Chronic non-specific low back pain (CNLBP) is a complex clinical syndrome with clinical mechanisms involving peripheral biomechanical alterations and central nervous system remodeling. This review explores the clinical mechanisms of CNLBP by biomechanics and central nervous system mechanisms. In terms of peripheral mechanisms, the impaired coordination among the three subsystems of spinal stability, namely the passive osseoligamentous system, the active muscular system, and the neuromuscular control system, constitutes the key pathophysiological basis for CNLBP, manifesting as restricted lumbar mobility, paraspinal muscle dysfunction, and postural control deficits. Biomechanical studies related to CNLBP spinal kinematics primarily address the roles of lumbar range of motion and lumbopelvic sagittal-plane motion in CNLBP biomechanics. Biomechanical studies of the trunk muscles in CNLBP primarily investigate the roles of muscle strength and endurance in CNLBP biomechanics. Biomechanical studies of posture control in CNLBP focus on proprioception and the integration of perceptual and visual information in CNLBP biomechanics. However, peripheral mechanisms alone are insufficient to fully account for the clinical heterogeneity of CNLBP. Neuroimaging studies have disclosed spontaneous neural activity and aberrant functional connectivity within the pain matrix of CNLBP patients. Specifically, the suppression of somatosensory nodes, such as the thalamus-somatosensory cortex pathway, results in abnormal pain signal transmission and modulation; the dysfunction of emotional nodes, such as the prefrontal-limbic system, is associated with the emotionalization of pain; and the diminished function of pain inhibition nodes, such as the periaqueductal gray matter, leads to a deficiency in endogenous analgesia.These central nervous system alterations are not only closely associated with the chronicification of pain but may also precipitate cognitive dysfunction and emotional disorders. The peripheral-central dual-dimensional framework offers a novel perspective for exploring the clinical mechanisms of CNLBP and facilitates the establishment of personalized, multidimensional precision rehabilitation programs.
Li et al. (Sun,) studied this question.