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 et al. (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 “co-morbid 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)i have been conducted in the context of chronic pain (7-9). 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. and Rybarczyk et al. studies utilized group formats, and only one study (Edinger et al.) 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-to-post) at 3 months for CBT was .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-to-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 co-morbid 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.