J Orthop Sports Phys Ther. 2019 Jun;49(6):402-414. doi: 10.2519/jospt.2019.8489.
Low back pain (LBP) is an important medical and socioeconomic problem. Impaired sensorimotor control has been suggested to be a likely mechanism underlying development and/or maintenance of pain. Although early work focused on the structural and functional abnormalities within the musculoskeletal system, in the past 20 years there has been an increasing realization that patients with LBP might also have extensive neuroplastic changes within the central nervous system. These include changes related to both the structure (eg, gray matter changes) and function (eg, organization of the sensory and motor cortices) of the nervous system as related to processing of pain and nociception and to motor and somatosensory systems. Moreover, clinical interventions increasingly aim to drive neuroplasticity with treatments to improve pain and sensorimotor function. This commentary provides a contemporary overview of neuroplasticity of the pain/nociceptive and sensorimotor systems in LBP. This paper addresses (1) defining neuroplasticity in relation to control of the spine and LBP, (2) structural and functional nervous system changes as they relate to nonspecific LBP and sensorimotor function, and (3) related clinical implications. Individuals with recurrent and persistent LBP differ from those without LBP in several markers of the nervous system's function and structure. Neuroplastic changes may be addressed by top-down cognitive-based interventions and bottom-up physical interventions. An integrated clinical approach that combines contemporary pain neuroscience education, cognition-targeted sensorimotor control, and physical or function-based treatments may lead to better outcomes in patients with recurrent and persistent LBP. This approach will need to consider variation among individuals, as no single finding/mechanism is present in all individuals, and no single treatment that targets neuroplastic changes in the sensorimotor system is likely to be effective for all patients with LBP. .
下腰痛（LBP）是一个重要的医学和社会经济问题。感觉运动控制受损被认为是疼痛发生和/或持续的一个可能机制。尽管早期的工作主要集中在肌肉骨骼系统的结构和功能异常上，但在过去的 20 年中，人们越来越意识到，LBP 患者的中枢神经系统可能也存在广泛的神经可塑性变化。这些变化包括与疼痛和伤害感受以及运动和躯体感觉系统处理相关的神经系统结构（例如，灰质变化）和功能（例如，感觉和运动皮层的组织）变化。此外，临床干预措施越来越旨在通过改善疼痛和感觉运动功能的治疗来驱动神经可塑性。本评论提供了 LBP 中疼痛/伤害感受和感觉运动系统神经可塑性的当代概述。本文讨论了（1）与脊柱和 LBP 控制相关的神经可塑性的定义，（2）与非特异性 LBP 和感觉运动功能相关的神经系统结构和功能变化，以及（3）相关的临床意义。反复和持续的 LBP 患者与没有 LBP 的患者在神经系统功能和结构的几个标志物上存在差异。神经可塑性变化可以通过自上而下的基于认知的干预措施和自下而上的物理干预措施来解决。一种综合的临床方法，结合当代疼痛神经科学教育、以认知为目标的感觉运动控制以及基于物理或功能的治疗方法，可能会改善反复和持续的 LBP 患者的结局。这种方法需要考虑个体之间的差异，因为并非所有个体都存在单一的发现/机制，也不太可能有一种针对感觉运动系统神经可塑性的单一治疗方法对所有 LBP 患者都有效。
