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Study objectivesTo evaluate the effects of digital cognitive behavior therapy for insomnia (dCBT-I) delivered during pregnancy on subjective sleep outcomes, depressive symptoms, and anxiety symptoms through 6 months postpartum.MethodsPeople up to 28 weeks gestation (N = 208) with insomnia were randomized to 6 weekly sessions of dCBT-I or standard care. We report follow-up data at 3 and 6 months postpartum. The primary outcome was insomnia symptom severity. Secondary sleep outcomes included global sleep quality and insomnia caseness. Mental health outcomes included depressive and anxiety symptom severity. We evaluated between-condition differences in change from baseline for each postpartum timepoint and categorical outcomes.ResultsdCBT-I participants did not experience significantly greater improvements in insomnia symptom severity relative to standard care participants, but they did experience higher rates of insomnia remission and lower rates of insomnia caseness at 6 months postpartum. dCBT-I participants experienced greater improvements in depressive symptom severity from baseline to both postpartum timepoints, and in anxiety symptom severity from baseline to 3 months postpartum. The proportion of participants with probable major depression at 3 months postpartum was significantly higher among standard care (18%) than dCBT-I (4%, p = 0.006) participants; this between-condition difference was pronounced among the subset (n = 143) with minimal depressive symptoms at baseline (18% vs 0%).ConclusiondCBT-I use during pregnancy leads to enduring benefits for postpartum insomnia remission. Findings provide strong preliminary evidence that dCBT-I use during pregnancy may prevent postpartum depression and anxiety, which is notable when considering the high frequency and importance of these problems.Clinical Trials: ClinicalTrials.gov, https://clinicaltrials.gov/ct2/show/NCT02805998, NCT02805998.

To compare cognitive behavioral therapy for insomnia (CBT-I) + antidepressant medication (AD) against treatments that target solely depression or solely insomnia. A blinded, randomized split-plot experimental study. Two urban academic clinical centers. 107 participants (68% female, mean age 42 ± 11) with major depressive disorder and insomnia. Randomization was to one of three groups: antidepressant (AD; escitalopram) + CBT-I (4 sessions), CBT-I + placebo pill, or AD + 4-session sleep hygiene control (SH). Subjective sleep was assessed via 2 weeks of daily sleep diaries (use of medication was covaried in all analyses); although there were no statistically significant group differences detected, all groups improved from baseline to posttreatment on subjective sleep efficiency (SE) and total wake time (TWT) and the effect sizes were large. Objective sleep was assessed via overnight polysomnographic monitoring at baseline and posttreatment; analyses revealed both CBT groups improved on TWT (p = .03), but the AD + SH group worsened. There was no statistically significant effect for PSG SE (p = .07). There was a between groups medium effect observed for the AD + SH and CBT + placebo group differences on diary TWT and both PSG variables. All groups improved significantly from baseline to posttreatment on the Hamilton Rating Scale for Depression (HAMD-17); the groups did not differ. Although all groups self-reported sleeping better after treatment, only the CBT-I groups improved on objective sleep, and AD + SH's sleep worsened. This suggests that we should be treating sleep in those with depression with an effective insomnia treatment and relying on self-report obscures sleep worsening effects. All groups improved on depression, even a group with absolutely no depression-focused treatment component (CBT-I + placebo). The depression effect in CBT-I only group has been reported in other studies, suggesting that we should further investigate the antidepressant properties of CBT-I.

This study examined whether individuals with insomnia and objective short sleep duration 6h.Secondary analyses of a randomized, clinical trial with 60 adults participants (n=31 women) from a single academic medical center. Outpatient treatment lasted 8 weeks, with a final follow-up conducted at 6 months. Mixed-effects models controlling for age, sex, CBT-I treatment group assignment, and treatment provider examined sleep parameters gathered via actigraphy, sleep diaries, and an Insomnia Symptom Questionnaire (ISQ) across the treatment and follow-up period.Six months post-CBT-I treatment, individuals with insomnia and normal sleep duration >6h fared significantly better on clinical improvement milestones than did those with insomnia and short sleep duration 80%; X2(1, N=60) =21, P50% decline in MWASO [X2(1, N=60) =60, P6h. Using an actigraphy TST cutoff of 6 hours to classify sleep duration groups was highly accurate and provided good discriminant value for determining insomnia remission.

