Biobehavioral Pain Management in TMD

描述(由申请人提供)：颞下颌关节紊乱病(TMD)是一种普遍且代价高昂的公共卫生挑战，影响到大量其他方面通常健康的成年人。然而，人们对它们的理解仍然很少。疼痛处理系统的外周和中枢变化导致TMD患者疼痛的严重程度和持续性存在很大的个体差异。这种复杂性和异质性要求一种全面的、多维的方法，系统地确定与临床疼痛的因果关系和机制联系。疼痛相关灾变(CAT)和睡眠连续性障碍(SCD)是TMD和其他特发性疼痛的两个可改变的危险因素，影响疼痛放大和临床疼痛的前感觉机制。这项拟议的研究考察了减少这些危险因素是否会改变TMD患者的疼痛调制系统和疼痛引发的炎症活动。符合RDC的TMD标准和研究进入标准的女性将随机接受灾难性认知治疗、睡眠连续性障碍的行为治疗或TMD疾病教育。除了全面的临床评估外，随机分组之前还将完成睡眠多导监测和疼痛敏感性和调节系统、炎症活动、自主活动和肾上腺皮质功能的实验室测量。CAT和SCD的减少有望减少疼痛引起的炎症活动并改善疼痛调制，这有望先于临床TMD疼痛的减轻。随着PSG和日记的加入，我们的方法允许我们检查CAT和SCD之间的潜在相互作用。具体地说，我们将研究CAT和SCD的减少是否会减少睡眠中的唤醒，以及这些影响是否通过特定治疗减少睡前唤醒来调节。由于睡眠障碍和灾难都是可改变的风险因素，我们的发现有望推动这种慢性疾病的新疗法和预防方法的发展，这种疾病影响着数百万正处于成年壮年的美国人。

DESCRIPTION (provided by applicant): Temporomandibular joint disorders (TMD) are a prevalent and costly public health challenge, affecting a large number of otherwise generally healthy adults. Yet they remain poorly understood. Peripheral and central alterations in pain processing systems contribute to the large individual differences seen in the severity and persistence of pain in TMD. This complexity and heterogeneity mandates a comprehensive, multidimensional approach that systematically determines causal and mechanistic linkages to clinical pain. Pain-related catastrophizing (CAT) and sleep continuity disturbance (SCD) are two modifiable risk factors for TMD and other idiopathic pain conditions that influence the pronociceptive mechanisms underlying pain amplification and clinical pain. The proposed study examines whether reducing these risk factors alters pain modulatory systems and pain-evoked inflammatory activity in patients with (TMD). Women meeting RDC criteria for TMD and study entry criteria will be randomized to receive cognitive therapy for catastrophizing, behavioral therapy for sleep continuity disturbance, or TMD disease education. In addition to a comprehensive clinical assessment, polysomnographic measures of sleep and laboratory measures of pain sensitivity and modulatory systems, inflammatory activity, autonomic activity, and adrenocortical function will be completed before after randomization. Reductions in CAT and SCD are expected to reduce pain-evoked inflammatory activity and improve pain modulation, which are expected to precede reductions in clinical TMD pain. With the inclusion of PSG and diaries, our methods allow us to examine potential interplay between CAT and SCD. Specifically, we will examine whether reductions in CAT and SCD to reduce arousal during sleep and whether these effects are mediated by treatment-specific reductions in pre-sleep arousal. Because both sleep disturbance and catastrophizing are modifiable risk factors, our findings promise to promote the development of new treatments and prophylactic approaches for this chronic illness that affects millions of Americans in the prime of their adult lives.