Arthrogenic Muscle Inhibition Following Anterior Cruciate Ligament Injury
Brian Pietrosimone, Adam S. Lepley, Christopher Kuenze, Matthew S. Harkey, Joseph M. Hart, J. Troy Blackburn, Grant E. Norte
Abstract
Arthrogenic muscle inhibition (AMI) is a common impairment in individuals who sustain an anterior cruciate ligament (ACL) injury. The AMI causes decreased muscle activation, which impairs muscle strength, leading to aberrant movement biomechanics. The AMI is often resistant to traditional rehabilitation techniques, which leads to persistent neuromuscular deficits following ACL reconstruction. To better treat AMI following ACL injury and ACL reconstruction, it is important to understand the specific neural pathways involved in AMI pathogenesis, as well as the changes in muscle function that may impact movement biomechanics and long-term structural alterations to joint tissue. Overall, AMI is a critical factor that limits optimal rehabilitation outcomes following ACL injury and ACL reconstruction. This review discusses the current understanding of the: (1) neural pathways involved in the AMI pathogenesis following ACL injury; (2) consequence of AMI on muscle function, joint biomechanics, and patient function; and (3) development of posttraumatic osteoarthritis. Finally, the authors review the evidence for interventions specifically used to target AMI following ACL injury.