The impact of insomnia and depression on asthma control.

BACKGROUND: Poor sleep quality is often reported by individuals with asthma, particularly by those who have poor asthma control overall. However, there is little understanding of how underlying sleep disorders such as insomnia may impact asthma control. Furthermore, given the frequent overlap of depression and insomnia, the incremental impact of mood disorders and insomnia on asthma control remains unclear. METHODS: We conducted a retrospective analysis of patients at a large asthma center to further elucidate connections between these disease processes. Asthma patients with and without a diagnosis of insomnia were matched by age, sex, Charlson comorbidity index, and biologic therapy. We evaluated the presence of concurrent obstructive sleep disorder, mood disorders, exacerbation frequency, and asthma control test (ACT) scores. RESULTS: From a cohort of 659 patients with an asthma diagnosis, 89 subjects with insomnia (13.5%) were matched 1:1 to patients without insomnia. Compared to those without insomnia, patients with insomnia were more likely to have a concurrent diagnosis of obstructive sleep apnea (57.3% vs. 18%, p < 0.001) and to have a diagnosis of depression or anxiety (68.5% vs. 11.4%, p < 0.001). Among insomnia patients, there was an average of 0.93 asthma exacerbations per year, compared to 0.59 exacerbations per year for those without insomnia (p = 0.039). CONCLUSION: Our data reveal a considerable interaction between insomnia, depression, and obstructive sleep apnea in individuals with asthma. The increased exacerbation rate suggests that underlying sleep and mood disorders negatively affect asthma control.

The relationship between sleep and opioids in chronic pain patients.

BACKGROUND: Sleep problems are common among chronic pain patients who take opioids. There are documented effects of opioids on sleep architecture; however, the long-term effects of opioids on sleep remain unknown. This study examined whether opioid-naïve participants have better sleep quality than current and previous chronic users of opioids. We also explored whether sleep differed between methadone and buprenorphine users, and whether amount of time since abstaining from opioids was associated with sleep quality. METHOD: Participants were 120 people with chronic pain (84.2% Caucasian, Mage = 42.0 years, SD = 11.44). They were in one of four groups of 30 participants each: (1) current users of methadone for opioid use disorder (OUD); (2) current users of buprenorphine for OUD; (3) a history of medication-assisted therapy for OUD but currently opioid-abstinent for at least 6 months; (4) those who have less than one month of cumulative lifetime opioids (opioid-naïve group). Only participants in group 1 and group 2 were taking opioids during the time of the study. Participants completed the Pittsburgh Sleep Quality Index and the SF-36. RESULTS: A MANCOVA revealed that all three groups with current or previous opioid use (i.e., groups 1-3) differed significantly from the opioid-naïve group (group 4) on sleep quality, sleep duration, sleep disturbances, and daytime dysfunction after controlling for sleep medications (all p < .05). For group 1 (methadone users), 2 (buprenorphine users), and 3 (prolonged abstinence), there were no statistically significant differences between each group. There was also a significant relationship between opioid-abstinent weeks and sleep disturbances in the opioid-abstinent group (r = - 0.604, p < .001). DISCUSSION: The results of this study suggest that opioids interfere with sleep quality, even after months of abstention. Further research into the long-term effects of opioids is warranted and may contribute further to the importance of addressing sleep problems in this population.

Neurocognitive performance in insomnia disorder: The impact of hyperarousal and short sleep duration.

Given the recent evidence on the association between hyperarousal in insomnia disorder and neurocognitive deficits, we aimed to examine the effect of short sleep duration on neurocognitive reaction time tests in insomnia disorder sufferers. We recruited subjects with insomnia disorder (n = 35, mean age = 40.6 years) who scored ≥29 on a Hyperarousal Scale, and a group of controls (n = 54, mean age = 31.5 years) who had no sleep disorders and scored <26 on the Hyperarousal Scale. Participants completed two in-home polysomnograms and four daytime trials of neurocognitive tests, including simple reaction time, choice reaction time, big circle-little circle, rapid visual information processing, attention switching task, and spatial working memory tests. Total sleep time divided study cohorts into subgroups of short (total sleep time <6 hr) and normal (total sleep time ≥6 hr) sleepers. ANCOVA showed a significant interaction between participant type (insomnia disorder versus controls) and sleep duration (short versus normal) for spatial working memory-latency (p = 0.020) and spatial working memory-errors (p = 0.025). The short-sleeping insomnia disorder group had longer spatial working memory-latencies and more spatial working memory-errors than did normal-sleeping controls. Regardless of sleep duration, those with insomnia disorder had more attentional deficits with longer attention switching task-latency (p = 0.011) and more attention switching task-incorrect trials (p = 0.015) than the control group. Normal-sleepers only had longer attention switching task-latency than short-sleepers (p = 0.004). A phenotype of insomnia disorder with hyperarousal and short sleep duration is associated with daytime cognitive deficits in complex attentional and spatial working memory tasks.

