Elsevier

Sleep Medicine

Volume 11, Issue 3, March 2010, Pages 302-309
Sleep Medicine

Original Article
The efficacy of cognitive-behavioral therapy for insomnia in patients with chronic pain

https://doi.org/10.1016/j.sleep.2009.05.018Get rights and content

Abstract

Study objectives

To assess the efficacy of cognitive-behavioral therapy for insomnia (CBT-I) in patients with non-malignant chronic pain.

Methods

Twenty-eight subjects with chronic neck and back pain were stratified according to gender, age, and ethnicity, then assigned to one of the two treatment groups: CBT-I or a contact control condition.

Intervention

Eight weeks of CBT-I including sleep restriction, stimulus control, sleep hygiene, and one session of cognitive therapy devoted to catastrophic thoughts about the consequences of insomnia.

Measurements and results

Outcomes included sleep diary assessments of sleep continuity, pre–post measures of insomnia severity (ISI), pain (Multidimensional Pain Inventory), and mood (BDI and POMS). Subjects receiving CBT-I (n = 19), as compared to control subjects (n = 9), exhibited significant decreases in sleep latency, wake after sleep onset, number of awakenings, and significant increase in sleep efficiency. The diary findings were paralleled by significant changes in the ISI (p = 0.05). Significant improvement (p = 0.03) was found on the Interference Scale of the Multidimensional Pain Inventory. The groups did not significantly differ on mood measures or measures of pain severity.

Conclusions

CBT-I was successfully applied to patients experiencing chronic pain. Significant improvements were found in sleep as well as in the extent to which pain interfered with daily functioning. The observed effect sizes for the sleep outcomes appear comparable to or better than meta-analytic norms for subjects with Primary Insomnia.

Introduction

In recent years there has been a growing interest in the veracity of the concept of “Secondary Insomnia” and the assumption that such forms of sleep continuity disturbance are likely to be more resistant to treatment than Primary Insomnia. This challenge has largely occurred at a theoretical level. Lichstein and co-worker [1], [2], have argued that it is nearly impossible to substantiate that insomnia is truly secondary and thus the distinction has little nosological value and should not be used to dictate when targeted treatment is warranted. This point of view is further buttressed by the Spielman Model [3], [4] which clearly suggests that chronic insomnia is maintained, irrespective of the original precipitants, by a common set of perpetuating factors which are largely cognitive and behavioral in nature. When taken together, these lines of thought suggest that treatments for Primary Insomnia should be effective for what is now considered “comorbid insomnia” [5], [6]. One very plausible exception to this perspective is in conditions where the comorbid illness may act as both a precipitating and perpetuating factor. This scenario is likely to be the case with insomnia comorbid with chronic pain. The unremitting nature of chronic pain may directly contribute to acute and chronic sleep initiation and maintenance problems via a form of hyperarousal that comes with the experience of pain. To date, three trials with cognitive-behavioral therapy for insomnia (CBT-I)1 have been conducted in the context of chronic pain [7], [8], [9]. The studies are briefly summarized below (see also Table 1).

The first study of CBT-I in chronic pain was conducted with 60 chronic pain patients [8]. Thirty-two of the subjects were randomized to group CBT-I and 28 were randomized to a self-monitoring/waiting-list control condition. The second study was conducted with 47 fibromyalgia patients who received individual therapy with CBT-I (n = 18), sleep hygiene (n = 18), or treatment-as-usual for fibromyalgia (n = 11) [9]. The third study was conducted in 92 elderly patients with insomnia occurring in association with one of three conditions: chronic pain due to osteoarthritis, chronic obstructive lung disease, or coronary artery disease. In this study, the effectiveness of CBT-I was compared to a control condition consisting of stress management [7]. All three of the studies included sleep restriction and stimulus control as the main components of their CBT-I regimens; the Currie et al. [8] and Rybarczyk et al. [7] studies utilized group formats, and only one study [9] had treatment conducted by expert therapists.

In the first study (Currie et al.), significant group differences were observed for self-reported sleep latency and wake after sleep onset. CBT-I was not associated with significant group differences in pain severity, although the mean changes were in a positive direction and the effects appeared to be in the moderate range. The pain reduction effect size (pre–post) at 3 months for CBT was 0.56 (moderate) compared to 0.15 for waitlist control (p = 0.12) [8]. In the second study (Edinger et al.), significant group differences were observed for self-reported sleep latency, total wake time, and sleep efficiency. A trend (p = 0.07) was evident for wake after sleep onset. CBT-I was not associated with significant changes in pain measures but here again there was a modest mean pre–post change with a moderate to large corresponding effect size (0.88). In the third study (Rybarczyk et al.), the three medical conditions responded to CBT-I in a comparable fashion and the aggregate of the samples significantly differed from the control condition for self-reported sleep latency, sleep efficiency, and wake after onset. Evaluating the effect of CBT-I on pain was not a focus of this study.

Taken together, these studies support the notion that CBT-I may be successfully utilized with insomnia that occurs comorbid with chronic pain. Further, two of the three studies provide data (when viewed as effect sizes) that suggest that CBT-I may also confer some clinical benefit with respect to pain.

The purpose of the present study was to (1) garner additional evidence regarding the efficacy of CBT-I in treating insomnia in the context of chronic pain and (2) assess whether CBT-I is associated with clinical changes with respect to pain severity and/or pain interference (daytime function). In the case of the first goal, our intent was to deploy a form of CBT-I that was more rigorous than that provided in the prior studies. In the present study, the intervention was delivered as individual therapy where treatment was conducted according to the specifications of a published treatment manual by a therapist who received intensive training and extensive supervision. In the case of the second goal, a broader measurement strategy was utilized to evaluate pain responses in a homogenous sample of chronic pain patients. In the present study, three measures were used to assess pain: the Pain Disability Index (PDI), The Multidimensional Pain Inventory (MPI), and a Likert scale score on the sleep/pain diaries.

Section snippets

Methods

This study was approved by the Research Subjects Review Board (RSRB) of the University of Rochester. All subjects signed informed consent before engaging in any research activities.

Subjects (sample acquisition and attrition)

Forty-seven subjects with chronic non-malignant pain located in the spinal region (neck and back) gave consent during the screening phase of the study. Twenty-eight subjects met study eligibility criteria and were randomized (∼2:1) to either CBT-I or a contact/measurement control condition (19 CBT-I, 9 controls). Study eligible subjects were double-match randomized by a blinded third party until the 16th subject was reached; at that point a stratification procedure according to gender, age, and

Discussion

In the present study, the efficacy of CBT-I was assessed in patients with chronic pain. Pre–post changes for sleep continuity, pain, and mood were assessed across two groups; a CBT-I group (n = 19) and a contact/measurement control group (n = 9). Overall, with a family-wise type I error controlled at the 0.05 level by the FDR method, SL, WASO, and NWAK were significantly decreased and SE was significantly increased in the group that received CBT-I, while TST and EMA were not significantly changed.

Acknowledgements

Funding/support: This research is supported by NINRNR5R21NR009080-02.

The authors would like to acknowledge support from the University of Rochester, School of Nursing Center for Research and Evidence Based Practice data management team and Xin Tu, Ph.D., Professor and Associate Chair of the University of Rochester, Department of Biostatistics.

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