Effects of different support surfaces on postural stability and sensorimotor cortex activation among individuals with chronic ankle instability.

Objectives: Chronic ankle instability (CAI) is characterized by recurrent ankle sprains and impaired postural control, which are particularly evident on unstable surfaces. Evidence indicates that the central nervous system undergoes adaptive plastic changes; however, the specific cortical mechanisms involved remain unclear. Therefore, this study aimed to investigate postural stability and cortical activation in individuals with CAI, especially on unstable surfaces, in order to identify compensatory cortical strategies underlying impaired postural control. Methods: Seventeen people with CAI and seventeen without CAI were recruited. Static postural control was measured under two experimental conditions: a stable surface and an unstable surface simulated by a foam pad. Static postural control was measured during single-leg standing and was represented by the root mean square (RMS) of the plantar center of pressure (COP). Cerebral cortex oxyhemoglobin concentration (ΔHbO₂) was measured using functional near-infrared spectroscopy (fNIRS). Two-way mixed ANOVA (between group: CAI vs. non-CAI, within group: stable vs. unstable surface) was used to analyze data. Results: Across different support surfaces, distinct patterns of between-group differences were observed. Under the stable surface condition, CAI group exhibited significantly lower sample entropy in the mediolateral direction of the center of pressure (SampEn_ML) compared with the non-CAI group. In contrast, under the unstable surface condition, the between-group differences were primarily reflected in increased COP sway magnitude and cortical activation. Moreover, during single-leg standing on the unstable surface, the CAI group demonstrated a significantly larger 95% confidence ellipse area (95%Area), greater root mean square of anteroposterior COP displacement (COP_RMS_AP), and higher ΔHbO₂ levels in the primary somatosensory cortex (S1), somatosensory association cortex (SAC), and the premotor and supplementary motor area (PMC & SMA) than the non-CAI group. Conclusions: Individuals with CAI exhibit impaired postural stability, particularly on unstable surfaces, accompanied by increased activation in the primary motor cortex, primary sensory cortex, somatosensory association cortex, and the premotor and supplementary motor area. These findings suggest a compensatory neural strategy, highlighting the critical role of cortical mechanisms in maintaining postural control in this population.