep profiles might emerge later in development as fawns transition from the socially isolated and vulnerable hider phase to the comparative safety of group living (Chapman & Chapman, 1997). ...
Inter‐individual differences are necessary for selection to act, while plasticity (intra‐individual variation) may buffer against selection. Sleep is a critical self‐maintenance behaviour but, unlike most behaviours, the causes and consequences of its inter‐ and intra‐individual variation in wild animals is poorly understood, particularly in neonates where sleep plays a key role in development. We have shown previously that free‐ranging neonate fallow deer (Dama dama) differ in sleep during the first few weeks of life. Here, we test whether individual variability in sleep is organised systematically across the population, and whether these individual differences are associated with chronic stress measured using hair cortisol, or the timing of birth.
Four dimensions of sleep behaviour (total sleep time, sleep fragmentation, sleep quality, and sleep distribution over 24‐h) were quantified using state‐of‐the‐art triaxial accelerometers. We then used a multivariate mixed‐effects model in a Bayesian framework to evaluate covariation between multiple dimensions of sleep behaviour, and quantify the relative importance of chronic stress and the timing of birth, while accounting for the confounding effects of environmental conditions and age.
We found that the timing of birth and chronic stress were not associated with changes in sleep between individuals. While both total sleep time and the number of bouts per day declined with age, their rate of development covaried, but no other sleep dimensions covaried.
Our results represent an in‐depth analysis of natural variation in sleep, and show that individual differences in four aspects of sleep architecture in free‐living fallow deer fawns are strong but independent of one another and unrelated to chronic stress or the timing of birth. We suggest that covariation between sleep dimensions might emerge later in life and effects of cortisol and birth timing might be very short and transient.
... Fragmentation has been shown to decrease psychomotor performance including tasks involving shortterm memory, reaction time, or vigilance. [16] One night of sleep fragmentation without deprivation has been shown to make normal subjects sleepy during the day and decrease mental flexibility and sustained attention. [17] When registrars or consultants were not contacted during on-calls, there was no measured difference in sleep quality compared with normal working days or off days. ...
Background: Shift work can lead to sleep deprivation and circadian misalignment. Sleep disturbances have implications for patient care, clinician well-being, and overall healthcare performance. In the United Kingdom, otolaryngology operates a non-resident on-call structure at registrar and consultant levels, necessitating availability for remote consultation and potential on-site attendance overnight. Objectives: Whilst resident on-call rotas have been shown to have a detrimental effect on sleep quality, the impact of non-resident on calls remains under investigated. This study aims to assess the impact of non-resident on-call structures on sleep quality using smart phone sleep-tracking. Materials and Methods: Three consultants and three registrars monitored their sleep quality using the mobile phone application 'Sleep cycle' over a ten week on call cycle at a district general hospital. Data was collected prospectively and results analysed anonymously. Results: Sleep length was longest during off days (when clinicians had no clinical commitments the following day). The average sleep length for consultants was 7.07 h versus 6.97 h for registrars. There were variations in sleep quality across different work and on-call scenarios. For consultants, the highest average sleep quality was during on-call hours (80.00%). Sleep quality was lowest when a consultant was called for advice after 22:00h (54.00%), however, this increased to 73.00% when a consultant was required on site after 22:00 h. For registrars, average sleep quality was highest during off days at 83.00%. When registrars were contacted for advice overnight, average sleep quality was 68.67% and was lowest when registrars were called on-site after 22:00h (57%). Conclusion: Sleep length and quality are negatively affected by non-resident on-calls when clinicians are contacted after 22:00h. There is no measurable impact on sleep quality when clinicians are not disturbed whilst on-call remotely. NHS trusts should monitor the wellbeing of their doctors and consider the implications of overnight commitments when structuring elective rotas.
... A person may experience multiple sleep episodes during the day due to several factors such as sleep fragmentation and daytime napping which can be interrelated [9]. Sleep fragmentation [10] involves frequent interruptions during the main sleep period at night, leading to diminished sleep continuity and quality. Fragmented sleep has significant health implications, including increased risks of metabolic disorders [11,12], cardiovascular diseases [13], and impaired cognitive function [14]. ...
Sleep disturbances are prevalent among elderly populations and are linked to various health complications. Understanding the underlying biological mechanisms contributing to sleep disorders is crucial for developing targeted interventions. In this study, we measured 355 plasma proteins in an elderly Japanese cohort ( n =77) using a high-throughput proteomic platform. Additionally, we collected over 25,000 person-days of physical activity and sleep behavior data from wrist-worn wearable devices, focusing on total sleep time (TST) across 24 h and daytime sleep. Fragmented sleep was observed as one of the most prevalent sleep disturbances in this population. In protein expression analysis, we identified 9 protein biomarkers associated with increased secondary sleep TST, defined as additional sleep episodes outside of the main sleep episode within 24 h. These findings may suggest disruptions in circadian rhythms or underlying health conditions. Functional analysis revealed that biological processes related to inflammation play a significant role in regulating sleep behavior. Further analysis showed an association of 12 proteins with daytime sleep and 5 proteins with afternoon sleep. Overall, this study identified inflammatory biomarkers and biological processes associated with sleep behavior in the elderly, presenting promising opportunities for developing diagnostic tools and targeted clinical interventions.
... Disregarding the eff ects of prolonged fatigue results in numerous psychophysical defi cits that may jeopardize crew safety [13,64]. Impairments of the central nervous system, including disturbances in short-term memory functioning, prolonged reaction time, loss of alertness, mood changes, and episodes of micro-sleep, are just some of the consequences [4,5]. As a result, specifi c skills such as radio communication, dexterity, or motor control during fl ight operations deteriorate [8]. ...
Introduction: Fatigue remains a significant challenge in the field of aviation safety. This is particularly the case in military aviation, where aircrews are expected to perform complex and cognitively demanding tasks, often with unpredictable working hours, insufficient sleep and disrupted circadian rhythms. The aim of the present study was to determine the effect of a single dose of modafinil on the physiological response (based on heart rate) to variable acceleration up to +3Gz during a limited period of sleep deprivation, compared with that of placebo and a single dose of galantamine. Methods: To determine the effect of stimulant use, 12 male volunteers with a mean age of 24 ± 2.5 years were tested under three night-time conditions, after an average of 27 hours of sleep deprivation. Participants received placebo, galantamine 10 mg, and modafinil 100 mg, and were tested in a human centrifuge during a daytime control session. Heart rate, blood pressure, core body temperature, and body hydration were measured in participants during the experiment. Results: As we expected, both galantamine and modafinil counteracted the effects of fatigue on the physiological response to variable acceleration up to +3Gz compared to placebo, with the beneficial effect of galantamine being greater than that of modafinil. A single administration of galantamine (10 mg) to participants after 27 hours of wakefulness resulted in a statistically significant reduction in heart rate relative to both placebo and modafinil. Conclusions: None of the drugs tested (modafinil or galantamine) at a single dose had a negative effect on the physiological response to variable acceleration reaching +3Gz. Therefore, if there are no contraindications to their use, they may be useful in combating the symptoms of fatigue in flight attendants exposed to overload during prolonged flights.
... In Study 2, disruptions to sleep continuity-affecting both sleep duration and sleep quality, but without imposing sleep restrictiondemonstrated a clear effect on state empathy. Our findings contribute to the growing evidence that, in some cases, disrupted sleep continuity impairs the mental and physical recovery typically supported by adequate sleep (Bonnet & Arand, 2003;Forbes et al., 2008;Hawkley et al., 2010;Kurina et al., 2011;Hoopes et al., 2021;Fjell et al., 2023). ...
Poor sleep is pervasive in modern society. Poor sleep is associated with major physical and mental health consequences, as well as with impaired cognitive function. Less is known about the relationship between sleep and emotional and interpersonal behavior. In this work, we investigate whether poor sleep impairs empathy, an important building block of human interaction and prosocial behavior. We aimed to capture the effects of poor sleep on the various aspects of empathy: trait and state, affect and cognition.
Study 1 (n = 155) assessed daily habitual sleep over several days, and global sleep quality in the past month. Participants who reported worse sleep quality exhibited lower empathic caring and perspective-taking traits. Study 2 (n = 347) induced a one-night disruption of sleep continuity to test a causal relationship between sleep and empathy. Participants in the sleep disrupted condition had to briefly wake up five times over the night, whereas the sleep-rested controls slept normally. In the next morning, participants’ empathy and prosocial intentions were assessed. Participants in the sleep disruption condition exhibited lower empathic sensitivity and less prosocial decision-making than sleep-rested controls.
The main contribution of this work is in providing a robust demonstration of the multi-faceted detrimental effects of poor sleep on trait and state empathy. Our findings demonstrate that poor sleep causally impairs empathic response to the suffering of others. These findings highlight the need for greater public attention to adequate sleep, which may impact empathy on a societal level.
... These convergent results indicate a consistent pattern of beta band modulation in response to cognitive demands. Engagement in tasks of varying difficulty leads to an increase in beta oscillatory activity, highlighting the dynamic nature of beta rhythms in response to cognitive workload variations and sleep quality [87]. Given that cognitive fatigue builds up over time, conducting the same TloadDback task over different durations (e.g., 16 min vs. 30 min) could allow us to determine whether the observed beta increase reflects an adaptive effort to maintain performance or a compensatory mechanism due to fatigue. ...
Cognitive fatigue (CF) is a critical factor affecting performance and well-being. It can be altered in suboptimal sleep quality conditions, e.g., in patients suffering from obstructive sleep apnea who experience both intermittent hypoxia and sleep fragmentation (SF). Understanding the neurophysiological basis of SF in healthy individuals can provide insights to improve cognitive functioning in disrupted sleep conditions. In this electroencephalographical (EEG) study, we investigated in 16 healthy young participants the impact of experimentally induced SF on the neurophysiological correlates of CF measured before, during, and after practice on the TloadDback, a working memory task tailored to each individual’s maximal cognitive resources. The participants spent three consecutive nights in the laboratory two times, once in an undisrupted sleep (UdS) condition and once in an SF condition induced by non-awakening auditory stimulations, counterbalanced and performed the TloadDback task both in a high (HCL) and a low (LCL) cognitive load condition. EEG activity was recorded during wakefulness in the 5 min resting state immediately before and after, as well as during the 16 min of the TloadDback task practice. In the high cognitive load under a sleep-fragmentation (HCL/SF) condition, high beta power increased during the TloadDback, indicating heightened cognitive effort, and the beta and alpha power increased in the post- vs. pre-task resting state, suggesting a relaxation rebound. In the low cognitive load/undisturbed sleep (LCL/UdS) condition, low beta activity increased, suggesting a relaxed focus, as well as mid beta activity associated with active thinking. These findings highlight the dynamic impact of SF on the neurophysiological correlates of CF and underscore the importance of sleep quality and continuity to maintain optimal cognitive functioning.
... Deterioration of sleep quality and impairment of sleep structure occur in a significant proportion in TMD patients, but their impact is not clearly known . [4,5,6] . ...
Temporomandibular joint (TMJ) disorders and sleep disturbances frequently coexist, yet their intricate relationship remains understudied. This review aims to comprehensively examine the bidirectional association between TMJ dysfunction and sleep disorders. A systematic search of relevant databases was conducted to identify studies investigating the prevalence, clinical manifestations, and underlying mechanisms of this complex interplay. The findings of this review will contribute to a deeper understanding of the pathophysiology, diagnostic criteria, and treatment strategies for TMJ-related sleep disorders. By delineating the shared risk factors, symptom overlap, and potential therapeutic interventions, this research seeks to improve patient outcomes and inform future research endeavors in this field.
... According to its duration, sleep deprivation can be classified into TSD and PSD. TSD refers to staying awake continuously throughout consecutive days and nights, with a minimum duration of 24 h of wakefulness between the end of the last sleep period and the beginning of the next sleep period (Bonnet & Arand, 2003;Cote et al., 2008;Dijk & Lazar, 2012). For instance, Salfi et al. (2020) kept participants awake from the morning of the first day until 9 AM the next day, achieving 24 h of TSD. ...
Sleep deprivation stands as a major threat to both physical and mental well-being, disrupting normal work and life. Given the ubiquity of risky decision making, it is crucial to comprehend how individuals make risky decisions when sleep-deprived. Although research on the effects of sleep deprivation on risky decision making has increased in recent years, it remains limited and lacks a unified conclusion. The current review attempted to elucidate the effects of sleep deprivation on risky decision making in healthy adults and clarify the regulatory mechanisms. The review showed that sleep deprivation had complex effects on risky decision making; that is, whether sleep deprivation led to riskier or more conservative decision-making behavior depended on factors such as sex, gain–loss frame, use of psychotropic drugs, time interval of sleep elimination, duration of sleep deprivation, and others. Additionally, the complexity of these effects might partly arise from the use of different tasks to measure risk-taking behavior. The review also discussed some limitations of existing research and put forth practical recommendations for future studies, aiming to resolve inconsistencies in the effects of sleep deprivation on risky decision making and enhance the ecological validity of conclusions.
... Nighttime interruptions leading to fragmentation can be caused by various factors, both physiological and pathological, resulting in increased objective sleepiness, decreased psychomotor performance in tasks involving short-term memory, increased reaction time, or vigilance [107]. For physiological causes, such as the need to drink or eat, it is advisable to regulate water and food intake throughout the day. ...
