Sleep Disturbance, Central Pain Modulation, and Clinical Pain in Osteoarthritis

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DESCRIPTION (provided by applicant): Osteoarthritis (OA) is one of the most common diseases and leading causes of disability in the world. Sleep disturbance, in addition to pain, is one of more frequent and disabling symptoms of OA. Numerous longitudinal and some experimental studies indicate that while poor sleep is a consequence of pain, sleep disturbance may also reciprocally feedback to cause hyperalgesia and exacerbate clinical pain. Recent conceptual models of chronic pain, including OA pain, implicate dysfunctional supraspinal pain processing mechanisms that modulate (amplify or inhibit) nociceptive transmission. Preliminary work by our group indicates that clinically relevant sleep disruptions directly impair these central pain processing mechanisms in healthy individuals. Empirical treatments for sleep disturbance in OA are lacking, as are data indicating whether normalization of sleep alters pain processing mechanisms and clinical pain. This proposal seeks to extend our work to investigate neurobehavioral causes and treatments of clinical pain in knee OA. Project aims are to: 1) determine the extent to which sleep maintenance insomnia and objective polysomnographic measures of sleep are associated with alterations in pain modulation and 2) evaluate whether improving sleep disturbance decreases clinical pain by improving pain modulation. Two inter-related studies are proposed. Study 1 is a factorial comparison of knee OA patients with and without insomnia versus matched controls with and without insomnia. These 4 groups will be compared on electroencephalographic measures of sleep, laboratory indices of pain modulation, and clinical pain ratings. Study 2 is a randomized, double-blinded, placebo controlled clinical trial of cognitive-behavior therapy for insomnia (CBT-I) in knee OA. Subjects from Study 1, meeting criteria for sleep maintenance insomnia will be randomized to a validated CBT-I protocol or a standardized behavioral placebo control. Primary endpoints measured half-way through treatment (4 weeks), at post-treatment, and 3 and 6 month follow-ups are: objective and subjective measures of sleep, laboratory measures of pain modulation, and clinical pain severity. This project will increase knowledge of the mechanisms by which sleep disturbance enhances pain sensitivity and lead to a critically needed empirical, non-pharmacological treatment approach for insomnia in OA. Osteoarthritis impacts approximately 29% of adults over the age of 44 and 50% of adults over the age of 64. Pain and insomnia are two of the most common and disabling symptoms associated with degenerative joint disease that cause substantial personal suffering and pose considerable burden on the healthcare system and the economy. This project will: 1) increase the scientific understanding of the mechanisms by which chronic sleep disturbance amplifies pain in arthritis and 2) rigorously test whether a much needed behavioral treatment for insomnia in arthritis not only improves sleep, but in turn reduces pain.