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Objective. Intra-esophageal pressure (Pes) measurement is the recommended gold standard to quantify respiratory effort during sleep, but used to limited extent in clinical practice due to multiple practical drawbacks. Respiratory inductance plethysmography belts (RIP) in conjunction with oronasal airflow are the accepted substitute in polysomnographic systems (PSG) thanks to a better usability, although they are partial views on tidal volume and flow rather than true respiratory effort and are often used without calibration. In their place, the pressure variations measured non-invasively at the suprasternal notch (SSP) may provide a better measure of effort. However, this type of sensor has been validated only for respiratory events in the context of obstructive sleep apnea syndrome (OSA). We aim to provide an extensive verification of the suprasternal pressure signal against RIP belts and Pes, covering both normal breathing and respiratory events. Approach. We simultaneously acquired suprasternal (207) and esophageal pressure (20) signals along with RIP belts during a clinical PSG of 207 participants. In each signal, we detected breaths with a custom algorithm, and evaluated the SSP in terms of detection quality, breathing rate estimation, and similarity of breathing patterns against RIP and Pes. Additionally, we examined how the SSP signal may diverge from RIP and Pes in presence of respiratory events scored by a sleep technician. Main results. The SSP signal proved to be a reliable substitute for both esophageal pressure (Pes) and respiratory inductance plethysmography (RIP) in terms of breath detection, with sensitivity and positive predictive value exceeding 75%, and low error in breathing rate estimation. The SSP was also consistent with Pes (correlation of 0.72, similarity 80.8%) in patterns of increasing pressure amplitude that are common in OSA. Significance. This work provides a quantitative analysis of suprasternal pressure sensors for respiratory effort measurements., (Creative Commons Attribution license.)

Study Objectives: Automatic sleep staging based on cardiorespiratory signals from home sleep monitoring devices holds great clinical potential. Using state-of-the-art machine learning, promising performance has been reached in patients with sleep disorders. However, it is unknown whether performance would hold in individuals with potentially altered autonomic physiology, for example under the influence of medication. Here, we assess an existing sleep staging algorithm in patients with sleep disorders with and without the use of beta blockers., Methods: We analyzed a retrospective dataset of sleep recordings of 57 patients with sleep disorders using beta blockers and 57 age-matched patients with sleep disorders not using beta blockers. Sleep stages were automatically scored based on electrocardiography and respiratory effort from a thoracic belt, using a previously developed machine-learning algorithm (CReSS algorithm). For both patient groups, sleep stages classified by the model were compared to gold standard manual polysomnography scoring using epoch-by-epoch agreement. Additionally, for both groups, overall sleep parameters were calculated and compared between the two scoring methods., Results: Substantial agreement was achieved for four-class sleep staging in both patient groups (beta blockers: kappa = 0.635, accuracy = 78.1%; controls: kappa = 0.660, accuracy = 78.8%). No statistical difference in epoch-by-epoch agreement was found between the two groups. Additionally, the groups did not differ on agreement of derived sleep parameters., Conclusions: We showed that the performance of the CReSS algorithm is not deteriorated in patients using beta blockers. Results do not indicate a fundamental limitation in leveraging autonomic characteristics to obtain a surrogate measure of sleep in this clinically relevant population., Citation: Hermans L, van Meulen F, Anderer P, et al. Performance of cardiorespiratory-based sleep staging in patients using beta blockers. J Clin Sleep Med . 2024;20(4):575-581., (© 2024 American Academy of Sleep Medicine.)

Objective . Unobtrusive long-term monitoring of cardiac parameters is important in a wide variety of clinical applications, such as the assesment of acute illness severity and unobtrusive sleep monitoring. Here we determined the accuracy and robustness of heartbeat detection by an accelerometer worn on the chest. Approach . We performed overnight recordings in 147 individuals (69 female, 78 male) referred to two sleep centers. Two methods for heartbeat detection in the acceleration signal were compared: one previously described approach, based on local periodicity, and a novel extended method incorporating maximum a posteriori estimation and a Markov decision process to approach an optimal solution. Main results estimation significantly improved performance, with a mean absolute error for the estimation of inter-beat intervals of only 3.5 ms, and 95% limits of agreement of -1.7 to +1.0 beats per minute for heartrate measurement. Performance held during posture changes and was only weakly affected by the presence of sleep disorders and demographic factors. a . The new method may enable the use of a chest-worn accelerometer in a variety of applications such as ambulatory sleep staging and in-patient monitoring.posteriori estimation significantly improved performance, with a mean absolute error for the estimation of inter-beat intervals of only 3.5 ms, and 95% limits of agreement of -1.7 to +1.0 beats per minute for heartrate measurement. Performance held during posture changes and was only weakly affected by the presence of sleep disorders and demographic factors. Significance . The new method may enable the use of a chest-worn accelerometer in a variety of applications such as ambulatory sleep staging and in-patient monitoring., (Creative Commons Attribution license.)

Sleep staging is the process by which an overnight polysomnographic measurement is segmented into epochs of 30 seconds, each of which is annotated as belonging to one of five discrete sleep stages. The resulting scoring is graphically depicted as a hypnogram, and several overnight sleep statistics are derived, such as total sleep time and sleep onset latency. Gold standard sleep staging as performed by human technicians is time-consuming, costly, and comes with imperfect inter-scorer agreement, which also results in inter-scorer disagreement about the overnight statistics. Deep learning algorithms have shown promise in automating sleep scoring, but struggle to model inter-scorer disagreement in sleep statistics. To that end, we introduce a novel technique using conditional generative models based on Normalizing Flows that permits the modeling of the inter-rater disagreement of overnight sleep statistics, termed U-Flow. We compare U-Flow to other automatic scoring methods on a hold-out test set of 70 subjects, each scored by six independent scorers. The proposed method achieves similar sleep staging performance in terms of accuracy and Cohen's kappa on the majority-voted hypnograms. At the same time, U-Flow outperforms the other methods in terms of modeling the inter-rater disagreement of overnight sleep statistics. The consequences of inter-rater disagreement about overnight sleep statistics may be great, and the disagreement potentially carries diagnostic and scientifically relevant information about sleep structure. U-Flow is able to model this disagreement efficiently and can support further investigations into the impact inter-rater disagreement has on sleep medicine and basic sleep research.

Objective. The accurate detection of respiratory effort during polysomnography is a critical element in the diagnosis of sleep-disordered breathing conditions such as sleep apnea. Unfortunately, the sensors currently used to estimate respiratory effort are either indirect and ignore upper airway dynamics or are too obtrusive for patients. One promising alternative is the suprasternal notch pressure (SSP) sensor: a small element placed on the skin in the notch above the sternum within an airtight capsule that detects pressure swings in the trachea. Besides providing information on respiratory effort, the sensor is sensitive to small cardiac oscillations caused by pressure perturbations in the carotid arteries or the trachea. While current clinical research considers these as redundant noise, they may contain physiologically relevant information. Approach. We propose a method to separate the signal generated by cardiac activity from the one caused by breathing activity. Using only information available from the SSP sensor, we estimate the heart rate and track its variations, then use a set of tuned filters to process the original signal in the frequency domain and reconstruct the cardiac signal. We also include an overview of the technical and physiological factors that may affect the quality of heart rate estimation. The output of our method is then used as a reference to remove the cardiac signal from the original SSP pressure signal, to also optimize the assessment of respiratory activity. We provide a qualitative comparison against methods based on filters with fixed frequency cutoffs. Main results. In comparison with electrocardiography (ECG)-derived heart rate, we achieve an agreement error of 0.06 ± 5.09 bpm, with minimal bias drift across the measurement range, and only 6.36% of the estimates larger than 10 bpm. Significance. Together with qualitative improvements in the characterization of respiratory effort, this opens the development of novel portable clinical devices for the detection and assessment of sleep disordered breathing., (Creative Commons Attribution license.)

