Mechanisms of Arthrogenic Muscle Inhibition

Arthrogenic muscle inhibition (AMI) continues to be a limiting factor in joint rehabilitation as the inability to volitionally activate muscle significantly dampens recovery. New evidence acquired at higher brain centers and in clinical populations continues to reshape our perspective of what AMI is and how to treat it. This review aims to stimulate discussion about the far-reaching effects of AMI by exploring the interconnected pathways by which it evolves.

To discuss how reflexive inhibition can lead to adaptations in brain activity, to illustrate how changes in descending motor pathways limit our ability to contract muscle following injury, and to summarize the emerging literature on the wide-reaching effects of AMI on other interconnected systems.

The databases PubMed, SPORTDiscus, and Web of Science were searched for articles pertaining to AMI. Reference lists from appropriate articles were cross-referenced.

AMI is a sequential and cumulative neurological process that leads to complex clinical impairments. Originating with altered afferent information arising from an injured joint, patients experience changes in afferent information, reflexive muscle inhibition, deficiencies in somatosensation, neuroplastic compensations in higher brain centers, and ultimately decreased motor output to the muscle surrounding the joint. Other aspects of clinical function, like muscle structure and psychological responses to injury, are also impaired and influenced by AMI. Removing, or reducing, AMI should continue to be a focus of rehabilitation programs to assist in the optimization of health after joint injury.