Cortical activation during single-leg stance in patients with chronic ankle instability.

Chronic ankle instability (CAI) has been considered a neurophysiological disease, having dysfunction in somatosensory and motor system excitability. However, few studies have so far explored the changes in cortical activation during balance tasks of CAI patients. To compare the cortical activity during single-leg stance among CAI, copers and uninjured controls and to compare dynamic balance across groups. Cross-sectional study. Biomechanics laboratory. Twenty-one uninjured controls (age = 25.0(10.5) years, height = 170.0(11.0) cm, mass = 64.0(16.5) kg), 17 copers (age = 27.0(14.0) years, height = 170.0(9.5) cm, mass = 66.5(16.5) kg) and 22 participants with CAI (age = 34.5(11.0) years, height = 170.0(15.8) cm, mass = 67.0(16.2) kg) participated in this study. Participants performed single-leg stance while testing cortical activation with functional near-infrared spectroscopy. The peak response of oxyhemoglobin of the activated cortex was calculated and compared across groups. Y-balance test outcomes and patient-reported outcomes were assessed and compared across groups. The CAI group had worse patient-reported outcomes and Y-balance test outcomes than copers and uninjured controls. Differences in the peak response of oxyhemoglobin were observed for the primary somatosensory cortex (S1, F(2,57)=4.347, p=0.017, η2p=0.132) and superior temporal gyrus (STG, F(2,57)=4.548, p=0.015, η2p=0.138). Specifically, copers demonstrated a greater activation in S1 and STG than CAI (d=0.73, p=0.034; d=0.69, p=0.043, respectively) and uninjured controls (d=0.77, p=0.036; d=0.88, p=0.022, respectively). No significant differences were found in the cortical activation between CAI participants and uninjured controls. Copers displayed significantly greater cortical activation in S1 and STG when compared with CAI participants and uninjured controls. Greater activation in S1 and STG suggested a better ability to perceive somatosensory stimuli and may represent a compensatory mechanism of the copers to maintain good functional ability after the initial severe ankle sprain.