Chronic Back Pain Linked to Sensory Cortex Hyperactivity During Walking

Patients with nonspecific low back pain show increased neural load in somatosensory regions and reduced gait velocity during dual tasks.

For Doctors in a Hurry

Clinicians lack clarity on the neural mechanisms driving gait alterations in patients with chronic nonspecific low back pain.
The researchers compared 18 patients with chronic low back pain against 18 healthy controls using functional near-infrared spectroscopy.
Patients showed significantly higher activation in the somatosensory association cortex and primary somatosensory cortex during walking and cognitive tasks.
The authors conclude that these cortical activity patterns indicate central sensitization, a state of heightened nervous system responsiveness.
These findings suggest that targeting sensory cortex activity may improve rehabilitation outcomes for patients with chronic back pain.

The Neural Burden of Chronic Nonspecific Low Back Pain

Chronic nonspecific low back pain represents the most frequent subtype of spinal pathology encountered in primary care, defined by a persistent lack of identifiable structural etiology and high rates of recurrence [1]. While clinical management traditionally prioritizes lumbar biomechanics and musculoskeletal stabilization, emerging evidence suggests that structural and functional alterations within the central nervous system, particularly the cortico-limbic and prefrontal networks, play a decisive role in the transition from acute to chronic pain [2]. These neuroplastic changes often manifest clinically as impaired postural control and disrupted muscle synergy, which is the coordinated, efficient activation of muscle groups required for fluid movement [3, 4]. To better understand these mechanisms, researchers are increasingly utilizing functional near-infrared spectroscopy (fNIRS), a non-invasive imaging modality that monitors hemodynamic responses (fluctuations in blood oxygenation and flow) within the cerebral cortex to observe neural activity during active movement [5, 6]. Recent data indicate that targeted clinical interventions can modulate activity in the frontal polar area (a region involved in high-level cognitive integration) and its connectivity with the insula, suggesting that cortical processing is a viable target for symptom management [7]. A new study now clarifies how these cortical shifts specifically impair gait and cognitive performance in patients with persistent symptoms.

Mapping Cortical Activity and Gait Biomechanics

Investigators utilized a cross-sectional study design to compare a cohort of 18 individuals with chronic nonspecific low back pain against 18 healthy controls. To evaluate the interplay between motor control and cognitive demand, participants were assessed under three distinct conditions: Task 1 (a single walking task), Task 2 (a single cognitive task), and Task 3 (a cognitive-walking dual task). This dual-task framework is particularly relevant for clinicians, as it mimics the real-world necessity of navigating environment-based motor challenges while processing mental information, a scenario that often exacerbates functional deficits in patients with chronic pain. Cortical activity was monitored via functional near-infrared spectroscopy (fNIRS), which tracks changes in oxygenated hemoglobin to identify which brain regions are being recruited during specific activities. The analysis focused on several critical regions of interest: the bilateral premotor cortex and supplementary motor area (PMC/SMA), which are responsible for planning and sequencing complex movements; the primary motor cortex (M1), the principal executor of voluntary motor commands; and the somatosensory association cortex (SAC), which integrates various sensory inputs to help the brain understand the body's orientation in space. Additionally, the researchers monitored the primary somatosensory cortex (S1), the main receptive area for tactile and proprioceptive feedback. Simultaneously, biomechanical performance was quantified using a three-dimensional gait analysis system. This technology provided high-resolution data on several parameters, including step duration, step length, stride length, velocity, cadence, swing power (the force generated during the forward phase of a step), and the overall gait cycle. By correlating these physical metrics with cortical hemodynamics, the study sought to determine if chronic pain forces the brain to over-recruit sensory resources for basic locomotion, especially when cognitive distractions are introduced.

Sensory Hyperactivation and Reduced Walking Velocity

Results from the single walking task (Task 1) demonstrated that patients with chronic nonspecific low back pain moved with a significantly lower velocity (p = 0.029) than healthy controls. This objective slowing of gait was linked to specific neural signatures in sensory processing regions. The chronic pain group exhibited higher activation in the left somatosensory association cortex (p = 0.001) and increased activity in the right primary somatosensory cortex (p = 0.018). These findings suggest that for patients with chronic pain, the act of walking is no longer a purely subcortical, automatic process; instead, it requires heightened cortical engagement in regions responsible for processing sensory and proprioceptive feedback. This neural burden extended into the cognitive domain during Task 2, where the chronic pain group showed significantly higher activation than controls in the left somatosensory association cortex (p = 0.028), the right somatosensory association cortex (p = 0.033), and the left primary somatosensory cortex (p = 0.032). The hyperactivation of these sensory zones during a purely mental task provides evidence of central sensitization, a clinical state where the central nervous system stays in a persistent state of high reactivity, lowering the threshold for sensory processing and potentially amplifying pain signals. Correlation analysis further revealed stronger associations between cortical activation patterns and gait parameters in the chronic pain group than in controls. For the practicing physician, this tighter coupling suggests a diminished neural reserve: these patients must exhaust more sensory processing 'bandwidth' to maintain basic gait stability, leaving them more vulnerable to functional decline when faced with additional stressors.

The Impact of Cognitive-Motor Interference

The introduction of a simultaneous cognitive load during walking (Task 3) further degraded motor performance, highlighting the clinical impact of cognitive-motor interference. In this dual-task condition, the chronic nonspecific low back pain group demonstrated a significantly lower step length (p = 0.031) and significantly lower stride length (p = 0.041) compared to healthy controls. These biomechanical deficits were accompanied by a significantly lower velocity (p = 0.016) and significantly lower swing power (p = 0.047). These data indicate that when neural resources are split between a mental task and locomotion, patients with chronic pain lack the compensatory capacity to maintain normal gait mechanics. This suggests that the brain regions managing cognitive tasks and those regulating gait are competing for the same limited pool of neural resources. The study concludes that central sensitization is a defining feature of chronic nonspecific low back pain, manifesting as increased responsiveness of central neurons during both daily cognitive and walking tasks. For clinicians, these findings emphasize that rehabilitation should move beyond simple biomechanical corrections. Effective recovery strategies may require interventions that address this sensory hyperactivation and aim to restore neural efficiency, potentially through dual-task training or cognitive-functional therapies that help the patient manage the increased neural load of routine activities.

Study Info

Cortical activity during cognitive and walking tasks in individuals with chronic nonspecific low back pain: a functional near-infrared spectroscopy study

Fan Jiang, Haiting Huang, Yifeng Chen, X B Li, et al.

Journal Frontiers in Neuroscience

Published April 23, 2026