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Introduction: Since insomnia and disturbed sleep may affect neuroplasticity, we aimed at reviewing their potential role as markers of disrupted neuroplasticity involved in mood disorders. Method: We performed a systematic review, according to PRIMA, on PubMed, PsycINFO and Embase electronic databases for literature regarding mood disorders, insomnia, sleep loss/deprivation in relation to different pathways involved in the impairment of neuroplasticity in mood disorders such as (1) alterations in neurodevelopment (2) activation of the stress system (3) neuroinflammation (4) neurodegeneration/neuroprogression, (5) deficit in neuroprotection. Results: Sixty-five articles were analyzed and a narrative/ theoretical review was conducted. Studies showed that insomnia, sleep loss and sleep deprivation might impair brain plasticity of those areas involved in mood regulation throughout different pathways. Insomnia and disrupted sleep may act as neurobiological stressors by over-activating the stress and inflammatory systems, which may affect neural plasticity causing neuronal damage. In addition, disturbed sleep may favor a deficit in neuroprotection hence contributing to impaired neuroplasticity. Conclusions: Insomnia and disturbed sleep may play a role as markers of alteration in brain plasticity in mood disorders. Assessing and targeting insomnia in the clinical practice may potentially play a neuroprotective role, contributing to “repairing” alterations in neuroplasticity or to the functional recovery of those areas involved in mood and emotion regulation.

Abstact Study Objectives The long-term effects of sleep health and shift work on cognitive performance are unclear. In addition, research has been limited by small sample sizes and short follow-up periods. We conducted one of the largest examinations of the longitudinal influence of sleep health dimensions and shift work on cognitive performance in people of middle and old age using data from the UK Biobank. The hypothesis was that poor sleep health and shift work would predict lower cognitive performance. Methods Self-reported sleep duration, daytime sleepiness, insomnia symptoms, chronotype, and shift work status were assessed as predictors at baseline. Cognitive performance was operationalized by a touchscreen test battery at follow-up between 7.4 ± 2.2 and 9.0 ± 0.9 years after baseline assessment, depending on the specific task. Models were performed for each cognitive domain including relevant confounders (e.g. depression). The alpha level was set at p Results The study sample comprised 9394 participants for the reasoning task, 30 072 for the reaction time task, 30 236 for the visual memory task, 2019 for the numeric memory task, and 9476 for the prospective memory task. Shift work without night shifts (β = −2.0 × 10−1 ± 6.5 × 10−2, p = 0.002) and with night shifts (β = −1.9 × 10−1 ± 7.2 × 10−2, p = 0.010) predicted a significantly reduced performance in the reasoning task. Short sleep duration (β = −2.4 × 10−1 ± 7.9 × 10−2, p = 0.003) and shift work without night shifts (β = −3.9 × 10−1 ± 1.2 × 10−1, p = 0.002) predicted a significantly lower performance in the task probing prospective memory. Conclusions Our results suggest that, after controlling for confounding variables, shift work, and short sleep duration are important predictors for cognitive performance in people of middle and old age. Further work is required to examine causal mechanisms of the observed associations.

Perfectionism is related to insomnia and objective markers of disturbed sleep. This study examined whether multidimensional perfectionism is related to dysfunctional beliefs about sleep, sleep-effort, pre-sleep arousal, and polysomnography-determined markers of sleep amongst individuals with insomnia. The effects of cognitive behavioral therapy for insomnia (CBT-I) on perfectionism was also examined. This was a secondary analysis of a randomized controlled trial on CBT-I. Forty-three insomnia patients were randomized to treatment (receiving CBT-I) or waitlist control groups. Sleep was recorded using polysomnography at baseline. Participants completed measures of perfectionism, dysfunctional beliefs about sleep, sleep-effort and pre-sleep arousal at baseline and post-treatment. Total perfectionism scores and doubts about action, concern over mistakes and personal standards were each significantly related to increased sleep effort, pre-sleep arousal and dysfunctional beliefs about sleep at baseline. Patients receiving treatment displayed increased total perfectionism scores post-treatment d=.49. In those receiving treatment, levels of organization d=.49 and parental expectations d=.47 were significantly increased post-treatment, relative to baseline. In line with the literature, our results confirm that perfectionism is related to insomnia. Here, insomnia was related to increased sleep effort, pre-sleep arousal and dysfunctional beliefs about sleep. The propensity to maintain a high standard of order and organization may be elevated following CBT-I, considering the treatment protocol expects patients to strictly adhere to a set of clearly defined rules. Levels of parental expectations may be increased following CBT-I since the patient-therapist-relationship may trigger implicitly expectations in the patients which are reminiscent of their relationship to their parents.

