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 2 mV vs HC = 11.3 ± 3.9 cm 2 mV) and map area (P = 0.046, CAI = 12.8 ± 6.0 cm 2 vs HC: 17.4 ± 6.9 cm 2) 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.