Objective. The recently-introduced hypnodensity graph provides a probability distribution over sleep stages per data window (i.e. an epoch). This work explored whether this representation reveals continuities that can only be attributed to intra- and inter-rater disagreement of expert scorings, or also to co-occurrence of sleep stage-dependent features within one epoch. Approach. We proposed a simplified model for time series like the ones measured during sleep, and a second model to describe the annotation process by an expert. Generating data according to these models, enabled controlled experiments to investigate the interpretation of the hypnodensity graph. Moreover, the influence of both the supervised training strategy, and the used softmax non-linearity were investigated. Polysomnography recordings of 96 healthy sleepers (of which 11 were used as independent test set), were subsequently used to transfer conclusions to real data. Main results. A hypnodensity graph, predicted by a supervised neural classifier, represents the probability with which the sleep expert(s) assigned a label to an epoch. It thus reflects annotator behavior, and is thereby only indirectly linked to the ratio of sleep stage-dependent features in the epoch. Unsupervised training was shown to result in hypnodensity graph that were slightly less dependent on this annotation process, resulting in, on average, higher-entropy distributions over sleep stages ( H unsupervised = 0.29). Moreover, pre-softmax predictions were, for both training strategies, found to better reflect the ratio of sleep stage-dependent characteristics in an epoch, as compared to the post-softmax counterparts (i.e. the hypnodensity graph). In real data, this was observed from the linear relation between pre-softmax N3 predictions and the amount of delta power. H This study provides insights in, and proposes new, representations of sleep that may enhance our comprehension about sleep and sleep disorders.supervised = 0.29). Moreover, pre-softmax predictions were, for both training strategies, found to better reflect the ratio of sleep stage-dependent characteristics in an epoch, as compared to the post-softmax counterparts (i.e. the hypnodensity graph). In real data, this was observed from the linear relation between pre-softmax N3 predictions and the amount of delta power. Significance. This study provides insights in, and proposes new, representations of sleep that may enhance our comprehension about sleep and sleep disorders., (Creative Commons Attribution license.)

Sleep is characterized by an intricate variation of brain activity over time. Measuring these temporal sleep dynamics is relevant for elucidating healthy and pathological sleep mechanisms. The rapidly increasing possibilities for obtaining and processing sleep registrations have led to an abundance of data, which can be challenging to analyze and interpret. This review provides a structured overview of approaches to represent temporal sleep dynamics, categorized based on the way the source data is compressed. For each category of representations, we describe advantages and disadvantages. Standard human-defined 30-s sleep stages have the advantages of standardization and interpretability. Alternative human-defined representations are less standardized but offer a higher temporal resolution (in case of microstructural events such as sleep spindles), or reflect non-categorical information (for example spectral power analysis). Machine-learned representations offer additional possibilities: automated sleep stages are useful for handling large quantities of data, while alternative sleep stages obtained from clustering data-driven features could aid finding new patterns and new possible clinical interpretations. While newly developed sleep representations may offer relevant insights, they can be difficult to interpret in for example a clinical context. Therefore, there should always be a balance between developing these sophisticated sleep analysis techniques and maintaining clinical explainability., Competing Interests: Conflicts of interest This work has been performed in the IMPULS framework of the Eindhoven MedTech Innovation Center (e/MTIC, incorporating Eindhoven University of Technology, Philips Research, Sleep Medicine Center Kempenhaeghe). The funders had no role in the study design, decision to publish, or preparation of the manuscript. Philips Research provided support in the form of a salary for authors LWAH, TRML and PF, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. This activity is in part funded by the PPS program research and innovation of the Dutch ministry of Economic affairs and Climate., (Copyright © 2022 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Rest-activity patterns are important aspects of healthy sleep and may be disturbed in conditions like circadian rhythm disorders, insomnia, insufficient sleep syndrome, and neurological disorders. Long-term monitoring of rest-activity patterns is typically performed with diaries or actigraphy. Here, we propose an unobtrusive method to obtain rest-activity patterns using smartphone keyboard activity. The present study investigated whether this proposed method reliably estimates rest and activity timing compared to daily self-reports within healthy participants. First-year students (n = 51) used a custom smartphone keyboard to passively and objectively measure smartphone use behaviours and completed the Consensus Sleep Diary for 1 week. The time of the last keyboard activity before a nightly absence of keystrokes, and the time of the first keyboard activity following this period were used as markers. Results revealed high correlations between these markers and user-reported onset and offset of resting period (r ranged from 0.74 to 0.80). Linear mixed models could estimate onset and offset of resting periods with reasonable accuracy (R 2 ranged from 0.60 to 0.66). This indicates that smartphone keyboard activity can be used to estimate rest-activity patterns. In addition, effects of chronotype and type of day were investigated. Implementing this method in longitudinal studies would allow for long-term monitoring of (disturbances to) rest-activity patterns, without user burden or additional costly devices. It could be particularly interesting to replicate these findings in studies amongst clinical populations with sleep-related problems, or in populations for whom disturbances in rest-activity patterns are secondary complaints, such as neurological disorders., (© 2021 Neurocast BV. Journal of Sleep Research published by John Wiley & Sons Ltd on behalf of European Sleep Research Society.)

Polysomnography (PSG) is the current gold standard for the diagnosis of sleep disorders. However, this multi-parametric sleep monitoring tool also has some drawbacks, e.g. it limits the patient's mobility during the night and it requires the patient to come to a specialized sleep clinic or hospital to attach the sensors. Unobtrusive techniques for the detection of sleep disorders such as sleep apnea are therefore gaining increasing interest. Remote photoplethysmography using video is a technique which enables contactless detection of hemodynamic information. Promising results in near-infrared have been reported for the monitoring of sleep-relevant physiological parameters pulse rate, respiration and blood oxygen saturation. In this study we validate a contactless monitoring system on eight patients with a high likelihood of relevant obstructive sleep apnea, which are enrolled for a sleep study at a specialized sleep center. The dataset includes 46.5 hours of video recordings, full polysomnography and metadata. The camera can detect pulse and respiratory rate within 2 beats/breaths per minute accuracy 92% and 91% of the time, respectively. Estimated blood oxygen values are within 4 percentage points of the finger-oximeter 89% of the time. These results demonstrate the potential of a camera as a convenient diagnostic tool for sleep apnea, and sleep disorders in general.

