Corticospinal activity during a single-leg stance in people with chronic ankle instability.

PURPOSE: The aim of the study was to determine whether corticospinal excitability and inhibition of the tibialis anterior during single-leg standing differs among individuals with chronic ankle instability (CAI), lateral ankle sprain copers, and healthy controls. METHODS: Twenty-three participants with CAI, 23 lateral ankle sprain copers, and 24 healthy control participants volunteered. Active motor threshold (AMT), normalized motor-evoked potential (MEP), and cortical silent period (CSP) were evaluated by transcranial magnetic stimulation while participants performed a single-leg standing task. RESULTS: Participants with CAI had significantly longer CSP at 100% of AMT and lower normalized MEP at 120% of AMT compared to lateral ankle sprain copers (CSP100%: p = 0.003; MEP120%: p = 0.044) and controls (CSP100%: p = 0.041; MEP120%: p = 0.006). CONCLUSION: This investigation demonstrate altered corticospinal excitability and inhibition of the tibialis anterior during single-leg standing in participants with CAI. Further research is needed to examine the effects of corticospinal maladaptations to motor control of the tibial anterior on postural control performance in those with CAI.

Potential Corticomotor Plasticity in Those with and without Chronic Ankle Instability.

INTRODUCTION: Quantifying corticomotor alterations is important to understand the neurophysiological mechanisms that likely contribute to the neuromuscular control deficits observed in patients with chronic ankle instability (CAI). Corticomotor output mapping provides further insight into the changes within the motor cortex and identifies potential changes in the area of the motor cortex associated with selected muscles. Therefore, this investigation compared the corticomotor map output for the fibularis longus (FL) muscle in patients with and without CAI. METHODS: Eighteen CAI patients and 16 healthy controls (HC) volunteered. Transcranial magnetic stimulation was used to map the motor cortex's representation of the FL. The normalized average of three motor evoked potentials at 100% of active motor threshold intensity was recorded for each scalp site on a 6 × 6 cm grid. Corticomotor output map was compared between groups through 1) the size of the corticomotor map area, 2) the volume of the corticomotor map, and 3) the location of cortical representation. Independent t-tests were used to assess group differences in each mapping outcome variable. Cohen's d effect sizes along with 95% confidence intervals were calculated using the pooled SD values. RESULTS: CAI patients exhibited less map volume (P = 0.018, CAI = 8.2 ± 3.2 cm mV vs HC = 11.3 ± 3.9 cm mV) and map area (P = 0.046, CAI = 12.8 ± 6.0 cm vs HC: 17.4 ± 6.9 cm) compared with HC. CONCLUSIONS: The smaller map area and volume suggest a more concentrated area of neurons communicating with the FL muscle in patients with CAI. Consequently, motor cortical cells on the border of the FL excitation area are less committed to the proper function of the FL muscle and may be recruited by other surrounding areas. This may explain altered movement strategies that lead to ankle reinjury.