Search

Background: During the first years of life, parental sleep strongly depends on child&rsquo, s sleep quality. Poor parental sleep may relate to increased stress and negative mood. However, there is a lack of sleep studies focusing on all family members. This study aimed to investigate the relationship between sleep, mood, and stress in mothers, fathers and children. Methods: Data were obtained from 65 parental couples and 65 children (2 to 36 months). Data on sleep for all family members and stress of parents were completed by both mothers and fathers through questionnaires and sleep diaries. Results: Toddlers&rsquo, positive mood before nocturnal sleep was significantly associated with reduced wake times after sleep onset. Mothers reported worse sleep quality compared to fathers. Shorter sleep onset latency in fathers and better sleep efficiency in mothers were linked with better self-reported mood upon awakening. In mothers, but not in fathers, poor sleep quality was associated with higher perceived stress. Conclusion: Results suggest bidirectional relationships between sleep and mood in children, mothers and fathers. Moreover, results evidence poorer sleep in mothers, compared to fathers, which was linked with increased parenting stress. This gender gap should be further considered in studies with larger samples and in clinical contexts.

Objectives Pre-sleep arousal and time monitoring behavior are two putative factors involved in the development and maintenance of insomnia. We investigate two questionnaires measuring these factors in good sleepers and patients with insomnia. Participants A sample of 96 patients with non-organic insomnia according to ICD-10 and 208 good sleepers completed the Pre-Sleep Arousal Scale (PSAS), the Time Monitoring Behavior-10 scale (TMB-10), the Beck Depression Inventory (BDI)-II, the Pittsburgh Sleep Quality Index (PSQI), the Insomnia Severity Index (ISI) and the State-Trait Anxiety Inventory (STAI). Methods In this study, 95% quantile cut-off scores were determined for good sleeper in the age and gender mathed subgroups of the insomnia group. Multiple logistic regression analysis was used to determine variables predicting above-threshold values in the two target questionnaires. Included predictors were age, gender as well as ISI, BDI-II, STAI-1 and -2 total scores. Results Good sleepers showed 95% quantiles between 12.2 and 23.8 for PSAS and between 7.5 and 12.7 for TMB-10. Approximately 40% of patients with insomnia had scores above these cut-offs for PSAS and ca. 25% for TMB-10. Female gender and anxiety were variables associated with scores above cut-off on the PSAS. Insomnia severity and anxiety were associated with scores above cut-off on the TMB-10. Conclusions These findings underline the importance of PSAS and TMB-10 in the diagnostic investigation of insomnia and indicate that time monitoring is related to increased insomnia severity. Further research may investigate the impact of the corresponding two constructs on response rates to cognitive-behavioral treatment for insomnia.

Animals and humans spend on average one third of their lives in sleep, but its functions remain to be specified. Distinct lines of research propose that sleep promotes local strengthening of information-bearing synapses (plasticity) and global downscaling of synaptic strength (stability) in neural networks-prerequisites for adaptive behavior in a changing environment. However, the potential orchestration of these processes, particularly in humans, needs to be further characterized. Here, we use electrophysiological, behavioral, and molecular indices to noninvasively study cortical plasticity and network stability in humans. We observe indices of local strengthening of prior induced long-term potentiation-like plasticity (paired associative stimulation induced change in motor-evoked potential) and global network stabilization (homeostatic regulation of wake EEG theta activity) after brief periods of nonrapid eye movement sleep compared with wakefulness. The interplay of local sleep slow oscillations and spindle activity, previously related to synaptic refinements during sleep, is identified as a potential mechanism. Our findings are consistent with the notion that sleep-specific brain activity patterns reduce the plasticity-stability dilemma by orchestrating local plasticity and global stability of neural assemblies in the human cortex. Future studies are needed to further decipher the neural mechanisms underlying our indirect observations.

The 21st century has brought with it a welcome call for increased rigor in observational research methods (1, 2). It is not that observational research methods are inherently flawed – they are not (3, 4). Observational studies can contribute valuable evidence supporting causal associations when designed and conducted using rigorous methods. The “flaws” are a result of reliance on outdated methodology, inadequate attention to threats to validity (such as confounding), opaque reporting of results, lack of replication, and a failure to interpret findings within the context of the limitations of observational research methodology. Aware of this situation and influenced by our experience as journal editors, we convened an ad hoc group of 47 editors of 35 respiratory, sleep, and critical care journals to offer guidance to authors, peer reviewers, and researchers on the design and reporting of observational causal inference studies. This guidance takes the form of a call for investigators to consider making major changes to their approach to such studies. This document represents our current best understanding of approaches to causal inference, an active area of research. We anticipate that best practice in this, as in any scientific endeavor, will continue to evolve, requiring this document to be updated every 5 to 10 years. We believe these changes will increase the rigor, validity, and value of the work we publish in our journals.