Sleep is a fundamental biological process that plays a pivotal role in the health and performance of physically active individuals (PAI). Sleep deprivation or poor sleep quality can negatively impact recovery capacity, concentration, coordination, and muscular strength, thereby compromising physical performance and increasing the risk of injuries. Objectives: This narrative literature review aims to examine the scientific evidence on the importance of sleep hygiene for the health and performance of PAI. A search was conducted for studies published on PubMed, Scopus, and Web of Science. Studies that investigated the effect of sleep hygiene on health and performance variables in athletes were included. The literature analysis highlighted that good sleep hygiene, adequate sleep duration (7–9 h per night), high sleep quality, and a regular sleep routine are associated with a range of benefits for the health and performance of PAI, including: (1) improved post-training recovery; (2) reduced risk of injuries; (3) enhanced concentration and attention; (4) improved coordination and muscle strength; (5) better mood and mental well-being; (6) reduced risk of chronic diseases. Sleep hygiene is a key factor for the health and performance of PAI. Implementing a comprehensive and personalized sleep hygiene routine can lead to significant improvements in the quality and quantity of sleep, with positive effects on physical and mental health, and overall well-being of PAI.
... These convergent results indicate a consistent pattern of beta band modulation in response to cognitive demands. Engagement in tasks of varying difficulty leads to an increase in beta oscillatory activity, highlighting the dynamic nature of beta rhythms in response to cognitive workload variations and sleep quality (Bonnet & Arand, 2003). ...
Cognitive fatigue (CF) is a critical factor affecting performance and well-being. It can be altered in suboptimal sleep quality conditions, e.g., in patients suffering from obstructive sleep apnea who experience both intermittent hypoxia and sleep fragmentation (SF). Understanding the neurophysiological basis of SF in healthy individuals can provide insights to improve cognitive functioning in disrupted sleep conditions. In this electroencephalographical (EEG) study, we investigated in 16 healthy young participants the impact of experimentally induced SF on the neurophysiological correlates of CF measured before, during, and after practice on the TloadDback, a working memory task tailored to each individual maximal cognitive resources. Participants spent two times three consecutive nights in the laboratory, once in an undisrupted sleep (UdS) condition and once in a SF condition induced by non-awakening auditory stimulations, counterbalanced, and performed the TloadDback task both in a high (HCL) and a low (LCL) cognitive load condition. EEG activity was recorded during wakefulness in the 5-minutes resting state immediately before and after, as well as during the 16-minutes of the TloadDback task practice. In the high cognitive load under sleep fragmentation (HCL-SF) condition, high beta power increased during the TloadDback indicating heightened cognitive effort, and beta and alpha power increased in the post- vs. pre task resting state, suggesting a relaxation rebound. In the low cognitive load/undisturbed sleep (LCL-UdS) condition, low beta activity increased suggesting a relaxed focus, as well as mid beta activity associated with active thinking. These findings highlight the dynamic impact of SF on the neurophysiological correlates of CF and underscore the importance of sleep quality and continuity to maintain optimal cognitive functioning.
... The prevailing consensus suggests that a night duration of seven to eight hours is adequate for maintaining the body aware and active during the day [3]. Nonetheless, it is imperative to recognize that the significance of sleep extends beyond mere quantity; the quality of sleep is equally pivotal [4,5]. In order to determine its quality, the analysis of sleep stages overnight is usually carried out. ...
... SD has been strongly associated with serious conditions including diabetes, hypertension, insulin resistance, obesity, obstructive sleep apnea, anxiety and depression. These medical and psychiatric comorbidities heighten the risk of heart attack and stroke for individuals [6,7]. A study conducted by Stanford University found that for every 5% decrease in deep sleep time, the risk of premature death increases by 13-17% [8]. ...
Sleep deprivation (SD) has emerged as a critical concern impacting human health, leading to significant damage to the cardiovascular system. However, the underlying mechanisms are still unclear, and the development of targeted drugs is lagging. Here, we used mice to explore the effects of prolonged SD on cardiac structure and function. Echocardiography analysis revealed that cardiac function was significantly decreased in mice after five weeks of SD. Real-time quantitative PCR (RT-q-PCR) and Masson staining analysis showed that cardiac remodeling marker gene Anp (atrial natriuretic peptide) and fibrosis were increased, Elisa assay of serum showed that the levels of creatine kinase (CK), creatine kinase-MB (CK-MB), ANP, brain natriuretic peptide (BNP) and cardiac troponin T (cTn-T) were increased after SD, suggesting that cardiac remodeling and injury occurred. Transcript sequencing analysis indicated that genes involved in the regulation of calcium signaling pathway, dilated cardiomyopathy, and cardiac muscle contraction were changed after SD. Accordingly, Western blotting analysis demonstrated that the cardiac-contraction associated CaMKK2/AMPK/cTNI pathway was inhibited. Since our preliminary research has confirmed the vital role of Casein Kinase-2 -Interacting Protein-1 (CKIP-1, also known as PLEKHO1) in cardiac remodeling regulation. Here, we found the levels of the 3’ untranslated region of Ckip-1 (Ckip-1 3’UTR) decreased, while the coding sequence of Ckip-1 (Ckip-1 CDS) remained unchanged after SD. Significantly, adenovirus-mediated overexpression of Ckip-1 3’UTR alleviated SD-induced cardiac dysfunction and remodeling by activating CaMKK2/AMPK/cTNI pathway, which proposed the therapeutic potential of Ckip-1 3’UTR in treating SD-induced heart disease.
... Sleep deprivation is related to various aspects of cognitive performance, namely tasks that require vigilant attention [4]. Various studies have shown that with the increase in sleep restrictions, behavioral lapses also increase during the performance [5]. Other studies have also indicated a reduction in the efficacy of cognitive processing, reaction time, and attentive responsiveness when sleep deprivation is present [6,7]. ...
Introduction
Sleep is a crucial biological need for all individuals, being reparative on a physical and mental level. Driving heavy vehicles is a task that requires constant attention and vigilance, and sleep deprivation leads to behavioral and physiological changes that can develop sleep disorders which can put lives at risk.
Objectives
The main objectives of this study are to describe and evaluate sleep quality, excessive daytime sleepiness, circadian preference, and risk of suffering from obstructive sleep apnea in a population of Portuguese professional drivers.
Methods
To fulfill the objectives, 43 Portuguese professional drivers, between 23 and 63 years old, answered validated questionnaires: Epworth Sleepiness Scale, Morningness–Eveningness, Stop-Bang Questionnaire, and Pittsburgh Sleep Quality Index.
Results
Results indicated that older drivers tend to experience higher daytime sleepiness (11 ± 3.4; p = 0.002) and obstructive sleep apnea risk (4.5 ± 1.5; p = 0.03). Regarding sleep quality, the majority of drivers were classified with poor sleep quality (74.4%). It was possible to infer statistical differences between groups based on body mass index (p = 0.037), the type of route (p = 0.01), and physical activity (p = 0.005).
Conclusion
Drivers have an indifferent circadian preference and small-course drivers have a worse sleep health perception. Therefore, it is essential to implement prevention programs, promoting the basic rules for better sleep quality as well as identifying sleep disorders to minimize possible road accidents.
... Sleep fragmentation (SF) is commonly found in both normal individuals and in patients with sleep disturbance [6]. SF usually caused by multiple frequent disorders such as sleep apnea, depression and asthma, or external environmental factors such as light, temperature, sound, caffeine, and pharmaceutical drugs [7,8]. ...
Objective
To evaluate the causal relationship between sleep fragmentation (SF) parameters with general and abdominal obesity in free-living conditions.
Methods
SF parameters were assessed by ActiGraph accelerometers for 7 consecutive days. Obesity was measured at baseline and 1-year follow-up with InBody S10 body composition analyzer.
Results
At baseline, the mean age of the study population was 18.7 years old (SD = 0.9) and 139 (35.7%) were male. Each 1-unit increase of baseline sleep fragmentation index (SFI) was associated with 0.08 kg/m²-increase of body mass index (BMI) (95% CI: 0.03, 0.14), 0.20%-increase of percentage of body fat (PBF) (95% CI: 0.07, 0.32), 0.15 kg-increase of fat mass (FM) (95% CI: 0.03, 0.27), 0.15 cm-increase of waist circumference (WC) (95% CI: 0.03, 0.26) and 0.91 cm²-increase of visceral fat area (VFA) (95% CI: 0.36, 1.46) at the 1-year follow-up. In addition, each 1-unit increase of baseline SFI was associated with 15% increased risk of general obesity (OR = 1.15, 95% CI = 1.04–1.28; p = 0.006) and 7% increased risk of abdominal obesity (OR = 1.07, 95% CI = 1.01–1.13; p = 0.021) in the following year.
Conclusions
Fragmented sleep is independently associated with an increased risk of both general and abdominal obesity. The result highlights SF as a modifiable risk factor for the prevention and treatment of obesity.
... The predawn meal is taken before the Fajir dawn pray (Suhoor), whereas the break of fasting (Iftar) occurs after sunset (Faris et al. 2020). Sharing similarities with social jet lag (Wittmann et al. 2006), the abrupt alteration and misalignment in eating habits combined with lifestyle and environmental changes, such as delays in school timings and postponed working hours for shopping malls and broadcasting programmes, play a role in causing problems of sleep deprivation, disruption, and fragmentation, having far-reaching health-related consequences (Bonnet and Arand 2003;Van Someren et al. 2015). Regardless of the total daily sleep intake, the fragmentation of a normal sleep cycle into short and heterogeneous sleep bouts, frequently interrupted by brief awakenings, is a typical pattern for the Ramadan predawn meal during the early morning hours (Qasrawi et al. 2017) as detrimental as curtailed sleep (Van Someren et al. 2015). ...
... The number of bouts over which TST is spread provides a measure of sleep efficiency, as repeated waking increases the time spent in transitional stages of sleep, and reduces time spent in deep sleep (Bonnet, 2004;Capellini et al., 2010). Finally, the duration of the longest sleep bout per day estimates sleep quality as it represents the best opportunity the individual has to gain the most restorative benefits of sleep (Bonnet & Arand, 2003). ...
An individual's future behaviour and fitness are strongly influenced by early life experience. Within the suite of factors that underpin juvenile development, sleep plays a particularly important role, fulfilling vital physiological and cognitive functions. Sleep ontogeny is the process by which sleep time becomes shorter and more consolidated into fewer bouts from in utero development to adulthood; however, how sleep quantity, fragmentation and quality develop in neonates in the wild is unknown. We investigated this question in 19 free-ranging fallow deer fawns, Dama dama, during the first 5 weeks of life. Specifically, we examined how sleep developed, how it differed between and within individuals, and how it was affected by environmental conditions, using accelerometer-derived estimates of sleep and a Bayesian hierarchical modelling approach. We showed that sleep duration rapidly decreased and became more consolidated, quickly approaching an adult-like condition. Moreover, fawns exhibited consistent individual differences in sleep quantity, fragmentation and quality, as well as in the rate at which sleep developed. Finally, environmental conditions affecting thermoregulation mediated sleep behaviour; sleep time was reduced and was of lower quality on warmer days, and sleep quality was further compromised in more humid conditions but was higher with greater rainfall. While sleep ontogeny in free-ranging fawns is partially shaped by the environment, our study reveals previously unknown individual differences in sleep behaviour present from birth, and in the rate of sleep development. We suggest that such individual differences may represent pace-of-life syndromes and may have important consequences for individual fitness later in life.
... Importantly, NHB has been shown to cause sleep disruption (also known as disturbed nocturnal sleep) that adversely affects quality of life and psychomotor performance, such as work productivity and driving [3][4][5]. The effect of NHB is of particular growing interest within the field of sleep medicine because of the negative clinical implications of chronic sleep disruption, including associated cognitive [6,7] and non-cognitive effects [8][9][10]. ...
Nocturnal heartburn (NHB) is a symptom that affects up to 25% of the general population and has been shown to cause sleep disruption that adversely affects quality of life and psychomotor performance. Few studies have evaluated the association between occasional NHB and sleep disturbances; therefore, this connection may be underappreciated and left untreated by the primary care provider and patient, with potentially significant negative clinical consequences and effects on quality of life. This review sought to describe what is currently known about the interplay between occasional NHB and sleep disruption, and identify whether acid suppression therapy can improve symptoms of occasional NHB and associated sleep disruptions. The pathophysiology of heartburn-induced sleep disruption appears to follow a bidirectional cycle due to the normal physiologic changes that occur in the upper gastrointestinal tract during sleep and due to the potential for heartburn symptoms to cause sleep arousal. The majority of the identified studies suggested that pharmacologic interventions for acid reduction, including proton pump inhibitors or histamine type-2 receptor antagonists (H2RAs), improved objective and/or subjective sleep outcomes among individuals with gastroesophageal reflux disease (GERD) and NHB. Several studies specific to famotidine demonstrated that treatment with 10 mg or 20 mg reduced nighttime awakenings due to NHB. In conclusion, NHB symptoms can cause sleep dysfunction that can have a profound adverse downstream effect on quality of life, next-day functioning, and health-related outcomes. The current approach to managing occasional NHB is similar to that associated with GERD, highlighting the need for studies specific to the occasional heartburn population. Health care providers should investigate NHB as one of the potential causes of sleep complaints, and patients with heartburn should be questioned about sleep quality, recalled arousals, next-day vitality, early fatigue, and next-day functioning.