Study Objectives: While poor sleep quality has been related to increased risk of Alzheimer's disease, long-time shift workers (maritime pilots) did not manifest evidence of early Alzheimer's disease in a recent study. We explored two hypotheses of possible compensatory mechanisms for sleep disruption: Increased efficiency in generating deep sleep during workweeks (model 1) and rebound sleep during rest weeks (model 2)., Methods: We used data from ten male maritime pilots (mean age: 51.6±2.4 years) with a history of approximately 18 years of irregular shift work. Subjective sleep quality was assessed with the Pittsburgh Sleep Quality Index (PSQI). A single lead EEG-device was used to investigate sleep in the home/work environment, quantifying total sleep time (TST), deep sleep time (DST), and deep sleep time percentage (DST%). Using multilevel models, we studied the sleep architecture of maritime pilots over time, at the transition of a workweek to a rest week., Results: Maritime pilots reported worse sleep quality in workweeks compared to rest weeks (PSQI = 8.2±2.2 vs. 3.9±2.0; p<0.001). Model 1 showed a trend towards an increase in DST% of 0.6% per day during the workweek (p = 0.08). Model 2 did not display an increase in DST% in the rest week (p = 0.87)., Conclusions: Our findings indicated that increased efficiency in generating deep sleep during workweeks is a more likely compensatory mechanism for sleep disruption in the maritime pilot cohort than rebound sleep during rest weeks. Compensatory mechanisms for poor sleep quality might mitigate sleep disruption-related risk of developing Alzheimer's disease. These results should be used as a starting point for future studies including larger, more diverse populations of shift workers., Competing Interests: The authors declare that Philips (Royal Philips, Amsterdam, The Netherlands) kindly lent us the home-EEG devices that were used in this study. This does not alter our adherence to PLOS ONE policies on sharing data and materials. Philips had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Introduction: Polysomnography (PSG) is the primary tool for sleep monitoring and the diagnosis of sleep disorders. Recent advances in signal analysis make it possible to reveal more information from this rich data source. Furthermore, many innovative sleep monitoring techniques are being developed that are less obtrusive, easier to use over long time periods and in the home situation. Here, we describe the methods of the Sleep and Obstructive Sleep Apnoea Monitoring with Non-Invasive Applications (SOMNIA) project, yielding a database combining clinical PSG with advanced unobtrusive sleep monitoring modalities in a large cohort of patients with various sleep disorders. The SOMNIA database will facilitate the validation and assessment of the diagnostic value of the new techniques, as well as the development of additional indices and biomarkers derived from new and/or traditional sleep monitoring methods., Methods and Analysis: We aim to include at least 2100 subjects (both adults and children) with a variety of sleep disorders who undergo a PSG as part of standard clinical care in a dedicated sleep centre. Full-video PSG will be performed according to the standards of the American Academy of Sleep Medicine. Each recording will be supplemented with one or more new monitoring systems, including wrist-worn photoplethysmography and actigraphy, pressure sensing mattresses, multimicrophone recording of respiratory sounds including snoring, suprasternal pressure monitoring and multielectrode electromyography of the diaphragm., Ethics and Dissemination: The study was reviewed by the medical ethical committee of the Maxima Medical Center (Eindhoven, the Netherlands, File no: N16.074). All subjects provide informed consent before participation.The SOMNIA database is built to facilitate future research in sleep medicine. Data from the completed SOMNIA database will be made available for collaboration with researchers outside the institute., Competing Interests: Competing interests: PF, TL, HM, RH, JWMB and LvdH are employees of Philips Research. CL is employee of 2M Engineering., (© Author(s) (or their employer(s)) 2019. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Objective: To date, there is little information on how lay people understand and discuss sleep in the context of daily life. Efforts to conceptualize sleep quality have been largely driven by clinical considerations of sleep disorders. As such, they are not necessarily of how normal sleepers without clinical expertise conceptualize sleep quality. A phenomenological approach was taken to understand the essence of the sleep experience and the concepts held by lay people without sleep disorders. A sentence completion questionnaire was developed and administered to a quota sample of 64 respondents who were selected aiming for sufficient representation of different gender, ages, and education levels., Results: Significant sentences and meaningful units were derived inductively, resulting in a classification of nine categories. The major facets of sleep experience of lay people were 'daytime functioning', 'interruptions during the night' and 'before bed state'. This implies that the experienced sleep quality is not only depending on the progress of the night. These results can guide future research to provide suitable psychometric measures for normal sleepers, as well as the design of sleep data visualization applications in the context of health self-monitoring.

Background: Upon awaking, many Parkinson's patients experience an improved mobility, a phenomenon known as 'sleep benefit'. Despite the potential clinical relevance, no objective correlates of sleep benefit exist. The discrepancy between the patients' subjective experience of improvement in absence of objective changes is striking, and raises questions about the nature of sleep benefit. We aimed to clarify what patients reporting subjective sleep benefit, actually experience when waking up. Furthermore, we searched for factors associated with subjective sleep benefit., Methods: Using a standardized topic list, we interviewed 14 Parkinson patients with unambiguous subjective sleep benefit, selected from a larger questionnaire-based cohort. A grounded theory approach was used to analyse the data., Results: A subset of the participants described a temporary decrease in their Parkinson motor symptoms after sleep. Others did experience beneficial effects which were, however, non-specific for Parkinson's disease (e.g. feeling 'rested'). The last group misinterpreted the selection questionnaire and did not meet the definition of sleep benefit for various reasons. There were no general sleep-related factors that influenced the presence of sleep benefit. Factors mentioned to influence functioning at awakening were mostly stress related., Conclusions: The group of participants convincingly reporting sleep benefit in the selection questionnaire appeared to be very heterogeneous, with only a portion of them describing sleep benefit on motor symptoms. The group of participants actually experiencing motor sleep benefit may be much smaller than reported in the literature so far. Future studies should employ careful inclusion criteria, which could be based on our reported data.

Monitoring of respiratory effort is paramount in the clinical diagnostic recording of sleep. Increased respiratory effort is a sign of obstructive sleep-disordered breathing and is associated with arousals from sleep. Respiration is the result of muscle activity that induces negative intrathoracic pressure and expansion of the thoracic and abdominal cavities. Therefore respiratory effort may be recorded from mechanical, electrical and electromechanical signals. Several techniques are available for the recording of respiratory effort. Monitoring of esophageal pressure is still the method of choice, as the pressure signal directly reflects the respiratory muscle force. However, esophageal pressure monitoring is cumbersome and may be replaced with noninvasive techniques. In order to be reliable, these techniques must be validated against the esophageal pressure standard. The present review presents a concise description of the technical principles and, if available, a comparison with esophageal pressure data, based on a systematic literature search. Most data are available on respiratory inductance plethysmography, and confirm that this technique is suitable for routine diagnostic investigation of respiratory effort during sleep. Pulse transit time, diaphragmatic electromyography, snoring loudness, suprasternal pressure monitoring, midsagittal jaw movement and forehead venous pressure monitoring are promising alternative techniques although only limited validation is available., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Study Objectives: Many people with Parkinson disease experience "sleep benefit": temporarily improved mobility upon awakening. Here we used quantitative motor tasks to assess the influence of sleep on motor functioning in Parkinson disease., Design: Eighteen Parkinson patients with and 20 without subjective sleep benefit and 20 healthy controls participated. Before and directly after a regular night sleep and an afternoon nap, subjects performed the timed pegboard dexterity task and quantified finger tapping task. Subjective ratings of motor functioning and mood/vigilange were included. Sleep was monitored using polysomnography., Results: On both tasks, patients were overall slower than healthy controls (night: F2,55 = 16.938, P < 0.001; nap: F2,55 = 15.331, P < 0.001). On the pegboard task, there was a small overall effect of night sleep (F1,55 = 9.695, P = 0.003); both patients and controls were on average slightly slower in the morning. However, in both tasks there was no sleep*group interaction for nighttime sleep nor for afternoon nap. There was a modest correlation between the score on the pegboard task and self-rated motor symptoms among patients (rho = 0.233, P = 0.004). No correlations in task performance and mood/vigilance or sleep time/efficiency were found., Conclusions: A positive effect of sleep on motor function is commonly reported by Parkinson patients. Here we show that the subjective experience of sleep benefit is not paralleled by an actual improvement in motor functioning. Sleep benefit therefore appears to be a subjective phenomenon and not a Parkinson-specific reduction in symptoms., (© 2015 Associated Professional Sleep Societies, LLC.)

Background: Parkinson's disease (PD) patients may experience 'sleep benefit' (SB): a temporarily improved mobility upon awakening. SB has mainly been studied retrospectively using questionnaires, but it remains unclear whether it is associated with actual changes in motor functioning., Methods: We performed a prospective study on sleep-related changes in motor functioning, using a PD symptom diary during 7 days in 240 randomly selected PD patients (140 men; 66.8 ± 9.6 years; disease duration 9.3 ± 6.2 years). Afterwards, patients received a questionnaire on the possible subjective experience of SB., Results: Using the PD symptom diary, a positive change in motor function was observed after 267 nights (17.8%) and after 138 daytime naps (23.4%). Based on these results, 75 patients (32%) were classified as having SB. In response to the subsequent questionnaire, 73 patients (31%) reported SB. Interestingly, the groups with SB according to either the diary or the questionnaire overlapped only partially: outcomes were congruent in 63% of subjects (both negative 49%, both positive 14%). In both the diary and questionnaire, patients with SB showed a longer disease duration and longer medication use. According to the questionnaire, there was a trend towards a shorter sleep duration and lower sleep efficiency in the SB group. The mean change in motor function after sleep as assessed using the diary was higher in patients reporting subjective SB., Conclusion: We show that the subjective experience of SB in PD is not always related to an actual increase in reported motor function after sleep. Defining SB using either a symptom diary or a questionnaire on subjective experience, results in only partly overlapping groups. These data suggest that SB may be a more heterogeneous phenomenon than previously thought and that subjective experience of symptom severity is not necessarily related to actual motor function.