Initially independent lines of research suggest that sleep-specific brain activity patterns, observed as electroencephalographic slow oscillatory and sleep spindle activity, promote memory consolidation and underlying synaptic refinements. Here, we further tested the emerging concept that specifically the coordinated interplay of slow oscillations and spindle activity (phase-amplitude coupling) support memory consolidation. Particularly, we associated indices of the interplay between slow oscillatory (0.16-1.25 Hz) and spindle activity (12-16 Hz) during non-rapid eye movement sleep (strength [modulation index] and phase degree of coupling) in 20 healthy adults with parameters of overnight declarative (word-list task) and procedural (mirror-tracing task) memory consolidation. The pattern of results supports the notion that the interplay between oscillations facilitates memory consolidation. The coincidence of the spindle amplitude maximum with the up-state of the slow oscillation (phase degree) was significantly associated with declarative memory consolidation (r = .65, p = .013), whereas the overall strength of coupling (modulation index) correlated with procedural memory consolidation (r = .45, p = .04). Future studies are needed to test for potential causal effects of the observed association between neural oscillations during sleep and memory consolidation, and to elucidate ways of modulating these processes, for instance through non-invasive brain-stimulation techniques.

The disorder insomnia represents a relevant and frequent condition in clinical care. Cognitive behavioral therapy of insomnia (CBT-I) is regarded as first line treatment. Pharmacotherapy can be considered if CBT-I is not available or effective. Therefore, pharmacological approaches for disturbed sleep are still among the most widely prescribed pharmacological treatments in clinical care.In this review, the authors highlight basic physiological pathways of sleep regulation to understand fundamental pharmacological principles of sleep medicine. Available guidelines and reviews are summarized and recommendations formulated regarding the use of benzodiazepines and hypnotic benzodiazepine receptor agonists, melatonin and melatonin receptor agonists, sedating antidepressants, antipsychotics and antihistamines, and orexin receptor antagonists in insomnia disorder. Variations in the treatment of insomnia disorder in subpopulations with increased prevalence of sleep disorders - childhood, pregnancy and old age - are specified.The well-established off-label use of hypnotic drugs should evocate a debate about a better alignment of clinical practice and scientific evidence and guidelines. Better understanding of sleep regulation could help in the development of completely new substance classes. Focusing subjective sleep disturbances, such as superficial sleep perception might help identify novel pathways.

Introduction Insomnia symptoms are very common in Bipolar Disorder. Our aim was to assess the potential association between insomnia, emotion dysregulation and suicidality in subjects with Bipolar Disorder. Methods Seventy-seven subjects with Bipolar Disorder type II with a depressive episode with mixed features were recruited. Patients were assessed with SCID-DSM-5, the Insomnia Severity Index (ISI), the Difficulties in Emotion Regulation Scale (DERS), the Scale for Suicide Ideation (SSI) while evaluating manic and depressive symptoms. Results Subjects with insomnia symptoms compared to those without showed higher scores in the DERS scale and subscales, including impulsivity, and in the SSI scale. Insomnia symptoms significantly predicted the severity of depressive symptoms, emotion dysregulation, and suicidality in subjects with bipolar disorder. In particular, insomnia was related to difficulties in some areas of emotion regulation including impulsivity. Emotion dysregulation significantly mediated the association between insomnia and depressive symptoms (Z = 2.9, p = 0.004). Furthermore, emotional impulsivity mediated the association between insomnia symptoms and suicidality (Z = 2.2, p = 0.03). Conclusion In our study, subjects with bipolar disorder suffering from insomnia experienced a greater severity of depressive symptoms and suicidality compared to subjects without insomnia. Insomnia was associated with emotion dysregulation, impulsivity and suicidality. Further research is necessary to investigate if these latter features may benefit from early insomnia treatment in subjects with bipolar disorder.

Previous research has identified insomnia as a predictor for the onset of depression. The aim of this meta-analysis is to investigate whether insomnia also predicts the onset of other mental disorders. Longitudinal studies were eligible for inclusion if they investigated insomnia at baseline (including nighttime- and daytime-symptoms) as a predictor of the later onset of psychopathology within a follow-up time-frame of at least 12 mo. Thirteen primary studies were included. The results suggest that insomnia is a significant predictor for the onset of depression (10 studies, OR 2.83, CI 1.55-5.17), anxiety (six studies, OR 3.23, CI 1.52-6.85), alcohol abuse (two studies, OR 1.35, CI 1.08-1.67, and psychosis (one study, OR 1.28, CI 1.03-1.59). The overall risk of bias in the primary studies was moderate. This meta-analysis provides evidence that insomnia increases the risk for psychopathology. A future research agenda should include more prospective studies using established diagnostic criteria, assessing insomnia at baseline and including long-term follow-up intervals evaluating a wider range of mental disorders. In addition, prospective long-term interventional studies investigating the efficacy of insomnia treatment for the prevention of mental disorders are called for.