Existing neuroimaging studies have reported divergent structural alterations in insomnia. Here, we performed a large-scale coordinated meta-analysis by pooling structural brain measures from 1,085 subjects with and without insomnia symptoms across three international ENIGMA-Sleep cohorts. The influence of insomnia on MRI-based brain morphometry using an insomnia brain score was assessed. We collected case-control data from two sites, as well as population-based data from another site. Within each cohort, we used an ordinary least-squares linear regression to investigate the link between the individual regional cortical thickness and subcortical volumes and the presence of insomnia symptoms. Then, we performed a fixed-effects meta-analysis across cohorts based on the first-level results. For the insomnia brain score, weighted logistic ridge regression was performed on one sample, which separated patients with insomnia disorder from controls to train a model based on the segmentation measurements. Afterward, the insomnia brain scores were validated using the other two samples. The model was used to predict the log-odds of the subjects with insomnia given individual insomnia-related brain atrophy. After adjusting for multiple comparisons, we did not detect any significant associations between insomnia symptoms and cortical or subcortical volumes, nor could we identify a global insomnia-related brain atrophy pattern. The current study found inconsistent brain morphology differences between individuals with and without insomnia across three independent cohorts. Further large-scale cross-sectional and longitudinal studies using both structural and functional neuroimaging data are warranted to decipher the pathophysiology of insomnia at the brain level.

An increasing number of studies harness resting-state fMRI functional connectivity analysis to investigate the neurobiological mechanisms of insomnia. The results to date are inconsistent and the detection of minor and widely distributed alterations in functional connectivity requires large sample sizes. The present study investigated associations between insomnia symptoms and resting-state functional connectivity at the whole-brain level in the largest sample to date. This cross-sectional analysis used resting-state imaging data from the UK Biobank, a large scale, population-based biomedical database. The analysis included 29,423 participants (age: 63.1 ± 7.5 years, 54.3% female), comprising 9210 with frequent insomnia symptoms and 20,213 controls without. Linear models were adjusted for relevant clinical, imaging, and socio-demographic variables. The Akaike information criterion was used for model selection. Multiple comparisons were corrected using the false discovery rate with a significance level of q 0.05. Frequent insomnia symptoms were associated with increased connectivity within the default mode network and frontoparietal network, increased negative connectivity between the default mode network and the frontoparietal network, and decreased connectivity between the salience network and a node of the default mode network. Furthermore, frequent insomnia symptoms were associated with altered functional connectivity between nodes comprising sensory areas and the cerebellum. These functional alterations of brain networks may underlie dysfunctional affective and cognitive processing in insomnia and contribute to subjectively and objectively impaired sleep. However, it must be noted that the item that was used to assess frequent insomnia symptoms in this study did not assess all the characteristics of clinically diagnosed insomnia.

Heatwaves are occurring more frequently and are known to affect particularly night-time temperatures. We review here literature on how night-time ambient temperature changes affect body temperature and sleep quality. We then discuss how these temperature effects impact particularly vulnerable populations such as older adults, children, pregnant women, and those with psychiatric conditions. Several ways of dealing with sleep problems in the context of heatwaves are then suggested, adapted from elements of cognitive behavioural therapy for insomnia, with more specific advice for vulnerable populations. By better dealing with sleep problems during heatwaves, general health effects of heatwaves may be more limited. However, given the sparse literature, many links addressed in this review on sleep problems affected by temperature changes should be the focus of future research.