Cognitive behavioral treatment is the gold standard treatment for insomnia, although a substantial group does not respond. We examined possible predictors for treatment outcome in psychophysiological insomniacs, with a focus on the presence of clearly defined psychiatric comorbidity. This was a longitudinal uncontrolled case series study comprising 60 patients with chronic psychophysiological insomnia consecutively referred to a tertiary sleep medicine center, to receive cognitive behavioral treatment for insomnia (CBT-I). Remission of insomnia was defined as a posttreatment Insomnia Severity Index score below 8. As an alternative outcome, we used a clinically relevant decrease on the Insomnia Severity Index (drop of > 7 points). Personality, coping, and social support questionnaires were assessed before the start of the treatment and were compared between treatment responders and nonresponders. To examine whether these variables were predictive for negative treatment outcome, logistic regression analyses were applied. Treatment nonresponders had a significantly higher prevalence of psychiatric comorbidity. Logistic regression analyses showed that the presence of psychiatric comorbidity was strongly predictive for negative treatment outcome (odds ratios: 20.6 and 10.3 for the 2 outcome definitions). Additionally, higher scores on the cognitive coping strategy called "refocus on planning" were associated with worse CBT-I outcome. Current psychiatric comorbidity is strongly predictive for negative treatment outcome. The presence of a psychiatric disorder must therefore be one of the leading arguments in the choice of treatment modalities that are being proposed to patients with insomnia.

Introduction: There is a need for prodromal markers to diagnose Parkinson's disease (PD) as early as possible. Knowing that most patients with overt PD have abnormal nocturnal movement patterns, we hypothesised that such changes might occur already in non-PD individuals with a potentially high risk for future development of the disease., Methods: Eleven patients with early PD (Hoehn & Yahr stage ≤2.5), 13 healthy controls and 33 subjects with a high risk of developing PD (HR-PD) were investigated. HR-PD was defined by the occurrence of hyperechogenicity of the substantia nigra in combination with prodromal markers (eg, slight motor signs, olfactory dysfunction). A triaxial accelerometer was used to quantify nocturnal movements during two nights per study participant. Outcome measurements included mean acceleration, and qualitative axial movement parameters, such as duration and speed., Results: Mean acceleration of nocturnal movements was lower in patients with PD compared to controls. Frequency and speed of axial movements did not differ between patients with PD and controls, but mean size and duration were lower in PD. The HR-PD group did not significantly differ from the control group in any of the parameters analysed., Conclusions: Compared with controls, patients with PD had an overall decreased mean acceleration, as well as smaller and shorter nocturnal axial movements. These changes did not occur in our potential HR-PD individuals, suggesting that relevant axial movement alterations during sleep have either not developed or cannot be detected by the means applied in this at-risk cohort., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

Importance: Increasing evidence suggests a relationship between poor sleep and the risk of developing Alzheimer disease. A previous study found an effect of sleep on β-amyloid (Aβ), which is a key protein in Alzheimer disease pathology., Objective: To determine the effect of 1 night of total sleep deprivation on cerebrospinal fluid Aβ42 protein levels in healthy middle-aged men., Design, Setting, and Participants: The Alzheimer, Wakefulness, and Amyloid Kinetics (AWAKE) study at the Radboud Alzheimer Center, a randomized clinical trial that took place between June 1, 2012, and October 1, 2012. Participants were cognitively normal middle-aged men (40-60 years of age) with normal sleep (n = 26) recruited from the local population., Interventions: Participants were randomized to 1 night with unrestricted sleep (n = 13) or 1 night of total sleep deprivation (24 hours of wakefulness) (n = 13)., Main Outcomes and Measures: Sleep was monitored using continuous polysomnographic recording from 3 pm until 10 am. Cerebrospinal fluid samples were collected using an intrathecal catheter at defined times to compare cerebral Aβ42 concentrations between evening and morning., Results: A night of unrestricted sleep led to a 6% decrease in Aβ42 levels of 25.3 pg/mL (95% CI [0.94, 49.6], P = .04), whereas sleep deprivation counteracted this decrease. When accounting for the individual trajectories of Aβ42 over time, a difference of 75.8 pg/mL of Aβ42 was shown between the unrestricted sleep and sleep deprivation group (95% CI [3.4, 148.4], P = .04). The individual trajectories of evening and morning Aβ42 concentrations differed between the unrestricted sleep and sleep deprivation groups (P = .04) in contrast to stable Aβ40, tau, and total protein levels., Conclusions and Relevance: Sleep deprivation, or prolonged wakefulness, interferes with a physiological morning decrease in Aβ42. We hypothesize that chronic sleep deprivation increases cerebral Aβ42 levels, which elevates the risk of Alzheimer disease., Trial Registration: clinicaltrials.gov Identifier: NCT01194713.

Sleep benefit in Parkinson's disease is characterized by restoration of mobility upon awakening from sleep and prior to drug intake. With this study, we aimed at assessing clinical and nocturnal sleep correlates of this phenomenon. We recorded motor and non-motor symptoms in 131 Parkinson patients with and without sleep benefit, as assessed by questionnaires. Polysomnography recordings were performed in 60 of these patients. Thirty-nine Parkinson patients (30%) reported sleep benefit. Motor symptoms, measures of sleepiness, fatigue, depression, anxiety, sleep-wake disorders, and dopaminergic treatment were not associated with sleep benefit, and most polysomnography measures were similar between both groups. However, Parkinson patients with sleep benefit had shorter total sleep times and longer sleep latencies at nocturnal polysomnography. The link between the occurrence of sleep benefit and shorter nocturnal sleep in Parkinson's disease remains unclear., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

A host of animal work demonstrates that the retention benefit for emotionally aversive over neutral memories is regulated by glucocorticoid action during memory consolidation. Particularly, glucocorticoids may affect systems-level processes that promote the gradual reorganization of emotional memory traces. These effects remain largely uninvestigated in humans. Therefore, in this functional magnetic resonance imaging study we administered hydrocortisone during a polysomnographically monitored night of sleep directly after healthy volunteers studied negative and neutral pictures in a double-blind, placebo-controlled, between-subjects design. The following evening memory consolidation was probed during a recognition memory test in the MR scanner by assessing the difference in brain activity associated with memory for the consolidated items studied before sleep and new, unconsolidated items studied shortly before test (remote vs. recent memory paradigm). Hydrocortisone administration resulted in elevated cortisol levels throughout the experimental night with no group difference at recent encoding or test. Behaviorally, we showed that cortisol enhanced the difference between emotional and neutral consolidated memory, effectively prioritizing emotional memory consolidation. On a neural level, we found that cortisol reduced amygdala reactivity related to the retrieval of these same consolidated, negative items. These findings show that cortisol administration during first post-encoding sleep had a twofold effect on the first 24h of emotional memory consolidation. While cortisol prioritized recognition memory for emotional items, it reduced reactivation of the neural circuitry underlying emotional responsiveness during retrieval. These findings fit recent theories on emotional depotentiation following consolidation during sleep, although future research should establish the sleep-dependence of this effect. Moreover, our data may shed light on mechanisms underlying potential therapeutic effects of cortisol administration following psychological trauma., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Sleep disorders are common among patients with Parkinson's disease (PD). However, there are also reports of PD patients experiencing a beneficial effect of sleep. Upon awaking in the morning some patients experience good mobility, as if they are in an "on" state induced by medication, contrary to what would be expected after a night without medication. This intriguing phenomenon is known as sleep benefit. Here, we review the available research on sleep benefit in PD, describing its prevalence, clinical effects and determinants. We also discuss the possible mechanisms underlying sleep benefit, and the potential clinical applicability. Finally, we propose a new definition of sleep benefit to allow for improved standardization and homogeneity in future research. Important research targets include the development of objective measures of sleep benefit, as a basis for obtaining a better understanding of sleep benefit, its underlying mechanisms and its potential therapeutic application., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

AD, sleep and circadian rhythm physiology display an intricate relationship. On the one hand, AD pathology leads to sleep and circadian disturbances, with a clear negative influence on quality of life. On the other hand, there is increasing evidence that both sleep and circadian regulating systems exert an influence on AD pathology. In this review we describe the impairments of both sleep regulating systems and circadian rhythms in AD and their link to clinical symptoms, as this may increase knowledge on appropriate diagnosis and adequate treatment of sleep problems in AD. Furthermore we discuss how sleep regulating systems, and especially neurotransmitters such as melatonin and hypocretin, may affect AD pathophysiology, as this may provide a role for lack of sleep and circadian rhythm deterioration in the onset of AD., (Copyright © 2012 Elsevier B.V. All rights reserved.)

