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Several randomized controlled trials have implemented cognitive behavioral therapy for insomnia (CBT-I) for patients with comorbid insomnia and chronic pain. This systematic review and meta-analysis investigated the effectiveness of CBT-I on patient-reported sleep, pain, and other health outcomes (depressive symptoms, anxiety symptoms, and fatigue) in patients with comorbid insomnia and chronic non-cancer pain. A systematic literature search was conducted using eight electronic databases. Upon duplicate removal, 6374 records were screened against the inclusion criteria. Fourteen randomized controlled trials were selected for the review, with twelve (N = 762 participants) included in the meta-analysis. At post-treatment, significant treatment effects were found on global measures of sleep (standardized mean difference = 0.89), pain (0.20), and depressive symptoms (0.44). At follow-up (up to 12 mo), CBT-I significantly improved sleep (0.56). Using global measures of sleep, we found a probability of 81% and 71% for having better sleep after CBT-I at post-treatment and final follow-up, respectively. The probability of having less pain after CBT-I at post-treatment and final follow-up was 58% and 57%, respectively. There were no statistically significant effects on anxiety symptoms and fatigue at either assessment point. Future trials with sufficient power, longer follow-up periods, and inclusion of CBT for pain components are warranted., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Sleep restriction therapy (SRT) is an established treatment for insomnia that has been used in clinical practise for over 30 y. It is commonly delivered as part of multicomponent cognitive-behavioural therapy (CBT-I) but has also been linked to beneficial effects as a standalone intervention. In order to quantify the efficacy of SRT we performed a comprehensive meta-analysis of randomised controlled trials (RCTs) comparing SRT to minimally active or non-active control groups. Primary outcomes were self-reported insomnia severity and sleep diary metrics at post-treatment. Weighted effect sizes were calculated with Hedges' g and risk of bias was assessed by two independent raters with the Cochrane tool. Our search yielded eight RCTs meeting inclusion/exclusion criteria. Random effects models revealed large treatment effects in favour of SRT versus control for insomnia severity measured with the insomnia severity index (g = -0.93; 95% CI = -1.15, -0.71), sleep efficiency (g = 0.91; 95% CI = 0.52, 1.31), sleep onset latency (g = -0.62; 95% CI = -0.84, -0.40), and wake-time after sleep onset (g = -0.83; 95% CI = -1.11, -0.55). No effects were found for total sleep time (g = 0.02; 95% CI = -0.29, 0.34). Results should be interpreted in the context of the small number of comparisons (≤6 per outcome), high risk of bias (6 out of 8 studies met criteria for high risk), and heterogeneity in study design and SRT administration. Only a small number of studies provided outcomes at follow-up (n ≤ 3), hindering assessment of long-term effects. Sleep restriction therapy effectively improves insomnia severity and sleep continuity in the short term; more studies are needed to assess if effects are sustained at long-term follow-up (>3 m). Post-treatment effect sizes appear as large as multicomponent CBT-I. To reduce risk of bias, future studies should consider testing the effects of SRT against control groups that are matched for non-specific treatment effects. Large-scale pragmatic trials are also needed to test if SRT is effective in clinical practise and to quantify effects on daytime functioning and quality of life., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

