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J. Ty Hopkins and Christopher D. Ingersoll


To define the concept of arthrogenic muscle inhibition (AMI), to discuss its implications in the rehabilitation of joint injury, to discuss the neurophysiologic events that lead to AMI, to evaluate the methods available to measure AM1 and the models that might be implemented to examine AMI, and to review therapeutic interventions that might reduce AMI.

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The databases MEDLINE, SPORTDiscus, and CIHNAL were searched with the terms reflex inhibition, joint mechanoreceptor, Ib interneuron, Hoffmann reflex, effusion, and joint injury. The remaining citations were collected from references of similar papers.


AMI is a limiting factor in the rehabilitation of joint injury. It results in atrophy and deficiencies in strength and increases the susceptibility to further injury. A therapeutic intervention that results in decreased inhibition, allowing for active exercise, would lead to faster and more complete recovery.

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Adam S. Lepley and Lindsey K. Lepley

an inhibitory effect on alpha motor neurons in the spinal cord. 11 – 13 Pain was also found to have similar inhibitory effects on alpha motor neurons due to the activation of type III and IV afferent nociceptors. 14 Researchers extended these basic insights by utilizing effusion models in humans

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Justin L. Rush, David A. Sherman, David M. Bazett-Jones, Christopher D. Ingersoll, and Grant E. Norte

not necessary to experience AMI. Previous literature has shown that altered joint receptor activity through artificial pain and effusion models can send inhibitory signals to the spinal cord, causing a reflexive shutdown of the musculature surrounding the injured joint. 5 , 8 However, previous

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Yu Konishi, Ryo Yoshii, and Christopher D. Ingersoll

swelling. In those studies, they used a knee effusion model induced by injecting saline solution into the undamaged knee joints of healthy subjects. As a result, attenuated H wave in the vastus medialis was observed. The measurement of the H-reflex can better detect the neural mechanism related to spinal

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Grant Norte, Justin Rush, and David Sherman

those with OA and ACLR compared with other disinhibitory modalities. 59 Following menisectomy 9 and ACL repair, 60 single bouts of TENS effectively increased quadriceps activation and maximal voluntary contractions. These findings have been reproduced in experimental effusion models 54 , 61 , 62 and

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Brian Pietrosimone, Adam S. Lepley, Christopher Kuenze, Matthew S. Harkey, Joseph M. Hart, J. Troy Blackburn, and Grant Norte

, and the neurophysiologic source of dysfunction. 103 This hypothesis is based on studies in which an experimental effusion model was utilized to mimic the effects of joint injury which indicated that an acute effusion alone resulted in increased hip and knee flexion along with knee-extensor moments