Altered Corticospinal Excitability During Single-leg Balance Following Acute Lateral Ankle Sprain

Patients with acute lateral ankle sprain (ALAS) present altered neural excitability associated with ankle joint dysfunction and disability. While postural control is often compromised following ALAS, information about neural alterations is primarily limited to the spinal level. PURPOSE: To determine the effects of ALAS on spinal and corticospinal excitability in the soleus muscle during single-leg balance (SLB). METHODS: Thirteen patients with ALAS (8 females; age=19.6±1.9 years; height=172.8±7.9 cm; mass=69.9±8.4 kg) and 13 uninjured controls (CON) without ankle sprain history (8 females; age=20.7±2.4 years; height=174.7±8.9 cm; mass=70.6±14.8 kg) participated. We conducted Hoffman reflex (H-reflex) and transcranial magnetic stimulation (TMS)-based motor evoked potential (MEP) tests during SLB to quantify neural excitability at spinal and corticospinal levels. Study outcomes included maximum H-reflex and MEP amplitudes at 100%, 120%, and 140% of the active motor threshold of TMS. To account for individual neural variations and the contribution of background EMG activity to study outcomes, normalization procedures were implemented. All H-reflex and MEP values were normalized by the maximum motor response and further adjusted relative to the background EMG activity recorded 50 ms prior to each stimulus. Independent t-tests were employed to assess group differences, with the alpha level set at <0.05. RESULTS: No significant group difference was found in spinal excitability: H-reflex: t(1,24)=0.44, P=0.67; ALAS=15.3±6.7, CON=13.9±9.2). However, significant differences were observed in corticospinal excitability at all levels: MEP100% (t(1,24)=4.16, P<0.001; ALAS=2.7±1.2, CON=1.2±0.6), MEP120% (t(1,24)=2.26, P=0.03; ALAS=3.9±1.1, CON=2.6±1.8), and MEP140% (t(1,24)=2.29, P=0.03; ALAS=3.9±1.9, CON=2.4±1.6). CONCLUSION: Patients with ALAS demonstrated higher corticospinal excitability, with no change in spinal excitability during SLB. This provides greater insight into neural mechanisms contributing to postural control deficits commonly observed following ALAS.