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Improving maternal's health is a worldwide priority. Sleep is a fundamental operating state of the central nervous system and it may be one of the most important psychophysiological processes for brain function and mental health. The study of maternal sleep problem including insomnia, however, implies deepening our understanding of family context. Family systems are dynamic and involve reciprocal interactions among members during day and night. So far, however, maternal and children's sleep has been rarely studied in a family perspective, and paternal sleep has often been neglected.The present work summarizes in a narrative review the state of the art of our current knowledge on the role of insomnia and poor quality of sleep for mental health in all family members in the peripartum period. The mother, the father, the child and the family interactive perspectives are considered.Insomnia and poor sleep problems are frequent in all family members during peripartum. Poor sleep and insomnia symptoms are recognized as important risk factors for mental health in adults and children. Despite this alarming evidence, sleep is rarely assessed in clinical contexts.Clinical implications include the utmost relevance of assessing sleep problems during pregnancy and early post-partum. Insomnia and poor sleep quality should be evaluated and treated in the clinical practice by using a "family perspective."

Background Therapeutic sleep deprivation (SD) presents a unique paradigm to study the neurobiology of major depressive disorder (MDD). However, the rapid antidepressant mechanism, which differs from today's slow first-line treatments, is not sufficiently understood. We recently integrated two prominent hypotheses of MDD and sleep, the synaptic plasticity hypothesis of MDD and the synaptic homeostasis hypothesis of sleep-wake regulation, into a synaptic plasticity model of therapeutic SD in MDD. Here, we further tested this model positing that homeostatically elevating net synaptic strength through therapeutic SD shifts the initially deficient inducibility of associative synaptic long-term potentiation (LTP)-like plasticity in patients with MDD into a more favorable window of associative plasticity. Methods We used paired associative stimulation (PAS), a transcranial magnetic stimulation protocol (TMS), to quantify cortical LTP-like plasticity after one night of therapeutic sleep deprivation in 28 patients with MDD. Results We demonstrate a significantly different inducibility of associative plasticity in clinical responders to therapeutic SD (> 50% improvement on the 6-item Hamilton-Rating-Scale for Depression, n=13) compared to non-responders (n=15), which was driven by a long-term depression (LTD)-like response in SD-non-responders. Indices of global net synaptic strength (wake EEG theta activity, intracortical inhibition and BDNF serum levels) were increased after SD in both groups, with responders showing a generally lower intracortical inhibition than non-responders. Limitations Repetitive assessments prior to and after treatment would be needed to further determine potential mechanisms. Conclusion After a night of therapeutic SD, clinical responders show a significantly higher inducibility of associative LTP-like plasticity than non-responders.

Postpartum depression (PPD) is a major public health problem that affects approximately 12-18% of women and is associated adverse maternal and infant outcome. Given that untreated maternal depression has negative consequences for both the mother and her child, it is important to deploy effective measures to treat or prevent PPD. Antidepressant treatment after delivery has been proposed for prophylaxis, however, this is not firmly established. Since insomnia is an early sign and a common symptom of PPD in this contribution we argue that management of insomnia may play a key role in the treatment and prevention of PPD. To this aim we by discussed the current evidence about the potential prophylactic role of antidepressants compared to that of insomnia treatment in PPD. We concluded that insomnia symptoms may be a better therapeutic target to prevent or treat PPD which is heterogeneous entity and may be more responsive to interventions addressing a common and early symptom such as insomnia.

Ovarian cancer is the leading cause of gynaecological cancer deaths and the seventh most commonly diagnosed cancer among women worldwide, so that, as it is related to substantial and increasing disease burden, the management of ovarian cancer survivors should be a priority. Such issues involve prevention and management of emotional distress, anxiety/depressive symptoms, and maintenance of quality of life from initial diagnosis to post-treatment. Within this framework, sleep disturbances, in particular insomnia, are emerging as modifiable determinants of mental health, also contributing to substantial morbidity among cancer, including ovarian cancer. To this aim we conducted a systematic review according to PRISMA guidelines on prevalence and management of insomnia and circadian sleep disorders in ovarian cancer, while selecting 22 papers. Insomnia was evaluated in ovarian cancer and, while circadian sleep disturbances were poorly assessed in ovarian cancer, insomnia increased from 14% to 60% of patients. Insomnia was associated with cancer-related comorbid conditions such as emotional distress, anxiety/depressive symptoms and low quality of life. Despite this evidence, no studies have been conducted about insomnia treatment in ovarian cancer. The burden of insomnia and circadian sleep disorders in patients with ovarian cancer still needs to be addressed, and requires a call to action for the evaluation and management of these potential modifiable factors that might contribute to ovarian cancer morbidity.