Cognitive behavioural therapy for insomnia reduces actigraphy and diary measured sleep discrepancy for individuals with comorbid insomnia and major depressive disorder: A report from the TRIAD study.

OBJECTIVE/BACKGROUND: Discrepancies between sleep diaries and actigraphy occur among individuals with insomnia. Cognitive behavioural therapy for insomnia (CBT-I) improves insomnia but the impact on discrepancy is unclear. This study examined CBT-I's effects on actigraphy-diary discrepancy and explored sleep-related beliefs and attitudes as a mediator. PATIENTS/METHODS: Participants were 108 (age M±SD = 47.23 ± 12.42, 67.60 % female) adults with insomnia and major depressive disorder from the Treatment of Insomnia and Depression study. They were randomized to 7 sessions of CBT-I or sham Quasi-Desensitization Therapy for Insomnia (DTI), plus 16 weeks of antidepressants. Two weeks of actigraphy and sleep diary were collected at baseline, mid-treatment, end-treatment. Differences between sleep diary and actigraphy total sleep time (TST), sleep onset latency (SOL), wake after sleep onset (WASO), and sleep efficiency (SE) were calculated. Participants completed Dysfunctional Beliefs and Attitudes about Sleep Scale (DBAS) at baseline and mid-treatment. RESULTS: At baseline, diary (versus actigraphy) TST was shorter (1.1 ± 1.41h), whilst SOL (21.64 ± 41.25min) and WASO (17.45 ± 61.99min) were longer. Mixed effects models using daily data showed that after adjusting for age and sex, participants in the CBT-I group (versus DTI) showed greater reduction in all actigraphy-diary discrepancy domains (all p-values<.01), reductions evident from mid-treatment. Group differences on actigraphy-diary discrepancy reductions in TST, SOL, and SE (not WASO) were mediated by changes in DBAS from baseline to mid-treatment (all p-values<.05). Changes in discrepancy did not mediate insomnia symptom changes (p-values>.39). CONCLUSIONS: CBT-I reduced actigraphy-diary discrepancy in individuals with comorbid insomnia and depression; this reduction was associated with improved sleep-related attitudes, a therapeutic target of CBT-I. CLINICAL TRIAL REGISTRATION: TRIAD (Treatment of Insomnia and Depression): Improving Depression Outcome by Adding Insomnia Therapy to Antidepressants. Prospectively registered with Clinical Trials (NCT00767624). SUPPORT (IF ANY): MH078924, MH078961, MH079256.

Cognitive behavior therapy for insomnia for untreated hypertension with comorbid insomnia disorder: The SLEEPRIGHT clinical trial.

Insomnia and poor sleep are associated with an increased risk of developing cardiovascular disease (CVD) and its precursors, including hypertension. In 2022, the American Heart Association (AHA) added inadequate sleep to its list of health behaviors that increase the risk for CVD. It remains unknown, however, whether the successful treatment of insomnia and inadequate sleep can reduce heightened CVD risk. SLEEPRIGHT is a single-site, prospective clinical trial designed to evaluate whether the successful treatment of insomnia results in improved markers of CVD risk in patients with untreated hypertension and comorbid insomnia disorder. Participants (N = 150) will undergo baseline assessments, followed by a 6-week run-in period after which they will receive cognitive behavior therapy for insomnia (CBT-I), comprised of 6 hourly sessions with an experienced CBT-I therapist over a 6-week period. In addition to measures of insomnia severity, as well as both subjective and objective measures of sleep, the primary outcome measures are nighttime blood pressure (BP) and BP dipping assessed by 24-h ambulatory BP monitoring (ABPM). Secondary outcomes include several CVD risk biomarkers, including clinic BP, lipid profile, vascular endothelial function, arterial stiffness, and sympathetic nervous system (SNS) activity. Data analysis will evaluate the association between improvements in insomnia and sleep with primary and secondary CVD risk biomarker outcomes. The SLEEPRIGHT trial (ClinicalTrials.Gov NCT04009447) will utilize CBT-I, the current gold standard treatment for insomnia disorder, to evaluate whether reducing insomnia severity and improving sleep are accompanied by improved biomarkers of CVD risk in patients with untreated hypertension.

Objective sleep duration and response to combined pharmacotherapy and cognitive behavioral insomnia therapy among patients with comorbid depression and insomnia: a report from the TRIAD study.

