The Brain-Behavior relationship after Anterior Cruciate Ligament Reconstruction

Abstract

Anterior cruciate ligament injury may induce neural adaptations that are unresolved with conventional reconstruction and rehabilitation techniques. Visual-motor function appears to be a key driver of this neuroplasticity. However, the relationship between the neuroplasticity after ACLR (anterior cruciate ligament reconstruction) and visually perturbed neuromuscular control is unknown. PURPOSE: To determine if a relationship exists between brain activation during knee movement and visually perturbed drop landing neuromuscular control, and if ACLR alters this relationship. METHODS:Participants consisted of 26 recreationally active individuals from the local university community (13 ACLR, 13 control matched on height, mass, extremity dominance, education level, history and current physical activity level). A drop vertical jump was completed to assess functional neuromuscular control (knee flexion and adduction). Stroboscopic eyewear provided a visually perturbed condition. The effect of disrupting visual feedback was calculated with a mean change score from the full vison to the disrupted condition. Brain functional magnetic resonance imaging was collected during a unilateral knee motor task of the involved or matched control knee consisting of repeated cycles of extension-flexion. The percent signal change of the motor cortex and lingual gyrus were calculated and correlated against the stroboscopic effect on knee flexion and adduction. RESULTS:Lingual gyrus activation was correlated with the stroboscopic effect on knee flexion for the ACLR (r=0.582, p=0.037) and control (r=0.688, p=0.009) cohorts. Motor cortex activation was correlated with the stroboscopic effect on knee adduction for only the ACLR (r=0.683, p=0.005) cohort. CONCLUSIONS: The motor neuroplasticity associated with ACLR is moderately related to visually perturbed drop landing neuromuscular control. These findings indicate visual-motor control maybe a driving factor behind neuromuscular control changes after ACLR, and a possible contributing mechanism to the continued poor neuromuscular control despite current therapy. Additional attention to the sensory-motor and visual-motor interaction after injury and during therapy may provide a means to improve neuromuscular therapy.