Neuromuscular control after injury to the knee: An anterior cruciate ligament injury and reconstruction model.

摘要

The goal of this series of investigations was to elucidate and characterize the changes in neuromuscular control that occur in response to ligament injury, surgical reconstruction, and subsequent rehabilitation. Comprehensive strength analysis of the ipsilateral and contralateral knee after ACL reconstruction identified regional changes in strength limited to joint angle, speed and contraction type that were dependent on graft selection (Study 1). The concept of neuromuscular balance about the knee is further developed using a comprehensive depiction of agonist and antagonist strength in both active healthy and surgical groups (Study 2). Strength deficits were identified in the contralateral uninjured limb after ACL reconstruction when compared to controls (Study 3). Neuromuscular changes in the contralateral limb are particularly important because of the widespread use of the contralateral limb as a control limb in both the clinical and research settings. Strength deficits in the contralateral limb were demonstrated immediately after ACL injury consistent with a neural nociceptive crossover etiology (Study 5). The lack of strength deficits of the hip extensors in the presence of large knee flexor strength deficits after hamstring ACL reconstruction suggest differential alteration of bi-articular muscles (Study 6). Finally, the role of proprioception, muscle fatigue and the implications for dynamic joint stabilization is presented (Study 4).; The possible underlying physiological mechanisms responsible for regional and global strength deficits could be muscular, mechanical or neural in origin. Changes in motor unit recruitment and/or activation patterns of the agonist and antagonist muscles that control motion about the knee and hip joints appear to be the most likely candidates to account for regional variations in resultant joint moment. Afferent feedback from the knee joint and peri-articular structures, spinal reflex changes and central and volitional mechanisms could mediate changes in neuromuscular activation.