STUDY OBJECTIVES: Several studies have shown that patients with short sleep duration show a poor response to cognitive behavioral therapy for insomnia (CBT-I), but such studies have not included patients with comorbid conditions. The current study was conducted to determine whether pretreatment sleep duration moderates the response of patients with major depression and insomnia disorders to a combined CBT-I and antidepressant medication treatment. METHODS: This study comprised a secondary analysis of a larger randomized trial that tested combined CBT-I/antidepressant medication treatment of patients with major depression and insomnia. Participants (n = 99; 70 women; Mage = 47.712.4 years) completed pretreatment polysomnography and then were randomly assigned to a 12-week treatment with antidepressant medication combined with CBT-I or a sham therapy. Short and longer sleepers were defined using total sleep time cutoffs of < 5, < 6, and < 7 hours for short sleep. Insomnia and depression remission ascertained respectively from the Insomnia Severity Index and Hamilton Rating Scale for Depression were used to compare treatment responses of short and longer sleepers defined by the cutoffs mentioned. RESULTS: Logistic regression analyses showed that statistically significant results were obtained only when the cutoff of < 5 hours of sleep was used to define "short sleep." Both the CBT-I recipients with < 5 hours of sleep (odds ratio = 0.053; 95% confidence interval = 0.006-0.499) and the sham-therapy group with ≥ 5 hours of sleep (odds ratio = 0.149; 95% confidence interval = 0.045-0.493) were significantly less likely to achieve insomnia remission than were CBT-I recipients with ≥ 5 hours of sleep. The shorter sleeping CBT-I group (odds ratio = 0.118; 95% confidence interval = 0.020-0.714) and longer sleeping sham-therapy group (odds ratio = 0.321; 95% confidence interval = 0.105-0.983) were also less likely to achieve insomnia and/or depression remission than was the longer sleeping CBT-I group with ≥ 5 hours of sleep. CONCLUSIONS: Sleeping < 5 hours may dispose comorbid major depression/insomnia patients to a poor response to combined CBT-I/medication treatments for their insomnia and depression. Future studies to replicate these findings and explore mechanisms of treatment response seem warranted. CLINICAL TRIAL REGISTRATION: Registry: ClinicalTrials.gov; Name: Treatment of Insomnia and Depression (TRIAD); URL: https://clinicaltrials.gov/ct2/show/results/NCT00767624; Identifier: NCT00767624. CITATION: Edinger JD, Smith ED, Buysse DJ, et al. Objective sleep duration and response to combined pharmacotherapy and cognitive behavioral insomnia therapy among patients with comorbid depression and insomnia: a report from the TRIAD study. J Clin Sleep Med. 2023;19(6):1111-1120.

Adherence to behavioral recommendations of cognitive behavioral therapy for insomnia predicts medication use after a structured medication taper.

STUDY OBJECTIVES: Cognitive behavioral therapy for insomnia (CBTI) has been paired with supervised medication tapering to help hypnotic-dependent individuals discontinue their hypnotics. This study examined the hypothesis that higher participant adherence to behavioral recommendations of CBTI will predict lower odds of using sleep medications 3 months after completion of a combined CBTI/sleep medication tapering protocol. METHODS: Fifty-eight individuals who used sedative hypnotics completed four CBTI sessions followed by sleep medication tapering. Logistic regression was used to examine the association of stability of time in bed and stability of rise time (measured as the within-person standard deviation) at completion of CBTI with two outcomes at 3-month follow-up: use of sedative hypnotics and use of any medication/substance for sleep. RESULTS: Participants with more stability in their rise time after CBTI than at baseline (ie, a decrease in their within-person standard deviation) had 69.5% lower odds of using sedative hypnotics at follow-up (odds ratio = 0.305, 95% confidence interval = 0.095-0.979, P = .046) than individuals who had no change or a decrease in the stability of their rise time. Results were similar for time in bed: participants with more stability in their time in bed after CBTI than at baseline had 83.2% lower odds of using sedative hypnotics (odds ratio = 0.168, 95% confidence interval = 0.049-0.580, P = .005). Increase in stability of rise time and stability of time in bed was also associated with reduced odds of using any medication/substance for sleep at follow-up. CONCLUSIONS: Participants who implement behavioral recommendations of CBTI appear to have more success with discontinuing use of sleep medications. CLINICAL TRIAL REGISTRATION: Registry: ClinicalTrials.gov; Name: The Role of Tapering Pace and Selected Traits on Hypnotic Discontinuation; URL: https://clinicaltrials.gov/ct2/show/NCT02831894; Identifier: NCT02831894. CITATION: Edinger JD, Wamboldt FS, Johnson RL, et al. Adherence to behavioral recommendations of cognitive behavioral therapy for insomnia predicts medication use after a structured medication taper. J Clin Sleep Med. 2023;19(8):1495-1503.

Effect of Psychological and Medication Therapies for Insomnia on Daytime Functions: A Randomized Clinical Trial.