Some patients with Parkinson's disease (PD) reportedly experience 'sleep benefit': an improved motor functioning upon awaking in the morning. In this questionnaire study, 114 out of 243 consecutive outpatients with PD (46.9%) subjectively experienced sleep benefit. Among those patients that regularly took an afternoon nap, 33.7% experienced sleep benefit after the nap as well. Between patients with and without sleep benefit, there were no differences in demographic or clinical variables, including age, disease duration, dopaminergic treatment, and nocturnal sleep quality. Sleep benefit remains an intriguing but elusive phenomenon, which deserves renewed attention and further research.

Narcolepsy is a sleep disorder caused by disruption of hypocretin (orexin) neurotransmission. Injection of hypocretin-1 acutely suppresses TRH and TSH release in rats. In contrast, subchronic administration does not appear to affect the hypothalamo-pituitary-thyroid ensemble in animals. We explored (in 7 patients and 7 controls) whether hypocretin deficiency impacts circulating TSH levels and circadian timing of TSH release in narcoleptic humans. Plasma TSH concentration profiles (blood samples taken at 10-min intervals during 24 h) and TSH levels in response to TRH injection were analyzed by Cluster, robust regression, approximate entropy (ApEn), and deconvolution. Circulating TSH levels were lower in patients, which was primarily attributable to lower pulse amplitude and nadir concentrations. TSH secretion correlated positively with mean 24-h leptin levels (R2 = 0.46, P = 0.02) and negatively with amount of sleep (R2 = 0.29, P = 0.048). Pattern-synchrony between 24-h leptin and TSH concentrations was demonstrated by significant cross-correlation and cross-ApEn analyses with no differences between controls and patients. Sleep onset was closely associated with a fall in circulating TSH. Features of diurnal rhythmicity of circulating TSH fluctuations were similar in patients and controls, with the acrophase occurring shortly after midnight. Thyroxine and triiodothyronine concentrations were similar in patients and controls and did not display a diurnal rhythm. The response of plasma TSH levels to TRH was also similar in both groups. Sleep patterns in narcoleptics were significantly disorderly compared with controls, as measured by ApEn (P = 0.006). In summary, circulating TSH concentrations are low in hypocretin-deficient narcoleptic men, which could be attributable to their low plasma leptin levels and/or their abnormal sleep-wake cycle.

Purpose of Review: Narcolepsy is a sleep disorder characterized by excessive daytime sleepiness and cataplexy. The discovery that the majority of human patients lack the hypothalamic neuropeptide hypocretin-1 has initiated a large body of new research., Recent Findings: Several studies on cerebrospinal fluid hypocretin-1 levels in narcolepsy and in various other sleep disorders have shown that hypocretin deficiency is both highly sensitive and specific for narcolepsy/cataplexy. Importantly, 15% of narcoleptic patients show low hypocretin levels, despite a negative multiple sleep latency test. Besides regulating sleep, the hypocretin system is involved in the regulation of energy balance, autonomic function and several neuroendocrine ensembles. Consequently, up to one-third of patients are obese (body mass index > 30). Furthermore, serum leptin levels are decreased in both nonoverweight and obese patients. The new rodent models for narcolepsy may aid in the further characterization of these endocrinological abnormalities. Finally, there is increasing insight into the physiological role of the hypocretin system in the regulation of sleep and wakefulness., Summary: Hypocretin measurements may now be applied as a new diagnostic tool, providing the results are interpreted within the clinical context. In the clinical care of narcoleptic patients, attention should be paid to the obesity that frequently accompanies the disorder. In the future, hypocretin agonists may become available. Further characterization of animal models for narcolepsy will undoubtedly increase our insight into the pathophysiology of the disorder., (Copyright 2002 Lippincott Williams & Wilkins)

Background: The reported prevalence of insomnia symptoms in people with intellectual disabilities varies greatly, possibly due to the lack of a common definition. This article provides an overview of the different definitions used and formulates key points for a general definition. Methods: A literature search was performed. An overview of the definitions used was given and compared to the third edition of the international classification of sleep disorders. Results: The search yielded 16 studies. No uniform definition was used. Terminology and cut-off points of insomnia symptoms differed. Insomnia symptoms were mostly described as night-time problems. A minority of studies incorporated daytime consequences. Conclusion: An insomnia disorder entails more than merely night-time complaints and should include daytime consequences. A general definition is warranted. This definition should focus on night-time and daytime insomnia symptoms, incorporate subjective features, and discuss the use of objective measurements and influence of environmental circumstances.

Summary: Automatic estimation of sleep structure is an important aspect in moving sleep monitoring from clinical laboratories to people's homes. However, the transition to more portable systems should not happen at the expense of important physiological signals, such as respiration. Here, we propose the use of cardiorespiratory signals obtained by a suprasternal pressure (SSP) sensor to estimate sleep stages. The sensor is already used for diagnosis of sleep‐disordered breathing (SDB) conditions, but besides respiratory effort it can detect cardiac vibrations transmitted through the trachea. We collected the SSP sensor signal in 100 adults (57 male) undergoing clinical polysomnography for suspected sleep disorders, including sleep apnea syndrome, insomnia, and movement disorders. Here, we separate respiratory effort and cardiac activity related signals, then input these into a neural network trained to estimate sleep stages. Using the original mixed signal the results show a moderate agreement with manual scoring, with a Cohen's kappa of 0.53 in Wake/N1–N2/N3/rapid eye movement sleep discrimination and 0.62 in Wake/Sleep. We demonstrate that decoupling the two signals and using the cardiac signal to estimate the instantaneous heart rate improves the process considerably, reaching an agreement of 0.63 and 0.71. Our proposed method achieves high accuracy, specificity, and sensitivity across different sleep staging tasks. We also compare the total sleep time calculated with our method against manual scoring, with an average error of −1.83 min but a relatively large confidence interval of ±55 min. Compact systems that employ the SSP sensor information‐rich signal may enable new ways of clinical assessments, such as night‐to‐night variability in obstructive sleep apnea and other sleep disorders. [ABSTRACT FROM AUTHOR]

The classification of sleep state in preterm infants, particularly in distinguishing between active sleep (AS) and quiet sleep (QS), has been investigated using cardiorespiratory information such as electrocardiography (ECG) and respiratory signals. However, accurately differentiating between AS and wake remains challenging; therefore, there is a pressing need to include additional information to further enhance the classification performance. To address the challenge, this study explores the effectiveness of incorporating video-based actigraphy analysis alongside cardiorespiratory signals for classifying the sleep states of preterm infants. The study enrolled eight preterm infants, and a total of 91 features were extracted from ECG, respiratory signals, and video-based actigraphy. By employing an extremely randomized trees (ET) algorithm and leave-one-subject-out cross-validation, a kappa score of 0.33 was achieved for the classification of AS, QS, and wake using cardiorespiratory features only. The kappa score significantly improved to 0.39 when incorporating eight video-based actigraphy features. Furthermore, the classification performance of AS and wake also improved, showing a kappa score increase of 0.21. These suggest that combining video-based actigraphy with cardiorespiratory signals can potentially enhance the performance of sleep-state classification in preterm infants. In addition, we highlighted the distinct strengths and limitations of video-based actigraphy and cardiorespiratory data in classifying specific sleep states. [ABSTRACT FROM AUTHOR]