Mood disorders are amongst the most prevalent and severe disorders worldwide, with a tendency to be recurrent and disabling. Although multiple mechanisms have been hypothesized to be involved in their pathogenesis, just a few integrative theoretical frameworks have been proposed and have yet to integrate comprehensively all available findings. As such, a comprehensive framework would be quite useful from a clinical and therapeutic point of view in order to identify elements to evaluate and target in the clinical practice. Because conditions of sleep loss, which include reduced sleep duration and insomnia, are constant alterations in mood disorders, the aim of this paper was to review the literature on their potential role in the pathogenesis of mood disorders and to propose a novel theoretical model. According to this hypothesis, sleep should be considered the main regulator of several systems and processes whose dysregulation is involved in the pathogenesis of mood disorders. The model may help explain why sleep disturbances are so strikingly linked to mood disorders, and underscores the need to evaluate, assess and target sleep disturbances in clinical practice, as a priority, in order to prevent and treat mood disorders.

Questionnaire studies suggest that stroke patients experience sustained problems with sleep and daytime sleepiness, but physiological sleep studies focussing specifically on the chronic phase of stroke are lacking. Here we report for the first time physiological data of sleep and daytime sleepiness obtained through the two gold-standard methods, nocturnal polysomnography and the Multiple Sleep Latency Test. Data from community-dwelling patients with chronic right-hemispheric stroke (>12 months) were compared to sex- and age-matched controls. Behavioural and physiological measures suggested that stroke patients had poorer sleep with longer sleep latencies and lower sleep efficiency. Patients further spent more time awake during the night, and showed greater high-frequency power during nonREM sleep than controls. At the same time the Multiple Sleep Latency Test revealed greater wake efficiency in patients than controls. Importantly these findings were not due to group differences in sleep disordered breathing or periodic limb movements. Post-stroke insomnia is presently not adequately addressed within the care pathway for stroke. A holistic approach to rehabilitation and care provision, that includes targeted sleep interventions, is likely to enhance long-term outcome and quality of live in those living with chronic deficits after stroke.

As the prevalence of sleep disorders is increasing, new methods for ambulatory sleep measurement are required. This paper presents electrodermal activity in different sleep stages and a sleep detection algorithm based on electrodermal activity. We analysed electrodermal activity and polysomnographic data of 43 healthy subjects and 48 patients with sleep disorders. Electrodermal activity was measured using an ambulatory device worn at the wrist. Two parameters to describe electrodermal activity were defined based on previous literature: EDASEF (electrodermal activity-smoothed feature) as parameter for skin conductance level; and EDAcounts (number of electrodermal activity-peaks) as skin conductance responses. Analysis of variance indicated significant EDASEF differences between the sleep stages wake versus N1, wake versus N2, wake versus slow-wave sleep, and wake versus rapid eye movement. The analysis of EDAcounts also showed significant differences, especially in the stages slow-wave sleep versus rapid eye movement. Between healthy subjects and patients, a significant disparity of EDAcounts was revealed in stage N1. Furthermore, the variances of EDASEF and EDAcounts in N1, N2 slow-wave sleep and rapid eye movement were higher in the patient group (p [F test] < .05). Next, an electrodermal activity-based sleep/wake discriminating algorithm was constructed. The optimized algorithm achieved an average sensitivity and specificity for sleep detection of 97% and 75%. The epoch agreement rate (average accuracy) was 86%. These outcomes are comparative to sleep detection algorithms based on actigraphy or heart rate variability. The results of this study indicate that electrodermal activity is not only a robust parameter for describing sleep, but also a potential suitable method for ambulatory sleep monitoring.

Beeinträchtigungen des Schlafes als Symptom psychischer Störungen sind ein wichtiges Forschungsfeld. Folgender Artikel wertet die Ergebnisse zweier Metaanalysen aus der Universität Freiburg aus, bei denen Polysomnographie als wichtige Methode zur Erkennung von Schlafauffälligkeiten eingesetzt wurde. Untersucht wurden die polysomnographischen Daten bei Insomnie sowie einer Reihe anderer psychischer Störungen: Affektive Störungen, Ess- Angst- und Persönlichkeitsstörungen, sowie ADHS, Asperger-Syndrom, Autismus und Schizophrenie.

Chronische Ein- und Durchschlafstörungen, die die Tagesbefindlichkeit beeinträchtigen, werden als Insomnie bezeichnet. Während die Insomnie nach ICD-10 nur dann diagnostiziert wird, wenn keine andere Erkrankung vorliegt, die die Schlafstörungen erklären könnte, kann eine Insomnie nach DSM 5 auch als komorbide Diagnose z.B. bei affektiven Störungen oder Angststörungen vergeben werden. Die Kognitive Verhaltenstherapie für Insomnie (KVT-I) ist eine wirksame Behandlung, mit der sowohl für Ein- als auch für Durchschlafstörungen gute Effekte erzielt werden können. Hier stellen wir achtsamkeitsbasierte Therapien vor, die in der letzten Zeit verstärkt als ergänzende oder alternative Behandlung diskutiert werden.

Sleep can foster the reorganization of memory, i.e. the emergence of new memory content that has not directly been encoded. Current neurophysiological and behavioral evidence can be integrated into a model positing that REM sleep particularly promotes the disintegration of existing schemas and their recombination in the form of associative thinking, creativity and the shaping of emotional memory. Particularly, REM sleep related dreaming might represent a mentation correlate for the reconfiguration of memory. In a final section, the potential relevance for psychiatry and psychotherapy is discussed.