... For this reason, perceived sleep quality may not reflect the actual sleep pattern in Antarctic camps. However, a worsening sleep pattern reduces cognitive capacity and physical performance 62,64 , which might affect expeditioners' working demands during Antarctic field. Therefore, individuals must be encouraged to engage in behaviors and use different strategies to improve sleep quality (e.g., thermal insulators and eye masks) and prevent the deleterious effects of ICE conditions. ...
Antarctic expeditions include isolation and exposure to cold and extreme photoperiods (with continuous natural light during summer) that may influence psychophysiological responses modulated by luminosity and sleep. We assessed changes in night sleep patterns by actigraphy, salivary biomarkers, and perceptual variables in seven participants in the following time points along a 50-day camping expedition in Antarctica (Nelson Island): Pre-Field (i.e., on the ship before camp), Field-1, Field-2, Field-3, Field-4 (from 1st to 10th, 11th to 20th, 21st to 35th and 36th to 50th days in camp, respectively), and Post-Field (on the ship after camp). We also characterized mood states, daytime sleepiness, and sleep quality by questionnaires. Staying in an Antarctic camp reduced sleep efficiency (5.2%) and increased the number of awakenings and wakefulness after sleep onset (51.8% and 67.1%, respectively). Furthermore, transient increases in time in bed (16.5%) and sleep onset latency (4.8 ± 4.0 min, from Pre- to Field-3) was observed. These changes were accompanied by an altered pattern of the emerging circadian marker β-Arrestin-1 and a trend to reduce nocturnal melatonin [57.1%; P = 0.066, with large effect size (ES) from Pre-Field to Field-2 (ES = 1.2) and Field-3 (ES = 1.2)]. All changes returned to Pre-Field values during the Post-Field. The volunteers reported sleep-related physical complaints (feeling of cold and pain, discomfort to breathe, and cough or loud snoring), excessive daytime sleepiness, and reduced vigor during the camp. Thus, a 50-day camp alters neuroendocrine regulation and induces physical discomfort, which may explain the impaired sleep pattern and the consequent daytime sleepiness and mood changes.
... Reviewing the evidence, however, Wesensten et al. (1999) concluded that sleep fragmentation only acted through reduction of deeper sleep phases, allowing its effect to be explained by sleep loss if stage N1 was not counted as sleep. These results still appear valid with newer studies (Benkirane et al., 2022;Bonnet & Arand, 2003;Finan et al., 2015;Laharnar et al., 2020;Lee et al., 2022). Despite this debate, healthy sleep disturbed by stimuli, in which N2 sleep duration is increased at the expense of N3 and REM sleep (Benkirane et al., 2022;Ko et al., 2015;Roehrs et al., 1994), may be a model for insomniac sleep to keep in mind. ...
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.
... Some researchers have found that these indicators affect the sleep quality of people who are awake for longer than the usual 16-18 h, or who do not get enough sleep every 24 h for one or more nights. The changes in subjective sleepiness, mood, and emotional processing (including the ability to read positive emotional expressions), as well as the decreased stress threshold, lead to increased stress responses [62][63][64][65]. Moreover, they are important risk factors for the development of burnout syndrome [51][52][53]. ...
Unlabelled:
Burnout syndrome (BS) is the result of chronic stress in the workplace. Moreover, chronic stress can affect sleep. A unidirectional relationship has been established between burnout and sleep, and it is known that white-collar workers with burnout syndrome have sleep fragmentation and marked daytime sleepiness.
Objective:
The aim of this study was to assess the relationships between burnout and sleep quality in elementary school teachers in Mexico.
Methods:
We collected data from more than 400 teachers who completed tests. Correlation analyses controlled for anxiety and depression, and Poisson logistic regression analyses were performed to examine the relationships of burnout with sleep quality, depression, and anxiety.
Results:
There was a significant correlation between burnout syndrome (mainly in the dimension of emotional exhaustion) and sleep disturbances; significant correlations were also observed with other burnout, depression, and anxiety dimensions. The strength of the correlations decreased after controlling for depression and anxiety.
Conclusions:
The symptoms of burnout syndrome in teachers can overlap with sleep disorders, so it is necessary to make a differential diagnosis to differentiate burnout syndrome from depression and anxiety, among others.
... Repeated respiratory obstructive events, accompanied by hypoxemia, trigger frequent arousals and wake transitions, thus reducing total sleep time in OSA. Insomnia impairs sleep via evening hyperarousal, or the failure to reduce wakefulness and enhance sleep drive [6] culminating in hallmark symptoms including (1) difficult sleep initiation, (2) difficulty staying asleep, and (3) waking too early [7]. Collectively, each of these symptoms may contribute to short total sleep time. ...
... Over the week, subjective sleepiness continued to increase and task performance decreased in a linear trend. It follows that individuals experience increased subjective sleepiness [77], more anxiety and depression, and some degree of cognitive impairment during sleep deprivation and that sleep deprivation may lead to impairments in higher cognitive functions, such as language and memory [56]. ...
Total sleep deprivation (TSD) leads to cognitive decline; however, the neurophysiological mechanisms underlying resting-state electroencephalogram (EEG) changes after TSD remain unclear. In this study, 42 healthy adult participants were subjected to 36 h of sleep deprivation (36 h TSD), and resting-state EEG data were recorded at baseline, after 24 h of sleep deprivation (24 h TSD), and after 36 h TSD. The analysis of resting-state EEG at baseline, after 24 h TSD, and after 36 h TSD using source localization analysis, power spectrum analysis, and functional connectivity analysis revealed a decrease in alpha-band power and a significant increase in delta-band power after TSD and impaired functional connectivity in the default mode network, precuneus, and inferior parietal lobule. The cortical activities of the precuneus, inferior parietal lobule, and superior parietal lobule were significantly reduced, but no difference was found between the 24 h and 36 h TSD groups. This may indicate that TSD caused some damage to the participants, but this damage temporarily slowed during the 24 h to 36 h TSD period.
... Repeated respiratory obstructive events, accompanied by hypoxemia, trigger frequent arousals and wake transitions, thus reducing total sleep time in OSA. Insomnia impairs sleep via evening hyperarousal, or the failure to reduce wakefulness and enhance sleep drive [6] culminating in hallmark symptoms including (1) difficult sleep initiation, (2) difficulty staying asleep, and (3) waking too early [7]. Collectively, each of these symptoms may contribute to short total sleep time. ...
Introduction:
Renal ischemia and reperfusion (IR) injury introduces cellular stress and is the main cause of acute kidney damage. Renal cells exposed to noxious stress induce the expression of the pleiotropic hormone leptin. As we have previously revealed a deleterious stress-related role for leptin expression, these results suggested that leptin is also involved in pathological renal remodeling. The systemic functions of leptin preclude the study of its local effects using conventional approaches. We have therefore designed a method to locally perturb leptin activity in specific tissues without affecting its systemic levels. This study explores whether local anti-leptin strategy is reno-protection in a post-IR porcine kidney model.
Methods:
We induced renal IR injury in pigs by exposing kidneys to ischemia and revascularization. Upon reperfusion, kidneys instantly received an intraarterial bolus of either a leptin antagonist (LepA) or saline solution. Peripheral blood was sampled to assess systemic leptin, IL-6, creatinine, and BUN levels, and post-operative tissue samples were analyzed by H&E histochemistry and immunohistochemistry.
Results:
Histology of IR/saline kidneys exhibited extensive necrosis of proximal tubular epithelial cells, as well as elevated levels of apoptosis markers and inflammation. In contrast, IR/LepA kidneys showed no signs of necrosis or inflammation, with normal IL-6 and TLR4 levels. LepA treatment led to upregulation in mRNA levels of leptin, leptin receptor, ERK1/2, STAT3, and transport molecule NHE3.
Conclusions:
Local, intrarenal post-ischemic LepA treatment at reperfusion prevented apoptosis and inflammation and was reno-protective. Selective intrarenal administration of LepA at reperfusion may provide a viable option for clinical implementation.
... While it is possible that sleep deprivation does not degrade simple reaction time, it negatively affects cognitive function or performance (Skurvydas et al., 2020). For examples, time pressure increases error rate and vigilance is deteriorated (Bonnet and Arand, 2003;Fullagar et al., 2015). Perceptual output for action capabilities is altered during prolonged wakefulness because sleep deprivation impairs the central executive processes, with adverse effects on attention and response inhibition (Daviaux et al., 2014). ...
This review addresses the effects of sleep deprivation on postural balance based on a comprehensive search of articles dealing with this relationship in the electronic databases PubMed, Google Scholar, and ScienceDirect. Evidence suggests that postural balance is sensitive to acute and chronic sleep deprivation for everyone, including young and healthy subjects. Pathologies, aging and the circadian pattern aggravate and/or accentuate the effects of sleep deprivation on postural balance. It turns out that the different systems of information taking, decision making, and motor execution of the postural balance function are negatively affected by sleep deprivation. For example, regarding the information taking system, the sensitivity of visual perception and visuo-spatial performance and the oculomotricity are disrupted and the vestibulo-ocular reflex and the sensory reweighting are altered. Regarding the decision making system, the different brain areas activated for the regulation of postural balance are less active after sleep deprivation and the executive function and perception of verticality are impaired. Regarding the motor execution system, the agonist-antagonist muscle coordination can be modified. However, the different detrimental effects induced for each system of the postural balance function are not yet fully known and deserve further exploration in order to better understand them.
... anxiety, parents of young children) and/or medical condition (e.g. sleep disorders: obstructive sleep apnoea, insomnia, circadian rhythm disorders; diabetes, neurodegenerative diseases, pain) [2,3]. www.journals.viamedica.pl/medical_research_journal ...
INTRODUCTION: Sleep disruption is commonly found in normal individuals and those with sleep disorders. Risk factors for sleep fragmentation involve a combination of lifestyle, environmental, psychosocial factors and/or medical conditions. The main objective of this study was to analyse the impact of acute, induced sleep fragmentation upon autonomic cardiovascular regulation, measured by a non-invasive haemodynamic measurement technique. MATERIAL AND METHODS: The authors analysed beat-to-beat measurements of haemodynamic and autonomic parameters at 5-time points during sleep fragmentation: 9:00 a.m. (baseline), 9:00 p.m., 00:30 a.m., 4:00 a.m., and 7:30 a.m. Differences in the mean values for chronotropic parameters, cardiac contractility, parameters related to blood pressure regulation and workload of the left ventricle, and autonomic parameters were examined in seventeen healthy male volunteers. Direct results obtained from every time point were analysed using analysis of variance with repeated measures or the Friedman rank sum test. RESULTS: Sleep fragmentation had a significant negative impact on haemodynamic parameters related to cardiac contractility (SV p < 0.001, IC p < 0.001, HI p < 0.001); parameters related to workload of the left ventricle (CO p < 0.001, LVWI p < 0.001, ACI p < 0.001); parameters related to blood pressure regulation (sBP p = 0.001, TPR p < 0.001); on chronotropic parameters (HR p < 0.001, PEP p < 0.001, LVET p < 0.001) and an indicator of cardiac autonomic regulation: LF-RRI (p = 0.001). CONCLUSIONS: Acute sleep fragmentation can modify haemodynamic control and autonomic cardiovascular regulation in healthy men; the most important changes were seen in the morning hours (4:00 a.m.). Therefore, conditions of chronic sleep fragmentation (e.g. shift work, uniformed services, clinicians), might lead to disturbance in the autonomic nervous system and therefore to problems with homeostasis in the cardiovascular system. Future research is needed in standardized conditions with large-scale studies to clarify the effects of chronic sleep fragmentation.
... Although sleep fragmentation does not necessarily reduce the total sleep time, as in our study, it has an impact on the sleep quality (Martin et al., 1997) and may negatively impact metabolic stability or endocrine and autonomous systems (Baud et al., 2013). Fragmentation of sleep can cause increased sleepiness, decreased psychomotory performance such as reduced short-term memory, reaction time, or vigilance (Bonnet andArand, 2003, Phillipson et al., 1980). Further, in humans sleep disturbance negatively affects cardiovascular health (Gangwisch et al., 2005). ...
Expansion of urban areas, landscape transformation and increasing human outdoor activities strongly affect wildlife behaviour. The outbreak of the COVID-19 pandemic in particular led to drastic changes in human behaviour, exposing wildlife around the world to either reduced or increased human presence, potentially altering animal behaviour. Here, we investigate behavioural responses of wild boar (Sus scrofa) to changing numbers of human visitors to a suburban forest near Prague, Czech Republic, during the first 2.5 years of the COVID-19 epidemic (April 2019-November 2021). We used bio-logging and movement data of 63 GPS-collared wild boar and human visitation data based on an automatic counter installed in the field. We hypothesised that higher levels of human leisure activity will have a disturbing effect on wild boar behaviour manifested in increased movements and ranging, energy spent, and disrupted sleep patterns. Interestingly, whilst the number of people visiting the forest varied by two orders of magnitude (from 36 to 3431 people weekly), even high levels of human presence (>2000 visitors per week) did not affect weekly distance travelled, home range size, and maximum displacement of wild boar. Instead, individuals spent 41 % more energy at high levels of human presence (>2000 visitors per week), with more erratic sleep patterns, characterised by shorter and more frequent sleeping bouts. Our results highlight multifaceted effects of increased human activities ('anthropulses'), such as those related to COVID-19 countermeasures, on animal behaviour. High human pressure may not affect animal movements or habitat use, especially in highly adaptable species such as wild boar, but may disrupt animal activity rhythms, with potentially detrimental fitness consequences. Such subtle behavioural responses can be overlooked if using only standard tracking technology.
