Neurophysiological Mechanisms Underlying Functional Knee Instability Following an Anterior Cruciate Ligament Injury

Abstract

PURPOSE Functional knee instability, which is defined as repetitive episodes of the knee “giving way” during physical activity, has received great attention to identify mechanisms due to serious pathological complications. Growing evidence suggests that insufficient neural adaptation in the central nervous system (CNS) may result in permanent functional deficits in patients with anterior cruciate ligament (ACL) injuries. The purpose of this review was to address neurophysiological mechanisms underlying functional joint instability following an anterior cruciate ligament rupture. METHODS Previous studies conducted from PubMed with particular emphasis on mechanisms underlying joint instability and neuromuscular control deficits after an anterior cruciate ligament were reviewed. RESULTS Inappropriate neuromuscular control, inconsistent correlations between joint laxity and functional outcomes, and altered neural activation in the brain during proprioceptive tasks may underscore the idea that persistent functional joint instability is an indication not only of the peripheral deafferentation input, but also neuromechanical decoupling between the injured ACL and CNS due to neuroplasticity. CONCLUSIONS Persistent functional instability can develop following knee joint injury due to altered neural processing in the CNS. Therefore, it must be considered for improving patient outcomes, minimizing functional disability, and returning to one’s chosen physical activity in ACL patients.

Keywords

• anterior cruciate ligament injury
• functional joint instability
• neuroplasticity
• neuromechanical decoupling
• joint laxity