Background:Arousal and sleep represent basic domains of behavior, and alterations are of high clinical importance. Objective/hypothesis:The aim of this study was to further elucidate the neurobiology of insomnia disorder (ID) and the potential for new treatment developments, based on the modulation of cortical activity through the non-invasivebrain stimulationtechnique transcranial direct current stimulation (tDCS). Specifically, we tested the hypotheses that bi-frontal anodal tDCS shortens and cathodal tDCS prolongs total sleep time in patients with ID, compared to sham stimulation. Furthermore, we tested for differences in indices of arousal between ID patients and healthy controls and explored their potential impact on tDCS effects. Methods:Nineteen ID patients underwent a within-subject repeated-measures sleep laboratory study with adaptation, baseline and three experimental nights. Bifrontal anodal, cathodal and sham tDCS was delivered in a counterbalanced order immediately prior to sleep. WakeEEGwas recorded prior to and after tDCS as well as on the following morning. Subsequently, we compared patients with ID to a healthy control group from an earlier dataset. Results:Against our hypothesis, we did not observe any tDCS effects on sleep continuity or sleep architecture in patients with ID. Further analyses of nights without stimulation demonstrated significantly increased levels of arousal in ID patients compared to healthy controls, as indexed by subjective reports, reduced total sleep time, increased wake after sleep onset and increased high frequency EEG power during wakefulness andNREM sleep. Of note, indices of increased arousal predicted the lack of effect of tDCS in ID patients. Conclusions:Our study characterizes for the first time differential effects of tDCS on sleep in patients with ID and healthy controls, presumably related to persistent hyperarousal in ID. These findings suggest that adapted tDCS protocols need to be developed to modulate arousal and sleep dependent on baseline arousal levels.

“Why treat insomnia?” This question grows out of the perspective that insomnia is a symptom that should only receive targeted treatment when temporary relief is needed or until more comprehensive gains may be achieved with therapy for the parent or precipitating medical or psychiatric disorders. This perspective, however, is untenable given recent data regarding the prevalence, course, consequences, and costs of insomnia. Further, the emerging data that the treatment of insomnia may promote better medical and mental health (alone or in combination with other therapies) strongly suggests that the question is no longer “why treat insomnia,” but rather “when isn’t insomnia treatment indicated?” This perspective was recently catalyzed with the American College of Physicians’ recommendation that chronic insomnia should be treated and that the first line treatment should be cognitive-behavioral therapy for insomnia (CBT-I).

Insomnia is defined as difficulties of initiating and maintaining sleep, early awakening and poor subjective sleep quality despite adequate opportunity and circumstances for sleep with impairment of daytime performance. These components of insomnia – namely persistent sleep difficulties despite of adequate sleep opportunity resulting in daytime dysfunction - appear secondary or co-morbid to neurological diseases. Comorbid insomnia originates from neurodegenerative, inflammatory, traumatic or ischemic changes in sleep regulating brainstem and hypothalamic nuclei with consecutive changes of neurotransmitters. Symptoms of neurological disorders (i.e motor deficits), co-morbidities (i.e. pain, depression, anxiety) and some disease-specific pharmaceuticals may cause insomnia and/or other sleep problems.This guideline focuses on insomnias in headaches, neurodegenerative movement disorders, multiple sclerosis, traumatic brain injury, epilepsies, stroke, neuromuscular disease and dementia.The most important new recommendations are: Cognitive behavioral therapy (CBTi) is recommended to treat acute and chronic insomnia in headache patients. Insomnia is one of the most frequent sleep complaints in neurodegenerative movement disorders. Patients may benefit from CBTi, antidepressants (trazodone, doxepin), melatonin and gaba-agonists. Insomnia is a frequent precursor of MS symptoms by up to 10 years. CBTi is recommended in patients with MS, traumatic brain injury and. Melatonin may improve insomnia symptoms in children with epilepsies. Patients with insomnia after stroke can be treated with benzodiazepine receptor agonists and sedating antidepressants. For patients with dementia suffering from insomnia trazodone, light therapy and physical exercise are recommended.

