Corticospinal Excitability and Inhibition of the Soleus in Individuals With Chronic Ankle Instability

Abstract

BackgroundUnderstanding the mechanisms of neurophysiological alterations with chronic ankle instability (CAI) may be essential in the development of the most-effective intervention programs to treat neuromuscular dysfunction in patients with CAI. Specifically, the presence of CAI may be associated with an altered supraspinal mechanism within the central nervous system to inhibit neural drive to the undamaged soleus surrounding the injured ankle joint. ObjectiveTo investigate the influence of CAI on corticospinal excitability and inhibition of the soleus. DesignA single-blinded, case-control study. SettingResearch laboratory. ParticipantsSixteen participants with self-reported CAI and 17 healthy control participants volunteered. MethodsTranscranial magnetic stimulation was used to assess corticospinal excitability and inhibition of the soleus muscle. Active motor threshold (AMT), defined as the lowest stimulator intensity required to elicit a peak-to-peak motor-evoked potential (MEP) amplitude ≥100 μV in at least four of 8 trials, was found to assess corticospinal excitability of the soleus. Eight stimuli were delivered at 120% of AMT, and peak-to-peak MEP amplitudes were recorded for each trial. The amplitude of 8 MEPs at 120% of AMP were averaged and normalized to the maximum M-response. Cortical silent period (CSP) was measured as the distance from the end of the MEP to a return of the mean electromyographic signal plus 2 times the standard deviation of the baseline (prestimulus) electromyographic signal. The ratio of the CSP to the MEP at 120% AMT (CSP:MEP120) were calculated to assess corticospinal inhibition. ResultsThe CAI group had a greater CSP:MEP120 ratio compared with the control group (P = .02). No significant differences between groups were observed for AMT (P = .67) and normalized MEP at 120% of AMT (P = .42). ConclusionsThe greater CSP:MEP120 ratio in participants with CAI suggests an altered balance in corticospinal inhibition and excitability to the soleus of the CAI cohort. Future research is needed to determine the role of corticospinal inhibition in physical and self-reported function in patients with CAI. Level of EvidenceIV