Sikdar Siddhartha, Srbely John, Shah Jay, Assefa Yonathan, Stecco Antonio, DeStefano Secili, Imamura Marta, Gerber Lynn H
Center for Adaptive Systems of Brain Body Interactions, George Mason University, Fairfax, VA, United States.
Department of Bioengineering, George Mason University, Fairfax, VA, United States.
Front Pain Res (Lausanne). 2023 Oct 13;4:1237802. doi: 10.3389/fpain.2023.1237802. eCollection 2023.
Low back pain (LBP) is the leading cause of disability worldwide. Most LBP is non-specific or idiopathic, which is defined as symptoms of unknown origin without a clear specific cause or pathology. Current guidelines for clinical evaluation are based on ruling out underlying serious medical conditions, but not on addressing underlying potential contributors to pain. Although efforts have been made to identify subgroups within this population based on response to treatment, a comprehensive framework to guide assessment is still lacking. In this paper, we propose a model for a personalized mechanism-based assessment based on the available evidence that seeks to identify the underlying pathologies that may initiate and perpetuate central sensitization associated with chronic non-specific low back pain (nsLBP). We propose that central sensitization can have downstream effects on the "myofascial unit", defined as an integrated anatomical and functional structure that includes muscle fibers, fascia (including endomysium, perimysium and epimysium) and its associated innervations (free nerve endings, muscle spindles), lymphatics, and blood vessels. The tissue-level abnormalities can be perpetuated through a vicious cycle of neurogenic inflammation, impaired fascial gliding, and interstitial inflammatory stasis that manifest as the clinical findings for nsLBP. We postulate that our proposed model offers biological plausibility for the complex spectrum of clinical findings, including tissue-level abnormalities, biomechanical dysfunction and postural asymmetry, ecological and psychosocial factors, associated with nsLBP. The model suggests a multi-domain evaluation that is personalized, feasible and helps rule out specific causes for back pain guiding clinically relevant management. It may also provide a roadmap for future research to elucidate mechanisms underlying this ubiquitous and complex problem.
下腰痛(LBP)是全球致残的主要原因。大多数下腰痛是非特异性的或特发性的,其定义为病因不明且无明确特定病因或病理的症状。当前的临床评估指南基于排除潜在的严重疾病,而非解决疼痛的潜在促成因素。尽管已努力根据治疗反应在这一人群中识别亚组,但仍缺乏指导评估的综合框架。在本文中,我们基于现有证据提出了一种基于个性化机制的评估模型,旨在识别可能引发并维持与慢性非特异性下腰痛(nsLBP)相关的中枢敏化的潜在病理。我们提出中枢敏化可对“肌筋膜单元”产生下游影响,“肌筋膜单元”被定义为一个整合的解剖和功能结构,包括肌纤维、筋膜(包括肌内膜、肌束膜和肌外膜)及其相关神经支配(游离神经末梢、肌梭)、淋巴管和血管。组织水平的异常可通过神经源性炎症、筋膜滑动受损和间质炎症停滞的恶性循环持续存在,这些表现为nsLBP的临床症状。我们推测,我们提出的模型为与nsLBP相关的复杂临床症状谱,包括组织水平异常、生物力学功能障碍和姿势不对称、生态及心理社会因素,提供了生物学合理性。该模型建议进行个性化、可行的多领域评估,并有助于排除背痛的特定原因,指导临床相关管理。它还可能为未来研究阐明这一普遍存在且复杂问题的潜在机制提供路线图。