Abstract
CONTEXT: Individuals with acute lateral ankle sprain (ALAS) demonstrate balance deficits and altered neural excitability associated with acute injury symptoms. However, it is unknown whether corticospinal excitability is altered during standing after ALAS and which factors are associated with neural change. OBJECTIVE: To investigate corticospinal excitability during single-legged standing and its relationship with postural control and acute injury symptoms after ALAS. DESIGN: Case-control study. SETTING: Research laboratory. PATIENTS OR OTHER PARTICIPANTS: A total of 14 individuals with ALAS (age = 19.8 ± 2.0 years, height = 171.9 ± 8.2 cm, mass = 69.7 ± 8.2 kg) and 14 uninjured matched controls (age = 20.7 ± 2.3 years, 174.2 ± 8.8 cm, mass = 69.5 ± 14.9 kg) participated. MAIN OUTCOME MEASURES: We measured the normalized motor-evoked potential (MEP) in the fibularis longus using transcranial magnetic stimulation at 100%, 120%, and 140% of the active motor threshold (AMT) while participants maintained a single-legged stance. Postural control was assessed using a 10-second single-legged stance immediately before transcranial magnetic stimulation testing. Center-of-pressure (COP) variables were recorded and analyzed. RESULTS: Individuals with ALAS demonstrated a trend toward facilitated corticospinal excitability of the fibularis longus during single-legged balance, with 64% (n = 9) of patients with ALAS exceeding the 95% CI upper limit for MEP at 100% of the AMT of the control group. Of the 4 patients with grade II ankle sprains, 75% (n = 3) exceeded this boundary for MEP at 100% of the AMT of the control group, and 100% (n = 4) exceeded the boundaries for all COP measures. Furthermore, correlation analyses revealed that a higher normalized MEP was associated with greater total COP velocity (r (s) = 0.543, P = .048). CONCLUSIONS: After ALAS, corticospinal excitability in the fibularis longus may have been facilitated during a single-legged stance, and the level of excitability tended to be associated with an increased rate of postural sway. The severity of ALAS appeared to influence both outcomes. These findings suggested a potential compensatory supraspinal mechanism for impaired postural control after ALAS.