Importance: Daytime functional impairments are the primary reasons for patients with insomnia to seek treatment, yet little is known about what the optimal treatment is for improving daytime functions and how best to proceed with treatment for patients whose insomnia has not remitted. Objectives: To compare the efficacy of behavioral therapy (BT) and zolpidem as initial therapies for improving daytime functions among patients with insomnia and evaluate the added value of a second treatment for patients whose insomnia has not remitted. Design, Setting, and Participants: In this sequential multiple-assignment randomized clinical trial conducted at institutions in Canada and the US, 211 adults with chronic insomnia disorder were enrolled between May 1, 2012, and December 31, 2015, and followed up for 12 months. Statistical analyses were performed on an intention-to-treat basis in April and October 2023. Interventions: Participants were randomly assigned to either BT or zolpidem as first-stage therapy, and those whose insomnia had not remitted received a second-stage psychological therapy (BT or cognitive therapy) or medication therapy (zolpidem or trazodone). Main Outcomes and Measures: Study outcomes were daytime symptoms of insomnia, including mood disturbances, fatigue, functional impairments of insomnia, and scores on the 36-item Short-Form Health Survey (SF-36) physical and mental health components. Results: Among 211 adults with insomnia (132 women [63%]; mean [SD] age, 45.6 [14.9] years), 104 were allocated to BT and 107 to zolpidem at the first stage. First-stage treatment with BT or zolpidem yielded significant and equivalent benefits for most of the daytime outcomes, including depressive symptoms (Beck Depression Inventory-II mean score change, -3.5 [95% CI, -4.7 to -2.3] vs -4.3 [95% CI, -5.7 to -2.9]), fatigue (Multidimensional Fatigue Inventory mean score change, -4.7 [95% CI, -7.3 to -2.2] vs -5.2 [95% CI, -7.9 to -2.5]), functional impairments (Work and Social Adjustment Scale mean score change, -5.0 [95% CI, -6.7 to -3.3] vs -5.1 [95% CI, -7.2 to -2.9]), and mental health (SF-36 mental health subscale mean score change, 3.5 [95% CI, 1.9-5.1] vs 2.5 [95% CI, 0.4-4.5]), while BT produced larger improvements for anxiety symptoms relative to zolpidem (State-Trait Anxiety Inventory mean score change, -4.1 [95% CI, -5.8 to -2.4] vs -1.2 [95% CI, -3.0 to 0.5]; P = .02; Cohen d = 0.55). Second-stage therapy produced additional improvements for the 2 conditions starting with zolpidem at posttreatment in fatigue (Multidimensional Fatigue Inventory mean score change: zolpidem plus BT, -3.8 [95% CI, -7.1 to -0.4]; zolpidem plus trazodone, -3.7 [95% CI, -6.3 to -1.1]), functional impairments (Work and Social Adjustment Scale mean score change: zolpidem plus BT, -3.7 [95% CI, -6.4 to -1.0]; zolpidem plus trazodone, -3.3 [95% CI, -5.9 to -0.7]) and mental health (SF-36 mental health subscale mean score change: zolpidem plus BT, 5.3 [95% CI, 2.7-7.9]; zolpidem plus trazodone, 2.0 [95% CI, 0.1-4.0]). Treatment benefits achieved at posttreatment were well maintained throughout the 12-month follow-up, and additional improvements were noted for patients receiving the BT treatment sequences. Conclusions and Relevance: In this randomized clinical trial of adults with insomnia disorder, BT and zolpidem produced improvements for various daytime symptoms of insomnia that were no different between treatments. Adding a second treatment offered an added value with further improvements of daytime functions. Trial Registration: ClinicalTrials.gov Identifier: NCT01651442.

Internight sleep variability: its clinical significance and responsiveness to treatment in primary and comorbid insomnia.

Although sleep diary and actigraphy data are usually collected daily for 1 or 2 weeks, traditional analytical approaches aggregate these data into mean values. Internight variability of sleep often accompanies insomnia. However, few studies have explored the relevance of this 'construct' in the context of diagnosis, clinical impact, treatment effects and/or whether having 'variable sleep' carries any prognostic significance. We explored these questions by conducting secondary analyses of data from a randomized clinical trial. The sample included primary (PI: n = 40) and comorbid insomnia (CMI: n = 41) sufferers receiving four biweekly sessions of cognitive-behavioural therapy (CBT) or sleep hygiene education. Using the within-subject standard deviations of diary- and actigraphy-derived measures collected for 2-week periods [sleep onset latency (SOL), wake after sleep onset (WASO), total sleep time (TST) and sleep efficiency (SE)], we found that CMI sufferers displayed more variable self-reported SOLs and SEs than PI sufferers. However, higher variability in diary and actigraphy-derived measures was related to poorer sleep quality only within the PI group, as measured by the Pittsburgh Sleep Quality Index (PSQI). Within both groups, the variability of diary-derived measures was reduced after CBT, but the variability of actigraphy-derived measures remained unchanged. Interestingly, the variability of actigraphy measures at baseline was correlated with PSQI scores at 6-month follow-up. Higher SOL variability was associated with worse treatment outcomes within the PI group, whereas higher WASO variability was correlated with better treatment outcomes within the CMI group. Sleep variability differences across insomnia diagnoses, along with their distinctive correlates, suggest that mechanisms underlying the sleep disruption/complaint and treatment response in both patient groups are distinct. Further studies are warranted to support variability as a useful metric in insomnia studies.