The relationship between insomnia and other mental disorders is still not fully understood. Yet, symptoms of insomnia are frequently observed in patients with other mental disorders and often precede the onset of other conditions. In some cases, symptoms of insomnia persist even after the successful treatment of other mental disorders. This observation has led to the assumption that the successful treatment of insomnia may prevent the future onset of other mental disorders. Since then, a considerable number of studies have lent further credibility to that hypothesis. This article reviews recent studies that shed further light on this issue with regard to depressive disorders, anxiety disorders, post-traumatic stress disorder, schizophrenia and alcohol dependence. While no studies have investigated whether cognitive behavioral therapy for insomnia (CBT-I) can prevent the future onset of mental disorders, there is evidence of a positive effect of CBT-I on a number of disorders. There is strong evidence of a positive effect of CBT-I on depression and anxiety disorders suggesting apreventive effect of CBT-I on these. Conversely, the current evidence does not suggest that CBT-I might prevent the onset of PTSD. Finally, research regarding the impact of CBT-I on schizophrenia and alcohol dependence is still at an early stage, and firm conclusions cannot yet be drawn.

In den vergangenen Jahren wurde eine beachtliche Anzahl an Studien publiziert, die nahelegen, dass Insomnien ein Risikofaktor fur korperliche Folgeerkrankungen sind, insbesondere fur kardiovaskulare Erkrankungen. Dies wirft die Frage auf, ob eine Behandlung von Schlafstorungen bei Patienten mit einer Insomnie als Praventionsmasnahme fur kardiovaskulare Erkrankungen eingesetzt werden kann. Die vorliegende Arbeit liefert eine Ubersicht uber empirische Studien, in denen diese Fragestellung bearbeitet wurde. Eine randomisierte kontrollierte klinische Studie legt nahe, dass die kognitive Verhaltenstherapie fur Insomnien zu einer Verbesserung von Laborparametern fuhrt, die fur das kardiovaskulare Risiko bedeutsam sind. Hierbei sollte jedoch angemerkt werden, dass eine unabhangige Replikation dieses Befundes wunschenswert ware. Zudem zeigen Register fur klinische Studien, dass aktuell einige Studien zu dem Thema durchgefuhrt werden bzw. kurzlich abgeschlossen wurden. Falls die kognitive Verhaltenstherapie fur Insomnien in Bezug auf kardiovaskulare Erkrankungen tatsachlich praventiv wirksam ist, wurde eine flachendeckende Verbreitung dieser Therapie sowohl den betroffenen Patienten helfen als auch zu einer erheblichen Reduktion der Versorgungskosten fuhren.

Insomnia is very common in the adult population and it includes a wide spectrum of sequelae, that is, neuroendocrine and cardiovascular alterations as well as psychiatric and neurodegenerative disorders. According to the conceptualization of insomnia in the context of the 3-P model, the importance of predisposing, precipitating, and perpetuating factors has been stressed. Predisposing factors are present before insomnia is manifested and they are hypothesized to interact with precipitating factors, such as environmental stressful events, contributing to the onset of insomnia. Understanding the early-life origins of insomnia may be particularly useful in order to prevent and treat this costly phenomenon. Based on recent evidence, prenatal-early-life stress exposure results in a series of responses that involve the stress system in the child and could persist into adulthood. This may encompass an activation of the hypothalamic-pituitary-adrenal axis accompanied by long-lasting modifications in stress reactivity. Furthermore, early-life stress exposure might play an important role in predisposing to a vulnerability to hyperarousal reactions to negative life events in the adult contributing to the development of chronic insomnia. Epigenetic mechanisms may also be involved in the development of maladaptive stress responses in the newborn, ultimately predisposing to develop a variety of (psycho-) pathological states in adult life.

Differences between subjective sleep perception and sleep determined by polysomnography (PSG) are prevalent, particularly in patients with primary insomnia, indicating that the two measures are partially independent. To identify individualized treatment strategies, it is important to understand the potentially different mechanisms influencing subjective and PSG-determined sleep. The aim of this study was to investigate to what extent three major components of insomnia models, i.e., sleep effort, dysfunctional beliefs and attitudes about sleep, and presleep arousal, are associated with subjective insomnia severity and PSG-determined sleep. A sample of 47 patients with primary insomnia according to DSM-IV criteria and 52 good sleeper controls underwent 2 nights of PSG and completed the Glasgow Sleep Effort Scale, the Dysfunctional Beliefs and Attitudes about Sleep Scale, the Pre-Sleep Arousal Scale and the Insomnia Severity Index. Regression analyses were conducted to investigate the impact of the three predictors on subjective insomnia severity and PSG- determined total sleep time. All analyses were adjusted for age, gender, depressive symptoms and group status. The results showed that subjective insomnia severity was associated positively with sleep effort. PSG-determined total sleep time was associated negatively with somatic presleep arousal and dysfunctional beliefs and attitudes about sleep. This pattern of results provides testable hypotheses for prospective studies on the impact of distinct cognitive and somatic variables on subjective insomnia severity and PSG-determined total sleep time.