... Sleep apnea is recognized as a sleep disorder that the respiration repeatedly stops and starts during the sleeping process [1]. As a common type of sleep apnea, obstructive sleep apnea (OSA) affects up to 38 % of the general population [2]. ...
... First, other characteristics relating to sleep-related metacognitive activity (e.g., beliefs about sleep; [8,58]), pre-sleep cognitive and somatic arousal (e.g., worries), and negative or positive emotions (e.g., [59]), not considered here, would help shed light on the role of thought control strategies at bedtime and sleep quality. In addition, because physiological arousal has been found to predict sleep disturbance [60,61], the perseverance of using a maladaptive strategy such as the worry strategy at bedtime can also be accompanied by physiological activation that can explain difficulty falling asleep (as reported above) and staying asleep throughout the night. Since sleep quality is also defined by other sleep indicators/parameters (e.g., nocturnal awakenings, nap frequency; [3]), future studies to better capture the nature of strategies should thus make the effort to consider a wider number of sleep quality indicators. ...
This study examined the associations between thought control strategies and subjective and objective sleep quality, across the adult lifespan. One hundred forty-nine individuals without insomnia (age range 18–86 years; M = 45.35, SD = 20.53) completed the Thought Control Questionnaire Insomnia–Revised for assessing sleep-related thought control strategies. Self-reported sleep quality was measured with the Pittsburgh Sleep Quality Index. Then, subjective and objective sleep parameters (i.e., total sleep time, sleep onset latency, sleep efficiency) were recorded through a sleep diary and an actigraph across 7 days. Results from linear mixed-effects models showed that a worry strategy was associated with longer subjective sleep latency and shorter subjective total sleeping time. An aggressive suppression strategy was associated with longer subjective total sleeping time. No such involvement of thought control strategies was detected for subjective sleep efficiency and all of the objective sleep parameters. Other individual differences (i.e., age, sex, circadian preference, self-reported sleep quality) also explained both subjective and objective sleep parameters, though to a different extent depending on the sleep parameter considered. The assessment of sleep-related thought control strategies, along with other individual characteristics, should be considered to account for individual differences in sleep quality and implement practices/interventions to support it in adulthood and older age.
... workplace deviance (Christian & Ellis, 2011), and decreased cognitive and motor performance (Bonnet, 1985;Bonnet & Arand, 2003;Pilcher & Huffcutt, 1996). Insufficient and disturbed sleep is also related to a variety of adverse health problems, including obesity (Cappuccio et al., 2008), cardiovascular disease (Ayas et al., 2003;Sabanayagam & Shankar, 2010), diabetes (Schultes et al., 2005), and mortality (Cappuccio et al., 2010). ...
Applying dynamic equilibrium theory (DET), we examined the temporal dynamics between role overload and three health behaviors (sleep, diet, physical activity). Participants (N = 781) completed five surveys, with 1-month lag between assessments, and the data were analyzed using general cross-lagged panel modeling (GCLM). Results indicated that people had stable health behavior patterns (i.e., there were strong unit effects) that were related to stable role overload patterns (i.e., the chronic role overload and health behavior factors were significantly related). Furthermore, while monthly increases (impulses) in role overload had a negative effect on health behaviors concurrently, health behaviors quickly adapted or regressed back toward previous levels (i.e., there were weak autoregressive and cross-lagged effects after accounting for chronic factors). Impulse response functions were created to show the specific proportion of the initial impulse effect that persisted on each health behavior over time. The results of these response functions indicated that diet and physical activity regressed back to previous levels within 1 month, whereas sleep regressed back to previous levels within 2 months. Collectively, our results suggest that people engage in fairly stable patterns of health behaviors and that these patterns are partly determined by chronic role overload. Our results also suggest that people are generally resilient to temporary changes in role overload, such that the resulting immediate changes in behavior do not persist or become habitual. These results underscore the strength of habits and the resistance to health behavior change, as well as provide support for the use of GCLM for studying DET. (PsycInfo Database Record (c) 2022 APA, all rights reserved).
... Sleep boosts the immune system 46 (Bonnet 2004, Capellini et al. 2009). Finally, the duration of the 128 longest daily sleep bout in a 24-hour period indicates sleep quality as it represents the best 129 opportunity for an individual to accrue the benefits of the most restorative stages of deep sleep 130 (Bonnet & Arand 2003). Combined, these three daily measures of sleep provide an ecologically 131 meaningful assessment of sleep quantity and quality. ...
Sleep is a fundamental behaviour as it serves vital physiological functions, yet how the sleep of wild animals is constrained by environmental conditions is poorly understood. Using non-invasive multi-sensor high-resolution biologgers and a robust classification approach, we quantified multiple dimensions of sleep in wild boar (Sus scrofa), a nocturnally active mammal, monitored for up to a full annual cycle. In support of the hypothesis that environmental conditions determining thermoregulatory challenges regulate sleep, we show that on warmer, longer, and more humid days sleep quality and quantity are reduced, whilst greater snow cover and rainfall promote sleep quality. Importantly, our study reveals large inter-and intra-individual variation in sleep durations, suggestive of pace-of-life syndromes. Given the major role that sleep plays in health, our results suggest that global warming and the associated increase in extreme climatic events are likely to negatively impact sleep, and consequently health in wildlife, particularly in nocturnal animals.
Falls remain the leading cause of unintentional injuries across all age groups, prompting many emergency room visits. The annual estimated cost associated with falls is believed to exceed 100 billion dollars. In addressing this trend, health professional team members emerge as key players and can assume a crucial role in bridging the gap between lifestyle medicine and fall prevention. By imparting strategies aligned with the 6 pillars of lifestyle medicine, these professionals can educate individuals on risk factors, assess fall risk, and offer activities to mitigate the likelihood of future falls. This collaborative approach empowers all to take immediate and informed action, fostering a proactive stance against the prevalent issue of fall-related injuries. Through the background and practical strategies described in this paper, health professionals of various disciplines will have access to tools and knowledge to enhance their role in preventing falls using the lens of lifestyle medicine.
Background
Sleep quality is very much affected in mothers in the postpartum period. Despite the high prevalence of poor sleep quality in the postpartum period, little effort is done in this field to help such mothers which is very much needed if their babies are admitted to a neonatal intensive care unit (NICU) which is an additional factor for their disturbed sleep.
Aim and Objectives
The objective of this study is to assess the quality of sleep and depression in mothers whose babies are admitted to the NICU by way of a cross-sectional study.
Methodology
This protocol tried to examine the research question whether there is any correlation between the quality of sleep and depression in mothers who had their delivery in a tertiary teaching hospital and whose babies were admitted to NICU for more than 7 days. This relationship, if any, was assessed using the Edinburgh Postnatal Depression Scale (EPDS) questionnaire whose domain is to find out any correlation between sleep quality and risk of postpartum depression.
Observations
Out of 106 mothers, 68 were primiparous and 38 were multiparous. Out of these mothers, 54% of mothers had EPDS score of >10 and the rest had score of <10. A total score >10 has been validated to have a strong predictive value for detecting women at risk for developing postpartum depression. Furthermore, it was found that as the duration of stay of babies increases in NICU, the number of mothers with EPDS score >10 increases which were found to be statistically significant.
Conclusion and Recommendations
Poor sleep quality is very common in the postpartum period, especially in females whose babies are admitted to NICU. The longer the stay of babies in NICU, worse the quality of sleep is. Hence, it should be kept in mind when the babies are admitted to NICU, some sort of support both psychological and medical should be available at hand for the mothers to cope with such a beautiful albeit stressful period of their lives and if detected to provide necessary treatment in time.
Obstructive sleep apnea is a sleep-related breathing disorder characterized by repetitive upper airway obstruction and is associated with significant morbidity and mortality. Obesity is one of the primary modifiable risk factors for the management of patients with sleep apnea as there is a positive association between the increasing obesity prevalence and sleep apnea prevalence. Several mechanisms link obesity and sleep apnea pathogenesis, including the potential increase in additional mechanical load on the upper and lower respiratory systems from regional adiposity, possible effects of obesity-related inflammation on neuromuscular and neuroventilatory function of the upper airway, or a combination of these effects. By examining the relationship between obesity and obstructive sleep apnea as well as the mechanisms by which obesity may contribute to the development of sleep apnea and its related comorbidities, we can evaluate the effect of weight reduction on the management of sleep apnea.
Accumulating evidence shows that most chronic neurological diseases have a link with sleep disturbances, and that patients with chronically poor sleep undergo an accelerated cognitive decline. Indeed, a single-night of sleep deprivation may increase metabolic waste levels in cerebrospinal fluid. However, it remains unknown how chronic sleep disturbances in isolation from an underlying neurological disease may affect the glymphatic system. Clearance of brain interstitial waste by the glymphatic system occurs primarily during sleep, driven by multiple oscillators including arterial pulsatility, and vasomotion. Herein, we induced sleep fragmentation in young wildtype mice and assessed the effects on glymphatic activity and cognitive functions. Chronic sleep fragmentation reduced glymphatic function and impaired cognitive functions in healthy mice. A mechanistic analysis showed that the chronic sleep fragmentation suppressed slow vasomotion, without altering cardiac-driven pulsations. Taken together, results of this study document that chronic sleep fragmentation suppresses brain metabolite clearance and impairs cognition, even in the absence of disease.
Rationale: Moderate-Severe Obstructive Sleep Apnea (OSA, AHI>15) disturbs sleep through frequent bouts of apnea and is associated with daytime sleepiness. However, many individuals without moderate-severe OSA (i.e., AHI<15) also report sleepiness. Objective: To test the hypothesis that sleepiness in the AHI<15 group is a consequence of substantial flow limitation, in the absence of overt reductions in airflow (i.e., apnea/hypopnea). Methods: N=1886 participants from the MESA sleep cohort were analyzed for frequency of flow limitation from polysomnogram recorded nasal airflow signal. Excessive daytime sleepiness (EDS) was defined by Epworth Sleepiness Scale ≥11. Covariate-adjusted logistic regression assessed the association between EDS (binary dependent variable) and frequency of flow limitation (continuous) in individuals with an AHI<15. Results: N=772 individuals with an AHI<15 were included in primary analysis. Flow limitation was associated with EDS (odds ratio of 2.04, CI95% [1.17-3.54], per 2 standard deviation (2SD) increase in flow limitation frequency) after adjusting for age, sex, BMI, race/ethnicity, and sleep duration. This effect size did not appreciably change after additionally adjusting for AHI. Conclusions: In individuals with an AHI<15, increasing flow limitation frequency by 2SD is associated with a 2-fold increase in risk of EDS. Future studies should investigate addressing flow limitation in low AHI individuals as a potential mechanism for ameliorating sleepiness.
Hospitalized patients are often characterized by various stress factors that can have an impact on their mental health and hospital experience. Improving the quality of life of these bedridden patients is an important task by relieving their anxiety, reducing their pain, and encouraging them in their fight against disease. Virtual reality has already been proved to be a novel and promising tool to improve the quality of life of hospitalized patients. Therefore, the purpose of this chapter is to focus on studies that gave evidence to the feasibility of virtual reality relaxation therapies for hospitalized patients, which virtual reality relaxation therapies are most used, and the benefits and limitations of this type of intervention.
Sleep disturbance is observed across species, resulting in neurocognitive dysfunction and poor impulse control/regulation of negative emotion. Understanding animal sleep disturbance is thus important to understand how environmental factors influence animal sleep and day-to-day welfare. Self-reporting tools for sleep disturbance are commonly used in human research to determine sleep quality, that cannot be transferred to non-verbal animal species research. Human research has, however, successfully used frequency of awakenings to create an objective measurement of sleep quality. The aim of this study was to utilise a novel sleep quality scoring system for a non-human mammalian species. Five separate sleep quality indices calculations were developed using frequency of awakenings and total sleep time/total time spent in different sleep states. These indices were applied to a pre-existing data set of equine sleep behaviour taken from a study investigating the effects of environmental change (lighting and bedding) on the duration of time in different sleep states. Significant treatment effects for index scores both differed and aligned to the original sleep quantity results, thus sleep quality may be a useful alternative measurement of sleep disturbance that could be used to investigate impactful (emotional, cognitive) effects on the animal.
Objective: The objective of this research was to determine the impact of circadian rhythm disorders on sleep disorders, fatigue and health problems of navy sailors from the perspective of their health behavior. During its voyage, navy crews have obvious problems such as sleep disorders and fatigue, among which the circadian rhythm disorder was the most common. Warning system, special environment at sea, pressure and other factors can lead to the occurrence of circadian rhythm disorders. Methods: The primary data was used in this research with a sample size of 278 and Smart PLS was used for statistical analysis. Results: According to empirical data, the impact of circadian rhythm disorders was significant on sleep disorders, fatigue and health problems of navy sailors. The research is novel in the literature because very few studies have discussed the circadian rhythm disorders in the context of navy sailors. Conclusion: The research implications in the theory are reliable to enhance the body of knowledge of circadian in the significant way. Furthermore, the study has some practical implications to work on to enhance the practices to improve the health of navy sailors during their long time in the sea.