Cognitive-behavioral therapy for the management of insomnia comorbid with mental disorders.

Insomnia is frequently comorbid with psychiatric conditions, mostly depression and anxiety disorders. Because disturbed sleep is a symptom of most major mental disorders, it has been traditionally assumed that effective treatment of the psychiatric condition will resolve the coincident insomnia also. However, insomnia often persists after successful treatment of the comorbid mental disorder, suggesting that insomnia often warrants separate treatment attention. Cognitive-behavioral therapy (CBT) is a well established and efficacious treatment for insomnia. Most evidence supporting the efficacy of CBT comes from studies conducted with patients suffering from primary insomnia, yet over the past 20 years there has been growing support for the use of cognitive-behavioral insomnia intervention for patients with comorbid psychiatric conditions. Overall, promising results have been obtained from these studies, not only with regard to insomnia improvement but also concurrent improvements in comorbid psychiatric conditions. In this article we review recent studies in this area with particular focus on treatment of insomnia in the context of depression, post-traumatic stress disorder, and alcohol dependence.

Hypnotic Discontinuation in Chronic Insomnia.

Insomnia disorder is common in adults and children. The estimated prevalence ranges from 9% to 15% in the general population, with higher prevalence in certain subpopulations. Hypnotic medications are those that tend to produce sleep and are frequently used to treat insomnia. Commonly used hypnotics in adults include benzodiazepines (BZDs), BZD receptor agonists, antihistamines, antidepressants, melatonin receptor agonists, orexin receptor antagonists, and antipsychotics. However, hypnotic discontinuation is difficult and often unsuccessful. This article discusses strategies to discontinue hypnotics and evidence supporting their use.

Overnight Delta Dynamics Associated with Daytime Psychomotor Performance in Adults with Insomnia and Healthy Controls.

PURPOSE: Sleep is vital to cognition, yet underlying mechanisms remain unclear. Although sleep duration and continuity are two well-established contributors, additional factors-including homeostatic sleep drive processes-may also underlie cognition-related sleep restoration. This study investigates the relative contributions of sleep EEG factors to psychomotor functioning in adults with insomnia and healthy controls (HC) to identify the most significant sleep factors supporting psychomotor functioning. MATERIALS AND METHODS: Adults with insomnia (n = 37) and HC (n = 39) completed 3 nights of polysomnography and a complex psychomotor task (switching attention task; SAT). Univariate correlations identified the most significant predictors (traditional PSG, spectral EEG, initial delta peak, and overnight delta decline) of SAT performance, which were then entered into multivariable linear regressions examining whether predictors remained significant after accounting for shortened/fragmented sleep and whether relationships differed across groups. RESULTS: In addition to greater wake after sleep onset (WASO; r = 0.33), a slower overnight delta decline (r = 0.50) and a lower initial delta peak (r = -0.38) were the most significant predictors of poorer SAT performance. Both overnight delta decline (F(7, 68) = 12.52, p < 0.001) and initial delta peak (F(7, 68) = 7.85, p = 0.007) remained significant predictors after controlling for demographics, total sleep time, and WASO. Relationships were analogous across subject groups. CONCLUSION: Findings suggest that, in addition to sleep duration and continuity, processes related to recovery from and dissipation of homeostatic sleep drive may support psychomotor performance and broadly support daytime functioning in individuals with and without insomnia. Future research may examine overnight delta dynamics as transdiagnostic processes supporting cognition-related sleep restoration across a range of clinical populations.

Association between insomnia patients' pre-treatment characteristics and their responses to distinctive treatment sequences.

STUDY OBJECTIVES: It is common to provide insomnia patients a second treatment when the initial treatment fails, but little is known about optimal treatment sequences for different patient types. This study examined whether pre-treatment characteristics/traits predict optimal treatment sequences for insomnia patients. METHODS: A community sample of 211 adults (132 women; Mage = 45.6 ± 14.9 years) with insomnia were recruited. Patients were first treated with behavioral therapy (BT) or zolpidem (Zol). Non-remitting BT recipients were randomized to a second treatment with either Zol or cognitive therapy; non-remitting Zol recipients underwent BT or Trazodone as a second treatment. Remission rates were assessed at the end of the first and second 6-week treatments. We then compared the remission rates of dichotomous groups formed on the basis of gender, age, pretreatment scores on SF36 and Multidimensional Fatigue Scale, the presence/absence of psychiatric/medical comorbidities or pain disorders, and mean subjective sleep duration and efficiency within and across treatment sequences. RESULTS: Lower remission rates were noted for those: with a pain disorder, poor mental health perceptions, high MFI fatigue scores, and lower sleep times and efficiencies. Patients with a pain disorder responded best to the BT-to-Zol sequence, whereas patients with more mental impairment, severe fatigue, short sleep, and low sleep efficiency responded poorly to treatment starting with BT. CONCLUSIONS: Pain, fatigue, poor mental health status, and subjective sleep duration and efficiency all affect response to different insomnia treatment sequences. Findings may guide clinicians in matching insomnia treatments to their patients. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT01651442, Protocol version 4, April 20, 2011, registered June 26, 2012, https://clinicaltrials.gov/ct2/show/NCT01651442?rslt=With&type=Intr&cond=Insomnia&cntry=US&state=US%3ACO&city=Denver&age=12&draw=2&rank=1.

