03/02/2026
Mechanisms of Arthrogenic Muscle Inhibition: Implications for Physiotherapy
Lepley, A. S., & Lepley, L. K. (2021).
Introduction
Arthrogenic muscle inhibition (AMI) represents a critical neurophysiological barrier in the rehabilitation of joint injuries. Despite advancements in therapeutic modalities, the persistent inability to achieve full volitional activation of periarticular musculature remains a significant impediment to functional recovery. Understanding the underlying mechanisms of AMI is essential for the development of targeted, evidence-based interventions that address not only peripheral impairments but also central nervous system adaptations.
Mechanistic Analysis
AMI is a multifactorial and progressive neurophysiological response initiated by altered afferent signaling from an injured joint. This aberrant sensory input triggers a cascade of neural adaptations that extend beyond the local joint environment. Initially, the disruption in afferent feedback induces reflexive inhibition of periarticular muscles, particularly those responsible for dynamic stabilization and load-bearing.
Concomitantly, somatosensory deficits emerge, further compromising neuromuscular control and proprioceptive acuity. Over time, these peripheral changes elicit neuroplastic modifications within supraspinal centers, including sensorimotor integration regions of the brain. These central adaptations can reinforce inhibitory patterns, leading to sustained reductions in motor output and prolonged deficits in voluntary muscle activation.
Beyond neuromuscular control, AMI influences broader aspects of clinical function. Changes in muscle morphology—such as atrophy, altered fiber-type distribution, and neuromuscular junction remodeling—are observed in conjunction with AMI. Psychological responses to injury, including fear-avoidance behavior and decreased confidence in joint stability, may also exacerbate inhibition and hinder the rehabilitation process.
Clinical Implications and Take-Home Message
AMI is not merely a local muscular issue but a systemic neurological phenomenon that disrupts the entire sensorimotor continuum. Effective rehabilitation must therefore incorporate strategies aimed at both peripheral and central contributors to inhibition. Techniques such as cryotherapy, neuromuscular electrical stimulation, proprioceptive training, and motor imagery may be employed to mitigate AMI and restore optimal muscle activation.
In summary, addressing AMI should remain a central focus in post-injury rehabilitation. A comprehensive, neuroscience-informed approach to reducing inhibition can significantly enhance clinical outcomes, improve functional performance, and accelerate the return to pre-injury activity levels.
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