Study Objectives Insomnia is defined by the subjective complaint of poor sleep as well as daytime impairments. Since polysomnography (PSG) typically shows only modest sleep impairment, some still unidentified property of sleep, not mirrored in PSG, may be modified in insomnia. One possible mechanistic hypothesis is that insomnia patients may be more sensitive to inevitably occurring internal or external stimuli during the night, causing brief sleep disruptions then perceived as wake time. Methods Auditory event-related potentials (ERP) to low intensity (50 dB SPL) synthesized guitar tones played continuously throughout two nights of polysomnographically registered sleep were obtained in fifty patients with insomnia disorder (ID, without comorbidities) and 50 age- and sex-matched good sleeper controls (GSC) for each sleep stage and NREM/REM cycle. Phasic and tonic REM were treated as separate stages. Latencies and amplitudes of components P1, N1 and P2 were measured and analyzed by multivariate repeated-measures ANCOVA including effects of group, night, cycle, and age. Results ID showed reduced P2 amplitudes relative to GSC specifically in phasic REM sleep. The same reduction also correlated with the amount of sleep misperception across groups. Independent component analysis showed a frontal negativity to contribute most to this group difference. Conclusions The present finding can be interpreted as increased mismatch negativity (MMN) in ID, reflecting automated detection of change in the auditory system and a concomitant orienting response. Specifically phasic REM sleep appears to be vulnerable to sensory afferences in ID patients, possibly contributing to the perception of being awake. Clinical Trial Information Short name “PERSLEEP 2,” URL https://www.drks.de/drks_web/navigate.do?navigationId=trial.HTML&TRIAL_ID=DRKS00008965, Registration DRKS00008965.

Background and purpose: Insomnia is a common and debilitating disorder that is frequently associated with important consequences for physical health and well-being. Methods: An international expert group considered the current state of knowledge based on the most relevant publications in the previous 5 years, discussed the current challenges in the field of insomnia and identified future priorities. Results: The association of trajectories of insomnia with subsequent quality of life, health and mortality should be investigated in large populations. Prospective health economics studies by separating the costs driven specifically by insomnia and costs attributable to its long-term effects are needed. Ignoring the heterogeneity of insomnia patients leads to inadequate diagnosis and inefficient treatment. Individualized interventions should be promoted. More data are needed on both the impact of sleep on overnight effects, such as emotion regulation, and the potential compensatory effort to counteract diurnal impairments. Another gap is the definition of neurocognitive deficits in insomnia patients compared to normal subjects after chronic sleep loss. There are also a number of key gaps related to insomnia treatment. Expert guidelines indicate cognitive–behavioural therapy for insomnia as first-line treatment. They neglect, however, the reality of major healthcare providers. The role of combined therapy, cognitive–behavioural therapy for insomnia plus pharmacological treatment, should be evaluated more extensively. Conclusion: Whilst insomnia disorder might affect large proportions of the population, there are a number of significant gaps in the epidemiological/clinical/research studies carried out to date. In particular, the identification of different insomnia phenotypes could allow more cost-effective and efficient therapies.

Background: Psychotherapy and pharmacotherapy are first-line treatments for mental disorders. Despite recent improvements, only approximately 50% of the patients reach sustained remission, indicating a need for novel developments. The main concept put forward in this systematic review and hypothesis article is the targeted co-administration of defined neurobiological interventions and specific psychotherapeutic techniques. Methods: We conducted a systematic literature search for randomized controlled trials comparing the efficacy of augmented psychotherapy to psychotherapy alone. Results: Thirty-five trials fulfilled the inclusion criteria. The majority (29 trials) used augmentation strategies such as D-cycloserine, yohimbine, or sleep to enhance the effects of exposure therapy for anxiety disorders. Fewer studies investigated noninvasive brain stimulation with the aim of improving cognitive control, psychedelic compounds with the aim of enhancing existentially oriented psychotherapy, and oxytocin to improve social communication during psychotherapy. Results demonstrate small augmentation effects for the enhancement of exposure therapy – however, some of the studies found negative results. Other methods are less thoroughly researched, and results are mixed. Conclusions: This approach provides an open matrix for further research and has the potential to systematically guide future studies.