Insomnien betreffen etwa 10 % der Menschen in westlichen Industrienationen. Für die psychotherapeutische Behandlung empfehlen Leitlinien die kognitiv-behaviorale Therapie für Insomnien (KVT-I). Diese Therapieform ist jedoch nur für die wenigsten Insomnie-Patienten verfügbar. Internetbasierte Selbsthilfeprogramme könnten erheblich zur Verbesserung der Versorgungssituation beitragen und wurden in den letzten Jahren in mehreren klinischen Studien positiv evaluiert.

The aim of this study was to assess the relationship between electroencephalogram (EEG) power spectral density and subjective sleep quality in healthy individuals. The sample was selected from the archival database of the Sleep Center at the Department for Psychiatry and Psychotherapy, Medical Center - University of Freiburg, and consisted of 206 healthy adults aged 19-73 years (85 male, 121 female) who underwent a polysomnographic examination for two consecutive nights. A multivariate analysis of variance (MANOVA) with spectral power variables of different frequency bands as dependent variables and subjective sleep quality, night number, age and gender as independent variables was statistically significant for subjective sleep quality, age and gender, but not for night number. In subsequent separate ANOVAs, higher subjective sleep quality was significantly related to decreased non-rapid eye movement (NREM) stage 2 sigma 2 and rapid eye movement (REM) delta 1; however, the relation between REM delta 1 and sleep quality did not remain significant when REM duration was accounted for. The effect sizes of the correlations between sleep quality and spectral power were small (r = -0.1). In contrast to common assumptions, the amount of variance in subjective sleep quality that can be explained through EEG power spectral density variables is small. This finding indicates that subjective and objective sleep are different constructs, the interrelations of which are not yet well understood.

Study Objectives: Perfectionism has been suggested to represent a predisposing factor for poor sleep. However, previous studies have relied upon self-report measures and the association between perfectionism and polysomnographic sleep warrants further investigation. Methods: The current retrospective exploratory study used the Frost Multidimensional Perfectionism Scale (FMPS) and polysomnography (PSG) in an unselected sample of 334 consecutive sleep laboratory patients (140 males, 194 females, 44.6 ± 15.9 years). Data was analysed using linear regression analyses. Results: High levels of perfectionism were associated with polysomnographically determined markers of poor sleep in the first sleep laboratory night. The total FMPS score was significantly associated with the number of nocturnal awakenings in the first sleep laboratory night. The sub-scales “concern over mistakes” and “personal standards” of perfectionism were significantly associated with markers of poor sleep. In contrast, there were only few associations between perfectionism and polysomnographic variables of the second sleep laboratory night. Conclusions: This pattern of results suggests that high levels of perfectionism may predispose individuals to sleep disturbances in the context of acute stressors. Thus the influence of perfectionism on poor sleep should be further investigated to improve treatment.

Objective: The relationship between insomnia symptoms and cognitive performance is unclear, particularly at the population level. We conducted the largest examination of this association to date through analysis of the UK Biobank, a large population-based sample of adults aged 40-69 yrs. We also sought to determine associations between cognitive performance and self-reported chronotype, sleep medication use, and sleep duration. Methods: This cross-sectional, population-based study involved 477,529 participants, comprising 133,314 with frequent insomnia symptoms (age: 57.4 ± 7.7 yrs; 62.1% female) and 344,215 controls without (age: 56.1 ± 8.2 yrs; 52.0% female). Cognitive performance was assessed through a touchscreen test battery probing reasoning, basic reaction time, numeric memory, visual memory and prospective memory. Adjusted models included relevant demographic, clinical and sleep variables. Results: Frequent insomnia symptoms were associated with cognitive impairment in unadjusted models, however these effects were reversed after full adjustment, leaving those with frequent insomnia symptoms showing statistically better cognitive performance over those without. Relative to intermediate chronotype, evening chronotype was associated with superior task performance, while morning chronotype was associated with the poorest performance. Sleep medication use and both long (>9hrs) and short (Conclusions: Our results suggest that after adjustment for potential confounding variables, frequent insomnia symptoms may be associated with a small statistical advantage, which is unlikely to be clinically meaningful, on simple neurocognitive tasks. Further work is required to examine mechanistic underpinnings of an apparent evening chronotype advantage in cognitive performance, as well as impairment associated with morning chronotype, sleep medication use, and sleep duration extremes.