Purpose:
To assess the impact of a 3-hour polysomnography (PSG)-recorded night of sleep deprivation on next-morning simulated microsurgical skills among vitreoretinal surgeons with different levels of surgical experience, and to associate the sleep parameters obtained by PSG with the Eyesi-generated performance.
Design:
Self-controlled cohort study.
Participants and controls:
Eleven junior vitreoretinal surgery fellows with less than 2 years' surgical experience and 11 senior surgeons with more than 10 years' surgical practice.
Methods:
Surgical performance was assessed at 7 a.m. after a 3-hour sleep-deprived night using the Eyesi simulator and compared to each subject's baseline performance.
Main outcome measures:
Changes in the Eyesi-generated score (0-700, worst-best), time for task completion (minutes), tremor-specific score (0-100, worst-best), and out-of-tolerance tremor percentage. PSG was recorded during sleep deprivation.
Results:
Novice surgeons had worse simulated surgical performance after sleep deprivation compared to self-controlled baseline dexterity in the total score (559.1 ± 39.3 vs. 593.8 ± 31.7, p=0.041), time for task completion (13.59 ± 3.87 minutes vs. 10.96 ± 1.95 minutes, p=0.027), tremor-specific score (53.8 ± 19.7 vs. 70.0 ± 15.3, p=0.031), and out-of-tolerance tremor (37.7% ± 11.9% vs. 28.0% ± 9.2%, p=0.031), while no performance differences were detected in those parameters among the senior surgeons before and after sleep deprivation (p≥0.05). The time for task completion increased by 26% (p=0.048) in the post-sleep deprivation simulation sessions for all participants with a high apnea-hypopnea index (AHI) and by 37% (p=0.008) among surgeons with fragmented sleep compared with those with normal AHI and fewer than 10 arousals/hour, respectively. Fragmented sleep was the only polysomnographic parameter associated with a worse Eyesi-generated score with a 10% (p=0.005) decrease the following morning.
Conclusion:
This study detected impaired simulated surgical dexterity among novice surgeons after acute sleep deprivation, while senior surgeons maintained their surgical performance, suggesting that the impact of poor sleep quality on surgical skills is offset by increased experience. When considering the two study groups together, sleep fragmentation and AHI were associated with jeopardized surgical performance after sleep deprivation.
Far more than a reversible state of unconsciousness, it would be more accurate to consider sleep as “the work of sleep.” This paper is designed to give the reader an understanding of the normal physiology of sleep. Because with an appreciation of normal, one can recognize and discern the implications associated with sleep-disordered breathing.
Study objectives:
Chronic noncancer pain (CP) commonly co-occurs with obstructive sleep apnea (OSA) and may contribute to greater symptom burden. The study aims were to (1) characterize CP among veterans with OSA; and (2) examine differences in sleepiness (Epworth Sleepiness Scale, ESS), insomnia symptoms (Insomnia Severity Index [ISI]), and quality of life (Short Form Health Survey 20, SF-20) in veterans with OSA with or without pre-existing CP.
Methods:
An observational, cross-sectional, study of 111 veterans with newly diagnosed, untreated OSA was conducted. Descriptive statistics characterized the sample and comorbid CP outcomes. Regression analyses were performed to investigate associations between self-reported CP and sleep-related symptoms or quality of life while controlling for potential confounders.
Results:
CP was reported by 69.5% (95% CI: 61.8, 76.2) of participants. Having CP was associated with increased ESS (12.7 ± 5.5 vs 10.2 ± 5.2; p = 0.021) and ISI scores (18.1 ± 6.2 vs. 13.7 ± 7.4; p = 0.002), and worse quality of life across all SF-20 domains.
Conclusions:
There is a high prevalence of CP among veterans with OSA and symptom burden is higher in patients with OSA and CP. Future investigations should address symptom response and burden to OSA treatment in comorbid OSA and CP to guide outcome expectancies and residual OSA symptom treatment plans.
O Brasil está entre os 10 países com maior número de óbitos por acidentes de trânsito. Esse problema diz respeito ao cenário em que atuam os Policiais Rodoviários Federais (PRFs), os quais realizam patrulhamento ostensivo visando à segurança e à preservação da vida. Com o objetivo de atualizar diretrizes institucionais de intervenção em saúde para esses profissionais, passamos a investigar qualidade do sono, estresse, fadiga e funcionamento executivo, utilizando como delineamento um estudo observacional do tipo transversal com abordagem descritiva analítica. Identificamos prevalência de profissionais com comprometimento na qualidade do sono, e presença de fadiga crônica e de vulnerabilidade ao estresse no trabalho, no item infraestrutura e rotina (teste EVENT). Esse fator está relacionado a questões como dobrar jornada de trabalho, problemas de saúde e acidentes de trabalho.
Sleep changes in new parents are widely observed but there is no extant meta-analysis of changes to sleep parameters in this group. We completed a meta-analysis of changes in actigraphy-measured parent sleep between pregnancy and the end of the first year of a child’s life. A search of six databases was completed. Following review using predetermined inclusion and exclusion criteria, 16 papers were left for review. Data were extracted, analysed and each paper was reviewed for methodological quality. Where possible, subgroup analysis was completed based on time since birth and location of the study, and meta-regression of parent age. Parents' total sleep time and sleep efficiency were shown to decrease following the birth of a child, with wake after sleep onset increasing. This change was most notably observed in the first four weeks after birth. Up to 16 weeks post-birth, differences were still apparent, but sleep parameters were beginning to return to pre-birth levels. New parents experience a significant change in multiple sleep parameters following the birth of a child. Future data collection, using best practice actigraphy measurement, reporting a broader range of variables and including fathers, as well as mothers, is warranted.
Both the human capital approach and the friction cost approach are frequently used to quantify the productivity costs associated with illness, disability or death in health economic evaluations. In this paper we argue that these approaches have one major, but common shortcoming: they only capture partial equilibrium (PE) effects and therefore underestimate the true potential productivity costs associated with health conditions. They neglect the sizable, indirect, ripple effects in the economy captured by general equilibrium (GE) models. To demonstrate our point, we compare a traditional PE with a GE approach for the application to nocturia, a condition characterized by the need to frequently wake up at night to urinate. Nocturia is associated with substantial impairment of daytime functioning and work productivity. We employ large‐scale United Kingdom (UK) employer‐employee survey data to estimate the prevalence and productivity loss. These estimates are then used as shared inputs to drive both approaches. We find that the traditional PE approach underestimates the annual productivity cost of clinically relevant nocturia by around 16%. We propose a generalized GE/PE multiplier to approximate the GE effect for other health conditions. Our findings stress the importance of accounting for sizable GE effects when conducting health economic evaluations.
It was hypothesized that the metabolic effects of caffeine, which can be objectively measured (i.e. physiological, "arousal"), could be used to develop a physiological arousal model of chronic insomnia in a group of normal young adults. Twelve normal young adult males participated for 11 nights after laboratory adaptation. Subjects received 400 mg of caffeine three times a day for 7 nights and days. As predicted, the use of caffeine resulted in increased metabolic rate. Sleep efficiency was significantly reduced by caffeine and multiple sleep latency tests (MSLTs) were significantly increased. Some adaptation to the metabolic, sleep efficiency, and MSLT effects of caffeine was seen over the week of administration. Withdrawal effects (i.e. rebound sleep or sleepiness) were not seen for metabolic, MSLT or sleep variables. The data indicated that caffeine was effective in producing significant metabolic and sleep effects and that those effects were related. The results were consistent with the interpretation that a chronic decrease in sleep efficiency associated with increased physiological arousal, although producing subjective dysphoria, does not produce a physiological sleep debt.
The usefulness of a 40-min per trial version of the maintenance of wakefulness test was assessed in 322 patients with obstructive sleep apnea. This test is a variant of the multiple sleep latency test in which patients are asked to remain awake in a quiet darkened room, and then monitored for electroencephalographic sleep onset. The four trials of the test are each stopped after 40 min. The mean sleep latency for all patients was 26.0 +/- 11.8 (SD) min. In a group of 24 patients who underwent treatment with nasal continuous positive airway pressure, the mean sleep latency increased from 18.0 +/- 12.3 to 31.9 +/- 10.4. The strongest nocturnal correlates of the MWT sleep latency were respiratory arousal index (r = -.35), mean oxygen saturation (r = .30), and weight/height ratio (r = -.25). These correlations were comparable to other studies using the MSLT. There were strong intercorrelations among the variables. In the more severe groups, measures of hypoxemia were more strongly correlated with MWT sleep latency. A two-factor analysis of variance using respiratory arousal index and several measures of oxyhemoglobin saturation indicated that both arousals from sleep and degree of hypoxemia contribute interactively to daytime dysfunction in patients with sleep apnea. The MWT appears useful in evaluating disability from daytime sleepiness.
Average metabolic data (O2 uptake and CO2 output) were obtained for each 3-min period during consecutive nights of normal, experimentally fragmented, and recovery sleep in a group of 12 normal young adult males. Naturally occurring arousals and awakenings resulted in a characteristic increase in metabolism on the baseline night. The placement of brief frequent experimental arousals on the following night resulted in significantly increased metabolism throughout the night and significantly decreased sleep restoration as measured by morning performance, mood, and alertness tests, even though total sleep time was minimally reduced. Metabolic variables were significantly decreased compared with baseline on the nondisturbed recovery night that followed the sleep fragmentation night. The data cannot be used to infer that increased metabolism during sleep causes nonrestorative sleep, but the direction and time course of metabolic change accompanying arousal are consistent with that hypothesis.
Many studies have shown a relationship between fragmented nocturnal sleep and daytime sleepiness. In the current study, 9 patients, aged 55-79, with fragmented nocturnal sleep secondary to periodic leg movements and objective daytime sleepiness, as verified by Multiple Sleep Latency Test (MSLT), had 12 weeks of treatment with 0.125 mg of triazolam following 2 screening nights and 2 placebo baseline nights; 2 final placebo nights were placed 5 nights following the last medication night. The medication increased total sleep time and sleep efficiency throughout the administration period, as compared to average placebo values; total leg movements were not changed. Generally, daytime performance, as measured by a vigilance task, and objective alertness, as measured by MSLT, were improved following the use of triazolam. No adverse reactions or significant side effects were noted. It was concluded that 0.125 mg triazolam, when used for up to 3 months, could improve sleep and daytime function in older patients with periodic leg movements, fragmented sleep, and daytime sleepiness.
To determine the effects of intermittent hypoxemia on daytime sleepiness in the clinical setting of obstructive sleep apnea syndrome, we enrolled seven patients in a prospective, randomized, crossover study. We had two experimental conditions with NCPAP treatment as follow: (1) to correct apneas, sleep fragmentation, and hypoxemia; and (2) to correct apneas and sleep fragmentation and at the same time, induce intermittent hypoxemia. The outcome variable, daytime sleepiness, was measured objectively with the multiple sleep latency test following completion of baseline and each treatment condition. Compared with sleep latencies in the untreated condition, both experimental treatment arms prolonged sleep latencies (p less than 0.05). We found no statistically significant differences between mean MSLT scores obtained after NCPAP treatment under hypoxemic and nonhypoxemic conditions. In summary, two nights of intermittent nocturnal hypoxemia during NCPAP treatment for OSAS did not diminish the objective improvement in daytime somnolence seen with NCPAP treatment in the absence of nocturnal hypoxemia. Results lend further support to the hypothesis relating excessive daytime sleepiness to sleep fragmentation.
Many studies have shown a relationship between fragmented nocturnal sleep and daytime sleepiness. In the current study, 11 patients, aged 55-75, were identified with fragmented nocturnal sleep secondary to periodic leg movements and objective daytime sleepiness as verified by the Multiple Sleep Latency Test (MSLT). In a double-blind, repeated measures, cross-over design, patients had three nights of treatment with placebo, 0.125 mg of triazolam, or 0.25 mg of triazolam following an adaptation night. Although total leg movements were not changed, the medication increased total sleep time and sleep efficiency while decreasing the number of stage changes. Generally, daytime performance and objective alertness were significantly improved following the use of triazolam. It was concluded that acute use of triazolam, particularly the 0.125 mg dose, could improve sleep and daytime function in older patients with periodic leg movements, fragmented sleep, and daytime sleepiness.
It was hypothesized that triazolam might decrease central apneas associated with arousal periods in patients with central sleep apnea by hastening the onset of consolidated sleep. Five male patients, diagnosed as having central sleep apnea on a screening night, participated in a double-blind randomized crossover study of the effect of placebo, 0.125 mg triazolam, and 0.25 mg triazolam on sleep, respiration, and daytime function. Results indicated that the medication increased total sleep and decreased central apnea index and number of brief arousals. Improved sleep quality was reflected in improved daytime psychomotor performance and alertness. These data, if replicated, imply that benzodiazepine use may be beneficial in patients with central sleep apnea.