Contains fulltext : 243961.pdf (Publisher’s version ) (Closed access) Neuroimaging and genetics studies have advanced our understanding of the neurobiology of sleep and its disorders. However, individual studies usually have limitations to identifying consistent and reproducible effects, including modest sample sizes, heterogeneous clinical characteristics and varied methodologies. These issues call for a large-scale multi-centre effort in sleep research, in order to increase the number of samples, and harmonize the methods of data collection, preprocessing and analysis using pre-registered well-established protocols. The Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) consortium provides a powerful collaborative framework for combining datasets across individual sites. Recently, we have launched the ENIGMA-Sleep working group with the collaboration of several institutes from 15 countries to perform large-scale worldwide neuroimaging and genetics studies for better understanding the neurobiology of impaired sleep quality in population-based healthy individuals, the neural consequences of sleep deprivation, pathophysiology of sleep disorders, as well as neural correlates of sleep disturbances across various neuropsychiatric disorders. In this introductory review, we describe the details of our currently available datasets and our ongoing projects in the ENIGMA-Sleep group, and discuss both the potential challenges and opportunities of a collaborative initiative in sleep medicine.

Objectives: One of the largest clusters of Covid-19 infections was observed in Italy. The population was forced to home confinement, exposing individuals to increased risk for insomnia, which is, in turn, associated with depression and anxiety. Through a cross-sectional online survey targeting all Italian adult population (≥18 yrs), insomnia prevalence and its interactions with relevant factors were investigated.Methods: The survey was distributed from 1st April to 4th May 2020. We collected information on insomnia severity, depression, anxiety, sleep hygiene behaviors, dysfunctional beliefs about sleep, circadian preference, emotion regulation, cognitive flexibility, perceived stress, health habits, self-report of mental disorders, and variables related to individual difference in life changes due to the pandemic's outbreak.Results: The final sample comprised 1,989 persons (38.4 ± 12.8 yrs). Prevalence of clinical insomnia was 18.6%. Results from multivariable linear regression showed that insomnia severity was associated with poor sleep hygiene behaviors [β = 0.11, 95% CI (0.07–0.14)]; dysfunctional beliefs about sleep [β = 0.09, 95% CI (0.08–0.11)]; self-reported mental disorder [β = 2.51, 95% CI (1.8–3.1)]; anxiety [β = 0.33, 95% CI (0.25–0.42)]; and depression [β = 0.24, 95% CI (0.16–0.32)] symptoms.Conclusion: An alarming high prevalence of clinical insomnia was observed. Results suggest that clinical attention should be devoted to problems of insomnia in the Italian population with respect to both prevention and treatment.

Insomnia disorder is defined as persistent difficulty with initiating or maintaining sleep, or early morning awakening accompanied by daytime impairment. Although insomnia disorder is a highly prevalent disorder and a major public health burden, the pathophysiology of the disorder is still not fully understood. Neurobiological as well as psychological models have been suggested highlighting genetic, behavioral, cognitive, emotional, and neurobiological factors. While psychological perspectives emphasize the role of dysfunctional sleep-related cognitions and a selective attention toward sleep-related stimuli, neurobiological perspectives particularly look at physiological alterations such as brain circuits that may be involved in the pathophysiology of insomnia. Relevant models explaining how insomnia develops and how it becomes chronic are described, and the evidence is summarized. Thus, this chapter provides an overview of important etiological models and further approaches dealing with the pathophysiology of insomnia disorder.

Aim The study aimed to investigate the potential pathways mediating early exposure to stressful events and the clinical manifestations of bipolar disorder (BD), such as severity of mood symptoms, hopelessness and suicidal ideation, focusing on the potential role of insomnia symptoms. Method A sample of 162 adult participants with BD I or II were assessed during depressed phase using the Structural Clinical Interview for DSM-5 (SCID-5), the Beck Depression Inventory-II (BDI-II), the Young Mania Rating Scale (YMRS), the Early Trauma Inventory Self Report-Short Form (ETISR-SF), the Beck Hopelessness Scale (BHS), the Insomnia Severity Index (ISI) and the Scale for Suicide Ideation (SSI). Participants with or without clinically significant insomnia were compared and we carried out correlations, regression and mediation analyses. Results Participants with insomnia showed a greater severity of depressive symptoms,of suicidal risk, of the cognitive component of hopelessness and of early life stressors. Insomnia symptoms mediated the association among early life stress and depressive symptoms (Z = 2.72, p = 0.0006), the cognitive component of hopelessness (Z = 3.02, p = 0.0001) and suicidal ideation and plans (Z = 2.07 p = 0.0006). Conclusion Insomnia may mediate the relationship between early life stress and clinical manifestations of BD. Assessing the evolution of insomnia symptoms could offer an approach to characterize BD and to formulate treatment strategies. In particular targeting insomnia symptoms might potentially modify the clinical features of BD in response to early life stressful events.

