Gamma Loop Dysfunction as a Possible Neurophysiological Mechanism of Arthrogenic Muscle Inhibition: A Narrative Review of the Literature

Quadriceps activation failure has been observed following various pathological conditions in a knee joint such as knee surgery, pain, effusion in knee, and osteoarthritis also could be aging matter. Those patients are unable to attain maximal quadriceps strength for a long period of time although their quadriceps itself is not damaged. This impairment is termed arthrogenic muscle inhibition (AMI). AMI has been of concern to clinicians because this weakness hinders the rehabilitation process considerably and delays recovery because strengthening protocols for the AMI could be largely ineffective. Clinically, it is important to understand neurophysiological mechanisms of the AMI to treat patients with the impairment.This is a narrative review of the literature. The purpose of this review is to understand the following: (1) Why investigations of only peripheral spinal reflexive pathways are not enough for elucidation of the mechanisms of the AMI? (2) What we know about the role of the gamma spindle system in AMI so far? (3) Could a dysfunctional gamma spindle system contribute to AMI lead neural changes in upper central nervous system? and (4) Concerns that a clinician should take into consideration when deciding whether to apply therapeutic interventions for AMI.The databases PubMed, MEDLINE, SPORTDiscus, and CINAHL were searched with the terms arthrogenic muscle inhibition (AMI), reflex inhibition, joint mechanoreceptor, gamma loop, corticospinal pathway, spinal 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. Motor unit recruitment could be hindered in patients with AMI as a result of a dysfunctional gamma spindle system. Clinicians should understand the mechanism of AMI well in order to establish effective rehabilitation programs for AMI. Indeed, AMI is not caused by a single factor, but rather, multiple neural factors can change over time following the appearance of AMI. Therefore, multiple interventions targeting different neural pathways should be combined to achieve the ideal therapeutic goal for the treatment of AMI.