A model for personalized diagnostics for non-specific low back pain: the role of the myofascial unit.
A model for personalized diagnostics for non-specific low back pain: the role of the myofascial unit.
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DOI：
10.3389/fpain.2023.1237802
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发表时间：
2023
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影响因子：
--
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中科院分区：
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下背痛（LBP）是全球残疾的主要原因。大多数LBP是非特异性或特发性的，其定义为没有明确的特定原因或病理的未知来源的症状。目前的临床评价指南是基于排除潜在的严重医疗条件，但没有解决潜在的疼痛因素。虽然已作出努力，根据对治疗的反应确定这一人群中的亚组，但仍然缺乏一个指导评估的综合框架。在本文中，我们提出了一个基于现有证据的个性化机制评估模型，该模型旨在确定可能引发和维持与慢性非特异性腰痛（nsLBP）相关的中枢致敏的潜在病理。我们认为中枢致敏可以对"肌筋膜单位"产生下游效应，"肌筋膜单位"被定义为包括肌纤维、筋膜（包括肌内膜、肌束膜和肌外膜）及其相关的神经支配（游离神经末梢、肌梭）、神经系统和血管的综合解剖和功能结构。组织水平的异常可以通过神经源性炎症、筋膜滑动受损和间质性炎症停滞的恶性循环持续存在，这些表现为nsLBP的临床结果。我们假设，我们提出的模型提供了复杂的临床研究结果，包括组织水平的异常，生物力学功能障碍和姿势不对称，生态和心理社会因素，与nsLBP的生物兼容性。该模型提出了一个多领域的评估，是个性化的，可行的，并有助于排除具体原因的背痛指导临床相关的管理。它也可能为未来的研究提供一个路线图，以阐明这一普遍存在的复杂问题的机制。
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.
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