The focus during rehabilitation for low back pain (LBP) is traditionally driven by the suspected structural cause of dysfunction. This approach primarily follows a biomechanical model of dysfunction, where only the peripheral musculoskeletal structure is responsible for the patient's experienced dysfunction and is the primary focus of our intervention(s). However, a growing body of evidence suggests that this approach neglects essential drivers of various dysfunction(s) in this population.
The biomechanical model of dysfunction suffices in cases of acute injuries, where the trauma and resultant physical dysfunction in the peripheral musculoskeletal structure are evident. However, this model is insufficient to explain chronic dysfunction that some patients experience. In such cases, it is important to look beyond the conventional and consider the emerging evidence regarding neuroplastic changes in LBP in order to achieve a better prognosis. Neuroplasticity is an intrinsic, fundamental neurophysiological feature that refers to change in the structure, function, and organization of the nervous system, which occurs throughout a person's life. Neuroplastic changes can occur in response to learning a new skill or as a result of any injury, which typically results in maladaptive changes.
Neuroplastic changes that occur in individuals with LBP discussed in this section are thought to be responsible for the chronicity of LBP, as well as poor prognoses such as persistent pain, altered sensorimotor deficits, and LBP recurrence. Neuroplastic changes include an increase in sensitivity of processing noxious stimuli. Neurophysiological changes within the peripheral receptors and dorsal horn of the spinal cord increase the responsiveness to noxious stimuli. This can result in an amplification of the pain transmission. This change is common and important, because it can lead to the development of allodynia (innocuous stimuli perceived as painful) and hyperalgesia (increased pain response). Both allodynia and hyperalgesia are associated with a poor outcome after an acute episode of LBP.
Motor changes include altered activation and coordination of trunk muscles in response to pain. There is greater activation of superficial muscles during movement, which is known as a bracing strategy to avoid pain. Altered activation is associated with long-term biomechanical alterations and eventual complete avoidance of certain movements and activities. In addition, there are changes in the higher processing centers, including a medial shift of the motor area representing the low back. This is directly proportional to the chronicity of the condition. The functional connectivity changes between the sensorimotor areas are associated with slowing sensorimotor task performance, such as a sit-to-stand. Structural changes include gray matter loss in the prefrontal cortex and thalamus that is equivalent to 10 to 20 years of aging. These areas are associated with pain processing. Traditional rehabilitation focusing on pain relief and strengthening does not address these neuroplastic changes. There is a need for interventions that can counteract these maladaptive neuroplastic changes, with evidence suggesting reversibility once the acute pain has resolved.
Rehabilitation strategies to address neuroplastic changes can focus on motor, sensory, or cognitive impairments. Motor control training focuses on incorporating exercises specific to particular muscle activation (for example, activating the transverse abdominis muscle under ultrasound guidance). Using ultrasound provides knowledge of whether appropriate muscles are contracting during a functional task with an external focus of attention. Sensory discrimination training involves providing the patient real-time visual feedback (eg, of their back) during movement (such as a spinal rotation), which has been shown to reduce the perception of intensity of pain and also reduce habitual pain. Cognitive training approaches include cognitive behavioral therapy, mindfulness, education, motor imagery, and peripheral sensory stimulation. Unfortunately, there is currently no method to differentiate which patients would benefit from which approach. However, trying any of these would be a great first step beyond the traditional approaches that don't consider neuroplastic changes at all.
There is a strong and continually growing body of evidence describing important neuroplastic changes in persons experiencing LBP that may explain the chronicity of the condition. Without targeting these neuroplastic changes with therapeutic interventions, the patient may struggle to achieve full recovery.
This post was authored by:
Srishti Banerjee serves as an Executive Committee member of the Environmental Physiotherapy Association and is a neurophysiotherapist currently working as an academician and researcher, with an interest in the presentation and rehabilitation of rare clinical conditions. Srishti's passion for physical therapy has led to physical therapy research at a grassroots level to improve clinical decision making and build physical therapy into a strong and sustainable health care profession.