Corticospinal and Spinal-Reflex Excitability during Unipedal Stance Following Acute Lateral Ankle Sprain

Acute lateral ankle sprains (ALAS) are linked to altered spinal-reflexive excitability that may predicate sensorimotor dysfunction. However, sensorimotor control is influenced by spinal and supraspinal mechanisms, necessitating examination of each following ALAS. We aimed to investigate the effects of ALAS on neural excitability during unipedal stance, relating these neural adaptations to clinical outcomes.

Twenty-six young adults were enrolled (13 ALAS: 19.6 ± 1.9 yr; 13 uninjured controls: 20.7 ± 2.4 yr). Spinal-reflex excitability was assessed at the soleus using the Hoffmann reflex, evoking maximal reflexive (H max ) and motor (M max ) responses from electrical stimulation. Corticospinal excitability was assessed via motor evoked potentials (MEP) from transcranial magnetic stimulation, recording responses at 100%, 120%, and 140% of active motor threshold, and normalized to background EMG prior to stimuli and M max . For clinical outcomes, area and velocity of unipedal center-of-pressure measurements were recorded, along with acute symptoms (pain and swelling) and ankle disability.

Independent t -tests revealed no significant differences in spinal-reflex excitability between ALAS and uninjured control (CON) groups. However, corticospinal excitability was significantly higher in patients with ALAS across all stimulus intensities (MEP 100% : ALAS = 2.7 ± 1.2, CON = 1.2 ± 0.6, P < 0.001; MEP 120% : ALAS = 3.9 ± 1.1, CON = 2.6 ± 1.8, P = 0.033; MEP 140% : ALAS = 3.9 ± 1.9, CON = 2.4 ± 1.6, P = 0.031). Patients with ALAS exhibited impaired postural control, as shown by larger area (ALAS = 2.9 ± 0.7, CON = 2.2 ± 0.6, P = 0.049) and higher velocity (ALAS = 3.3 ± 1.0, CON = 2.7 ± 0.5, P = 0.005). Pearson's product - moment correlations found that increased corticospinal excitability did not significantly correlate with impaired postural control or acute symptoms; however, higher corticospinal excitability was associated with more severe ankle disability ( r = -0.607 to -0.721, P = 0.028 to 0.005).

This study provides initial evidence that ALAS affects neural excitability during unipedal stance predominantly at the corticospinal level, which may contribute to ankle disability.