Study objectivesTo examine the relationship between hypertension prevalence in individuals with insomnia who have short total sleep duration < 6 h or sleep duration ≥ 6 h, using both objective and subjective measures of total sleep duration.MethodsUsing a cross-sectional, observational design, 255 adult volunteers (n = 165 women; 64.7%) meeting current diagnostic criteria for insomnia disorder (MAge = 46.2 y, SDAge = 13.7 y) participated in this study at two large university medical centers. Two nights of polysomnography, 2 w of sleep diaries, questionnaires focused on sleep, medical, psychological, and health history, including presence/absence of hypertension were collected. Logistic regressions assessed the odds ratios of hypertension among persons with insomnia with short sleep duration < 6 h compared to persons with insomnia with a sleep duration ≥ 6 h, measured both objectively and subjectively.ResultsConsistent with previous studies using objective total sleep duration, individuals with insomnia and short sleep duration < 6 h were associated with a 3.59 increased risk of reporting hypertension as a current medical problem as compared to individuals with insomnia with sleep duration ≥ 6 h. Increased risk for hypertension was independent of major confounding factors frequently associated with insomnia or hypertension. No significant risk was observed using subjectively determined total sleep time groups. Receiver operating characteristic curve analysis found that the best balance of sensitivity and specificity using subjective total sleep time was at a 6-h cutoff, but the area under the receiver operating characteristic curve showed low accuracy and did not have good discriminant value.ConclusionsObjectively measured short sleep duration increased the odds of reporting hypertension more than threefold after adjusting for potential confounders; this relationship was not significant for subjectively measured sleep duration. This research supports emerging evidence that insomnia with objective short sleep duration is associated with an increased risk of comorbid hypertension.

Study objectivesInsomnia, which is very common in patients with chronic low back pain (LBP), has long been viewed as a pain symptom that did not merit specific treatment. Recent data suggest that adding insomnia therapy to pain-targeted treatment should improve outcome; however, this has not been empirically tested in LBP or in any pain condition treated with a standardized pain medication regimen. We sought to test the hypothesis that adding insomnia therapy to pain-targeted treatment might improve sleep and pain in LBP.DesignDouble-blind, placebo-controlled, parallel-group, 1-mo trial.SettingDuke University Medical Center Outpatient Sleep Clinic.PatientsFifty-two adult volunteers with LBP of at least 3 mo duration who met diagnostic criteria for insomnia (mean age: 42.5 y; 63% females).InterventionsSubjects were randomized to eszopiclone (ESZ) 3 mg plus naproxen 500 mg BID or matching placebo plus naproxen 500 mg twice a day.Measurements and resultsESZ SIGNIFICANTLY IMPROVED TOTAL SLEEP TIME (MEAN INCREASE: ESZ, 95 min; placebo, 9 min) (primary outcome) and nearly all sleep measures as well as visual analog scale pain (mean decrease: ESZ, 17 mm; placebo, 2 mm) (primary pain outcome), and depression (mean Hamilton Depression Rating Scale improvement ESZ, 3.8; placebo, 0.4) compared with placebo. Changes in pain ratings were significantly correlated with changes in sleep.ConclusionsThe addition of insomnia-specific therapy to a standardized naproxen pain regimen significantly improves sleep, pain, and depression in patients with chronic low back pain (LBP). The findings indicate the importance of administering both sleep and pain-directed therapies to patients with LBP in clinical practice and provide strong evidence that improving sleep disturbance may improve pain.Trial registrationclinicaltrials.gov identifier: NCT00365976.

ObjectiveTo examine the association between physiological hyperarousal and response accuracy on reaction time tasks among individuals with insomnia.Design and settingThis study was conducted at affiliated Veterans Administration (VA) and academic medical centers using a matched-group, cross-sectional research design.ParticipantsEighty-nine individuals (48 women) with primary insomnia, PI (MAge = 49.8 ± 17.2 y) and 95 individuals (48 women) who were well-screened normal sleepers, NS (MAge = 46.9 ± 17.0 y).Methods and measuresParticipants underwent 3 nights of polysomnography followed by daytime testing with a four-trial Multiple Sleep Latency Test (MSLT). Before each MSLT nap, they rated their sleepiness and completed computer-administered reaction time tasks. The mean number of correct and error responses made by each participant across testing trials served as dependent measures. The PI and NS groups were each subdivided into alert (e.g., MSLT mean onset latency > 8 min) and sleepy (e.g., MSLT mean onset latency ≤ 8 min) subgroups to allow for testing the main and interaction effects of participant type and level of alertness.ResultsAlert participants had longer MSLT latencies than sleepy participants (12.7 versus 5.4 min), yet both alert and sleepy individuals with PI reported greater sleepiness than NS. Alert participants also showed lower sleep efficiencies (83.5% versus 86.2%, P = 0.03), suggesting 24-h physiological hyperarousal particularly in the PI group. Individuals with PI had fewer correct responses on performance testing than did NS, whereas a significant group × alertness interaction (P = 0.0013) showed greater error rates among alert individuals with PI (mean = 4.5 ± 3.6 errors per trial) than among alert NS (mean = 2.6 ± 1.9 errors per trial).ConclusionsPhysiological hyperarousal in insomnia may lead to more apparent daytime alertness yet dispose individuals with insomnia to higher error rates on tasks requiring their attention.