- Arthrogenic muscle inhibition manifests as a condition in which the non-injured muscle of a corresponding injured joint becomes voluntarily inhibited, ultimately impeding the ability to resolve requisite neurophysiological muscle qualities.
BACKGROUND & OBJECTIVE
Arthrogenic muscle inhibition (AMI) can be defined as the reduction in the ability to voluntarily activate non-injured musculature neighbouring an injured joint, most notably the knee joint (1). The mitigation of this neurophysiological phenomenon should be approached with distinct solutions as it can be a significant performance inhibitor.
While the inflammatory cascade, pain, joint effusion and of course joint laxity and mechanoreceptor alterations via structural insult are instigators into the development of AMI, this does not explain the mechanistic processes that underpin the phenomenon, ultimately warranting distinct strategies (2).
The main purpose of this paper was to provide an overview of the neurophysiological processes involved in the development of AMI; but more importantly, offer solutions to course correct AMI or simply to implement when initiating rehabilitation, thus altogether avoiding AMI.
It appears that intervening on the initial instigators of arthrogenic muscle inhibition - pain, joint effusion, and inflammation - limits the negative proliferation of system wide neurophysiological effects.
Focal Joint Cooling