01-04-2015 | Knee
Quadriceps corticomotor excitability following an experimental knee joint effusion
Published in: Knee Surgery, Sports Traumatology, Arthroscopy | Issue 4/2015
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Purpose
Deficits in quadriceps strength and voluntary activation are common following knee injury. These deficits are hypothesized to generate from a neural level, however, it remains unclear how corticomotor pathways are affected following acute injury. The purpose of this investigation was to examine whether corticomotor alterations of the quadriceps were present following a simulated knee joint injury using an experimental effusion model.
Methods
Participants completed two testing sessions, an experimental knee effusion and control session, separated by 7 days. The central activation ratio was used to assess change in quadriceps activation. Corticomotor excitability was assessed pre- and post-intervention via active motor thresholds (AMTs) and motor evoked potentials (MEPs) normalized to maximal muscle responses. MEPs were assessed at different percentages of AMT, and associated slopes between these percentages were analysed. Paired-sample t tests were performed on percentage change scores calculated from pre-intervention outcome measures to assess change in corticomotor excitability and changes in the slope of MEP values as percentage of AMT increased.
Results
Quadriceps activation significantly decreased during the effusion session. AMT and MEP change scores were not different between effusion and control conditions. No substantial differences were found in slope between any percentages of AMT.
Conclusions
An experimental knee effusion did not induce changes in corticomotor excitability. Further research is needed to understand how corticomotor pathways are affected following joint injury. Corticomotor excitability alterations may not be the cause of acute changes in neuromuscular activation following joint effusion. Future research should determine whether clinically altering corticomotor excitability will improve physical function.
Level of evidence
II.