Insomnia disorder comprises symptoms during night and day that strongly affect quality of life and wellbeing. Prolonged sleep latency, difficulties to maintain sleep and early morning wakening characterize sleep complaints, whereas fatigue, reduced attention, impaired cognitive functioning, irritability, anxiety and low mood are key daytime impairments. Insomnia disorder is well acknowledged in all relevant diagnostic systems: Diagnostic and Statistical Manual of the American Psychiatric Association, 5th revision, International Classification of Sleep Disorders, 3rd version, and International Classification of Diseases, 11th revision. Insomnia disorder as a chronic condition is frequent (up to 10% of the adult population, with a preponderance of females), and signifies an important and independent risk factor for physical and, especially, mental health. Insomnia disorder diagnosis primarily rests on self-report. Objective measures like actigraphy or polysomnography are not (yet) part of the routine diagnostic canon, but play an important role in research. Disease concepts of insomnia range from cognitive-behavioural models to (epi-) genetics and psychoneurobiological approaches. The latter is derived from knowledge about basic sleep-wake regulation and encompass theories like rapid eye movement sleep instability/restless rapid eye movement sleep. Cognitive-behavioural models of insomnia led to the conceptualization of cognitive-behavioural therapy for insomnia, which is now considered as first-line treatment for insomnia worldwide. Future research strategies will include the combination of experimental paradigms with neuroimaging and may benefit from more attention to dysfunctional overnight alleviation of distress in insomnia. With respect to therapy, cognitive-behavioural therapy for insomnia merits widespread implementation, and digital cognitive-behavioural therapy may assist delivery along treatment guidelines. However, given the still considerable proportion of patients responding insufficiently to cognitive-behavioural therapy for insomnia, fundamental studies are highly necessary to better understand the brain and behavioural mechanisms underlying insomnia. Mediators and moderators of treatment response/non-response and the associated development of tailored and novel interventions also require investigation. Recent studies suggest that treatment of insomnia may prove to add significantly as a preventive strategy to combat the global burden of mental disorders.

Insomnia and circadian dysregulation during adolescence represent important risk factors for emotional and psychological problems. Recent studies have shown that the coronavirus disease 2019 (COVID-19) pandemic has been linked to a high prevalence of behavioural sleep problems in the general population. This study aimed to provide two pictures of two different time points of the pandemic regarding the prevalence of sleep problems in adolescents and their association with psychological health variables. Two different independent large samples of Italian adolescents aged 13-17 years were recruited at two pandemic time points. A total of 1,146 adolescents at Time 1 (T1; April 2020) and 1,406 at Time 2 (T2; April 2021) took part in the study. Measures of insomnia symptoms, sleep hygiene, chronotype, psychological distress and emotion regulation were collected. Prevalence of insomnia was 12.13% at T1 and 23.19% at T2. Furthermore, high levels of poor sleep habits (late bedtime, poor sleep hygiene, use of electronic devices at bedtime) were also detected at both time points. Insomnia symptoms strongly correlated with poor sleep hygiene, higher psychological distress, and emotional suppression at both time points. Results highlighted an alarming picture for two large samples at two different time points of the pandemic that showed a potential negative impact of the COVID-19 pandemic, in both the first outbreak and in the later phase of the pandemic, on sleep habits, psychological distress and insomnia symptoms in adolescents. This strongly suggests the need for monitoring these variables and their interaction in the post-pandemic period and to develop and promote interventions for insomnia and circadian disturbances during adolescence.