Instantaneous heart rate (IHR) has been investigated for sleep applications, such as sleep apnea detection and sleep staging. To ensure the comfort of the patient during sleep, it is desirable for IHR to be measured in a contact-free fashion. In this work, we use speckle vibrometry (SV) to perform on-skin and on-textile IHR monitoring in a sleep setting. Minute motions on the laser-illuminated surface can be captured by a defocused camera, enabling the detection of cardiac motions even on textiles. We investigate supine, lateral, and prone sleeping positions. Based on Bland–Altman analysis between SV cardiac measurements and electrocardiogram (ECG), with respect to each position, we achieve the best limits of agreement with ECG values of [−8.65, 7.79] bpm, [−9.79, 9.25] bpm, and [−10.81, 10.23] bpm, respectively. The results indicate the potential of using speckle vibrometry as a contact-free monitoring method for instantaneous heart rate in a setting where the participant is allowed to rest in a spontaneous position while covered by textile layers. [ABSTRACT FROM AUTHOR]

Introduction: Excessive daytime sleepiness (EDS) associated with narcolepsy or obstructive sleep apnea (OSA) can impair vigilance/attention. Solriamfetol, a dopamine/norepinephrine reuptake inhibitor, is approved to treat EDS associated with narcolepsy (75–150 mg/day) or OSA (37.5–150 mg/day). The analysis reported here explored the use of the Sleep, Activity, Fatigue, and Task Effectiveness (SAFTE) model (used in transport industries to model performance based on accumulated sleep and circadian variability) as a substitute for healthy controls using psychomotor vigilance task (PVT) data collected during clinical studies. Methods: Data were analyzed from two phase 2 studies of solriamfetol in adults with OSA (NCT02806895, EudraCT 2015-003930-28) or narcolepsy (NCT02806908, EudraCT 2015-003931-36). Participants were randomly assigned 1:1 to solriamfetol 150 mg/day (3 days) followed by 300 mg/day (4 days), or placebo (7 days), then crossed over to the other treatment. Actual task effectiveness scores were calculated from average PVT inverse reaction time (pre-dose; 2 h post-dose; 6 h post-dose). Actigraphy-derived sleep intervals were used in SAFTE to determine modeled healthy control task effectiveness scores. Results: In participants with OSA (N = 31) on placebo or solriamfetol, actual and modeled healthy control task effectiveness did not differ at any time point. In participants with narcolepsy (N = 20) on placebo, actual task effectiveness at 2 h post-dose was lower than modeled healthy control task effectiveness (nominal P = 0.03), a difference not present with solriamfetol. There was no main effect of solriamfetol on actual or modeled healthy control task effectiveness across time points. Conclusion: This study represents a novel application of the SAFTE biomathematical model to approximate healthy controls in sleep disorder research and provides valuable lessons that may optimize future research. Future studies should perform a priori power analyses for model-tested outcomes and use sleep measures that capture sleep fragmentation characteristic of sleep disorders for sleep input (e.g., total sleep time rather than time in bed). Trial Registration: NCT02806895, EudraCT 2015-003930-28: A Randomized, Double-Blind, Placebo-Controlled, Crossover On-Road Driving Study Assessing the Effect of JZP-110 on Driving Performance in Subjects With Excessive Sleepiness Due to Obstructive Sleep Apnea. NCT02806908, EudraCT 2015-003931-36: A Randomized, Double-Blind, Placebo-Controlled, Crossover On-Road Driving Study Assessing the Effect of JZP-110 on Driving Performance in Subjects With Excessive Sleepiness Due to Narcolepsy. [ABSTRACT FROM AUTHOR]

Acute total sleep deprivation and partial sleep deprivation have negative impacts on cognitive performance. Studies in subjects who regularly experience sleep loss, however, are rare and often restricted to examination of internal sleeping disorders. To address this issue, we set up a pilot study to explore the effects of a week characterized by sleep disruption on cognitive functioning, using a case–control setting in a maritime pilot group with chronic exposure to intermittent extrinsic, work‐related sleep disruption. Twenty maritime pilots (aged 30–50 years) were compared to sex‐ and education‐matched controls with normal sleep behaviour, from the same age range. We assessed subjective and objective cognitive function, including attention, psychomotor speed, memory and executive function using the Cambridge Neuropsychological Test Automated Battery (CANTAB). Although we were able to confirm poorer sleep in maritime pilots and subjective complaints in some cognitive domains, we did not find objective cognitive deficits in the maritime pilot group compared to controls without sleep disruption. This could suggest that in this group of healthy, young maritime pilots, exposure to sleep disruption resulted in some subjective cognitive complaints, but objective deficits of cognitive function were not detected in comparison with a non‐pilot control group. However, given the small sample size, the absence of an effect does not exclude the possibility that sleep disruption could result in cognitive deficits in general. Therefore, our findings have to be confirmed in future prospective studies with a larger sample size and matched controls, regarding age, education and work history. [ABSTRACT FROM AUTHOR]

Rationale: The mechanisms underlying impaired sleep quality in insomnia are not fully known, but an important role for sleep fragmentation has been proposed. Objectives: The aim of this study is to explore potential mechanisms of sleep fragmentation influencing alterations of perceived sleep quality. Methods: We analyzed polysomnography (PSG) recordings from a double-blind crossover study with zopiclone 7.5 mg and placebo, in elderly participants with insomnia complaints and age-matched healthy controls. We compared survival dynamics of sleep and wake across group and treatment. Subsequently, we used a previously proposed model to estimate the amount of sleep onset latency (SOL) misperception from PSG-defined sleep fragmentation. Self-reported and model-estimated amount of SOL misperception were compared across group and treatment, as well as model prediction errors. Results: In the zopiclone night, the average segment length of NREM sleep was increased (group F = 1.16, p = 0.32; treatment F = 8.89, p< 0.01; group x treatment F = 0.44, p = 0.65), while the segment length of wake was decreased (group F = 1.48, p = 0.23; treatment F = 11.49, p< 0.01; group x treatment F = 0.36, p = 0.70). The self-reported and model-estimated amount of SOL misperception were lower during the zopiclone night (self-reported group F = 6.08, p< 0.01, treatment F = 10.8, p< 0.01, group x treatment F = 2.49, p = 0.09; model-estimated F = 1.70, p = 0.19, treatment F = 16.1, p< 0.001, group x treatment F = 0.60, p = 0.55). The prediction error was not altered (group F = 1.62, p = 0.20; treatment F = 0.20, p = 0.65; group x treatment F = 1.01, p = 0.37). Conclusions: Impaired subjective sleep quality is associated with decreased NREM stability, together with increased stability of wake. Furthermore, we conclude that zopiclone-induced changes in SOL misperception can be largely attributed to predictable changes of sleep architecture. [ABSTRACT FROM AUTHOR]

