Chronic Pain, Motor Output and Motor Learning in Knee Osteoarthritis

 描述（由申请人提供）：据估计，到2030年，美国将有6700万人患有骨关节炎（OA），其中大多数人将在中年时开始患有膝关节OA。患者在接受全膝关节置换术之前要忍受多年的疼痛。膝关节OA患者忍受疼痛的年数会影响他们的膝关节功能和生活质量，但也会影响神经系统处理疼痛信号的方式。疼痛的中枢敏感性是对疼痛刺激的高度反应，这是一种保护机制，旨在使身体愈合。在正常情况下，当组织愈合完成时，中枢致敏消退。然而，有时中枢致敏持续存在，疼痛被夸大或不再源于外周源。这种异常的感觉处理可能导致误诊和治疗效果不佳，因为疼痛的来源是中枢神经系统而不是外周组织。已在膝关节OA患者中证实了疼痛的中枢致敏性，并且另一种异常疼痛机制加剧了疼痛：条件性疼痛调制（CPM）减少。CPM涉及应用疼痛的“条件刺激”，其消除疼痛感知的减少。中枢致敏和条件性疼痛调制减少的存在可能使膝关节OA更难治疗，然而临床医生现在正在通过认知行为治疗和身心治疗等治疗来增强传统的物理治疗干预，这些治疗可以影响中枢神经系统如何处理疼痛信号。不幸的是，这些干预措施不会影响人们使用的运动模式，这些运动模式会加速关节退化，包括膝关节运动减少和肌肉共同收缩增加以及屈曲。这些运动在膝关节中产生更大的负荷和更高的剪切力，这对关节软骨特别有害。最近，已经开发了物理治疗干预措施来解决异常运动和肌肉激活模式，但没有一种比传统的有氧运动或强化运动更有效。这可能是由于学习新的运动程序以稳定膝关节的能力不足，这是非常合理的 考虑到运动输出和运动学习依赖于准确的感觉反馈，我们知道膝关节OA患者的感觉反馈受损。本研究将调查中枢敏感化和CPM减少的存在及其对该人群运动适应和学习的影响。这些结果将为运动控制提供有价值的见解，可用于进一步开发改善膝关节功能同时减缓疾病进展的治疗方法。

 DESCRIPTION (provided by applicant): By 2030, it is estimated that 67 million people will have osteoarthritis (OA) in the US and the majority of them will have OA in the knee that begins in middle age. Patients endure pain for many years before they have a total knee replacement. The number of years that knee OA patients endure pain takes a toll on their knee function and quality of life but it also impacts how the nervous system processes pain signals. Central sensitization of pain is a heightened response to painful stimuli that is a protective mechanism designed to allow the body to heal. Under normal circumstances, central sensitization subsides when tissue healing is complete. However, sometimes central sensitization persists and pain is exaggerated or no longer originates from a peripheral source. This abnormal sensory processing can lead to misdiagnosis and poor outcomes to treatments because the source of the pain is in the central nervous system not in peripheral tissues. Central sensitization of pain has been demonstrated in people with knee OA and it is exacerbated by another anomalous pain mechanism: reduced conditioned pain modulation (CPM). CPM involves the application of a painful "conditioning stimulus" that elicits a reduction in the perception of pain. The presence of central sensitization and reduced conditioned pain modulation can make knee OA much harder to treat, however clinicians are now augmenting traditional physical therapy interventions with treatments like cognitive behavioral therapy and mind-body treatments that can influence how the central nervous system processes the pain signals. Unfortunately, those interventions do not influence the movement patterns used by people that can hasten joint degeneration including reduced knee motion and higher muscle co-contraction combined with buckling. These movements produce greater loads and higher shear forces in the knee that are particularly detrimental to articular cartilage. Recently physical therapy interventions have been developed to address the abnormal movement and muscle activation patterns but none have been shown to be any more effective than traditional aerobic or strengthening exercises. This may be due to deficits in the ability to learn new motor programs to stabilize the knee which is highly plausible considering that motor output and motor learning rely on accurate sensory feedback that we know is impaired in people with knee OA. This study will investigate the presence of central sensitization and reduced CPM and their influence on motor adaptation and learning in this population. The results will provide valuable insight into motor control that can be used to furthe develop treatments that will improve knee function while slowing progress of the disease.