Insomnia is the most frequent sleep disorder and a public health concern that increased during the Covid 19 pandemic. Fully restrictive lockdowns during Covid are interesting periods to examine the impact of environmental and behavioural changes on the emergence of insomnia symptoms. In this cross-sectional study we aimed to (1) determine the main factors associated with insomnia symptoms during a Covid-19 fully restrictive lockdown examining the associated daily life alterations and (2) create a predictive model of insomnia symptoms. We used the data drawn from the "Covid-RythmE" study that reached volunteers from the general French population through an online survey during the last 2 weeks of the 2 month full lockdown. Associations with insomnia symptoms were tested and significant associations were entered in a Backward Stepwise Logistic Regression (BSLR) to assess the best combination to classify individuals with or without insomnia symptoms. From the 1624 participants, 50.64% suffered from mild to severe insomnia symptoms as assessed by the ISI. The best combination for explaining insomnia symptoms with 74.26% of accuracy included: age (OR = 1.15), females (OR = 1.26), smaller home sizes (OR = 0.77), environmental noises (OR = 1.59), anxiety symptoms (OR = 1.24), depressive symptoms (OR = 1.15), regularity of sleep-wake schedules (OR = 1.25), exposure to screen during the morning (OR = 1.13), and LED light during the evening (OR = 1.17). Thus, lifestyle schedule and exposure to natural synchronizers such as light, are primordial in considering in insomnia physiopathology, prevention and treatment, as well as the associated mental health status.

Insomnia symptoms are frequent during peripartum and are considered risk factors for peripartum psychopathology. Assessing and treating insomnia and related conditions of sleep loss during peripartum should be a priority in the clinical practice. The aim of this paper was to conduct a systematic review on insomnia evaluation and treatment during peripartum which may be useful for clinicians. The literature review was carried out between January 2000 and May 2021 on the evaluation and treatment of insomnia during the peripartum period. The PubMed, PsycINFO, and Embase electronic databases were searched for literature published according to the PRISMA guidance with several combinations of search terms “insomnia” and “perinatal period” or “pregnancy” or “post partum” or “lactation” or “breastfeeding” and “evaluation” and “treatment.” Based on this search, 136 articles about insomnia evaluation and 335 articles on insomnia treatment were found and we conducted at the end a narrative review. According to the inclusion/exclusion criteria, 41 articles were selected for the evaluation part and 22 on the treatment part, including the most recent meta-analyses and systematic reviews. Evaluation of insomnia during peripartum, as for insomnia patients, may be conducted at least throughout a clinical interview, but specific rating scales are available and may be useful for assessment. Cognitive behavioral therapy for insomnia (CBT-I), as for insomnia patients, should be the preferred treatment choice during peripartum, and it may be useful to also improve mood, anxiety symptoms, and fatigue. Pharmacological treatment may be considered when women who present with severe forms of insomnia symptoms do not respond to nonpharmacologic therapy.

Improving our learning abilities is important for numerous aspects of our life. Several studies found beneficial effects of presenting cues (odor or sounds) during learning and during sleep for learning performance. A recent study applying a real-life paradigm indicated that additional odor cueing during a Final Test can further increase this cueing effect. The present online study builds on these findings with the following questions: (1) Can we replicate beneficial memory effects of additional odor cueing during tests? (2) How many odor cueing learning units and odor cueing nights of sleep maximize the learning success? (3) Can odor cueing also reduce the amount of forgetting over time? 160 Participants learned 40 German Japanese word pairs in four groups with separate experimental conditions over three days. group N received no odor during the whole study. Group LS received odor cueing during learning and sleep, group LT during learning and testing and group LST during learning, sleep and testing. Participants performed intermediate tests after each learning unit plus three Final Tests 1, 7 and 28 days after the last learning unit. Results: (1) Group LST learned 8.5% more vocabulary words than the other groups overall. (2) This odor cueing effect increased across the three days of cued learning. (3) We found no clear evidence for effects of odor cueing on the forgetting dynamics. Our findings support the notion of a beneficial effect of odor cueing. They further suggest to use at least 3 days and nights of odor cueing. Overall, this study indicates that there is an easy, efficient and economical way to enhance memory performance in daily life.