For over 30 y sleep restriction therapy (SRT) has been used to treat insomnia but we know very little about how this therapy exerts its effects. When SRT was first described, it was hypothesised to treat insomnia by addressing four key factors: strengthening homeostatic sleep pressure, inhibiting perpetuating practices (excessive time in bed), attenuating hyperarousal and tightening regulatory control of sleep by the endogenous circadian pacemaker. We conducted a systematic literature review in search of evidence for these putative mechanisms-of-action. A total of 15 randomised and non-randomised studies investigating SRT met inclusion criteria. For each study, we extracted all variables associated with the proposed mechanisms and assessed study quality using a structured appraisal tool. The extracted variables were: time in bed (TIB), napping, variability in sleep, markers of circadian rhythmicity, measurements of sleep pressure/sleepiness, and assessments of arousal. Overall study quality was poor as indicated by a mean quality score of 17 (out of a possible range of 0-31). No study indicated, or indeed was designed to test, whether changes in the proposed mechanisms act as mediators of treatment outcomes. Of all reviewed studies, most reported a reduction in TIB (10/10) and/or revealed a decrease in sleep onset latency (10/14), indexing increased sleep pressure. However, such changes were most often reported at the end of treatment, reflecting an outcome and not a mechanism of SRT per se. Evidence for reduction in arousal (4/4) and night-to-night sleep variability (2/2) was found in only a small number of uncontrolled studies while there was no evidence for change in circadian phase or periodicity (0/1). Our review suggests that SRT targets some of the hypothesised processes but specifically-designed mechanistic evaluations are needed. We introduce a new testable model of SRT mechanism-of-action (Triple-R) and set out a research agenda aimed at stimulating prospective investigations., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Sleep and emotion are closely linked, however the effects of sleep on socio-emotional task performance have only recently been investigated. Sleep loss and insomnia have been found to affect emotional reactivity and social functioning, although results, taken together, are somewhat contradictory. Here we review this advancing literature, aiming to 1) systematically review the relevant literature on sleep and socio-emotional functioning, with reference to the extant literature on emotion and social interactions, 2) summarize results and outline ways in which emotion, social interactions, and sleep may interact, and 3) suggest key limitations and future directions for this field. From the reviewed literature, sleep deprivation is associated with diminished emotional expressivity and impaired emotion recognition, and this has particular relevance for social interactions. Sleep deprivation also increases emotional reactivity; results which are most apparent with neuro-imaging studies investigating amygdala activity and its prefrontal regulation. Evidence of emotional dysregulation in insomnia and poor sleep has also been reported. In general, limitations of this literature include how performance measures are linked to self-reports, and how results are linked to socio-emotional functioning. We conclude by suggesting some possible future directions for this field., (Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Sleep restriction therapy is a core element of contemporary cognitive-behavioural therapy for insomnia and is also effective as a single-component therapeutic strategy. Since its original description, sleep restriction therapy has been applied in several different ways, potentially limiting understanding of key therapeutic ingredients, mode of action, evidence synthesis, and clinical implementation. We sought to examine the quality of reporting and variability in the application of sleep restriction therapy within the context of insomnia intervention trials. Systematic literature searches revealed 88 trials of cognitive-behavioural therapy/sleep restriction therapy that met pre-defined inclusion/exclusion criteria. All papers were coded in relation to their description of sleep restriction therapy procedures. Findings indicate that a large proportion of papers (39%) do not report any details regarding sleep restriction therapy parameters and, for those papers that do, variability in implementation is present at every level (sleep window generation, minimum time-in-bed, sleep efficiency titration criteria, and positioning of sleep window). Only 7% of papers reported all parameters of sleep restriction treatment. Poor reporting and variability in the application of sleep restriction therapy may hinder progress in relation to evidence synthesis, specification of mechanistic components, and refinement of therapeutic procedures for patient benefit. We set out guidelines for the reporting of sleep restriction therapy as well as a research agenda aimed at advancing understanding of sleep restriction therapy., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

Sleep restriction therapy is routinely used within cognitive behavioral therapy to treat chronic insomnia. However, the efficacy for sleep restriction therapy as a standalone intervention has yet to be comprehensively reviewed. This review evaluates the evidence for the use of sleep restriction therapy in the treatment of chronic insomnia. The literature was searched using web-based databases, finding 1344 studies. Twenty-one were accessed in full (1323 were deemed irrelevant to this review). Nine were considered relevant and evaluated in relation to study design using a standardized study checklist and levels of evidence. Four trials met adequate methodological strength to examine the efficacy of therapy for chronic insomnia. Weighted effect sizes for self-reported sleep diary measures of sleep onset latency, wake time after sleep onset, and sleep efficiency were moderate-to-large after therapy. Total sleep time indicated a small improvement. Standalone sleep restriction therapy is efficacious for the treatment of chronic insomnia for sleep diary continuity variables. Studies are insufficient to evaluate the full impact on objective sleep variables. Measures of daytime functioning in response to therapy are lacking. Variability in the sleep restriction therapy implementation methods precludes any strong conclusions regarding the true impact of therapy. A future research agenda is outlined., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Insomnia is a common health complaint world-wide. Insomnia is a risk factor in the development of other psychological and physiological disorders. Therefore understanding the mechanisms which predispose an individual to developing insomnia has great transdiagnostic value. However, whilst it is largely accepted that a vulnerable phenotype exists there is a lack of research which aims to systematically assess the make-up of this phenotype. This review outlines the research to-date, considering familial aggregation and the genetics and psychology of stress-reactivity. A model will be presented in which negative affect (neuroticism) and genetics (5HTTLPR) are argued to lead to disrupted sleep via an increase in stress-reactivity, and further that the interaction of these variables leads to an increase in learned negative associations, which further increase the likelihood of poor sleep and the development of insomnia., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

