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Summary: Insomnia is a primary symptom of shift work disorder, yet it remains undertreated. This randomised‐controlled pilot trial examined the efficacy of a digital, guided cognitive behavioural therapy for insomnia adapted to shift work (SleepCare) in nurses with shift work disorder. The hypothesis was that SleepCare reduces insomnia severity compared with a waitlist control condition. A total of 46 unmedicated nurses suffering from shift work disorder with insomnia (age: 39.7 ± 12.1 years; 80.4% female) were randomised to the SleepCare group or the waitlist control group. The primary outcome measure was the Insomnia Severity Index. Other questionnaires on sleep, mental health and occupational functioning, sleep diary data and actigraphy data were analysed as secondary outcomes. Assessments were conducted before (T0), after the intervention/waitlist period (T1), and 6 months after treatment completion (T2). The SleepCare group showed a significant reduction in insomnia severity from T0 to T1 compared with the control condition (β = −4.73, SE = 1.12, p < 0.001). Significant improvements were observed in sleepiness, dysfunctional beliefs about sleep, pre‐sleep arousal, sleep effort, self‐reported sleep efficiency and sleep onset latency. No significant effect was found in actigraphy data. Depressive and anxiety symptoms, cognitive irritation and work ability improved significantly. Overall, satisfaction and engagement with the intervention was high. SleepCare improved insomnia severity, sleep, mental health and occupational functioning. This is the first randomised‐controlled trial investigating the efficacy of digital cognitive behavioural therapy for insomnia in a population suffering from shift work disorder with insomnia. Future research should further explore these effects with larger sample sizes and active control conditions. [ABSTRACT FROM AUTHOR]

Objective: Insomnia can be a contributing factor, a comorbid disorder, or a transdiagnostic element to several mental disorders, including mood disorders (MDs). A recent meta-analysis has already shown the effectiveness of cognitive behavioral treatment (CBT) for insomnia that is comorbid with MDs. This work aimed to systematically review data on pharmacological insomnia treatment in the context of MDS. In agreement with the current guidelines, pharmacological interventions for insomnia include gamma-aminobutyric acid (GABA)A receptor agonists such as short-medium acting benzodiazepines and benzodiazepine receptor agonists - Z-drugs, melatonergic receptors agonists, specifically melatonin 2 mg Prolonged Release (PR) and ramelteon, and dual orexin receptors antagonists (DORA) such as daridorexant, lemborexant, and suvorexant. Method: A systematic search was carried out on PUBMED database, according to the PRISMA Guidelines. Results: Thirty-three papers, 15 on gabaergic receptor agonists, 14 on melatonergic receptor agonists and 4 on DORA, were selected. Conclusions: Available data suggests that the treatment of insomnia symptoms with specific pharmacological options can improve both insomnia and comorbid conditions. Specifically, eszopiclone and melatonin 2 mg PR have demonstrated promising outcomes. Moreover, daridorexant and suvorexant, both belonging to the DORA class, have demonstrated efficacy in treating insomnia and mood symptoms. To summarize, current literature would suggest that targeting insomnia could potentially regulate the sleep system and, as such, improve mood symptoms. [ABSTRACT FROM AUTHOR]

