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.

Circadian misalignment and sleep disruption in mild cognitive impairment.

BACKGROUND: While it is evident that Alzheimer's disease is associated with disturbed sleep and circadian rhythms, the extent to which such changes are evident in older people 'at risk' of developing dementia is unknown. OBJECTIVE: In this study, we aimed to determine whether patients with mild cognitive impairment (MCI) demonstrated significant alterations in the timing of melatonin secretion onset and amount, as well as sleep architecture. METHODS: Thirty patients with MCI and 28 age-matched controls underwent psychiatric, medical, and neuropsychological assessment, followed by overnight polysomnography and dim light melatonin onset assessment. Participants also performed an episodic memory task while in the laboratory. Dim light melatonin onset was computed using a standardized algorithm, and area under the curve was computed for melatonin secretion. Sleep architecture measures including wake after sleep onset and latency to rapid eye movement sleep were derived. RESULTS: Patients with MCI had advanced timing of their melatonin secretion onset relative to controls, but the levels of melatonin secreted did not differ between groups. The MCI group also had greater wake after sleep onset and increased rapid eye movement sleep latency. There were differential associations between dim light melatonin onset and cognition between the two groups, with earlier dim light melatonin onset being associated with poorer memory performance in MCI patients. CONCLUSION: Circadian misalignment and sleep disruption is evident in patients with MCI, and is consistent with changes observed in Alzheimer's disease. Such findings could be a marker for disease trajectory, and may even be implicated in disease pathogenesis.