Stepped care management of insomnia co-occurring with sleep apnea: the AIR study protocol.

BACKGROUND: Obstructive sleep apnea (OSA) and insomnia are commonly co-occurring conditions that amplify morbidity and complicates the management of affected patients. Unfortunately, previous research provides limited guidance as to what constitutes the best and most practical management approach for this comorbid patient group. Some preliminary studies show that when cognitive behavioral insomnia therapy (CBT-I) is combined with standard OSA therapies for these patients, outcomes are improved. However, the dearth of trained providers capable of delivering CBT-I has long served as a pragmatic barrier to the widespread use of this therapy in clinical practice. The emergence of sophisticated online CBT-I (OCBT-I) programs could improve access, showing promising reductions in insomnia severity. Given its putative scalability and apparent efficacy, some have argued OCBT-I should represent a 1st-stage intervention in a broader stepped care model that allocates more intensive and less assessable therapist-delivered CBT-I (TCBT-I) only to those who show an inadequate response to lower intensity OCBT-I. However, the efficacy of OCBT-I as a 1st-stage therapy within a broader stepped care management strategy for insomnia comorbid with OSA has yet to be tested with comorbid OSA/insomnia patients. METHODS/DESIGN: This dual-site randomized clinical trial will use a Sequential Multiple Assignment Randomized Trial (SMART) design to test a stepped care model relative to standard positive airway pressure (PAP) therapy and determine if (1) augmentation of PAP therapy with OCBT-I improves short-term outcomes of comorbid OSA/insomnia and (2) providing a higher intensity 2nd-stage CBT-I to patients who show sub-optimal short-term outcomes with OCBT-I+PAP improves short and longer-term outcomes. After completing baseline assessment, the comorbid OSA/insomnia patients enrolled will be randomized to a 1st-stage therapy that includes usual care PAP + OCBT-I or UC (usual care PAP + sleep hygiene education). Insomnia will be reassessed after 8 weeks. OCBT-I recipients who meet "remission" criteria (defined as an Insomnia Severity Index score < 10) will continue PAP but will not be offered any additional insomnia intervention and will complete study outcome measures again after an additional 8 weeks and at 3 and 6 month follow-ups. OCBT-I recipients classified as "unremitted" after 8 weeks of treatment will be re-randomized to a 2nd-stage treatment consisting of continued, extended access to OCBT-I or a switch to TCBT-I. Those receiving the 2nd-stage intervention as well as the UC group will be reassessed after another 8 weeks and at 3- and 6-month follow-up time points. The primary outcome will be insomnia remission. Secondary outcomes will include subjective and objective sleep data, including sleep time, sleep efficiency, fatigue ratings, PAP adherence, sleepiness ratings, sleep/wake functioning ratings, and objective daytime alertness. DISCUSSION: This study will provide new information about optimal interventions for patients with comorbid OSA and insomnia to inform future clinical decision-making processes. TRIAL REGISTRATION: ClinicalTrials.gov, NCT03109210 , registered on April 12, 2017, prospectively registered.

A randomized controlled trial of cognitive behavioral therapy for insomnia and PAP for obstructive sleep apnea and comorbid insomnia: effects on nocturnal sleep and daytime performance.