In the current global home confinement situation due to the COVID-19 outbreak, most individuals are exposed to an unprecedented stressful situation of unknown duration. This may not only increase daytime stress, anxiety and depression levels, but also disrupt sleep. Importantly, because of the fundamental role that sleep plays in emotion regulation, sleep disturbance can have direct consequences upon next day emotional functioning. In this paper, we summarize what is known about the stress-sleep link and confinement as well as effective insomnia treatment. We discuss those effects of the current home confinement situation that can disrupt sleep but also those that could benefit sleep quality. We suggest adaptions of cognitive behavioural therapy elements that are feasible to implement for those facing changed work schedules and requirements, those with health anxiety and those handling childcare and home-schooling, whilst also recognizing the general limitations imposed on physical exercise and social interaction. Managing sleep problems as best as possible during home confinement can limit stress and possibly prevent disruptions of social relationships.

Summary Repetitive negative thinking (RNT), i.e., worry, rumination, and transdiagnostic repetitive thinking, is thought to exacerbate and perpetuate insomnia in cognitive models. Moreover, RNT is a longitudinal precursor of depression and anxiety, which are often co-present alongside insomnia. Whilst accumulating evidence supports the efficacy of cognitive behavioural therapy for insomnia (CBT-I) in reducing depression and anxiety symptoms, the literature on the effects of CBT-I on RNT has never been systematically appraised. Importantly, preliminary evidence suggests that reduction of RNT following CBT-I may be associated with reduction of depression and anxiety. Therefore, we aimed to conduct a systematic review and meta-analysis on the effects of CBT-I on RNT. Seven databases were searched, and 15 randomised controlled trials were included. Results showed moderate-to-large effects of CBT-I on worry (Hedge's g range: −0.41 to g = −0.71) but small and non-reliable effects on rumination (g = −0.13). No clear evidence was found for an association between post-treatment reduction in RNT and post-treatment reduction in depression and anxiety. Although the literature is small and still developing, CBT-I seems to have a stronger impact on sleep-related versus general measures of RNT. We discuss a research agenda aimed at advancing the study of RNT in CBT-I trials.

Perfectionism is one of several personality traits associated with insomnia. Whilst research has examined the relationships between perfectionism and insomnia, the mediating role of dysfunctional sleep-related cognition (i.e. sleep-related worry and dysfunctional beliefs about the biological attribution of and consequences of poor sleep) has yet to be examined. This study aimed to determine whether aspects of multidimensional perfectionism were related to increased reporting of insomnia symptoms. In addition, the potential mediating role of dysfunctional sleep-related cognition and anxiety symptoms was examined. Members of the general population (N = 624) completed the Dysfunctional Beliefs and Attitudes About Sleep Scale, the Insomnia Severity Index, the Hospital Anxiety and Depression Scale, and the Multidimensional Perfectionism Scale. The results showed that perfectionism dimensions, anxiety symptoms, and dysfunctional sleep-related cognition were significantly associated with insomnia symptoms. Regression-based mediation analyses further showed that both dysfunctional sleep-related cognition and anxiety significantly mediated the associations between insomnia symptoms and three perfectionism dimensions (i.e. doubts about action, parental expectations, and parental criticism). The experience of perfectionistic tendencies, anxiety, and dysfunctional sleep-related cognition may initiate behavioural strategies (e.g. daytime napping) when faced with an acute sleep problem. However, these strategies may serve to transition insomnia from an acute to a chronic condition. Electronic supplementary material The online version of this article (10.1007/s10339-019-00937-8) contains supplementary material, which is available to authorized users.

Trauma-induced insomnia is a symptom of posttraumatic stress disorder (PTSD), and is reported to be particularly distressing and often persists even after remission of the core symptoms of PTSD. Recently, it has been suggested that fear of sleep plays an important role in the development and maintenance of trauma-induced insomnia. The aim of this review is to propose a conceptual model of fear of sleep as a maintaining factor of trauma-induced insomnia. After a brief overview of the role of sleep in PTSD, the concept of fear of sleep is introduced. Theoretical considerations and empirical findings on the role of fear of sleep for trauma-induced insomnia in the context of PTSD are summarized and integrated. Specifically, links between PTSD symptoms and fear of sleep are presented, as well as possible consequences of fear of sleep leading to trauma-induced insomnia. Finally, we highlight methodological issues, identify areas for future research, and discuss potential clinical implications.

