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

CBT 治疗失眠对纤维肌痛疼痛症状和中枢敏化的影响。

• 批准号: 10163918
• 负责人: Christina S McCrae
• 金额: $ 59.41万
• 依托单位: UNIVERSITY OF MISSOURI-COLUMBIA
• 依托单位国家: 美国
• 财政年份: 2018
• 资助国家: 美国
• 起止时间: 2018-08-27 至 2023-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10163918
• 关键词: Affect; Affective; Aftercare; Anterior; Area; Arousal; Brain; Brain region; Characteristics; Chronic Insomnia; Cognition; Cognitive; Cognitive Therapy; Collection; Dimensions; Exhibits; Feedback; Fibromyalgia; Goals; Healthcare Systems; Inferior frontal gyrus; Insula of Reil; Lateral; Lead; Link; Long-Term Effects; Medial; Mediating; Mediator of activation protein; Methodology; Modeling; Nervous System Physiology; Neuraxis; Neuronal Plasticity; Outcome; Pain; Pattern; Peripheral; Prefrontal Cortex; Public Health; Resolution; Rest; Role; Sleep; Sleep disturbances; Sleeplessness; Stimulus; Stress; Structure; Suggestion; Testing; Thick; Thinness; Time; active comparator; base; blood oxygen level dependent; brief intervention; central sensitization; chronic pain; chronic pain patient; cingulate cortex; cingulate gyrus; clinical pain; cognitive testing; fibromyalgia pain; fibromyalgia patients; gray matter; heart rate variability; improved; improvement on sleep; neuroimaging; neuromechanism; novel; pain processing; pain sensitivity; pain symptom; pilot trial; poor sleep; relating to nervous system; response; sleep health; sleep onset; theories; white matter

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.

项目概要 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具有共同的神经元 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 和疼痛。 CATS 声称持续的唤醒和缺乏唤醒解决（通过安宁的睡眠）会导致严重的后果 中枢神经系统功能（又名中枢敏化，CS）的变化导致疼痛敏感性增加。我们最近 检查了纤维肌痛 (FM) 中失眠 (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，减少与疼痛相关的认知情感 唤醒和神经可塑性变化提示 CS 逆转（即疼痛处理中的大脑功能正常化） 区域）与 CBT-I 后疼痛的改善相关。这是此类的第一个证据。 与 CATS 一致，我们假设疼痛的改善是通过改善 CBT-I 后立即进行唤醒、睡眠和 CS。在本文提出的试验中，我们检查了小说 假设觉醒、睡眠和 CS 改善的持续反馈循环将导致持续（或 随着时间的推移，疼痛会有所改善。 拟议的研究有四个具体目标。目标 1 检查 CBT-I 对觉醒、睡眠和疼痛的影响 FM 患者。纳入外周唤醒是新颖的，因为我们之前的试验中没有对其进行测试。目标 2 检查 治疗相关的静息状态大脑活动变化以及功能性大脑的神经激活模式 相关区域对疼痛刺激的网络和血氧水平依赖性（BOLD）反应 疼痛处理。目标 3 研究治疗对与以下疾病相关的大脑结构的纵向影响 疼痛。目标 4 检查觉醒、睡眠和 CS 对疼痛的中介影响，并评估这些是否 中介效应解释了疼痛改善的独特差异，超越了全球中介效应 或可能是疼痛和/或睡眠特定的认知情感因素。所有测试的假设都与我们的一致 概念模型——CATS。 公共卫生影响：证明相对简短的干预措施可以扭转甚至解决问题 疼痛相关的适应不良神经可塑性，改善甚至解决临床疼痛将具有立竿见影的效果 对数百万慢性疼痛患者以及美国医疗保健系统和经济产生深远影响。