In the first of two experiments, 12 normal young adults had their sleep periodically disturbed for two nights in the laboratory at three different rates: 10 min of sleep followed by 20 min of disturbance, 20 min of sleep followed by 40 min of disturbance and 40 min of sleep followed by 80 min of disturbance. Sleep and disturbance alternated throughout the night. While all disturbance conditions resulted in decreased daytime performance and increased sleepiness, the disturbance conditions did not differ from each other. In the second experiment, sleep was periodically disturbed for two nights at three new rates to act as control conditions for Experiment 1. The three conditions were: 2 min of sleep followed by 4 min of disturbance, 20 min of sleep followed by a single awakening, and 40 min of sleep followed by a single awakening. Sleep and disturbance again alternated throughout the night. As expected, sleep was less disturbed and daytime decrements were smaller in the conditions allowing 20 and 40 min of sleep followed by a single awakening. The data from both experiments were interpreted as support for sleep continuity theory; i.e., as the length of periods of consolidated sleep decrease, residual decrements increase.
The daytime sleepiness of a large sample (n = 129) of healthy, young (age 18-29) adults with no sleep-wake complaints was measured and compared with that of a sample (n = 47) of older (age 30-80) healthy, normal sleeping, subjects. Each spent 8 h in the laboratory on 1 night and received the Multiple Sleep Latency Test (MSLT) the following day. Sleep latency was measured at 1000, 1200, 1400, and 1600 h. Mean sleep latency ranged from 2 to 20 min within each group, but the shape of the distribution of latency between groups was different. The mean latency of young subjects (particularly college students) was shorter than that of the older subjects, with the differences occurring between the sleepiest 80% of each distribution. Among the college students, those with higher nocturnal sleep efficiencies (the previous night) were sleepier the following day than those with lower sleep efficiencies. The relation between nocturnal sleep efficiency and daytime sleepiness suggests that the increased sleepiness of average young adults is due to mild sleep restriction.
The recuperative effects of naps fragmented by different rates of electroencephalographic (EEG) arousal were evaluated. Forty healthy subjects with normal hearing and daytime sleep tendency (measured by the Multiple Sleep Latency Test at 10:00 a.m., 12:00 p.m., 2:00 p.m., and 4:00 p.m.) were randomly assigned to one of five conditions. Each was deprived of sleep for one night and then at 8:30 a.m. was given 100 min of natural sleep, sleep with arousals 1/5 min, 1/3 min, 1/1 min, or no sleep. After the recovery nap at 12:00 p.m., 2:00 p.m., 4:00 p.m., and 6:00 p.m., sleep latencies were again evaluated. Mean sleep latencies increased linearly as the rate of arousal during the recuperative nap decreased. Latency in the high-arousal condition was similar to no sleep and lower than natural sleep. The sleep latency of the low-arousal condition was similar to natural sleep and higher than no sleep, whereas latency in the medium arousal condition was intermediate to and differed from both natural sleep and no sleep. Although the natural sleep provided recuperation relative to no sleep or fragmented sleep, it did not restore daytime sleepiness to the screening level.
Many changes occur in sleep as a function of aging, but it is not known whether these changes result in sleep being less restorative. To examine the sleep restorative process, groups of 12 normal young adults and 12 normal and 12 insomniac male subjects, age 55-71, were totally sleep deprived for 64 hours and then allowed recovery sleep. Response speed, immediate recall, sleepiness, and body temperature were tested at approximately 2300, 0115, 0330, 0530 and 0800 during baseline, sleep loss, and recovery nights. Significant group (age or insomnia) by sleep loss condition interactions were found for reaction time and immediate recall performance measures. Similar significant interactions were found for oral temperature and all EEG sleep variables except total time in bed, percent stage 1, and percent REM. It was concluded that performance recovery following sleep loss was no slower in older subjects than in younger subjects despite very different recovery sleep stage parameters. This implied that aging effects on sleep are developmental rather than degenerative.
Eleven young adults had their sleep briefly disturbed following each 2 min of accumulated sleep for 2 consecutive nights in 3 different weeks. During 1 week the disturbance was a brief awakening followed by a subjective response. During another week subjects were required to make a quarter-body turn response. During the final week, the disturbance was an ongoing electroencephalographic (EEG) change. As expected, the three disturbance conditions differentially impacted sleep, with the most sleep disturbance seen in the awakening condition and the least disturbance seen in the EEG change condition. Morning vigilance performance and nap latency were decreased and fatigue was increased as compared with baseline following all three disturbance conditions. However, no significant condition interaction was found for any performance variable or for morning nap latency. For the mood scales, significant condition interactions indicated that subjects reported being sleepier only after the awakening condition. The data were interpreted as providing evidence that the restorative function of sleep is equally impaired by any periodic change in ongoing EEG and that impairment does not require a return to waking consciousness. However, mood, as a subjective rating, is dependent upon conscious events that occur during the sleep period.
Eight normal young adult sleepers spent 4 nonconsecutive weeks in the laboratory. Each week consisted of a baseline night followed by 2 consecutive nights of disrupted sleep, followed by 2 recovery nights. Disruption conditions included: a) brief awakening after each minute of accumulated sleep, b) brief awakening after each 10 min of accumulated sleep, c) 2.5 hrs of normal sleep followed by a brief awakening at each sleep onset, and d) total sleep deprivation. Morning testing revealed that all disruption conditions decreased sleep latency in a morning nap test. Performance after 1-min disruptions approximated that seen after total sleep loss. Performance decrements were less in the 10-min condition and least in the 2.5-hr sleep condition. Performance under baseline and total sleep loss conditions was used to predict performance during the sleep deprivation condition using four sleep stage rules. Total time asleep and total time asleep minus stage 1 predicted performance poorly. Total SWS plus REM predicted performance best but could not differentiate the 10-min and 2.5-hr conditions. Therefore, it was concluded that the data were most parsimoniously explained by the Sleep Continuity Theory—i.e., that periods of uninterrupted sleep in excess of 10 min are required for sleep to be restorative.
Recent studies have shown that periodically disrupted sleep resulted in significant daytime sleepiness and performance loss in normal young adults. One study suggested that the periodicity of disturbance rather than the total number of sleep disturbances was the primary factor in causing degraded function. However, in that study, increased performance levels could have been associated with increased levels of slow wave sleep. The present study was designed to determine whether the amount of SWS rather than the periodic disruption of sleep accounts for decreased performance of Ss with disrupted sleep. Twelve normal young adults spent two 4-night periods in the laboratory. During one 4-night series, Ss were briefly aroused either following each 10 min of sleep or whenever they entered stage 3 sleep (No SWS condition). During the second series of nights, Ss were briefly aroused after each 10 min of sleep (SWS condition). In the second series, additional arousals were performed after 5-min periods (but not when Ss were in SWS) to equalize the total number of arousals in the SWS conditions with those in the No SWS condition. Total experimental arousals were equal in the disruption conditions, and the experimental manipulation was successful in reducing total SWS to infrequent epochs of stage 3 in the No SWS condition while allowing significantly more SWS in the SWS condition. In terms of sleep stages, this difference was balanced by increased stage 2 in the No SWS condition. Despite the differential occurrence of SWS, no performance, mood, or nap latency measure was different in the SWS vs.(ABSTRACT TRUNCATED AT 250 WORDS)
Fifty-eight geriatric normal and chronic insomniac sleepers were screened with sleep recordings to define groups of 12 Normal (Sleep Efficiency greater than 85%) and Insomniac (Sleep Efficiency less than 80%) sleepers. All subjects then had 4 baseline sleep nights, 64 hours of total sleep loss, and 4 recovery nights. Insomniacs, had lower sleep efficiencies and less REM than Normals during baseline. Sleep efficiency was high (97%) in both groups on the first recovery night but decreased toward baseline values in both groups between the second (Normal) and fourth (Insomniac) recovery night. The groups had relatively little slow wave sleep, but had a significant increase on the first recovery night. Five Normals and one Insomniac had REM latency of less than 15 min on their first recovery night. This REM latency was found to be significantly correlated with the amount of slow wave sleep on baseline. Decreased REM latency in initial recovery sleep was interpreted as evidence of decreased pressure for slow wave sleep in aging.
Eleven young adult subjects were briefly awakened after each minute of electroencephalographic-defined sleep for 2 consecutive nights after undisturbed laboratory adaptation and baseline nights. Two undisturbed recovery nights followed disruption nights. On disruption nights, subjects were awakened with an audiometer and signaled the awakening by subjective rating of sleep state or button push response. The disruption procedure resulted in severely fragmented sleep with only very small amounts of slow-wave and REM sleep. Total sleep time was reduced by approximately 1 h on each night. Arousal threshold increased 56 dB across the disruption nights. Following disruption, subjects performed more poorly and rated themselves sleepier than on baseline. The level of decline was similar to that seen after periods of total sleep loss of 40-64 h. Recovery sleep was also similar to that seen after total sleep loss. It was concluded that periodic disruption of sleep, perhaps by destroying sleep continuity, quickly results in impaired function. These data may help explain function loss in severe sleep apneics.
The periods of apnea during sleep that characterize the upper-airway obstructive sleep apnea syndromes are usually terminated by electroencephalographic (EEG) and behavioral evidence of brief arousal, followed by an increase in tone of the upper-airway muscles and restoration of airflow (Guilleminault et al., 1976; Remmers et al., 1978). The specific stimuli that lead to arousal probably include hypercapnia and hypoxia, both of which are known to produce reticular stimulation and cortical activation (Bonvallet et al., 1955; Hugelin et al., 1959). However, the degree of asphyxia that develops in such patients during the periods of apnea before producing arousal is often profound; and we have suggested previously that impaired arousal responses to respiratory stimuli may be a feature of the sleep apnea syndromes (Phillipson and Sullivan, 1978). Furthermore, it is reasonable to speculate that such defects in arousability might result from the severe fragmentation of nocturnal sleep (by multiple arousals) that is characteristic of patients with this disorder. Accordingly, the purpose of this study was to test the hypothesis that sleep fragmentation per se may result in impaired arousal responses to respiratory stimuli.
Patients with obstructive sleep apnea (OSA) have impaired health status that Improves with nasal continuous positive airway pressure (nCPAP). The study reported here explored the relationships between health status, its improvement with nCPAP, sleep fragmentation, and daytime sleepiness. In the study, 51 patients (46 male, five female) ranging from nonsnorers to individuals with severe OSA (median apnea/hypopnea index [AHI] 25, 90% central range: 1 to 98) had polysomnography with microarousal scoring, respiratory arousal scoring, and measurement of pulse transit time. The Short Form-36 Health Survey (SF-36) questionnaire was administered before and after 4 wk of nCPAP treatment; daytime sleepiness was also measured before starting nCPAP. Relationships between pretreatment health status and sleep fragmentation were weak, but significant associations were found between all sleep fragmentation indices and health status improvement with nCPAP (e.g., arousals according to the criteria of the American Sleep Disorders Association versus change in the physical component summary, r = 0.44, p < 0.001). Compared with general population data, the dimensions of energy and vitality and physical role limitation were abnormal before nCPAP (p < 0.05) and normalized with treatment. Sleepiness and pretreatment SF-36 values correlated significantly (Epworth Sleepiness Scale versus energy and vitality, r = -0.47, p < 0.001; modified Maintenance of Wakefulness Test versus energy and vitality, r = 0.32, p < 0.05). We conclude that the health status of patients with OSA improves with nCPAP and this improvement correlates with sleep fragmentation severity. However, the correlation is not very close, which may reflect the improvement with nCPAP of other symptoms not directly related to disease severity.
This authoritative guide to sleep medicine is also available as an e-dition, book (ISBN: 1416003207) plus updated online reference! The new edition of this definitive resource has been completely revised and updated to provide all of the latest scientific and clinical advances. Drs. Kryger, Roth, and Dementand over 170 international expertsdiscuss the most recent data, management guidelines, and treatments for a full range of sleep problems. Representing a wide variety of specialties, including pulmonary, neurology, psychiatry, cardiology, internal medicine, otolaryngology, and primary care, this whos who of experts delivers the most compelling, readable, and scientifically accurate source of sleep medicine available today. Includes user-friendly synopses of important background information before all basic science chapters. Provides expert coverage of narcolepsy * movement disorders * breathing disorders * gastrointestinal problems * neurological conditions * psychiatric disturbances * substance abuse * and more. Discusses hot topics such as the genetic mechanisms of circadian rhythms * the relationship between obesity, hormones, and sleep apnea * sleep apnea and arterial hypertension * and more. Includes a new section on Cardiovascular Disorders that examines the links between sleep breathing disorders and cardiovascular abnormalities, as well as the use of sleep related therapies for congestive heart failure. Provides a new section on Womens Health and Sleep Disorders that includes information on the effects of hormonal changes during pregnancy and menopause on sleep. Features the fresh perspectives of 4 new section editors. Employs a more consistent chapter organization for better readability and easier navigation.
Study Objective: In the last two decades there has been an increase in the awareness of and professional expertise in sleep disorders. The objective of this study was to determine the spectrum of sleep-related disorders diagnosed in regional sleep centers and compare this to a previous survey published in 1982. Design: A two-month prospective point-prevalence survey Setting: Nineteen accredited regional sleep centers in the United States Participants: Patients evaluated at regional sleep centers during a two-month period. Interventions: NA Results: Obstructive sleep apnea, narcolepsy, and restless legs syndrome were the top three reported primary diagnoses with a prevalence of 67.8%, 4.9%, and 3.2%, respectively. The entire range of sleep disorders, however, was represented in the study sample. Nearly a third of patients had either a primary or secondary diagnosis of a non-respiratory sleep disorder. Referral physicians were most likely to be from internal medicine, pulmonary medicine, and otolaryngology. Compared to the previous survey from 1982, there has been an absolute increase in patient referrals/center with a two- to four-fold increase in the number of patients/center with a final diagnosis of a non-respiratory sleep-related problem. Moreover, there has been a greater than twenty-fold increase in the diagnosis of obstructive sleep apnea. Conclusion: Regional sleep centers are encountering increasing patient referrals and a broad range of sleep-related disorders. The predominant reasons for referral are related to obstructive sleep apnea, narcolepsy, and restless legs syndrome.