Sleep problems during pregnancy are prevalent and could be linked to negative outcomes during pregnancy or post-partum. However, these complaints are often underdiagnosed and undertreated. This review aimed to systematically assess the effectiveness of different interventions to ameliorate poor sleep quality and insomnia during pregnancy. Pubmed, PsycINFO and Medline databases were systematically searched without publication period restriction until 3rd May 2019. Eligible studies had to: include pregnant women of any age and gestational age; use clinical intervention designs targeted at improving sleep outcome; report pre- and post-treatment data for one or more sleep-related outcomes; be published in English, Italian, German, Spanish, or French. Sixteen studies were selected including 1252 expecting mothers. Studies evaluated the efficacy of various interventions: cognitive behavioral interventions for insomnia (4); pharmacotherapy (1); acupuncture (1); mindfulness and yoga (3); relaxation (5) and herbal medication (2). Only six were randomized controlled trials, and only four evaluated longitudinal outcomes. Preliminary support was found for all interventions, but our knowledge is still too limited by lack of evidence. There is an utmost urgency to perform high-quality randomized controlled trials for insomnia interventions during pregnancy and to implement effective programs in standard gynecological care.

Since ancient times it is known that melancholia and sleep disturbances co-occur. The introduction of polysomnography into psychiatric research confirmed a disturbance of sleep continuity in patients with depression, revealing not only a decrease in Slow Wave Sleep, but also a disinhibition of REM (rapid eye movement) sleep, demonstrated as a shortening of REM latency, an increase of REM density, as well as total REM sleep time. Initial hopes that these abnormalities of REM sleep may serve as differential-diagnostic markers for subtypes of depression were not fulfilled. Almost all antidepressant agents suppress REM sleep and a time-and-dose-response relationship between total REM sleep suppression and therapeutic response to treatment seemed apparent. The so-called Cholinergic REM Induction Test revealed that REM sleep abnormalities can be mimicked by administration of cholinomimetic agents. Another important research avenue is the study of chrono-medical timing of sleep deprivation and light exposure for their positive effects on mood in depression. Present day research takes the view on insomnia, i.e., prolonged sleep latency, problems to maintain sleep, and early morning awakening, as a transdiagnostic symptom for many mental disorders, being most closely related to depression. Studying insomnia from different angles as a transdiagnostic phenotype has opened many new perspectives for research into mechanisms but also for clinical practice. Thus, the question is: can the early and adequate treatment of insomnia prevent depression? This article will link current understanding about sleep regulatory mechanisms with knowledge about changes in physiology due to depression. The review aims to draw the attention to current and future strategies in research and clinical practice to the benefits of sleep and depression therapeutics.

Insomnia, the most prevalent sleep disorder worldwide, confers marked risks for both physical and mental health. Furthermore, insomnia is associated with considerable direct and indirect healthcare costs. Recent guidelines in the US and Europe unequivocally conclude that cognitive behavioural therapy for insomnia (CBT‐I) should be the first‐line treatment for the disorder. Current treatment approaches are in stark contrast to these clear recommendations, not least across Europe, where, if any treatment at all is delivered, hypnotic medication still is the dominant therapeutic modality. To address this situation, a Task Force of the European Sleep Research Society and the European Insomnia Network met in May 2018. The Task Force proposed establishing a European CBT‐I Academy that would enable a Europe‐wide system of standardized CBT‐I training and training centre accreditation. This article summarizes the deliberations of the Task Force concerning definition and ingredients of CBT‐I, preconditions for health professionals to teach CBT‐I, the way in which CBT‐I should be taught, who should be taught CBT‐I and to whom CBT‐I should be administered. Furthermore, diverse aspects of CBT‐I care and delivery were discussed and incorporated into a stepped‐care model for insomnia. publishedVersion

According to the diathesis-stress model of insomnia, insomnia may develop in vulnerable individuals in response to stress. Resilience is a psychobiological factor that determines an individual's capacity to adapt successfully to stressful events and low resilience increases vulnerability for development of mental disorders. The aim was to explore resilience in subjects with insomnia and its relationship with the factors that contribute to its development and perpetuation.The study consisted of 58 subjects with Insomnia Disorder according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition and 38 good sleepers. Resilience Scale for Adults (RSA), Ford Insomnia Response to Stress Test (FIRST), Pre-sleep Arousal Scale (PSAS), and Difficulties in Emotion Regulation Scale (DERS) were administered while taking into account psychiatric symptoms. Differences in means between groups were assessed usingSubjects with insomnia (24 females, mean age 49 ± 2.1 years) had lower RSA and higher FIRST, DERS, and PSAS scores than good sleepers (22 females, mean age 47.2 ± 1.2 years). After controlling for anxiety/depressive symptoms, low resilience correlated with high stress-related sleep reactivity (Subjects with insomnia showed low resilience, which was related to high stress-related sleep reactivity, emotional dysregulation, and hyperarousal. If resilience helps to minimize the extent of pathogenesis in the developmental process, an early identification of vulnerable candidates should be useful for preventing insomnia development and maintenance.A commentary on this article appears in this issue on page 709.

