Neuroplasticity of sensorimotor control in low back pain

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 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