Study Objectives
This study investigated changes in MSLT scores and recovery sleep following total sleep deprivation in subjects with insomnia as compared to normal sleepers.
Design
Matched-groups design.
Setting
A sleep disorders center in a large medical center.
Participants
Ten individuals with psychophysiological insomnia and ten age- and sex-matched normal sleepers served as subjects.
Interventions
Subjects underwent total sleep deprivation after baseline polysomnography and MSLT. A post-deprivation MSLT was obtained, as well as polysomnography on the recovery night and an MSLT after the recovery night.
Measurements and Results
Both groups showed significant decreases in MSLT scores following total sleep deprivation, as compared to baseline. Both groups had significantly shorter scores on a nighttime MSLT compared to a daytime MSLT. The insomnia group also showed a significant increase in total sleep time on the recovery night compared to baseline.
Conclusions
The MSLT is sensitive to changes in sleepiness associated with total sleep deprivation in individuals with primary insomnia.
Obstructive sleep apnea syndrome is a well recognized cause of excessive sleepiness; however, the relation of sleepiness to mild sleep-disordered breathing (SDB), which affects as much as half the adult population, is uncertain. In order to explore this relation, we conducted a cross-sectional cohort study of community-dwelling adults participating in the Sleep Heart Health Study, a longitudinal study of the cardiovascular consequences of SDB. The study sample comprises 886 men and 938 women, with a mean age of 65 (SD 11) yr. Sleepiness was quantified using the Epworth Sleepiness Scale (ESS). Sleep-disordered breathing was quantified by the respiratory disturbance index (RDI), defined as the number of apneas plus hypopneas per hour of sleep, measured during in-home polysomnography. When RDI was categorized into four groups ( < 5, 5 to < 15, 15 to < 30, ⩾ 30), a significantly progressive increase in mean ESS score was seen across all four levels of SDB, from 7.2 (4.3) in subjects with RDI < 5 to 9.3 (4.9) in subjects with RDI ⩾ 30 (p < 0.001). There was no significant modification of this effect by age, sex, body mass index, or evidence of chronic restriction of sleep time or periodic limb movement disorder. The percentage of subjects with excessive sleepiness, defined as an ESS score ⩾ 11, increased from 21% in subjects with RDI < 5 to 35% in those with RDI ⩾ 30 (p < 0.001). We conclude that SDB is associated with excess sleepiness in community-dwelling, middle-aged and older adults, not limited to those with clinically apparent sleep apnea.
To determine whether a cumulative sleep debt (in a range commonly experienced) would result in cumulative changes in measures of waking neurobehavioral alertness, 16 healthy young adults had their sleep restricted to an average 4.98 hrs per night for 7 consecutive nights. Ss slept in the laboratory, and sleep and waking were monitored. Three times each day, Ss were assessed for subjective sleepiness and mood and were evaluated on a brief performance battery that included psychomotor vigilance (PVT), probed memory (PRM), and serial-addition testing. Once each day they completed a series of visual analog scales (VASs) and reported sleepiness and somatic and cognitive/emotional problems. Sleep restriction resulted in statistically robust cumulative effects on waking functions. Subjective sleepiness ratings, subscale scores for fatigue, confusion, tension, and total mood disturbance from the mood and VAS ratings of mental exhaustion and stress were elevated across days of restricted sleep. PVT performance parameters were also significantly increased by restriction. Significant time-of-day effects were evident in subjective sleepiness and PVT data. Findings suggest that cumulative nocturnal sleep debt had a dynamic and escalating analog in cumulative daytime sleepiness and that asymptotic or steady-state sleepiness was not achieved in response to sleep restriction. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
A review was made of the literature relating sleep apnoea to sympathetic nervous system (SNS) activity, as inferred from catecholamine levels or muscle sympathetic nerve activity (MSNA). Twenty-four studies were located. Most studies reported an elevation of norepinephrine and MSNA, both during sleep and wakefulness among individuals with sleep apnoea. However, studies rarely controlled for known confounders of sympathetic activity, making the validity of the findings questionable.
SUMMARY Upper airway obstructions during sleep cause recurrent brief awakenings or microarousals. Standard criteria exist for sleep and respiratory event scoring, however, there are different definitions currently used to score microarousals. We therefore compared three definitions of microarousal (ranging from 1.5-3 s in duration) and one of awakening (> 15 s). We examined their occurrence at the termination of apnoeas and hypopnoeas and their correlation with daytime sleepiness in patients with sleep apnoea/hypopnoea syndrome (SAHS). Sixty-three patients (aged 49, SD 10) had overnight polysomnography, multiple sleep latency tests (MSLT) and Epworth Sleepiness Scales (ESS). There were significantly more microarousals by any definition than there were awakenings (P<0.001) and there were more 1.5 s than 3 s microarousals (P<0.001). Significantly more apnoeas and hypopnoeas were terminated by 1.5 s microarousals (83% and 81%) than by 3 s microarousals (75%) (all P<0.001). Apnoea/hypopnoea index (AHI) correlated significantly with objective daytime sleepiness (p = -0.30, P<0.01). There were weakly significant relationships between all three microarousal definitions (-0.24<P< -0.22, 0.03<P<0.04) and objective daytime sleepiness. None of the arousal definitions correlated with Epworth Sleepiness Scales scores. These results suggest that although 1.5 s microarousals are found at the end of more respiratory events, relationships between 3 and 1.5 s definitions, and daytime sleepiness are similar. This indicates that any of the three microarousal definitions can be used for visual assessment of sleep fragmentation.
Objectives/hypothesis:
A large sector of the population of the United States has sleep deprivation directly leading to excessive daytime sleepiness. The prevalence of excessive daytime sleepiness in this population ranges from 0.3% to 13.3%. The consequences of even 1 to 2 hours of sleep loss nightly may result in decrements in daytime functions resulting in human error, accidents, and catastrophic events. The magnitude of risks in the workplace or on the highways resulting from sleepiness is not fully understood or appreciated by the general population. Hence, to more clearly emphasize the magnitude of these risks, we question whether mild sleep deprivation may have the same effect as alcohol on reaction times and driving performance.
Study design:
Nonrandomized prospective cohort investigation.
Methods:
Sixteen healthy matched adult subjects (50% women) were stratified into two groups, sleep deprived and alcohol challenged. The sleep-deprived group was further subdivided into acute (one night without sleep) and chronic (2 h less sleep nightly for 7 d) sleep deprivation. Each group underwent baseline reaction time testing and then drove on a closed course set up to test performance. Seven days later, the group repeated this sequence after either sleep deprivation or alcohol intake.
Results:
There were no significant between-group differences (sleep deprivation or alcohol challenged) in the changes before and after intervention for all 11 reaction time test metrics. Moreover, with few exceptions, the magnitude of change was nearly identical in the two groups, despite a mean blood alcohol concentration of 0.089 g/dL in the alcohol-challenged group. On-track driving performances were similar (P =.724) when change scores (hits and errors) between groups were compared (baseline minus final driving trial).
Conclusion:
This comparative model suggests that the potential risks of driving while sleepy are at least as dangerous as the risks of driving illegally under the influence of alcohol.
Sleep and daytime sleepiness were evaluated in 10 young adult subjects to determine whether restricting nocturnal step by a constant amount produces cumulative impairment. Subjects were studied for 12 consecutive days, including 3 baseline days with a 10-hr time in bed, 7 days with sleep restricted to 5 hrs, and 2 recovery days. In 5 subjects, recovery included a 10-hr time in bed; in the remaining subject, recovery induced a 5-hr time in bed with a 1-hr daytime nap. Sleepiness was measured using two self-rating scales and the multiple sleep latency test. During sleep restriction, nocturnal stage 2 and REM sleep were reduced and slow wave sleep was unaffected. Stanford Sleepiness Scales showed an immediate increase in daytime sleepiness that reached a plateau after 4 days. An analog sleepiness rating scale showed increased sleepiness after 2 restricted nights and leveled off after the fourth restricted night. The multiple sleep latency tests showed no effect of sleep restriction until the second day, followed by a progressive increase in sleepiness that persisted through the seventh sleep restriction day. During the recovery period, daytime sleepiness returned to basal values on all three measures following one full night of sleep; with a daytime nap, no further cumulative effects of sleep restriction were seen.
Plasma prolactin (PRL) concentration exhibits a sleep-dependent pattern, with highest levels during sleep and lowest levels during the waking period. The syndrome of obstructive sleep apnoea (OSA) is associated with severe hypoxaemia and chronic sleep fragmentation, both of which could affect the sleep-entrained PRL rhythm. Treatment with nasal continuous positive airway pressure (CPAP) immediately restores a normal sleep structure by successful abolition of the apnoeas. In the present study, seven OSA patients underwent two night studies, once when no treatment was given and once during the first night of CPAP treatment. Sleep was recorded polygraphically in all experiments. Plasma PRL was measured at 10 min intervals and secretory rates were calculated by a deconvolution procedure. CPAP treatment greatly reduced hypoxaemia and improved sleep quality. The secretory pulse amplitude and the total amount of PRL secreted during the night remained constant regardless of whether patients were treated or not. The only difference found was a lower pulse frequency in untreated OSA patients as compared to treated patients, which may be attributed either to hypoxaemia or to sleep disturbance or to the combined action of both. Treatment may be considered to normalize PRL release by restoring pulse frequency to values similar to those observed for normal subjects.
This experiment was designed to test the effects on subsequent sleep of a restriction in sleep length on the previous night. Eight male subjects were studied. After baseline recordings were made, sleep was restricted to either a period between 4-8 am or to a period between 6–8 am. On the night following the restriction of sleep the subjects retired at 11 pm and they were permitted to sleep ad lib in the morning.
The restricted sleep periods resulted in differential sleep deprivation. Stages REM and 2 were markedly reduced whereas stages 3 and 4 showed little or no reduction in amount. There were significant reductions in sleep latencies and in the amount of lime spent in stages 0 and 1. The first 8 hrs of ad lib sleep following the 2 restricted sleep periods did not differ in any significant way from the 8 hrs of baseline sleep. When sleep was permitted to continue until the subjects awakened spontaneously, the sleep after the restriction of sleep to‘i hrs was significantly longer and displayed significantly more of stages REM and 2 when compared with the baseline ad lib sleep condition. The ad lib sleep period following the 4 hr condition showed similar changes although the differences were not statistically significant.
The significant reductions in stages KEM and 2 during the restricted sleep periods were attributed to the effects of reduced steep length per se. The increases in sleep length and specifically the increases in stages REM and 2 during the ad lib sleep periods were attributed to a differential sleep “debt” accruing from restricted sleep length.
Six studies on sleep/wake patterns and circadian rhythms were carried out. In summary: (1) Adrenaline excretion, self-rated activation, and body temperature rhythms persisted during sleep deprivation, resisted adjustment to rotating shift work, but adjusted rather well to permanent night work. Noradrenaline adjusted to most schedules and lost its rhythm during sleep deprivation. When night sleep was reintroduced the noradrenaline rhythm reappeared while the existing adrenaline rhythm was accentuated. (2) Exposure to a performance stressor at the trough raised adrenaline to daytime levels. An equally large response was seen at the peak. (3) Interindividual day-to-day consistency of 3 and 24 hour levels was high for both catecholamines. Intraindividual consistency of the 24-hour pattern was high for adrenaline but low for noradrenaline. Cosine estimates of adrenaline phase showed a considerable intraindividual consistency while interindividual consistency was poor. Noradrenaline had poor cosine fit. (4) Sleep deprivation did not change catecholamine excretion either during the vigil or during recovery sleep. (5) It was concluded that adrenaline excretion, rated alertness, and body temperature exhibited self-sustained circadian rhythms which made adjustment to new sleep/wake patterns very difficult, and that the noradrenaline excretion rhythm depended on exogenous factors.
Recent studies have provided evidence that nocturnal cortisol secretion is coupled to ultradian rhythms of sleep. The present study was designed to specify how exogenous and sleep-related endogenous factors influence nocturnal adrenocorticotropin (ACTH) and cortisol secretion. We compared the influences of (1) temporary sleep deprivation, (2) arousals continuously induced during sleep and, (3) undisturbed sleep (baseline) on pituitary-adrenocortical activity in 10 healthy men. Sleep deprivation (DS) and continuous arousals during sleep (AS) were introduced at the beginning of the second rapid eye movement (REM) sleep period which is an epoch close to the first significant nocturnal rise in plasma cortisol. Compared with the baseline nights, plasma cortisol significantly increased immediately after continuous arousals were started or the subject was awakened and remained awake. Despite this exogenously provoked first cortisol peak, average cortisol release during DS and AS was no higher than during undisturbed sleep. The arousal-induced cortisol burst was followed by a temporary inhibition of cortisol secretion, suggesting that once the subject is aroused (i.e., in stage 1 sleep or awake), the hypothalamus-pituitary-adrenal (HPA) system becomes highly sensitive to negative feedback inhibition. Spontaneously occurring endogenous cortisol peaks of comparable size during undisturbed sleep did not exhibit such a temporary inhibition of cortisol secretion. We hypothesize that sleep attenuates negative feedback inhibition within the HPA system, whereas wakefulness (or stage 1 sleep) reflects increased feedback sensitivity of this system.
