Alterations in Cortical Activation Among Individuals With Chronic Ankle Instability During Single-Limb Postural...

Chronic ankle instability (CAI) is characterized by repetitive ankle sprains and perceived instability. Whereas the underlying cause of CAI is disputed, alterations in cortical motor functioning may contribute to the perceived dysfunction.

To assess differences in cortical activity during single-limb stance among control, coper, and CAI groups.

Cross-sectional study.

Biomechanics laboratory.

A total of 31 individuals (10 men, 21 women; age = 22.3 ± 2.4 years, height = 169.6 ± 9.7 cm, mass = 70.6 ± 11.6 kg), who were classified into control (n = 13), coper (n = 7), and CAI (n = 11) groups participated in this study.

Participants performed single-limb stance on a force platform for 60 seconds while wearing a 24-channel functional near-infrared spectroscopy system. Oxyhemoglobin (HbO₂) changes in the supplementary motor area (SMA), precentral gyrus, postcentral gyrus, and superior parietal lobe were measured.

Differences in averages and standard deviations of HbO₂ were assessed across groups. In the CAI group, correlations were analyzed between measures of cortical activation and Cumberland Ankle Instability Tool (CAIT) scores.

No differences in average HbO₂ were present for any cortical areas. We observed differences in the standard deviation for the SMA across groups; specifically, the CAI group demonstrated greater variability than the control (r = 0.395, P = .02; 95% confidence interval = 0.34, 0.67) and coper (r = 0.38, P = .04; 95% confidence interval = -0.05, 0.69) groups. We demonstrated a strong correlation that was significant in the CAI group between the CAIT score and the average HbO₂ of the precentral gyrus (ρ = 0.64, P = .02) and a strong correlation that was not significant between the CAIT score and the average HbO₂ of the SMA (ρ = 0.52, P = .06).

The CAI group displayed large differences in SMA cortical-activation variability. Greater variations in cortical activation may be necessary for similar static postural-control outcomes among individuals with CAI. Consequently, variations in cortical activation for these areas provide evidence for an altered neural mechanism of postural control among populations with CAI.