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

项目总结 与对照组相比，慢性疼痛患者表现出适应不良的神经可塑性。此外，失眠还会影响 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 因此，改善睡眠可能会逆转疼痛相关的适应不良神经可塑性并改善 临床疼痛。压力的认知激活理论(CATS)提供了一个将慢性失眠联系起来的模型 和痛苦。猫认为持续的唤醒和缺乏唤醒解决(通过安宁的睡眠)会导致严重的 中枢神经系统功能的改变(又名中枢敏感化，CS)，导致疼痛敏感度增加。我们最近 研究了纤维肌痛(FM)患者失眠(CBT-I)和疼痛(CBT-P)的认知行为疗法 病人。我们发现了新的初步证据，可以改善睡眠，减少与疼痛相关的认知情感 觉醒和神经可塑性变化提示CS逆转(即疼痛处理过程中正常的大脑功能 区域)与CBT-I后疼痛改善有关。这是这类证据中的第一个。 与猫一致，我们假设疼痛的改善是通过改善 CBT-I后立即进行觉醒、睡眠和CS检查。在这里提出的审判中，我们审查了这部小说 假设觉醒、睡眠和CS的持续反馈循环将导致持续(或 可能增加)疼痛随着时间的推移而改善。 这项拟议的研究有四个具体目标。目的1研究CBT-I对性唤醒、睡眠和疼痛的影响 在FM患者中。包括外周唤醒是新的，因为它没有在我们之前的试验中进行测试。AIM 2考试 静息状态脑活动及功能脑神经激活模式的治疗相关变化 与疼痛刺激相关区域的网络和血氧水平依赖(BOLD)反应 疼痛处理。目的3研究治疗对脑结构的纵向影响 疼痛。目标4考察了唤醒、睡眠和CS对疼痛的中介影响，并评估了这些因素 中介效应解释了疼痛改善的独特差异，超过了全球 或者可能是疼痛和/或睡眠特有的认知情感因素。所有经过测试的假设都与我们的 概念模型-猫。 对公共卫生的影响：证明相对短暂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立即和 对数百万慢性疼痛患者以及美国医疗体系和经济的深远影响。

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.