Study objectives Insomnia disorder (ID) is a frequent sleep disorder coupled with increased risks for somatic and mental illness. Although subjective complaints are severe, polysomnography (PSG) parameters show only modest differences between groups. Rapid eye movement (REM) sleep as the most aroused sleep state may be especially vulnerable to be perceived as wake. To directly assess possible differences, we determined auditory waking thresholds and sleep perception in patients with ID and healthy control participants (good sleeper controls [GSC]) in N2 and REM sleep. Methods In case-control study, 27 patients with ID and 27 age- and gender-matched controls were included. Four consecutive nights were assessed in the sleep laboratory, with nights 3 and 4 each containing three awakenings either from stable N2 or REM sleep. Awakening thresholds in patients with ID did not differ from GSC, but decreased over the course of the night. Patients with ID indicated significantly more frequently than GSC having been awake when woken from REM sleep but not from N2 and were less sure when indicating they had been asleep. Additionally, participants with ID rated their REM sleep mentation as more emotionally negative compared with GSC. Conclusions This study presents direct evidence that the subjective experience of insomnia might be specifically coupled to the REM sleep state. Assuming chronic hyperarousal as a central pathophysiologically relevant pathway for insomnia, this might become especially evident during REM sleep, thus reflecting a hybrid sleep state in insomnia being coupled with altered sleep perception.

Insomnia and circadian rhythm sleep disorders affect large proportions of the population and have pronounced effects on quality of life and daytime performance. While the neurobiology of insomnia is not yet fully understood, circadian rhythm sleep disorders are assumed to be caused by a mismatch between the individual circadian phase position and the desired sleep-wake schedule. Benzodiazepines and non-benzodiazepine positive allosteric GABA

Study Objectives: Objective sleep impairments in insomnia disorder (ID) are insufficiently understood. The present study evaluated whether whole-night sleep stage dynamics derived from polysomnography (PSG) differ between people with ID and matched controls and whether sleep stage dynamic features discriminate them better than conventional sleep parameters.Methods: Eighty-eight participants aged 21-70 years, including 46 with ID and 42 age- and sex-matched controls without sleep complaints, were recruited through www.sleepregistry.nl and completed two nights of laboratory PSG. Data of 100 people with ID and 100 age- and sex-matched controls from a previously reported study were used to validate the generalizability of findings. The second night was used to obtain, in addition to conventional sleep parameters, probabilities of transitions between stages and bout duration distributions of each stage. Group differences were evaluated with nonparametric tests.Results: People with ID showed higher empirical probabilities to transition from stage N2 to the lighter sleep stage N1 or wakefulness and a faster decaying stage N2 bout survival function. The increased transition probability from stage N2 to stage N1 discriminated people with ID better than any of their deviations in conventional sleep parameters, including less total sleep time, less sleep efficiency, more stage N1, and more wake after sleep onset. Moreover, adding this transition probability significantly improved the discriminating power of a multiple logistic regression model based on conventional sleep parameters.Conclusions: Quantification of sleep stage dynamics revealed a particular vulnerability of stage N2 in insomnia. The feature characterizes insomnia better than-and independently of-any conventional sleep parameter.

This European guideline for the diagnosis and treatment of insomnia was developed by a task force of the European Sleep Research Society, with the aim of providing clinical recommendations for the management of adult patients with insomnia. The guideline is based on a systematic review of relevant meta-analyses published till June 2016. The target audience for this guideline includes all clinicians involved in the management of insomnia, and the target patient population includes adults with chronic insomnia disorder. The GRADE (Grading of Recommendations Assessment, Development and Evaluation) system was used to grade the evidence and guide recommendations. The diagnostic procedure for insomnia, and its co-morbidities, should include a clinical interview consisting of a sleep history (sleep habits, sleep environment, work schedules, circadian factors), the use of sleep questionnaires and sleep diaries, questions about somatic and mental health, a physical examination and additional measures if indicated (i.e. blood tests, electrocardiogram, electroencephalogram; strong recommendation, moderate-to high-quality evidence). Polysomnography can be used to evaluate other sleep disorders if suspected (i.e. periodic limb movement disorder, sleep-related breathing disorders), in treatment-resistant insomnia, for professional at-risk populations and when substantial sleep state misperception is suspected (strong recommendation, high-quality evidence). Cognitive behavioural therapy for insomnia is recommended as the first-line treatment for chronic insomnia in adults of any age (strong recommendation, high-quality evidence). A pharmacological intervention can be offered if cognitive behavioural therapy for insomnia is not sufficiently effective or not available. Benzodiazepines, benzodiazepine receptor agonists and some antidepressants are effective in the short-term treatment of insomnia (

This chapter evaluates evidence-based treatment options for chronic insomnia. Insomnia is a common sleep disorder characterized by sleep onset and maintenance difficulties and daytime impairment such as reduced concentration and motivation. Cognitive behavioral therapy for insomnia (CBTI) is the first-line treatment for chronic primary and comorbid insomnia. CBTI comprises behavioral treatment (sleep restriction, stimulus control), relaxation, cognitive therapy, and sleep education. Its effects are of medium to large size and are stable up to two years after treatment. Benzodiazepines and benzodiazepine receptor agonists are equally effective for short-term treatment. However, because of their adverse effects, especially in the elderly, and their potential for tolerance and dependence, they are only recommended for a treatment period up to four weeks. Low doses of sedating antidepressants are commonly prescribed for treating chronic insomnia and have shown promising results in clinical trials. However, more research on their long-term efficacy and safety is needed.