Introduction: Suicide is a widespread problem, with risk factors still a challenge. The aim was to assess correlations among insomnia, circadian rhythm, and inflammatory markers in individuals who attempted suicide. Materials and Methods: Consecutive patients hospitalised following an attempted suicide, were assessed. Psychiatric diagnosis (DSM-5-TR Criteria), lethality of the suicide attempt (Suicide Intent Scale-SIS), and inflammatory parameters NLR (neutrophil-lymphocyte ratio) PLR (platelet-lymphocyte ratio), and SII (systemic inflammation index/neutrophil-to-platelet ratio on lymphocytes), were computed. Depressive and manic symptoms (Beck Depression Inventory-BDI-II, Young Mania Rating Scale- YMRS), circadian rhythms disturbances (Biological Rhythms Interview of Assessment in Neuropsychiatry-BRIAN), insomnia symptoms (Insomnia Severity Index-ISI) were assessed together with socio-demographic, clinical and pharmacological data. Results: The final sample included 52 individuals. Patients who experienced insomnia during the preceding two weeks utilised high lethality methods, reported heightened dysregulation of chronobiological rhythms, heightened severity of depression, and elevated levels of inflammatory markers. High lethality was best predicted by insomnia symptoms (OR = 20.1, CI-95% 4.66-87.25, p = 0.001), by disturbances of circadian rhythms (OR = 6.97, CI-95% 1.82-26.66, p = 0.005), and by NLR indices (OR 4.00, CI-95% 1.14-13.99, p = 0.030). Conclusions: Sleep disturbances may be a risk factor for suicidal lethality, along with markers of inflammation. It is plausible that insomnia and circadian sleep dysregulation may contribute to inflammation, thereby promoting suicidal risk. [ABSTRACT FROM AUTHOR]

Summary: Several professional societies have provided recommendations for prescribing medications for insomnia. None has provided an integrative analysis that concurrently quantifies safety and efficacy (e.g., risk–benefit ratios). This represents an important gap for informing clinician decision‐making. Accordingly, the aim of the present review is to provide such an analysis for five classes of sleep‐promoting medications. Adverse event data values were extracted from the most recent FDA‐approved package inserts and converted to an integer before being placebo‐adjusted and standardized as a rate per 1000 (AEr). Efficacy data, pre‐to‐post self‐reported data for active and placebo conditions were acquired from pivotal trials identified in "white papers" and systematic reviews/meta‐analyses. Weighted effect sizes were calculated for subjective sleep latency, wake time after sleep onset and total sleep time, and then were averaged by medication class for each sleep continuity variable. Overall efficacy was represented by a single variable, SWT (sleep latency + wake time after sleep onset + total sleep time). Risk–benefit was represented using a simple ratio value. For safety, it was found that melatonin receptor agonists had the lowest adverse event rate (AEr = 43.1), and non‐benzodiazepine benzodiazepine receptor agonists had the highest rate (AEr = 255.0). For efficacy, it was found that the pre‐to‐post placebo adjusted effect sizes were largest for benzodiazepines (effect size = 1.94) and smallest for melatonin receptor agonists (effect size = 0.109). For risk–benefit, histamine antagonist had the most favourable profile (risk–benefit = 69.5), while melatonin receptor agonist had the least favourable profile (risk–benefit = 395.7). Overall, the combined metric for risk–benefit suggests that treatment with a histamine antagonist is optimal and potentially represents the best first‐line therapy for the medical management of insomnia. [ABSTRACT FROM AUTHOR]

Summary The world‐wide prevalence of insomnia disorder reaches up to 10% of the adult population. Women are more often afflicted than men, and insomnia disorder is a risk factor for somatic and mental illness, especially depression and anxiety disorders. Persistent hyperarousals at the cognitive, emotional, cortical and/or physiological levels are central to most theories regarding the pathophysiology of insomnia. Of the defining features of insomnia disorder, the discrepancy between minor objective polysomnographic alterations of sleep continuity and substantive subjective impairment in insomnia disorder remains enigmatic. Microstructural alterations, especially in rapid eye movement sleep (“rapid eye movement sleep instability”), might explain this mismatch between subjective and objective findings. As rapid eye movement sleep represents the most highly aroused brain state during sleep, it might be particularly prone to fragmentation in individuals with persistent hyperarousal. In consequence, mentation during rapid eye movement sleep may be toned more as conscious‐like wake experience, reflecting pre‐sleep concerns. It is suggested that this instability of rapid eye movement sleep is involved in the mismatch between subjective and objective measures of sleep in insomnia disorder. Furthermore, as rapid eye movement sleep has been linked in previous works to emotional processing, rapid eye movement sleep instability could play a central role in the close association between insomnia and depressive and anxiety disorders. [ABSTRACT FROM AUTHOR]