# Exploratory EEG-TMS Study Reveals Altered Behavioral Function in Individuals Following Anterior Cruciate Ligament Reconstruction

## TL;DR

This study shows that ACLR patients have altered brain activity and increased muscle response, which could lead to higher re-injury risk.

## Contribution

The study explores neural adaptations in ACLR patients using EEG and TMS, revealing new insights into corticospinal excitability and motor cortex inhibition.

## Key findings

- ACLR patients showed significantly greater motor-evoked torque compared to healthy controls.
- ACLR patients had lower P200 TEP amplitude in the motor cortex, suggesting neural inhibition.

## Abstract

Background: Following anterior cruciate ligament reconstruction (ACLR), ACLR patients often experience quadriceps dysfunction, potentially linked to increased corticospinal excitability. However, the role of motor cortex neuroadaptations in persistent quadriceps strength deficits remains unclear. Purpose: The purpose of this study is to investigate neural behavior during a force reproduction task using transcranial magnetic stimulation (TMS) in ACLR participants compared to healthy controls (CONT). Methods: Electrocortical activation of 16 ACLR (10F and 6M, 20.0 ± 1.2 years, 171.9 ± 7.2 cm, 75.8 ± 17.1 kg) and 16 CONT (10F and 6M, 20.6 ± 1.4 yrs, 168.0 ± 9.9 cm, 66.3 ± 11.0 kg) was measured using a 64-channel EEG system during an isometric force reproduction task. Sixty TMS pulses (≥120% active motor threshold) were delivered to the primary motor cortex while participants maintained 10% of quadriceps maximal voluntary isometric contraction (QMVIC10%). Motor-evoked torque (METnorm, %), normalized to 100% TMS intensity, was measured to assess neuroadaptation in the corticospinal tract. EEG data was processed to compute N100 (80–200 ms) and P200 (160–300 ms) TMS-evoked event-related potentials (TEPs, µV) at three regions of interest (ROI): the motor (ROI1), parietal (ROI2), and frontal (ROI3) cortices. MET and TEP comparisons were conducted using independent and unpaired two-sample permutation-based t-tests, respectively. Results: The ACLR group exhibited a significantly greater MET than CONT. Although exploratory, differences were found in P200 TEP at ROI1 with lower power in ACLR than CONT. Conclusions: Lower TEP amplitude at ROI1 implies neural inhibition in the motor cortex, while heightened MET in ACLR suggests greater corticospinal excitability. Neural adaptations in the corticospinal tract in ACLR patients may contribute to excessive quadriceps activation in response to unanticipated stimuli, potentially increasing the risk of re-injury.