Insomnia, i.e., difficulties initiating and/or maintaining sleep, is one of the most common sleep disorders. To study underlying mechanisms for insomnia, we studied autonomic activity changes around sleep onset in participants without clinical insomnia but with varying problems with initiating or maintaining sleep quantified as increased sleep onset latency (SOL) and wake after sleep onset (WASO), respectively. Polysomnography and electrocardiography were simultaneously recorded in 176 participants during a single night. Cardiac autonomic activity was assessed using frequency domain analysis of RR intervals and results show that the normalized spectral power in the low frequency band (LF nu ) after sleep onset was significantly higher in participants with long SOL compared to participants with short SOL. Furthermore, the normalized spectral power in the high frequency band (HF nu ) was significantly lower in participants with long SOL as compared to participants with short SOL over 3 time periods (first 10 min in bed intending to sleep, 10 min before, and 10 min after sleep onset). These results suggest that participants with long SOL are more aroused in all three examined time periods when compared to participants with short SOL, especially for young adults (20–40 years). As there is no clear consensus on the cutoff for an increased WASO, we used a data-driven approach to explore different cutoffs to define short WASO and long WASO groups. LF nu , HF nu , and LF / HF differed between the long and the short WASO groups. A higher LF nu and LF / HF and a lower HF nu was observed in participants with long WASO for most cutoffs. The highest effect size was found using the cutoff of 66 min. Our findings suggest that autonomic cardiac activity has predictive value with respect to sleep characteristics pertaining to sleep onset and maintenance. [ABSTRACT FROM AUTHOR]

Chronic insomnia is known to have a negative influence on quality of life (QOL). To date, most studies on chronic insomnia have focused on health-related aspects of QOL. General QOL, which is a different construct, has not been studied in detail. Moreover, it is not known which factors are associated with general QOL in insomnia, and whether the presence of mental disorders, a condition known as comorbid insomnia, affects these variables. The present study focused on identifying sleep and psychosocial variables that might be associated with general QOL in primary and comorbid insomnia. Personality traits, coping variables, anxiety and depressive symptoms, fatigue and subjective sleep variables were assessed in 218 consecutive well-characterized patients with primary and comorbid insomnia, referred to a third line centre for sleep medicine. In primary insomnia, higher extraversion and lower discrepancies in social support were associated with higher QOL. Surprisingly, insomnia severity was not significantly associated with QOL in this group. However, lower fatigue, which can be seen as an important daytime consequence of insomnia was correlated with higher QOL in patients with primary insomnia. In both insomnia groups, low anxiety and depressive symptoms and low fatigue were associated with higher general QOL. In contrast with the primary insomnia group, lower insomnia severity was correlated with higher QOL in patients with comorbid insomnia. These results stress the importance of assessing and treating daytime fatigue in insomnia. In primary insomnia, improving social support might be an important treatment goal. Furthermore, this study supports the concept that treatment of insomnia should not be neglected in patients with comorbid insomnia. Indeed, both insomnia and indices of psychiatric disease are strongly associated with general QOL in this condition. [ABSTRACT FROM AUTHOR]

We assessed subjective sleep measures in a cohort of 146 patients with chronic insomnia and hypothesized that these measures may differ depending on the presence as well as the type of comorbid psychiatric disorders. All patients were consecutively referred to a third line sleep medicine center and underwent an extensive clinical intake by both a sleep physician and a psychologist. Psychodiagnostics were performed according to the DSM-IV criteria. Subjective sleep was assessed by sleep diaries and the insomnia severity index. Insomniacs with anxiety disorders showed a relatively higher total sleep time and higher sleep efficiency than the two other groups. Furthermore, the number of awakenings was higher and time in bed after the final awakening was lower in patients with comorbid anxiety disorders when compared to the two other groups. Although subjective total bedtimes where comparable, patients with comorbid anxiety disorders on average reported a striking 2 h more sleep per night and around a 20% higher sleep efficiency than patients with comorbid mood disorders. Patients with comorbid mood disorders showed a trend towards a higher Insomnia Severity Index-score when compared to primary insomniacs. Insomniacs with comorbid anxiety disorders present with a markedly higher sleep efficiency and total sleep time. On the other hand, these patients describe more fragmented sleep. Our findings may have practical implications for more tailored cognitive behavioral treatment in insomniacs with and without different types of psychiatric comorbidity. [ABSTRACT FROM AUTHOR]

Objectives To study the relationship between nocturnal hypokinesia and sleep quality in Parkinson's disease ( PD). Design Questionnaire study using intergroup analysis. Setting Parkinson Centre Nijmegen, a tertiary university referral center. Participants Two hundred forty individuals with Parkinson's disease. Measurements Clinical and demographic data were obtained. Nocturnal hypokinesia was assessed using Question 35 of the Parkinson's Disease Quality of Life Questionnaire and rated on a 5-point Likert scale (1 = all of the time to 5 = never). The Pittsburgh Sleep Quality Index ( PSQI) was used to quantify sleep quality, higher scores indicating poorer sleep quality. Results One hundred thirty-five of 240 participants had difficulties turning over in bed. Mean PSQI scores were significantly higher in participants with nocturnal hypokinesia (7.7 ± 4.1) than in those without (6.1 ± 3.4, P = .001). A regression model correcting for age, disease duration, and Hoehn and Yahr stage showed a significant influence of nocturnal hypokinesia on sleep quality (coefficient of determination = 0.042, standardized-beta = 0.163, P = .03). There was a linear relationship between frequency of nocturnal hypokinesia and sleep quality. Conclusion This is the first study that documents that nocturnal hypokinesia negatively affects sleep quality in PD. Nocturnal hypokinesia therefore merits therapeutic attention, including optimal nighttime dopaminergic treatment and education about turning strategies in bed. [ABSTRACT FROM AUTHOR]

Hypocretin deficiency causes narcolepsy and may affect neuroendocrine systems and body composition. Additionally, growth hormone (GH) alterations my influence weight in narcolepsy. Symptoms can be treated effectively with sodium oxybate (SXB; γ-hydroxybutyrate) in many patients. This study compared growth hormone secretion in patients and matched controls and established the effect of SXB administration on GH and sleep in both groups. Eight male hypocretin-deficient patients with narcolepsy and cataplexy and eight controls matched for sex, age, BMI, waist-to-hip ratio, and fat percentage were enrolled. Blood was sampled before and on the 5th day of SXB administration. SXB was taken two times 3 g/night for 5 consecutive nights. Both groups underwent 24-h blood sampling at 10-min intervals for measurement of GH concentrations. The GH concentration time series were analyzed with AutoDecon and approximate entropy (ApEn). Basal and pulsatile GH secretion, pulse regularity, and frequency, as well as ApEn values, were similar in patients and controls. Administration of SXB caused a significant increase in total 24-h GH secretion rate in narcolepsy patients, but not in controls. After SXB, slow-wave sleep (SWS) and, importantly, the croβ-correlation between GH levels and SWS more than doubled in both groups. In conclusion, SXB leads to a consistent increase in nocturnal GH secretion and strengthens the temporal relation between GH secretion and SWS. These data suggest that SXB may alter somatotropic tone in addition to its consolidating effect on nighttime sleep in narcolepsy. This could explain the suggested nonsleep effects of SXB, including body weight reduction. [ABSTRACT FROM AUTHOR]

In the first column of table 2, it says: 'REM Weibull scale, 1/ʎ'. NREM Weibull scale 1/ʎ, and Wake Weibull scale 1/ʎ. [ABSTRACT FROM AUTHOR]

Background: Recent evidence indicates that disrupted sleep could contribute to the development of Alzheimer's disease by influencing the production and/or clearance of the amyloid-β protein. We set up a case-control study to investigate the association between long-term work-induced sleep disruption, cognitive function, and brain amyloid-β burden. Methods: Nineteen male maritime pilots (aged 48–60 years) with chronic work-related sleep disruption and a sex-, age-, and education-matched control sample (n = 16, aged 50–60 years) with normal sleep completed the study. Primary sleep disorders were ruled out with in-lab polysomnography. Additional sleep measurements were obtained at home using actigraphy, sleep-wake logs, and a single-lead EEG device. Cognitive function was assessed with a neuropsychological test battery, sensitive to early symptomatic Alzheimer's disease. Brain amyloid-β burden was assessed in maritime pilots using 18F-flutemetamol amyloid PET-CT. Results: Maritime pilots reported significantly worse sleep quality (Pittsburgh Sleep Quality Index (PSQI) = 8.8 ± 2.9) during work weeks, compared to controls (PSQI = 3.2 ± 1.4; 95% CI 0.01 to 2.57; p = 0.049). This was confirmed with actigraphy-based sleep efficiency (86% ± 3.8 vs. 89.3% ± 4.3; 95% CI 0.43 to 6.03; p = 0.03). Home-EEG recordings showed less total sleep time (TST) and deep sleep time (DST) during work weeks compared to rest weeks (TST 318.56 (250.21–352.93) vs. TST 406.17 (340–425.98); p = 0.001; DST 36.75 (32.30–58.58) vs. DST 51.34 (48.37–69.30); p = 0.005)). There were no differences in any of the cognitive domains between the groups. For brain amyloid-β levels, mean global cortical standard uptake value ratios of 18F-flutemetamol were all in the normal range (1.009 ± 0.059; 95% CI 0.980 to 1.037), confirmed by visual reads. Conclusions: Capitalizing on the particular work-rest schedule of maritime pilots, this study with a small sample size observed that long-term intermittent sleep disruption had no effects on global brain amyloid-β levels or cognitive function. [ABSTRACT FROM AUTHOR]