Objective/Background: Sleep-related attentional bias has been suggested to represent an important factor for the maintenance of chronic insomnia. However, little is known about potentially underlying psychological mechanisms such as threat or craving. As these are associated with distinguishable brain activation patterns, we performed a functional neuroimaging study. Participants/Methods: Functional magnetic resonance imaging was used to investigate brain reactivity to sleep-related words in 20 patients with primary insomnia according to DSM-IV criteria and 35 good sleeper controls according to Research Diagnostic Criteria. In addition, an emotional Stroop task was performed in all participants outside the scanner to investigate sleep-related attentional bias. Results: Contrary to the hypotheses, patients with chronic insomnia did not differ from good sleeper controls in terms of threat- or craving-related brain reactivity to sleep-related words. In addition, the emotional Stroop task did not reveal any significant group difference in sleep-related attentional bias. Exploratory analyses did not show any significant correlations between brain reactivity/selective attention to sleep-related words and questionnaire scores/PSG parameters. Conclusions: The results from the present study call into question that attentional bias to sleep-related stimuli is a core feature of chronic insomnia. Future studies may use pictorial stimuli and larger sample sizes for investigating sleep-related information processing in insomnia.

In diesem Beitrag hat sich unter „Einhaltung ethischer Richtlinien“ ein Fehler bei der Angabe der Interessenkonflikte eingeschlichen. Korrekt ist: David D. Ebert und Dirk Lehr sind Gesellschafter des GET.ON Instituts. Die fehlende Nennung dieses Interessenkonflikts wurde durch einen …

Chronische Insomnie, d. h. Klagen über Ein- und Durchschlafstörungen, frühmorgendliches Erwachen und damit verbundene Beeinträchtigung der Befindlichkeit während des Tages betreffen etwa 10 % der Bevölkerung in den meisten westlichen Industrienationen. Ursächlich für chronische Schlaflosigkeit können körperliche Erkrankungen, psychische Erkrankungen, die Einnahme von Medikamenten, Genussmittel oder Drogen sein. Ein Drittel aller chronischen Insomnien wird als primäre Insomnie oder insomnische Störung bezeichnet, wenn keiner der oben genannten Faktoren ursächlich identifiziert werden kann. Üblicherweise werden chronische Insomnien in der ärztlichen Praxis medikamentös mit Hypnotika oder anderen sedierenden Substanzen, wie etwa sedierenden Antidepressiva behandelt. In den letzten 20 Jahren hat sich gezeigt, dass kognitiv-verhaltenstherapeutische Ansätze (KVT) bei chronischen Insomnien auch unabhängig von der Ursache erfolgreich eingesetzt werden können. Zu den Methoden der kognitiven Verhaltenstherapie gehört die Aufklärung über Schlaf und Schlafhygiene (Psychoedukation), Entspannungstechniken wie etwa die progressive Muskelentspannung, spezifische verhaltenstherapeutische Techniken wie etwa die Stimuluskontrolle oder die Schlafrestriktion sowie kognitive Techniken zur Reduktion nächtlicher Grübeleien. Aufgrund von mehreren, in den letzten Jahren veröffentlichten Meta-Analysen können diese Techniken insbesondere in ihrer Applikation als Kombinationstherapie, als evidenz-basiert und der pharmakologischen Therapie als kurzzeitig gleichwertig und langfristig überlegen angesehen werden. Die kognitiv-verhaltenstherapeutischen Techniken der Insomniebehandlung können von darin geschulten Ärzten und Psychotherapeuten mit Erfolg eingesetzt werden.

Insomnia is one of the most common sleep disorders, and it frequently co‐occurs with several other psychiatric conditions. The relationship between insomnia and eating disorders is supported by cli...

Im Alter nehmen REM-Schlaf und Tiefschlaf ab: Der REM-Schlaf-Anteil betragt bei Erwachsenen ca. 20%, Tiefschlaf ist bei 40- bis 50-Jahrigen oft gar nicht mehr nachweisbar. Schlafstorungen werden mittels ICD-10, DSM-V sowie ICSD-3 klassifiziert.Epidemiologischen Studien zufolge leiden ca. 10–20% der Bevolkerung an insomnischen Beschwerden. Das macht die Insomnie zu einem der haufigsten Krankheitsbilder uberhaupt.Eine chronische Insomnie stellt ein erhohtes Risiko fur psychische Erkrankungen dar, v. a. fur die Entwicklung einer Depression.Zu den psychotherapeutischen Interventionen gehoren u. a. Psychoedukation, Stimuluskontrolle, Schlafrestriktion, Entspannungstechniken und kognitive Techniken.In der medikamentosen Therapie werden Benzodiazepine, sedierende Antidepressiva, Neuroleptika, Phytotherapeutika und Melatonin eingesetzt. Hier liegen unterschiedliche Wirksamkeitsnachweise vor.