STUDY OBJECTIVES: This study examines the impact of cognitive behavioral therapy for insomnia (CBT-I) and positive airway pressure (PAP) therapy for comorbid insomnia and sleep apnea on nocturnal sleep and daytime functioning. METHODS: A partial factorial design was used to examine treatment pathways with CBT-I and PAP and the relative benefits of each treatment. One hundred eighteen individuals with comorbid insomnia and sleep apnea were randomized to receive CBT-I followed by PAP, self-monitoring followed by CBT-I concurrent with PAP, or self-monitoring followed by PAP only. Participants were assessed at baseline, PAP titration, and 30 and 90 days after PAP initiation. Outcome measures included sleep diary- and actigraphy-measured sleep, Flinders Fatigue Scale, Epworth Sleepiness Scale, Functional Outcome of Sleep Questionnaire, and cognitive emotional measures. RESULTS: A main effect of time was found on diary-measured sleep parameters (decreased sleep onset latency and wake after sleep onset; increased total sleep time and sleep efficiency) and actigraphy-measured sleep parameters (decreased wake after sleep onset; increased sleep efficiency) and daytime functioning (reduced Epworth Sleepiness Scale, Flinders Fatigue Scale; increased Functional Outcome of Sleep Questionnaire) across all arms (all P < .05). Significant interactions and planned contrast comparisons revealed that CBT-I was superior to PAP and self-monitoring on reducing diary-measured sleep onset latency and wake after sleep onset and increasing sleep efficiency, as well as improving Functional Outcome of Sleep Questionnaire and Flinders Fatigue Scale compared to self-monitoring. CONCLUSIONS: Improvements in sleep and daytime functioning were found with PAP alone or concomitant with CBT-I. However, more rapid effects were observed on self-reported sleep and daytime performance when receiving CBT-I regardless of when it was initiated. Therefore, concomitant treatment appears to be a favorable approach to accelerate treatment outcomes. CLINICAL TRIAL REGISTRATION: Registry: ClinicalTrials.gov; Name: Multidisciplinary Approach to the Treatment of Insomnia and Comorbid Sleep Apnea (MATRICS); URL: https://clinicaltrials.gov/ct2/show/NCT01785303; Identifier: NCT01785303. CITATION: Tu AY, Crawford MR, Dawson SC, et al. A randomized controlled trial of cognitive behavioral therapy for insomnia and PAP for obstructive sleep apnea and comorbid insomnia: effects on nocturnal sleep and daytime performance. J Clin Sleep Med. 2022;18(3):789-800.

Daytime symptom patterns in insomnia sufferers: is there evidence for subtyping insomnia?

The type and severity of daytime symptoms reported by insomnia sufferers may vary markedly. Whether distinctive daytime symptom profiles are related to different insomnia diagnoses has not been studied previously. Using profile analysis via multidimensional scaling, we investigated the concurrent validity of ICSD-2 insomnia diagnoses by analysing the relationship of prototypical profiles of daytime symptoms with a subset of ICSD-2 diagnoses, such as insomnia associated to a mental disorder, psychophisiological insomnia, paradoxical insomnia, inadequate sleep hygiene, idiopathic insomnia, obstructive sleep apnea and restless legs syndrome. In a sample of 332 individuals meeting research diagnostic criteria for insomnia (221 women, M(age) =46 years.), the profile analysis identified four prototypical patterns of daytime features. Pearson correlation coefficients indicated that the diagnoses of insomnia associated to a mental disorder and idiopathic insomnia were associated with a daytime profile characterized by mood disturbance and low sleepiness; whereas the diagnoses of psychophysiological insomnia and inadequate sleep hygiene were related to a profile marked by poor sleep hygiene, daytime tension and low fatigue. Furthermore, whereas paradoxical insomnia was consistently associated to lower daytime impairment, insomnia associated to a mental disorder appeared as the most severe daytime form of insomnia. This classification of insomnia sufferers along multiple defining dimensions provides initial validation for two basic insomnia subtypes, with a presumably distinct aetiology: insomnia characterized mainly by an 'internal' component, and a 'learned' insomnia. Research to determine which dimensions are critical for inclusion or differential weighting for defining a general typological system for insomnia sufferers is warranted.

Optimizing computation of overnight decline in delta power: Evidence for slower rate of decline in delta power in insomnia patients.

OBJECTIVE: To determine the best of commonly used methods for computing the rate of decline in non-rapid eye movement (NREM) sleep EEG delta power overnight (Delta Decline) in terms of vulnerability to missing data and to evaluate whether this rate is slower in insomnia patients than healthy controls (HC). METHODS: Fifty-one insomnia patients and 53 HC underwent 6 nights of polysomnography. Four methods for estimating Delta Decline were compared (exponential and linear best-fit functions using NREM (1) episode mean, (2) peak, and (3) total delta power and (4) delta power for all available NREM epochs). The best method was applied to compare groups on linear and exponential rates of Delta Decline. RESULTS: Best-fit models using all available NREM epochs were significantly less vulnerable to deviation due to missing data than other methods. Insomnia patients displayed significantly slower linear and exponential Delta Decline than HC. CONCLUSIONS: Computing Delta Decline using all available NREM epochs was the best of the methods studied for minimizing the effects of missing data. Insomnia patients display slower Delta Decline, which is not explained by differences in total sleep time or wake after sleep onset. SIGNIFICANCE: This study supports using all available NREM epochs in Delta Decline computation and suggests a slower rate in insomnia.

Impact of daytime sleepiness and insomnia on simple and complex cognitive task performances.

