Evaluating Specific and Non-Specific Mechanisms in Two Distinct Complementary/Int

评估两个不同的互补/整合中的特异性和非特异性机制

• 批准号: 9981631
• 负责人: Stephen Bruehl
• 金额: $ 91.3万
• 依托单位: RUSH UNIVERSITY MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2018
• 资助国家: 美国
• 起止时间: 2018-08-01 至 2023-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9981631
• 关键词: Acupuncture Therapy; Address; Affect; Attention; Categories; Chronic low back pain; Cognition; Data; Early treatment; Etiology; Integrative Therapy; Intervention; Knowledge; Link; Mindfulness Training; Moods; Outcome; Outcome Measure; Pain; Pain management; Patient Participation; Patients; Procedures; Proliferating; Public Health; Randomized; Research; Resources; Role; Science; Self Efficacy; Spinal; Spinal Manipulation; System; Testing; Theoretical model; Therapeutic; Time; Treatment Efficacy; Work; chronic pain; comparative; conditioned pain modulation; endogenous opioids; mindfulness; neglect; outcome prediction; pain catastrophizing; patient expectation; public health relevance; theories; treatment effect

Modified Project Summary/Abstract Section Chronic low back pain (CLBP) is a major public health concern. Complementary/integrative (C/I) chronic pain interventions have proliferated (eg, Mindfulness Training [MT], spinal manipulation therapy [SMT]), and some approaches have strong support for efficacy. Most research has focused on questions regarding treatment efficacy. However, important questions regarding treatment mechanisms have been neglected. A parsimonious approach to uncovering C/I treatment mechanisms may start from the hypothesis that C/I treatments work to a large extent via non-specific mechanisms that may be shared across treatments. Candidate non-specific mechanisms can be grouped into at least 3 categories: endogenous pain inhibitory systems (endogenous opioid function; conditioned pain modulation), pain-related cognition (pain catastrophizing; self-efficacy), and therapy factors (therapeutic relationship, patient expectations). The general hypothesis is that treatment-induced changes in these non-specific mechanisms will predict outcomes across different C/I interventions. At the same time, the contribution of specific mechanisms must be addressed. For MT, this would be changes in mindfulness, whereas for SMT, this would be changes in spinal stiffness. The proposed study will compare the degree to which MT and SMT activate specific and non-specific mechanisms, and the degree to which these mechanisms affect pain-related outcomes. Comparing the activation and effects of mechanisms in these 2 interventions in a single trial will allow us to test the degree to which effects of certain mechanisms are shared across treatments or are unique to a given treatment. 240 people with CLBP will be randomly assigned to MT, or SMT. All mechanism and outcome measures will be assessed frequently across all treatments. We expect the 2 treatments to produce significant changes in pain, mood and function. Aim 1 will test to what degree MT and SMT produce changes in non-specific mechanisms. Aim 2 will test to what degree MT and SMT produce changes in treatment-specific mechanisms (MT: mindfulness; SMT: spinal stiffness). Aim 3 will test to what degree changes in non-specific and specific mechanisms predict changes in pain, mood and function, and whether these relationships depend on the treatment received, and the degree to which changes in non-specific and specific mechanisms account for unique and shared variance in predicting outcomes. Addressing questions of mechanism is critical to the science and practice of C/I pain interventions because it: (1) tests theory validity, (2) provides empirically-supported rationale for asking people with pain to devote the resources needed to participate in treatment, (3) identifies the effective mechanisms of pain treatments and reveals those that may be redundant or inert, and (4) provides theoretical and empirical principles by which to enhance those C/I mechanisms that are most closely linked to the largest benefits.

修改后的项目摘要/摘要部分 慢性腰痛（CLBP）是一个主要的公共卫生问题。补充/综合（C/I）慢性疼痛干预措施已经激增（例如正念训练[MT]、脊柱推拿疗法[SMT]），并且一些方法对疗效有强有力的支持。大多数研究都集中在有关治疗效果的问题上。然而，有关治疗机制的重要问题却被忽视了。 揭示 C/I 治疗机制的简约方法可能始于这样的假设：C/I 治疗在很大程度上通过可能在不同治疗中共享的非特异性机制发挥作用。候选非特异性机制可分为至少 3 类：内源性疼痛抑制系统（内源性阿片类药物功能；条件性疼痛调节）、疼痛相关认知（疼痛灾难化；自我效能）和治疗因素（治疗关系、患者期望） ）。一般假设是，治疗引起的这些非特异性机制的变化将预测不同 C/I 干预措施的结果。同时，必须解决具体机制的贡献。对于 MT 来说，这将是正念的变化，而对于 SMT 来说，这将是脊柱僵硬的变化。拟议的研究将比较 MT 和 SMT 激活特定和非特定机制的程度，以及这些机制影响疼痛相关结果的程度。在单个试验中比较这两种干预措施中机制的激活和效果将使我们能够测试某些机制的效果在不同治疗方法中共享的程度或对于给定治疗来说是独特的程度。 240 名 CLBP 患者将被随机分配到 MT 或 SMT。 所有治疗方法中的所有机制和结果指标都将经常进行评估。我们预计这两种治疗会对疼痛、情绪和功能产生显着的变化。 目标 1 将测试 MT 和 SMT 在多大程度上产生非特定机制的变化。 目标 2 将测试 MT 和 SMT 在多大程度上对特定治疗机制产生变化（MT：正念；SMT：脊柱僵硬）。目标 3 将测试非特异性和特异性机制的变化在多大程度上预测疼痛、情绪和功能的变化，以及这些关系是否取决于所接受的治疗，以及非特异性和特异性机制的变化在多大程度上解释了独特的机制。以及预测结果的共同方差。 解决机制问题对于 C/I 疼痛干预的科学和实践至关重要，因为它：(1) 测试理论有效性，(2) 为要求疼痛患者投入参与治疗所需的资源提供经验支持的基本原理， (3) 确定疼痛治疗的有效机制，并揭示那些可能多余或惰性的机制，(4) 提供理论和经验原则，通过这些原则来增强与最大效益最密切相关的 C/I 机制。