Studies show that unhelpful cognitive processes play a role in insomnia, whereas interpersonal factors have been less studied in insomnia. Attachment theory can be used as a cognitive-interpersonal framework for understanding insomnia. Because attachment insecurity (vs security) is related to psychiatric disorders the objective was to study the attachment style in insomnia. To this aim sixty-four subjects with Insomnia Disorder (DSM-5) and 38 good sleepers were evaluate in a cross-sectional study with: Attachment Style Questionnaire (ASQ), Arousal Predisposition Scale (APS), Pre-Sleep Arousal Scale (PSAS) and Difficulties in Emotion Regulation Scale (DERS). Differences in means between groups were assessed using t-test or Mann-Whitney U/Wilcoxon test. Linear/multiple regression analyses were performed. Subjects with insomnia (mean age 47.1 + 13 yrs) presented an insecure attachment style and higher scores in all the scales (ASQ, APS, PSAS, DERS p < 0.0001) than good sleepers (mean age 48.2 + 14 yrs). After taking into account anxiety/depressive symptoms, insecure attachment was related to hyperarousal trait (p = 0.02), pre-sleep hyperarousal (p = 0.04) and emotion dysregulation (p = 0.002). In conclusion subjects with insomnia showed an insecure attachment which was related to hyperarousal trait, pre-sleep hyperarousal and emotion dysregulation. It may intervene in the trajectory of insomnia starting from predisposition to perpetuation. Clinical implications are discussed.

Summary This review aimed to assess the impact of behavioural therapy for insomnia administered alone (BT-I) or in combination with cognitive techniques (cognitive-behavioural therapy for insomnia, CBT-I) on depressive and fatigue symptoms using network meta-analysis. PubMed, Scopus and Web of Science were searched from 1986 to May 2015. Studies were included if they incorporated sleep restriction, a core technique of BT-I treatment, and an adult insomnia sample, a control group and a standardised measure of depressive and/or fatigue symptoms. Face-to-face, group, self-help and internet therapies were all considered. Forty-seven studies were included in the meta-analysis. Eleven classes of treatment or control conditions were identified in the network. Cohen's d at 95% confidence interval (CI) was calculated to assess the effect sizes of each treatment class as compared with placebo. Results showed significant effects for individual face-to-face CBT-I on depressive ( d = 0.34, 95% CI: 0.06–0.63) but not on fatigue symptoms, with high heterogeneity between studies. The source of heterogeneity was not identified even after including sex, age, comorbidity and risk of bias in sensitivity analyses. Findings highlight the need to reduce variability between study methodologies and suggest potential effects of individual face-to-face CBT-I on daytime symptoms.

Background : Bipolar disorders are complex disorders involving the interaction of multiple factors. Affective temperaments, insomnia, and chronobiological rhythms desynchronization may all contribute to bipolar disorder. Since there is a paucity of research examining this topic we aimed to study how they are interrelated and collectively associated with clinical features of bipolar disorder. Method : One-hundred patients with Bipolar Disorder type II depressive episode with and without mixed features were recruited and compared. Subjects were evaluated with SCID -5, the Biological Rhythms Interview of Assessment in Neuropsychiatry (BRIAN), the Insomnia Severity Index (ISI), and the Temperament Evaluation of Memphis, Pisa, Paris, and San Diego Auto-questionnaire (TEMPS-A) while evaluating depressive (Beck Depression Inventory-BDI-II) and manic (Young Mania Rating Scale-YMRS) symptoms. Logistic regression and mediation analyses were conducted. Results : Subjects with mixed features showed a higher scores in both insomnia and chronobiological rhythms scores. When considering affective temperaments not only depressive, cyclothymic and irritable temperaments predicted mood symptoms but also insomnia (depressive symptoms O.R. 4.17, p = 0.043) and chronobiological sleep de-synchronization (manic symptoms O.R. 8.69, p = 0.001). Insomnia symptoms and chronobiological alterations mediated the association between affective temperaments and mood symptoms. Limitations : the cross-sectional design limited any causal interpretation. Conclusion : Subjects with mixed features showed a greater severity of insomnia and chronobiological rhythm de-synchronization compared to subjects without. Insomnia and chronobiological alterations may contribute to mood disorders together with affective temperaments in a complex interplay also mediating their effect on mood. Preventive strategies for bipolars should also act on the dysregulation of sleep and circadian rhythms.