To explore sleep structure in participants with obstructive sleep apnea (OSA) and comorbid insomnia (COMISA) and participants with OSA without insomnia (OSA-only) using both single-night polysomnography and multi-night wrist-worn photoplethysmography/accelerometry. Multi-night 4-class sleep-staging was performed with a validated algorithm based on actigraphy and heart rate variability, in 67 COMISA (23 women, median age: 51 years) and 50 OSA-only (15 women, median age: 51) participants. Sleep statistics were compared using linear regression models and mixed-effects models. Multi-night variability was explored using a clustering approach and between- and within-participant analysis. Polysomnographic parameters showed no significant group differences. Multi-night measurements, during 13.4 ± 5.2 nights per subject, demonstrated a longer sleep onset latency and lower sleep efficiency for the COMISA group. Detailed analysis of wake parameters revealed longer mean durations of awakenings in COMISA, as well as higher numbers of awakenings lasting 5 min and longer (WKN ≥5min) and longer wake after sleep onset containing only awakenings of 5 min or longer. Within-participant variance was significantly larger in COMISA for sleep onset latency, sleep efficiency, mean duration of awakenings and WKN ≥5min. Unsupervised clustering uncovered three clusters; participants with consistently high values for at least one of the wake parameters, participants with consistently low values, and participants displaying higher variability. Patients with COMISA more often showed extended, and more variable periods of wakefulness. These observations were not discernible using single night polysomnography, highlighting the relevance of multi-night measurements to assess characteristics indicative for insomnia. • Single-night sleep measurements show limited value in the differentiation between OSA and COMISA. • COMISA patients more often show extended periods of wakefulness over multiple nights. • Combined photoplethysmography and actigraphy can adequately capture these differences. • Multi-night assessment is useful to objectively identify comorbid insomnia and prompt further investigation. [ABSTRACT FROM AUTHOR]

Palpitations occurring in specific body positions are often reported by patients, but the effect of body position on arrhythmia has received little research attention. We hypothesize that resting body position can exert pro-arrhythmogenic effects in various ways. For example, lateral body position is known to increase change atrial and pulmonary vein dimensions. This observational study capitalizes on overnight polysomnography (PSG) recordings from a tertiary sleep clinic. PSGs were retrieved based on any mention of cardiac arrhythmia in the clinical report, irrespective of primary sleep diagnosis or (cardiac) comorbidities. Every instance of atrial ectopy was annotated and subgroups with a homogenous rate of atrial ectopy were created based on the Dunn index. A generalized linear mixed-effects model using age, sex, gender, sleep stage and body position was used to analyse the total amount of atrial ectopy in each combination of sleep stage and body position. Backward elimination was then performed to select the best subset of variables for the model. Presence of a respiratory event was then added to the model for the subgroup with a high atrial ectopy rate. PSGs of 22 patients (14% female, mean age 61y) were clustered and analysed. Body position, sleep stage, age or sex did not have a significant effect on atrial ectopy in the subgroup with a low rate of atrial ectopy (N = 18). However, body position did significantly affect the rate of atrial ectopy in the subgroup with a high rate of atrial ectopy (N = 4; 18%). Respiratory events significantly altered the atrial ectopy rate in only three body positions across two patients. In each individual with a high rate of atrial ectopy, the rate of atrial ectopy was significantly higher in either left or right decubital or supine position. Increase in atrial wall stretch in lateral decubital position and obstructive respiratory events in positional sleep apnea are two possible pathophysiological mechanisms, while avoidance of a body position due to symptomatic atrial ectopy in that position is an important limitation. In a selected cohort of patients with a high rate of atrial ectopy during overnight polysomnography, the occurrence of atrial ectopy is related to resting body position. • Body position can be arrhythmogenic in patients with a high rate of atrial ectopy. • Sleep apnea and changes in atrial wall strain could potentially explain this. • Symptomatic positional atrial ectopy could cause patients to avoid body positions. [ABSTRACT FROM AUTHOR]

Study Objective: To study sleep EEG characteristics associated with misperception of Sleep Onset Latency (SOL).Methods: Data analysis was based on secondary analysis of standard in-lab polysomnographic recordings in 20 elderly people with insomnia and 21 elderly good sleepers. Parameters indicating sleep fragmentation, such as number of awakenings, wake after sleep onset (WASO) and percentage of NREM1 were extracted from the polsysomnogram, as well as spectral power, microarousals and sleep spindle index. The correlation between these parameters during the first sleep cycle and the amount of misperceived sleep was assessed in the insomnia group. Additionally, we made a model of the minimum duration that a sleep fragment at sleep onset should have in order to be perceived as sleep, and we fitted this model to subjective SOLs of both subject groups.Results: Misperception of SOL was associated with increased percentage of NREM1 and more WASO during sleep cycle 1. For insomnia subjects, the best fit of modelled SOL with subjective SOL was found when assuming that sleep fragments shorter than 30 min at sleep onset were perceived as wake. The model indicated that healthy subjects are less sensitive to sleep interruptions and perceive fragments of 10 min or longer as sleep.Conclusions: Our findings suggest that sleep onset misperception is related to sleep fragmentation at the beginning of the night. Moreover, we show that people with insomnia needed a longer duration of continuous sleep for the perception as such compared to controls. Further expanding the model could provide more detailed information about the underlying mechanisms of sleep misperception. [ABSTRACT FROM AUTHOR]

Abstract: Sleep disturbances in Alzheimer''s disease (AD) patients are associated with the severity of dementia and are often the primary reason for institutionalization. These sleep problems partly resemble core symptoms of narcolepsy, a sleep disorder caused by a general loss of the neurotransmitter hypocretin. AD is a neurodegenerative disorder targeting different brain areas and types of neurons. In this study, we assessed whether the neurodegenerative process of AD also affects hypothalamic hypocretin/orexin neurons. The total number of hypocretin-1 immunoreactive neurons was quantified in postmortem hypothalami of AD patients (n = 10) and matched controls (n = 10). In addition, the hypocretin-1 concentration was measured in postmortem ventricular cerebrospinal fluid of 24 AD patients and 25 controls (including the patients and controls in which the hypothalamic cell counts were performed). The number of hypocretin-1 immunoreactive neurons was significantly decreased by 40% in AD patients (median [25th–75th percentiles]); AD 12,935 neurons (9972–19,051); controls 21,002 neurons (16,439–25,765); p = 0.049). Lower cerebrospinal fluid (CSF) hypocretin-1 levels were found in AD patients compared with controls (AD: 275 pg/mL [197–317]; controls: 320 pg/mL [262–363]; p = 0.038). Two AD patients with documented excessive daytime sleepiness showed the lowest CSF hypocretin-1 concentrations (55 pg/mL and 76 pg/mL). We conclude that the hypocretin system is affected in advanced AD. This is reflected in a 40% decreased cell number, and 14% lower CSF hypocretin-1 levels. [Copyright &y& Elsevier]