To date, continuous positive airway pressure (CPAP) is the most effective intervention in the treatment of obstructive sleep apnoea, but adherence to this treatment is often less than optimal. A variety of factors and interventions that influence and improve CPAP use have been examined. There is increasing recognition of the multifaceted nature of CPAP adherence: the patient's psychological profile and social environment have been recognised, in addition to the more extensively researched patient's treatment and physiological profile. Understanding how these multiple factors impact on CPAP use in an integrative fashion might provide us with a useful holistic model of CPAP adherence. This concept of integration--a biopsychosocial (BPS) approach to health and illness--has previously been described to understand care provision for various chronic health disorders. This paper proposes an adherence framework, whereby variables integrally affect CPAP use. The BPS model has been considered for nearly 35 years; the presence of poor CPAP adherence was acknowledged in the early 1990s--it is timely to incorporate this approach into our care pathway of CPAP users., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Despite significant contributions made in the area of persistent/chronic insomnia, especially with regard to the underlying mechanisms driving its maintenance, the area of acute insomnia has received comparatively little attention. The aim of this paper is to review the literature with regard to understanding the situational and personaological circumstances that surround the development of acute insomnia. The review begins by examining how the existing diagnostic systems conceptualise acute insomnia. Theoretical models that explain, or inferentially explain, the transition between normal sleep and acute insomnia are then explored and evaluated. The review then examines the current evidence base in terms of the pathogenesis of acute insomnia from naturalistic and experimental studies. Overall, the findings from the review confirm the paucity of evidence available but perhaps more importantly highlight the need for a structured diagnosis of acute insomnia as the first step in a research and treatment strategy. To this end a diagnostic system, drawing on the existing literature on stress and the systems used to diagnose depression, is forwarded and justified and a research agenda advanced., (Crown Copyright © 2011. Published by Elsevier Ltd. All rights reserved.)

Health-related Quality of Life (HRQoL) has become an important construct in contemporary medicine and health care, permitting assessment of disorder burden and evaluation of interventions on various aspects of functioning, in a standardized manner. Here we review literature on the measurement of HRQoL in insomnia populations, and the extent to which insomnia treatment improves domains of HRQoL. It is concluded from the relatively small literature that insomnia impacts on diverse areas of HRQoL, and that both pharmacological and non-pharmacological interventions can produce, to varying degrees, improvements in domains spanning physical, social and emotional functioning. Limitations of the current literature are identified; with particular emphasis on measurement and conceptual shortcomings. Suggestions are made in relation to improving the quality of future research, and how to further shed light on the impact of insomnia - and treatment thereof - on both HRQoL and global quality of life., (Copyright 2009 Elsevier Ltd. All rights reserved.)

Psychophysiologic insomnia (PI) is the most common form of persistent primary insomnia. Its 'behavioral phenotype', comprising elements such as conditioned arousal, sleep-incompatible behavior and sleep preoccupation, has not changed markedly across several generations of diagnostic nosology. Moreover, a substantial outcome literature demonstrates that PI can be treated effectively using a range of psychological interventions. It seems evident that behavioral and cognitive factors play a part. What is less clear is exactly how PI develops and what are its crucial maintaining factors. This paper proposes an explanatory model, that we call the attention-intention-effort pathway. The argument is that sleep normalcy is a relatively automatic process. Consequently, it is vulnerable, and may be inhibited, by focused attention and by direct attempts to control its expression. Drawing upon parallels in the literature on adult psychopathology, and upon recent clinical and experimental studies on insomnia, the evidence for this pathway is considered and a research agenda is outlined. In particular, computerized tests of cognitive bias are seen as offering an objective means of appraising mental processes in insomnia. These may be applied concurrently with somatic measurements in future studies to better understand this common psycho-physiologic condition.