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.

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.

Therapeutic sleep deprivation (SD) is a rapid acting treatment for major depressive disorder (MDD). Within hours, SD leads to a dramatic decrease in depressive symptoms in 50-60% of patients with MDD. Scientifically, therapeutic SD presents a unique paradigm to study the neurobiology of MDD. Yet, up to now, the neurobiological basis of the antidepressant effect, which is most likely different from today's first-line treatments, is not sufficiently understood. This article puts the idea forward that sleep/wake-dependent shifts in synaptic plasticity, i.e., the neural basis of adaptive network function and behavior, represent a critical mechanism of therapeutic SD in MDD. Particularly, this article centers on two major hypotheses of MDD and sleep, the synaptic plasticity hypothesis of MDD and the synaptic homeostasis hypothesis of sleep-wake regulation, and on how they can be integrated into a novel synaptic plasticity model of therapeutic SD in MDD. As a major component, the model proposes that therapeutic SD, by homeostatically enhancing cortical synaptic strength, shifts the initially deficient inducibility of associative synaptic long-term potentiation (LTP) in patients with MDD in a more favorable window of associative plasticity. Research on the molecular effects of SD in animals and humans, including observations in the neurotrophic, adenosinergic, monoaminergic, and glutamatergic system, provides some support for the hypothesis of associative synaptic plasticity facilitation after therapeutic SD in MDD. The model proposes a novel framework for a mechanism of action of therapeutic SD that can be further tested in humans based on non-invasive indices and in animals based on direct studies of synaptic plasticity. Further determining the mechanisms of action of SD might contribute to the development of novel fast acting treatments for MDD, one of the major health problems worldwide.

Insomnia is defined as a difficulty initiating or maintaining sleep with daytime impairments like increased fatigue, decreased attention, and increased mood irritability for at least three nights a week for a period of 3 months. DSM 5 has established a new overarching category of insomnia disorder, thus replacing the old primary vs. secondary dichotomy. Insomnia has been traditionally viewed as a symptom or consequence of somatic or mental disorders. The last decade has seen a paradigm shift, focusing more on the question whether insomnia as an independent diagnostic entity may be predictive for other disorders/diseases, especially in the cardiovascular and mental area. There is now strong evidence that insomnia is a risk factor for cardiovascular disorders on the one hand and for mental disorders, especially depression, on the other hand. These data raise the question, whether early and adequate treatment of insomnia may be preventive for the somatic or mental sequelae of the disorder. The first-line treatment for insomnia is cognitive behavioral treatment (CBT-I) which comprises techniques like education about sleep, behavioral recommendations, relaxation training and cognitive restructuring. These techniques are usually delivered as a treatment package in one to eight sessions. CBT-I has been shown to be very effective for the treatment of insomnia. There is now also growing evidence that this type of treatment is effective in comorbid insomnia, i.e. insomnia coupled with mental or somatic disorders. First tentative data indicate that insomnia treatment may be effective as prevention for mental and somatic disorders.

Insomnia disorder, defined by nocturnal and daytime symptoms, is highly prevalent worldwide and is associated with the onset of mental illness. Although daytime symptoms are often the reason insomnia patients seek help, it is not clear whether recommended treatment is effective on daytime symptoms. We aimed to investigate the efficacy of cognitive and behavior therapies for insomnia (CBT–I) on all daytime symptoms explored in the literature using both direct and indirect data. 86 studies (15,578 participants) met inclusion criteria. Results showed significant effects of CBT-I administered face-to-face individually, in group and different self-help settings on depressive symptoms, anxiety, daytime sleepiness, fatigue, quality of life, daytime and social functioning and mental state, with Cohen's d's ranging from −0.52 and 0.81. Our results suggest that CBT-I is effective in the treatment of daytime symptoms, albeit with predominantly small to moderate effects compared to far stronger effects on the core symptoms of insomnia. Effects may be biased for depressive and anxiety symptoms, since many included studies excluded patients with severe levels of these complaints. Further, small to moderate effects may reflect that CBT–I, by improving nighttime symptoms, has a positive effect on daytime symptoms, but it does not target the daytime symptoms directly. Future studies may benefit from adding therapeutic techniques that address daytime symptoms more directly.

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.

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.

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.

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.