Arthrogenic Muscle Inhibition After Anterior Cruciate Ligament Injury and Reconstruction: Neurophysiological Mechanism, Assessment and Rehabilitation

Background: Persistent quadriceps weakness is a common consequence of joint injury, particularly following anterior cruciate ligament (ACL) injury and reconstruction. While traditionally attributed to muscle atrophy and disuse, growing evidence suggests that neural mechanisms play a central role. Arthrogenic Muscle Inhibition (AMI) is a neurally mediated impairment in the ability to voluntarily activate periarticular musculature following joint injury, occurring within a broader neurophysiological response involving altered joint-related afferent input, spinal mechanisms, and supraspinal adaptations. Methods: A narrative review of the literature was conducted using PubMed and Scopus databases. Studies investigating the peripheral, spinal, and supraspinal mechanisms of AMI, as well as its clinical manifestations, assessment methods, and rehabilitation strategies, were reviewed. Experimental, observational, and neurophysiological studies focusing on ACL injury and related joint disorders were included. Results: Current evidence indicates that AMI is a multifactorial neurophysiological process involving altered afferent signaling, spinal reflex inhibition, and central nervous system adaptations. These mechanisms contribute to persistent quadriceps activation failure, impaired motor control, biomechanical asymmetries, and functional and biomechanical alterations that may persist during recovery. Neuroimaging and electrophysiological studies further demonstrate cortical reorganization and neuroplastic changes that may persist despite restoration of joint stability and muscle strength. Conclusions: AMI should be considered a multilevel sensorimotor dysfunction rather than an isolated muscular deficit. Recognition of its neurophysiological basis may improve rehabilitation strategies by promoting interventions that target both neural and muscular components of recovery.