Impact of CBT for Insomnia on Pain Symptoms and Central Sensitization in Fibromyalgia.

项目摘要 慢性疼痛患者表现出适应不良的神经可塑性相比，控制。此外，失眠影响 67-88%的慢性疼痛患者。我们假设疼痛处理和睡眠共享共同的神经元 因此，改善睡眠可以逆转疼痛相关的适应不良神经可塑性， 临床疼痛压力的认知激活理论（CATS）提供了一个模型， 和痛苦. CATS声称持续的唤醒和缺乏唤醒解决（通过休息睡眠）导致严重的 中枢神经系统功能的变化（又称中枢致敏，CS）导致疼痛敏感性增加。我们最近 检查了纤维肌痛（FM）患者失眠（CBT-I）和疼痛（CBT-P）的认知行为治疗 患者我们发现了新的初步证据，可以改善睡眠，减少疼痛相关的认知情感障碍， 唤醒和暗示CS逆转的神经可塑性变化（即，疼痛处理中的正常化脑功能 区域）与CBT-I后疼痛改善相关。这是第一个此类证据。 与CATS一致，我们假设疼痛的改善是由以下因素介导的： CBT-I后即刻的觉醒、睡眠和CS。在这里提出的审判中，我们审查了小说 假设唤醒、睡眠和CS改善的持续反馈回路将导致持续（或 可能增加）随着时间的推移疼痛改善。 拟议的研究有四个具体目标。目的1检查CBT-I对觉醒、睡眠和疼痛的影响 FM患者纳入外周觉醒是新的，因为在我们之前的试验中没有进行测试。目标2检查 静息状态脑活动以及功能性脑的神经激活模式的治疗相关变化 网络和血氧水平依赖（BOLD）反应疼痛刺激相关的区域 疼痛处理目的3：研究治疗对脑结构的纵向影响， 痛苦目的4检查唤醒、睡眠和CS对疼痛的中介影响，并评估这些影响是否与疼痛相关。 中介效应解释了疼痛改善的独特差异，并超出了全球的中介效应 或者可能是疼痛和/或睡眠特异性认知情感因素。所有测试的假设都与我们的假设一致。 概念模型- CATS。 公共卫生影响：证明相对简短的干预可以逆转甚至解决 疼痛相关的适应不良神经可塑性，并改善甚至解决临床疼痛将有立即和 这将对数百万慢性疼痛患者以及美国医疗体系和经济产生深远影响。

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.