OBJECTIVE: To examine the individual and combined effects of daytime sleepiness and insomnia disorder (ID) on measures of cognitive functioning. DESIGN AND SETTING: This study was conducted at a medical center using a cross-sectional research design. PARTICIPANTS: 35 persons with ID (Mage = 40.6 years; 25 women) and 54 normal sleepers (NS; Mage = 31.5 years; 38 women). METHODS AND MEASURES: Participants underwent two nights of home-based polysomnography (PSG) followed by daytime testing with a four-trial Multiple Sleep Latency Test (MSLT). Before each MSLT nap, they completed a computer-administered battery of reaction time tasks. Measures of response latencies and response accuracy were tabulated and used as dependent measures. The ID and NS groups were each subdivided into "alert" (eg, MSLT mean latency > 8 min) and "sleepy" (eg, MSLT mean latency ≤ 8 min) subgroups to identify hyperaroused persons with ID and allow for their comparisons with the other participant subgroups. RESULTS: Multivariate analyses of variance showed a significant main effect for level of daytime sleepiness (F [1, 84] = 8.52, p = 0.0045) on simpler performance tasks and a significant main effect for presence vs. absence of ID (F [1,84] = 6.62, p = 0.012) on complex tasks. A lack of significant participant type x MSLT alertness level interactions in study analyses suggested those ID participants with presumed hyperaousal were not relatively more impaired than the other participant subgroups. CONCLUSIONS: Daytime performance deficits on simple tasks seem most dependent on individuals' levels of daytime sleepiness, whereas performance deficits on more complex tasks appears related to the presence of ID. Therefore, it seems best to use complex performance measures both to document cognitive deficits among those with ID and to determine if insomnia treatments reduce such impairments. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02290405.

Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine systematic review, meta-analysis, and GRADE assessment.

INTRODUCTION: The purpose of this systematic review is to provide supporting evidence for a clinical practice guideline on the use of behavioral and psychological treatments for chronic insomnia disorder in adult populations. METHODS: The American Academy of Sleep Medicine commissioned a task force of 9 experts in sleep medicine and sleep psychology. A systematic review was conducted to identify randomized controlled trials that addressed behavioral and psychological interventions for the treatment of chronic insomnia disorder in adults. Statistical analyses were performed to determine if the treatments produced clinically significant improvements in a range of critical and important outcomes. Finally, the Grading of Recommendations Assessment, Development, and Evaluation process was used to evaluate the evidence for making specific treatment recommendations. RESULTS: The literature search identified 1,244 studies; 124 studies met the inclusion criteria, and 89 studies provided data suitable for statistical analyses. Evidence for the following interventions is presented in this review: cognitive-behavioral therapy for insomnia, brief therapies for insomnia, stimulus control, sleep restriction therapy, relaxation training, sleep hygiene, biofeedback, paradoxical intention, intensive sleep retraining, and mindfulness. This review provides a detailed summary of the evidence along with the quality of evidence, the balance of benefits vs harms, patient values and preferences, and resource use considerations.

Behavioral and psychological treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine clinical practice guideline.

INTRODUCTION: This guideline establishes clinical practice recommendations for the use of behavioral and psychological treatments for chronic insomnia disorder in adults. METHODS: The American Academy of Sleep Medicine (AASM) commissioned a task force of experts in sleep medicine and sleep psychology to develop recommendations and assign strengths based on a systematic review of the literature and an assessment of the evidence using Grading of Recommendations Assessment, Development and Evaluation (GRADE) methodology. The task force evaluated a summary of the relevant literature and the quality of evidence, the balance of clinically relevant benefits and harms, patient values and preferences, and resource use considerations that underpin the recommendations. The AASM Board of Directors approved the final recommendations. RECOMMENDATIONS: The following recommendations are intended as a guide for clinicians in choosing a specific behavioral and psychological therapy for the treatment of chronic insomnia disorder in adult patients. Each recommendation statement is assigned a strength ("strong" or "conditional"). A "strong" recommendation (ie, "We recommend…") is one that clinicians should follow under most circumstances. A "conditional" recommendation is one that requires that the clinician use clinical knowledge and experience, and to strongly consider the patient's values and preferences to determine the best course of action. 1. We recommend that clinicians use multicomponent cognitive behavioral therapy for insomnia for the treatment of chronic insomnia disorder in adults. (STRONG). 2. We suggest that clinicians use multicomponent brief therapies for insomnia for the treatment of chronic insomnia disorder in adults. (CONDITIONAL). 3. We suggest that clinicians use stimulus control as a single-component therapy for the treatment of chronic insomnia disorder in adults. (CONDITIONAL). 4. We suggest that clinicians use sleep restriction therapy as a single-component therapy for the treatment of chronic insomnia disorder in adults. (CONDITIONAL). 5. We suggest that clinicians use relaxation therapy as a single-component therapy for the treatment of chronic insomnia disorder in adults. (CONDITIONAL). 6. We suggest that clinicians not use sleep hygiene as a single-component therapy for the treatment of chronic insomnia disorder in adults. (CONDITIONAL).