IMPORTANCE Cognitive behavioral therapy for insomnia (CBT-I) is the most prominent nonpharmacologic treatment for insomnia disorders. Although meta-analyses have examined primary insomnia, less is known about the comparative efficacy of CBT-I on comorbid insomnia.OBJECTIVE To examine the efficacy of CBT-I for insomnia comorbid with psychiatric and/or medical conditions for ( 1) remission from insomnia; (2) self-reported sleep efficiency, sleep onset latency, wake after sleep onset, total sleep time, and subjective sleep quality; and (3) comorbid symptoms. DATA SOURCES A systematic search was conducted on June 2, 2014, through PubMed, PsycINFO, the Cochrane Library, and manual searches. Search terms included (1) CBT-I or CBT or cognitive behavioral [and its variations] or behavioral therapy [and its variations] or behavioral sleep medicine or stimulus control or sleep restriction or relaxation therapy or relaxation training or progressive muscle relaxation or paradoxical intention; and (2) insomnia or sleep disturbance.STUDY SELECTION Studies were included if they were randomized clinical trials with at least one CBT-I arm and had an adult population meeting diagnostic criteria for insomnia as well as a concomitant condition. Inclusion in final analyses (37 studies) was based on consensus between 3 authors' independent screenings. DATA EXTRACTION AND SYNTHESIS Data were independently extracted by 2 authors and pooled using a random-effects model. Study quality was independently evaluated by 2 authors using the Cochrane risk of bias assessment tool. MAIN OUTCOMES AND MEASURESA priori main outcomes (ie, clinical sleep and comorbid outcomes) were derived from sleep diary and other self-report measures.RESULTS At posttreatment evaluation, 36.0% of patients who received CBT-I were in remission from insomnia compared with 16.9% of those in control or comparison conditions (pooled odds ratio, 3.28; 95% CI, 2.30-4.68; P < .001). Pretreatment and posttreatment controlled effect sizes were medium to large for most sleep parameters (sleep efficiency: Hedges g = 0.91 [95% CI, 0.74 to 1.08]; sleep onset latency: Hedges g = 0.80 [95% CI, 0.60 to 1.00]; wake after sleep onset: Hedges g = 0.68; sleep quality: Hedges g = 0.84; all P < .001), except total sleep time. Comorbid outcomes yielded a small effect size (Hedges g = 0.39 [95% CI, 0.60-0.98]; P < .001); improvements were greater in psychiatric than in medical populations (Hedges g = 0.20 [95% CI, 0.09-0.30]; χ 2 test for interaction = 12.30; P < .001). CONCLUSIONS AND RELEVANCECognitive behavioral therapy for insomnia is efficacious for improving insomnia symptoms and sleep parameters for patients with comorbid insomnia. A small to medium positive effect was found across comorbid outcomes, with larger effects on psychiatric conditions compared with medical conditions. Large-scale studies with more rigorous designs to reduce detection and performance bias are needed to improve the quality of the evidence.

OBJECTIVE Although cognitive-behavioral therapy is effective for treating anxiety disorders, little is known about its effect on quality of life. To conduct a meta-analysis of cognitive-behavioral therapy for anxiety disorders on quality of life, we searched for relevant studies in PubMed, PsycINFO and the Cochrane Library, and conducted manual searches. METHOD The search identified 44 studies that included 59 CBT trials, totaling 3,326 participants receiving cognitive-behavioral therapy for anxiety disorders. We estimated the controlled and within-group random effects of the treatment changes on quality of life. RESULTS The pre-post within-group and controlled effect sizes were moderately strong, Hedges’ g = 0.54 and Hedges’ g = 0.56, respectively. Improvements were greater for physical and psychological domains of quality of life than for environmental and social domains. The overall effect sizes decreased with publication year and increased with treatment duration. Face-to-face treatments delivered individually and in groups produced significantly higher effect sizes than internet-delivered treatments. CONCLUSION Cognitive-behavioral therapy for anxiety disorders is moderately effective for improving quality of life, especially in physical and psychological domains. Internet-delivered treatments are less effective in improving quality of life than face-to-face treatments.

Research on future-oriented cognition in generalized anxiety disorder (GAD) has primarily focused on worry, while less is known about the role of episodic future thinking (EFT), an imagery-based cognitive process. To characterize EFT in this disorder, we used the experimental recombination procedure, in which 21 GAD and 19 healthy participants simulated positive, neutral and negative novel future events either once or repeatedly, and rated their phenomenological experience of EFT. Results showed that healthy controls spontaneously generated more detailed EFT over repeated simulations. Both groups found EFT easier to generate after repeated simulations, except when GAD participants simulated positive events. They also perceived higher plausibility of negative—not positive or neutral—future events than did controls. These results demonstrate a negativity bias in GAD individuals’ episodic future cognition, and suggest their relative deficit in generating vivid EFT. We discuss implications for the theory and treatment of GAD.

The goal of this review is to examine the clinical studies on d-cycloserine, a partial glutamatergic N-methyl-D-aspartate agonist, as an augmentation strategy for exposure procedures during cognitive behavioral therapy for anxiety disorders. Although cognitive behavioral therapy and anxiolytic medications are more effective than placebo for treating anxiety disorders, there is still considerable room for further improvement. Traditional combination strategies typically yield disappointing results. However, recent studies based on translational research have shown promise to augment the neural circuitry underlying fear extinction with pharmacological means. We discuss the current state of the literature, including inconsistencies of findings and issues concerning the drug mechanism, dosing, and dose timing. D-cycloserine is a promising combination strategy for cognitive behavioral therapy of anxiety disorders by augmenting extinction learning. However, there is also evidence to suggest that d-cycloserine can facilitate reconsolidation of fear memory when exposure procedures are unsuccessful.

Background Cognitive impairment is a common and debilitating symptom of Parkinson's disease (PD), and its etiology is likely multifactorial. One candidate mechanism is circadian disruption. Although there is evidence of circadian abnormalities in PD, no studies have directly assessed their association with cognitive impairment. Objectives Investigate whether circadian rest‐activity rhythm is associated with cognitive function in PD independently of sleep. Methods Thirty‐five participants with PD wore wrist actigraph monitors and completed sleep diaries for 7 to 10 days, then underwent neuropsychological testing. Rest‐activity rhythm was characterized using nonparametric circadian rhythm analysis of actigraphy data. Objective sleep parameters were also estimated using actigraphy data. Hierarchical regression models assessed the independent contributions of sleep and rest‐activity rhythm to cognitive performance. Results Less stable day‐to‐day rest‐activity rhythm was associated with poorer executive, visuospatial, and psychomotor functioning, but not with memory. Hierarchical regressions showed that interdaily stability's contribution to cognitive performance was independent of sleep's contributions. Whereas sleep contributed to executive function, but not psychomotor or visuospatial performance, rest‐activity rhythm stability significantly contributed to variance in all three of these domains, uniquely accounting for 14.4% to 17.6% of their performance variance. Conclusions Our findings indicate that circadian rest‐activity rhythm is associated with cognitive impairment independently of sleep. This suggests the possible utility of rest‐activity rhythm as a biomarker for circadian function in PD. Future research should explore interventions to stabilize behavioral rhythms in order to strengthen circadian function, which, in turn, may reduce cognitive impairment in PD.