Improvement of Knowledge About the Arthrogenic Muscle Inhibition in the Aftermath of Knee Trauma.

Overview

Arthrogenic Muscle Inhibition (AMI) is one of the classic complications occurring in the aftermath of knee trauma; AMI is grossly defined as a lack of extension due to quadriceps inhibition and hamstring contracture. However, its origins remains unknown with a strong suspicion for a central brain origin. It could be the missing link explaining this lack of extension following an anterior cruciate ligament (ACL) rupture. The primary hypothesis of this study is that a difference in activation of motor brain areas exists in patients with an ACL rupture, between those with AMI or without. The second hypothesis is that this difference could be seen on brain functional MRI.

AMI leads to quadriceps atrophy, persistent knee pain, dynamic instability, and a higher rate of osteoarthritis. A recent literature review suggests that the AMI phenomenon is multifactorial, but not widely known and poorly understood. Known mechanisms include impaired motor function at rest, impaired transmission of information from joint sensory receptors, impaired excitability of the spinal reflex and impaired cortical activity. Several studies have suggested a link between ACL rupture and central nervous system reorganization. Among the neurophysiological investigations explored are the evoked somesthesic potentials, electroencephalography, and transcranial magnetic stimulation (TMS). However, these mechanisms alone do not explain the phenomenon in its entirety, suggesting that there are other mechanisms. Furthermore, no study has used functional brain MRI to assess the existence of similar changes in AMI. This study plans to compare two groups of patients with an ACL rupture: a group with AMI, and a group without AMI. Both groups will undergo a functional brain MRI in order to analyse any modification of the sensory-motor network connectivity that could occur.