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Original Investigation |

Cognitive Behavioral Therapy for Insomnia Comorbid With Psychiatric and Medical Conditions A Meta-analysis

Jade Q. Wu, MA1; Erica R. Appleman, MA1; Robert D. Salazar, MA1; Jason C. Ong, PhD2
[+] Author Affiliations
1Department of Psychological and Brain Sciences, Boston University, Boston, Massachusetts
2Sleep Disorders Service and Research Center, Department of Behavioral Sciences, Rush University Medical Center, Chicago, Illinois
JAMA Intern Med. 2015;175(9):1461-1472. doi:10.1001/jamainternmed.2015.3006.
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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 Measures  A 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]; χ2 test for interaction = 12.30; P < .001).

Conclusions and Relevance  Cognitive 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.

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Figure 1.
Selection Process for Trials Included in the Meta-analyses

The total number of trials is greater than the total number of studies (n = 37) because 1 study24 included 2 trials (ie, 2 cognitive behavioral therapy for insomnia [CBT-I] conditions, each with an independent control/comparison condition).

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Figure 2.
Remission from Insomnia at Posttreatment

Variation in data marker size indicates relative weighting by sample size. CBT-I indicates cognitive behavioral therapy for insomnia; COPD, chronic obstructive pulmonary disease; ISI, Insomnia Severity Index; PD, Parkinson disease; PSQI, Pittsburgh Sleep Quality Index; and PTSD, posttraumatic stress disorder.

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Figure 3.
Sleep Efficiency (SE)–Controlled Effect Sizes From Baseline to Posttreatment

All outcomes were derived from sleep diaries. Variation in data marker size indicates relative weighting by sample size. CBT-I indicates cognitive behavioral therapy for insomnia; COPD, chronic obstructive pulmonary disease; PD, Parkinson disease; PLMD, periodic limb movement disorder; and PTSD, posttraumatic stress disorder.

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Figure 4.
Comorbid Outcomes–Controlled Effect Sizes From Baseline to Posttreatment

Variation in data marker size indicates relative weighting by sample size. BDI indicates Beck Depression Inventory; CBT-I, cognitive behavioral therapy for insomnia; COPD, chronic obstructive pulmonary disease; CPS, Chronic Pain Scale; FSS, Fatigue Severity Scale; HRSD, Hamilton Rating Scale for Depression; MFSI-SF, Multidimensional Fatigue Inventory–Short Form; MPQ, McGill Pain Questionnaire; OSA, obstructive sleep apnea; PCL-M, PTSD Checklist–Military Version; PFS, Piper Fatigue Scale; PHQ-9, Patient Health Questionnaire; PLMD, periodic limb movement disorder; POMS-SF, POMS–Short-Form; and PTSD, posttraumatic stress disorder.

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