Fifteen subjects (9 men and 6 women) exhibiting objective evidence of excessive daytime somnolence and periodic leg movements in sleep underwent 4-7 days of treatment with triazolam (0.25 or 0.50 mg) and placebo in a double-blind crossover design. One night of polysomnography followed by daytime multiple sleep latency testing were conducted on the first and last days of each treatment block. By the last day of treatment, the mean multiple sleep latency test score after triazolam (9.0 minutes) was significantly greater than that after placebo (5.7 minutes). Thus, triazolam treatment led to a decrease in daytime somnolence. Triazolam also improved sleep architecture and continuity; it increased total sleep time, decreased the number of awakenings and arousals, and decreased stage 1 and increased stage 2 percentages. Although the frequency of periodic electromyographic bursts remained unchanged, the frequency of associated arousals decreased after treatment. Short-term treatment with triazolam is thus effective in diminishing daytime sleepiness and in improving sleep architecture, continuity and duration in patients with periodic leg movements in sleep. These effects do not seem to be mediated through a decrease in periodic leg movement activity.
We report the relationship between periodic leg movements during sleep and recurrent rises in systemic blood pressure in a patient with narcolepsy. The mean increase in systolic blood pressure following leg movements was 23%, which is ofthe same order as the rises seen in patients with obstructive sleep apnea. Following treatment with temazepam, the swings in blood pressure were unchanged despite considerably less electroencephalographic evidence of cortical arousal. Key Words: Periodic movement of the legs-Hypertension.
It has been postulated that sleep disruption may change ventilatory chemoresponsiveness to hypercapnia and hypoxia and thereby contribute to the development of respiratory failure in some patients with obstructive sleep apnea syndrome (OSAS) or with other respiratory disorders. Some studies have demonstrated a reduction in ventilatory chemoresponsiveness in normal subjects after one night of total sleep deprivation. However, sleep fragmentation rather than total sleep deprivation is usual in patients. In this study, therefore, we measured hypercapnic ventilatory responsiveness (HCVR) and spirometry in 13 healthy male subjects (18 to 30 yr of age) after two consecutive nights of severe sleep fragmentation (arousal to an auditory stimulus after each minute of sleep) and compared the results with those obtained in the same subjects after normal sleep. Sleep fragmentation and normal sleep were separated by a week, and the order of intervention was randomized from patient to patient. No significant differences were observed in the slope or position of the HCVR curve after sleep fragmentation or in forced expiratory volumes. Although it is possible that a more prolonged period of sleep fragmentation than that used in this study may have an effect on HCVR, the results suggest that sleep fragmentation is an unlikely cause of progressive respiratory failure in patients with OSAS or with other respiratory disorders.
During sleep, mild reduction in inspiratory airflow is associated with snoring, whereas obstructive hypopneas and apneas are associated with more marked reductions in airflow. We determined whether the degree of inspiratory airflow reduction was associated with differences in the collapsibility of the upper airway during sleep. Upper airway collapsibility was defined by the critical pressure (Pcrit) derived from the relationship between maximal inspiratory airflow and nasal pressure. In 10 asymptomatic snorers, six patients with obstructive hypopneas, and 10 patients with obstructive apneas, during nonrapid eye movement sleep, Pcrit ranged from -6.5 +/- 2.7 cm H2O to -1.6 +/- 1.4 and 2.5 +/- 1.5 cm H2O, respectively (mean +/- SD, p less than 0.001). Moreover, higher levels of Pcrit were associated with lower levels of maximal inspiratory airflow during tidal breathing during sleep (p less than 0.005). We conclude that differences in upper airway collapsibility distinguish among groups of normal subjects who snore and patients with periodic hypopneas and apneas. Moreover, the findings suggest that small differences in collapsibility (Pcrit) along a continuum are associated with reduced airflow and altered changes in pattern of breathing.
This study was designed to determine the effects of sleep deprivation on respiratory events during sleep in healthy infants. Ten unsedated full-term infants (1-6 mo) were monitored polygraphically during "afternoon naps" on a control day and on the day after sleep deprivation. Respiratory events, i.e., central apnea, obstructive apnea and hypopnea, and periodic breathing were tabulated. Results for respiratory events were expressed as 1) indexes of the total number of respiratory events and of specific respiratory events per hour of total sleep (TST), "quiet" sleep (QS) and "active" sleep (AS) times; 2) total duration of total and specific respiratory events, expressed as a percentage of TST, QS, and AS times. After sleep deprivation, significant increases were observed for 1) respiratory event (P less than 0.001), central apnea (P less than 0.05), and obstructive respiratory event (P less than 0.01) indexes; 2) respiratory event time as a percentage of TST (P less than 0.002) and as a percentage of AS time (P less than 0.001); 3) obstructive respiratory event time as a percentage of TST (P less than 0.01), QS (P less than 0.05), and AS times (P less than 0.002). The present study shows that short-term sleep deprivation in healthy infants increases the number and timing of respiratory events, especially obstructive events in AS.
Despite the subjective reports of patients with difficulty initiating and maintaining sleep (DIMS) that they are impaired during the day, consistent differences in daytime functions have not been found between normal sleepers and patients with insomnia. The present study compares polysomnography and Multiple Sleep Latency Test (MSLT) data from 70 clinic patients seeking evaluation for chronic insomnia with data from a group of 45 asymptomatic sleepers. The DIMS group was found to sleep significantly less than the control group; yet they were also significantly more alert than the control group the following day, as measured by MSLT. Within the insomnia diagnostic subgroups, a correlation of -0.67 (p less than 0.05) was found between nocturnal total sleep time and mean MSLT. The results are interpreted as supporting the existence of a tendency towards physiological hyperarousal in patients with chronic insomnia. This tendency may be exacerbated by other factors (e.g., personality disorder, periodic leg movements) also associated with insomnia.
Recent research has suggested that sleep fragmentation in the absence of sleep loss is an important cause of excessive daytime sleepiness in certain clinical populations (e.g., sleep apnea syndrome or periodic leg movements). This study experimentally varied the number and rate of arousals in sleep to define more clearly the relation of sleep fragmentation and daytime sleepiness. Five male subjects participated in the study. Data from each were recorded for three consecutive nights (one baseline followed by two experimental nights) under three experimental conditions. All nocturnal polysomnograms were followed by a Multiple Sleep Latency Test (MSLT) the next day. The experimental conditions consisted of three different schedules of arousal produced by series of tones presented to subjects over headphones. The MSLT showed statistically significant changes after two nights of fragmented sleep, but the three fragmentation schedules did not differ from each other. Arousal threshold also changed significantly with sleep fragmentation from night one to night two.
The effects of two levels of sleep fragmentation on sleep and daytime sleepiness were investigated in young adult males. Experimental subjects were informed while awake that tones would be presented periodically throughout the night and that their task was to terminate the tone by taking a deep breath. Eight subjects received tones after each minute of sleep and 8 received tones after each 4 min of sleep. Control subjects (N=8) HI did not receive (ones. The subjects were tested for daytime sleepiness using the Multiple Steep latency Test. It was found that: 1) subjects responded reliably lo tones presented during sleep; 2) behavioral control was accompanied by brief electro-physiological indices of arousal on almost all trials, and occasionally led to fall awakenings; 3) sleep was markedly altered in the 1-min condition; 4) a relatively small effect on sleep (reduced stage 4 sleep) was produced by the 4-min condition, and 5) daytime sleepiness was increased by the 1-min condition but not the 4-min condition. It was concluded that the most parsimonious explanation of these results is (he Continuity of Sleep hypothesis.
Upper airway obstruction is recognized to cause apnoea in newborns as well as in adults. However, very little is known about factors that influence the arousal response from sleep during upper airway obstruction in newborns. Experiments were therefore done to investigate the effect of short-term sleep fragmentation on the arousal response to upper airway obstruction in six lambs aged 8 to 14 days. Each lamb was anaesthetized and instrumented for recordings of electrocorticogram, electro-oculogram, nuchal and diaphragm electromyograms and measurements of systemic arterial blood pressure and oxygen saturation (fiberoptic catheter oximeter). A tracheostomy was done and a fenestrated tracheostomy tube placed in the trachea. Experiments were not done before the third postoperative day. During a study, a 5F balloon tipped catheter was inserted into the tube so that airflow could be obstructed by inflating the balloon. Measurements were made during 30 s control periods and during experimental periods of upper airway obstruction in at least three epochs of quiet sleep and active sleep in each animal. These measurements were made following a period of uninterrupted sleep and repeated following a 36-42 h period of sleep fragmentation. Sleep fragmentation was produced by 30 s of noise separated by 2 min of quiet. Sleep fragmentation produced small but statistically significant increases in the time to arousal and decreases in the haemoglobin oxygen saturation at arousal during upper airway obstruction in quiet sleep but not active sleep. However, these changes, although consistent, were small and are of questionable biological significance. Therefore, I believe it is unlikely that short-term sleep fragmentation per se significantly impairs the arousal response to respiratory stimuli in newborns.
We have previously shown that one night of sleep deprivation results in significant deterioration of spirometric performance and ventilatory responsiveness to inhaled carbon dioxide in normal people. Since even a small decrease in pulmonary function may be clinically important in patients with chronic limitation of airflow, we undertook the present study to assess the effects of sleep loss on breathing in patients with chronic obstructive pulmonary disease (COPD). Criteria for inclusion in this study were a ratio of the forced expiratory volume in one second over the forced vital capacity (FEV1/FVC) of less than 60 percent, no hospital admission for pulmonary disease within two weeks of testing, stable (less than 30 percent variation) in tests of pulmonary function on two occasions within three months of testing, and no history of asthma. We studied 15 men (mean age, 57 +/- 3 years) on two consecutive mornings. Patients were studied with and without sleep deprivation in a randomized fashion. Patients were hospitalized for the study so that sleep deprivation, medications, smoking, and diet could be monitored and enforced. We found small but statistically significant falls in FEV1 (1.06 +/- 0.11 to 1.00 +/- 0.09 L; p less than 0.05) and in FVC (2.56 +/- 0.20 to 2.43 +/- 0.17 L; p less than 0.05) following sleep deprivation. Changes of similar magnitude which were not statistically significant occurred in maximal voluntary ventilation (MVV) and response to carbon dioxide. The arterial oxygen (PaO2) and carbon dioxide (PaCO2) tensions were not affected. Maximal expiratory pressure at the mouth increased slightly, but there was a fall in maximal inspiratory pressure (MIP) at the mouth. We conclude that sleep loss is associated with small but significant falls in FEV1 and FVC, as well as changes of similar magnitude in MVV, minute ventilation, and MIP in patients with severe COPD. Although the sleep loss which frequently accompanies exacerbations of COPD may be a slight additional stress of pulmonary reserve, a single night's loss of sleep in the patient with stable chronic airflow obstruction does not have major clinical consequences.
Ten nonobese, healthy elderly adults (M = 73.3 years) were monitored polygraphically during sleep for sleep state changes, breathing, and the development of cardiac arrhythmias. All participated in 2 baseline nights and 1 night of flurazepam 30 mg ingestion; six underwent 1 night of sleep deprivation; four received ethyl alcohol (.6 mg/kg); and four whose apnea worsened significantly with flurazepam 30 mg were pretreated for 3 days with acetazolamide, taking acetazolamide and flurazepam 30 mg on the fourth night. Elderly adults with an Apnea Index (the number of apneas per sleep hour) between 5 and 7 at baseline experienced a worsening of their apnea with each manipulation. Acetazolamide did not protect individuals whose Apnea Index increased after flurazepam ingestion. One person developed premature ventricular contractions in conjunction with an increased Apnea Index after each manipulation.
To better understand the relation of sleep complaint to sleep continuity and periodic movements during sleep (PMS), two groups of patients were studied retrospectively. One group of 51 patients, 26 men and 25 women, with a mean age of 56.4 years, complained of insomnia. The other group of 29 patients, 20 men and nine women, with a mean age of 55.8 years, complained of excessive daytime sleepiness. Sleepy patients differed significantly from insomnia patients in that they fell asleep faster and slept longer. They showed more frequent arousals (shifts to stage 1 sleep and number of awakenings) than insomnia patients who had longer arousals (mean duration of awakenings). Insomnia patients had more series of PMS, but sleepy patients had more PMS bursts per series.
Sleep in the elderly is known to be disturbed, and many elderly persons also complain of daytime sleepiness. The present study assessed sleep and waking behavior in 12 male (aged 63 to 86) and 12 female (ages 63 to 82) subjects. Sleep stages, respiration, and movement were recorded at night, and daytime sleep tendency was measured using the Multiple Sleep Latency Test during a single 24-hour period. Daytime sleepiness did not correlate with total sleep time or any sleep stage, but was significantly correlated with measures of sleep fragmentation. The latter included transient arousals, a measure of less than 15-sec awakenings, and sleep-related respiration disturbance. These findings suggest that fragmented nocturnal sleep is a significant cause of reduced daytime well-being in elderly individuals. The continuity of both sleep and wakefulness appears to be disrupted with age. Experimental strategies for achieving a rational sleep hygiene are discussed.