Sleep disturbances have been documented across a range of mental disorders, particularly depression. However, studies that have examined sleep quality in large samples of different diagnostic groups and that report how sleep quality changes during inpatient treatment have been scarce. This retrospective, observational study examined changes in sleep quality during inpatient treatment at a psychosomatic hospital in Germany from admission to discharge as a function of 10 diagnostic groups. Data of 11,226 inpatients were analysed who completed the Pittsburgh Sleep Quality Index as part of the routine diagnostic assessment at admission and discharge. All diagnostic groups showed impaired sleep quality (Pittsburgh Sleep Quality Index score 5). Patients with trauma-related disorders had the lowest sleep quality and patients with obsessive-compulsive disorder had the highest sleep quality. While sleep quality significantly improved in each diagnostic group, changes differed in size, with patients with trauma-related disorders showing the smallest improvement and patients with eating disorders showing the largest improvement. The current study documents impaired sleep quality in inpatients with mental disorders and shows that sleep problems are a transdiagnostic feature in this population. Results also resonate with earlier suggestions that sleep disturbances represent a key feature of trauma-related disorders in particular and the need for trauma-specific sleep interventions. Although sleep quality significantly improved during disorder-specific inpatient treatment in all diagnostic groups, average scores were still clinically elevated at discharge. Thus, a future avenue would be to examine whether adding sleep-specific treatment elements fosters both short- and long-term success in the treatment of mental disorders.

While sleep serves important regulatory functions for mental health, sleep disturbances, in particular insomnia, may favour a state of allostatic overload impairing brain neuroplasticity and stress immune pathways, hence contributing to mental disorders. In this framework, the aim of this work was to link current understanding about insomnia mechanisms with current knowledge about mental health dysregulatory mechanisms. The focus of the present work was on mood, anxiety, and psychotic disorders, which represent important challenges in clinical practice. Literature searches were conducted on clinical, neurobiological, and therapeutic implications for insomnia comorbid with these mental disorders. Given the complexity and heterogeneity of the existing literature, we ended up with a narrative review. Insomnia may play an important role as a risk factor, a comorbid condition and transdiagnostic symptom for many mental disorders including mood/anxiety disorders and schizophrenia. Insomnia may also play a role as a marker of disrupted neuroplasticity contributing to dysregulation of different neurobiological mechanisms involved in these different mental conditions. In this framework, insomnia treatment may not only foster normal sleep processes but also the stress system, neuroinflammation and brain plasticity. Insomnia treatment may play an important preventive and neuroprotective role with cognitive behavioural therapy for insomnia being the treatment with important new evidence of efficacy for insomnia, psychopathology, and indices of disrupted neuroplasticity. On the other hand, pharmacological pathways for insomnia treatment in these mental conditions are still not well defined. Therapeutic options acting on melatonergic systems and new therapeutic options acting on orexinergic systems may represents interesting pathways of interventions that may open new windows on insomnia treatment in mental disorders.

Introduction The hyperarousal model suggests that insomnia is characterized by increased cortical, cognitive, and physiological arousal. However, the relationship between these domains of arousal remains insufficiently studied. The aim of the current observational study was to investigate pre-sleep cognitive arousal, cortical arousal during the night, and the relationship between these domains. Methods 109 patients with insomnia disorder (ID) and 109 age-and gender matched healthy controls (GSC) were investigated on two sleep laboratory nights. As a measure of cortical arousal, EEG spectral power was analyzed during NREM and REM sleep. In addition, participants completed the Pre-Sleep Arousal Scale (PSAS), which consists of a subscale for cognitive arousal (PSAS-CA) and another subscale for self-reported somatic arousal (PSAS-SA). The relationship between the subscale scores and EEG spectral power was calculated by multivariate and univariate analyses of variance. Results The total sample consisted of 218 participants. ID patients had a mean age of 44.7 years (± 10.6 years) and GSC had a mean age of 44.4 years (± 12.6 years). Both groups consisted of 78 women and 31 men.During NREM and REM sleep, patients with ID showed significantly increased spectral power in the EEG gamma band (NREM: p < .001; REM: p = .002). In addition, patients with ID showed significantly increased scores on the PSAS-SA (ID: M = 12.4, SD = 4.4; GSC: M = 10.7, SD = 3.3; t(216) = 3.34, p = .001, d = 0.45) and the PSAS-CA (ID: M = 18.3, SD = 7.2; GSC: M = 10.6, SD = 2.9; t(216) = 10.33, p < .001, d = 1.40). The PSAS-CA score was significantly associated with increased NREM (p = .001) and REM gamma power (p = .004), whereas PSAS-SA was associated with significant decreases in NREM (p < .001) and REM gamma power (p = .001). Conclusion In line with our hypothesis, patients with ID showed increased cortical and cognitive arousal. Moreover, there was a relationship between pre-sleep cognitive arousal and high-frequency EEG activity during the night. This might suggest that the latter is caused (at least in part) by pre-sleep worry and rumination. Support (if any)

