Motor cortex inhibition and facilitation changes within two weeks of anterior cruciate ligament reconstruction (ACLR): A case series

Purpose: Anterior cruciate ligament reconstruction (ACLR) can cause arthrogenic muscle inhibition (AMI) or persistent muscle weakness that impairs physical function and return to sport. Deficits in voluntary activation (one method to measure AMI) are thought to contribute to AMI, however, the specific neurophysiological underpinnings remain inconclusive. The primary objective of this study was to explore changes in intracortical excitability (inhibition and facilitation) of the quadriceps representation in the primary motor cortex pre- and post-ALCR. Our secondary objective was to explore changes in hamstrings intracortical excitability pre- and post-ALCR. Methods: Prospective case-series pre-post-ACLR. Single- and paired-pulse transcranial magnetic stimulation (TMS) was delivered over the motor cortex with responses recorded via surface electromyography from the active vastus medialis (quadriceps) and semitendinosus (hamstrings). TMS outcomes were short- and long-interval-intracortical-inhibition (SICI, LICI) and short-interval-intracortical-facilitation (SICF). Data are reported as median (interquartile range [IQR]) and analysed using non-parametric analysis of variance, with significance accepted when p ​< ​0.05. Results: Twenty-one participants (38% female) with a mean (standard deviation) age of 24.5 (4.7) years were included. Following ACLR participants had increased quadriceps inhibition (SICI, p ​= ​0.005) and facilitation at all SICF peaks (Peak 1: p ​< ​0.05, Peak 2: p ​= ​0.016, Peak 3: p ​< ​0.05). There were no changes following ACLR in quadriceps LICI (p ​= ​0.108). No differences were detected in hamstring excitability. Conclusion: In the acute post-operative period following ACLR, there is increased activity within some intracortical pathways. The altered excitability of SICI and SICF circuits might contribute to long-term issues, such as impaired voluntary activation resulting in arthrogenic muscle inhibition, in post-ACLR patients.