Short sleep duration, poor sleep quality, and insomnia frequently characterize sleep in pregnancy during all three trimesters. We aimed: (i) to review the clinical evidence of the association between conditions of sleep loss during pregnancy and adverse pregnancy outcomes; and (ii) to discuss the potential pathophysiological mechanisms that may be involved. A systematic search of cross-sectional, longitudinal studies using Medline, Embase, and PsychINFO, and MeSH headings and key words for conditions of sleep loss such as ‘insomnia’, ‘poor sleep quality’, ‘short sleep duration’, and ‘pregnancy outcome’ was made for papers published between January 1, 1960 and July 2013. Twenty studies met inclusion criteria for sleep loss and pregnancy outcome: seven studies on prenatal depression, three on gestational diabetes, three on hypertension, pre-eclampsia/eclampsia, six on length of labor/type of delivery, eight on preterm birth, and three on birth grow/birth weight. Two main results emerged: (i) conditions of chronic sleep loss are related to adverse pregnancy outcomes; and (ii) chronic sleep loss yields a stress-related hypothalamic– pituitary–adrenal axis and abnormal immune/inflammatory, reaction, which, in turn, influences pregnancy outcome negatively. Chronic sleep loss frequently characterizes sleep throughout the course of pregnancy and may contribute to adverse pregnancy outcomes. Common pathophysiological mechanisms emerged as being related to stress system activation. We propose that in accordance to the allostatic load hypothesis, chronic sleep loss during pregnancy may also be regarded as both a result of stress and a physiological stressor per se, leading to stress ‘overload’. It may account for adverse pregnancy outcomes and somatic and mental disorders in pregnancy.

Im DSM-5 wird eine Klassifikation von Schlaf-Wach-Storungen dargestellt, die fur den Bereich der Psychiatrie und Psychotherapie gut geeignet ist. Auf eine uberflussige Undifferenziertheit wurde verzichtet und Storungen, bei denen die Atiologie beziehungsweise die Pathophysiologie gut bekannt sind, wurden im Sinne eigenstandiger Krankheitsbilder aufgewertet. Vollkommen aufgegeben wurde die im DSM-IV vorgeschlagene Einteilung in primare versus sekundare versus andere Schlafstorungen. Fur den Bereich der Psychiatrie und Psychotherapie am meisten relevant ist die Einfuhrung der Kategorie „Insomnische Storung“ (insomnia disorder).

Sleep, depression and insomnia have manifold associations. Psychiatric sleep research in affective disorders has demonstrated that sleep in depression is characterized by an impairment of sleep continuity, deficits in slow wave sleep and a disinhibition of REM sleep (including shortened REM latency and increased REM density). Traditionally, insomnia, i.e. prolonged latency to fall asleep and increased frequency of nocturnal wake periods, was considered as an unspecific symptom of affective disorders. In the meantime, a shift in clinical and scientific focus has taken place viewing insomnia in addition as an independent diagnostic entity and as a clinical predictor of depression. Unfortunately, the neurobiological processes underlying the relationships between sleep, insomnia and depression have not been fully identified yet. It is clear that both insomnia and depression are characterized by alterations in the arousal system in the CNS presenting as hyperarousal. Moreover, insomniac patients display reduced and fragmented REM sleep periods, which might interfere negatively with basal processes of emotion regulation. The alterations in the arousal system and the interaction of it with the affect-regulatory system over the course of time might influence cognitive systems and hence lead to the clinical picture of depression. Given the suggestion of insomnia symptoms as possibly involved in the causation and the maintenance of psychopathology in general, this type of sequence might also be found in relation to other mental disorders.

According to self-report questionnaire studies, insomnia patients differ from healthy controls with respect to several personality traits. The current study aimed at exploring how these personality traits may translate into behavior. Insomnia patients' behavior during psychometric testing (n = 163) was investigated in comparison to healthy controls (n = 81), patients with other sleep disorders (n = 80), and patients with obsessive-compulsive disorder (n = 36). In line with our hypotheses, insomnia patients made more additional comments than healthy controls and more corrections than patients with other sleep disorders during sleep-related questionnaire completion. Furthermore, insomnia patients calculated the sum score of a depression questionnaire more frequently than both healthy controls and patients with other sleep disorders. These findings further support the assumption of an altered personality profile in patients with primary insomnia. Future work should aim to elucidate what personality factors these novel behavioral markers may reflect.

Nicotine may affect sleep by influencing sleep-regulating neurotransmitters. Sleep disorders can increase the risk for depression and substance dependency. To detect the influence of sleep disturbances on the effect of smoking cessation, we investigated polysomnographically (PSG) the sleep of smoking subjects during a period of smoking, during withdrawal and after a period of abstinence from nicotine. Thirty-three smokers (23 male, 10 female, median age 29 years, Fagerstrom Test for Nicotine Dependence score 6.3) were examined during smoking, 24-36 hours after smoking and 3 months after cessation. All subjects had an adaptation night followed by the PSG night. Compared with the smoking state, we found increased arousal index and wake time during nicotine withdrawal. Smokers who later relapsed (11) presented a higher degree of nicotine dependence and more withdrawal symptoms than those who abstained (22) and were characterized by less rapid eye movement (REM) sleep, a longer REM latency as well as by more intense sleep impairments in the subjective sleep rating during the withdrawal. Impairments of sleep during the withdrawal phase may reflect more severe nicotine dependence and may contribute to earlier relapse into smoking behaviours.