Introduction Hypnotics continue to be preferentially used in practice for the treatment of chronic insomnia, yet the comparative safety and efficacy of medication options are unclear. While several position statements and network meta-analyses have provided some guidance, none have provided a quantitative assessment of risk-benefit. In the present analysis, each therapeutic class commonly used for chronic insomnia is quantitatively ranked with respect to safety, efficacy, and risk-benefit. Methods Safety data for FDA-approved hypnotics were extracted from the package insert adverse event tables and standardized to form a placebo-adjusted adverse event rate per 1000 (AEr). Efficacy data were extracted from randomized controlled trials identified in professional society position statements and published systematic reviews. The efficacy metric was computed from placebo adjusted pre-post change scores for self-reported sleep continuity (i.e., sleep latency [SL], wake after sleep onset [WASO], and total sleep time [TST]) and represented as a summed composite effect size score (SWT). Risk-benefit (R/B) was represented as a ratio between AEr and SWT. Comparative safety, efficacy, and risk-benefit metrics were calculated for five therapeutic classes: Benzodiazepines (BZs), non-benzodiazepine benzodiazepine receptor agonists (BZRAs), dual orexin receptor antagonists (DORAs), melatonin receptor agonists (MELAs), and sedating antidepressants (SADs). Results With respect to safety, MELAs had the lowest adverse event rate (AEr=43.1) and BZRAs had the highest rate (AEr=255.0). With respect to efficacy, BZs were the most efficacious (SWT=1.94, Mean ES=0.59) and MELAs were least efficacious (SWT=0.11, Mean ES=0.02). Overall, with respect to risk-benefit, SADs had the most favorable profile (R/B=69.5), while MELAs had the least favorable profile (R/B=395.7). Conclusion The optimal selection of hypnotics requires consideration of both risk and benefit. Findings suggest that SADs can be considered the first-line pharmacotherapeutic option due to the superior risk-benefit profile. If treatment responses are inadequate or if SADs are contraindicated, risk-benefit rankings may serve as a decision tree as part of a medical algorithm protocol to guide treatment selection for patients with chronic insomnia. Support (If Any) Sleep Research Society Mentor-Mentee Award (Cheung); K24AG055602 & R01AG054521 (Perlis)

Insomnia is a highly prevalent disorder and a state of 24 h hyperarousal is considered as a key factor of this condition. Various physiological markers of hyperarousal have been investigated, including the activity of the HPA axis. However, these studies yielded heterogenous results. The aim of this study was to qualitatively and quantitatively evaluate whether there are differences in cortisol levels, the hormonal end product of the HPA axis, between patients with insomnia and good sleeper controls (GSC). The databases PubMed, Cinahl, PsycInfo, PsycArticles and Web of Science were searched for case-control studies comparing cortisol levels in patients with insomnia and GSC. Twenty studies (449 patients with insomnia, limited to ages 18-70 not taking any medications; 357 GSC) met the inclusion criteria. For each study, standardized mean differences (SMD) were calculated as a measure of effect size. Results suggest that patients with insomnia show moderately increased cortisol levels (SMD = 0.50, 95% CI: [0.21-0.80]). Higher effect sizes were found by including only studies using blood samples in the analysis (SMD = 0.67, 95% CI: [0.15-1.18]). Furthermore, a positive, but insignificant association was found between the extent of objective sleep loss in insomnia patients and group differences in cortisol levels.