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

修改项目摘要/摘要部分 慢性腰痛（CLBP）是一个主要的公共卫生问题。补充/整合（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]），一些方法具有强有力的疗效支持。大多数研究都集中在治疗效果方面。然而，关于治疗机制的重要问题被忽视了。 揭示C/I治疗机制的一种简约方法可能始于这样的假设，即C/I治疗在很大程度上通过非特异性机制起作用，这些机制可能在治疗中共享。候选的非特异性机制可以分为至少3类：内源性疼痛抑制系统（内源性阿片功能;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）。一般的假设是，这些非特异性机制的治疗诱导的变化将预测不同C/I干预的结果。与此同时，必须解决具体机制的贡献问题。对于MT，这将是正念的变化，而对于SMT，这将是脊柱刚度的变化。拟议的研究将比较MT和SMT激活特异性和非特异性机制的程度，以及这些机制影响疼痛相关结果的程度。在一项试验中比较这两种干预措施中机制的激活和影响，将使我们能够测试某些机制的影响在多大程度上是跨治疗共享的，或者是特定治疗所独有的。240名CLBP患者将被随机分配到MT或SMT。 将在所有治疗中频繁评估所有机制和结局指标。我们希望这两种治疗能在疼痛、情绪和功能方面产生显著的变化。 目的1将测试MT和SMT在非特异性机制中产生何种程度的变化。 目标2将测试MT和SMT在治疗特定机制（MT：正念; SMT：脊柱僵硬）中产生多大程度的变化。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预测结果的独特和共享方差。 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了有力支持的理由，（3）确定了疼痛治疗的有效机制，并揭示了那些可能是多余的或惰性的机制，（4）提供了理论和经验原则，通过这些原则来加强那些与最大利益联系最紧密的C/I机制。

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.