Quadriceps Arthrogenic Muscle Inhibition: The Effects of Experimental Knee Joint Effusion on Motor Cortex Excitability

Date
2014
Authors
Rice, DA
McNair, PJ
Lewis, GN
Dalbeth, N
Supervisor
Item type
Journal Article
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Journal Title
Journal ISSN
Volume Title
Publisher
BioMed Central
Abstract

Introduction Marked weakness of the quadriceps muscles is typically observed following injury, surgery or pathology affecting the knee joint. This is partly due to ongoing neural inhibition that prevents the central nervous system from fully activating the quadriceps, a process known as arthrogenic muscle inhibition (AMI). This study aimed to further investigate the mechanisms underlying AMI by exploring the effects of experimental knee joint effusion on quadriceps corticomotor and intracortical excitability.

Methods Seventeen healthy volunteers participated in this study. Transcranial magnetic stimulation was used to measure quadriceps motor evoked potential area, short-interval intracortical inhibition, intracortical facilitation and cortical silent period duration before and after experimental knee joint effusion. Joint effusion was induced by the intraarticular infusion of dextrose saline into the knee.

Results There was a significant increase in quadriceps motor evoked potential area following joint infusion, both at rest (P = 0.01) and during voluntary muscle contraction (P = 0.02). Cortical silent period duration was significantly reduced following joint infusion (P = 0.02). There were no changes in short interval intracortical inhibition or intracortical facilitation over time (all P > 0.05).

Conclusions The results of this study provide no evidence for a supraspinal contribution to quadriceps AMI. Paradoxically, but consistent with previous observations in patients with chronic knee joint pathology, quadriceps corticomotor excitability increased after experimental knee joint effusion. The increase in quadriceps corticomotor excitability may be at least partly mediated by a decrease in gamma-aminobutyric acid (GABA)-ergic inhibition within the motor cortex.

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Source
Arthritis Research & Therapy, 16(6), 502.
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© 2014 Rice et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.