Friday, April 19, 2024
4/19/2024
PROJECT SUMMARY Chronic pain patients exhibit maladaptive neural plasticity compared to controls. Further, insomnia affects 67-88% of chronic pain patients. We hypothesize that pain processing and sleep share common neural underpinnings and thus, improving sleep may reverse pain related maladaptive neural plasticity and improve clinical pain. The Cognitive Activation Theory of Stress (CATS) provides a model linking chronic insomnia and pain. CATS asserts sustained arousal and lack of arousal resolution (through restful sleep) lead to critical changes in CNS functioning (aka Central Sensitization, CS) that result in increased pain sensitivity. We recently examined cognitive behavioral treatments for insomnia (CBT-I) and pain (CBT-P) in fibromyalgia (FM) patients. We found novel preliminary evidence that improved sleep, decreased pain-related cognitive-affective arousal, and neural plastic changes suggestive of CS reversal (i.e., normalized brain function in pain processing areas) were associated with improved pain following CBT-I. This is the first evidence of its kind. Consistent with CATS, we hypothesize that pain improvements are mediated by improvements in arousal, sleep, and CS immediately following CBT-I. In the trial proposed herein, we examine the novel hypothesis that a sustained feedback loop of improvements in arousal, sleep, and CS will result in sustained (or possibly increased) pain improvements over time. The proposed study has four specific aims. Aim 1 examines the effects of CBT-I on arousal, sleep, and pain in FM patients. Inclusion of peripheral arousal is novel as it was not tested in our previous trial. Aim 2 examines treatment related changes in resting state brain activity as well as neural activation patterns of functional brain networks and Blood-Oxygen-Level Dependent (BOLD) responses to painful stimuli in regions associated with pain processing. Aim 3 investigates the longitudinal impact of treatment on brain structures associated with pain. Aim 4 examines the mediating impact of arousal, sleep, and CS on pain and evaluates whether these mediating effects explain unique variance of pain improvement over and beyond the mediating effects of global or possibly pain- and/or sleep-specific cognitive-affective factors. All hypotheses tested are consistent with our conceptual model – CATS. Public Health Implications: Demonstration that a relatively brief intervention can reverse or even resolve pain related maladaptive neural plasticity, and improve or even resolve clinical pain would have immediate and far-reaching implications for millions of chronic pain sufferers and the US healthcare system and economy.
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