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Quadriceps arthrogenic muscle inhibition: the effects of experimental knee joint effusion on motor cortex excitability
Authors:David Andrew Rice  Peter John McNair  Gwyn Nancy Lewis  Nicola Dalbeth
Affiliation:.Health and Rehabilitation Research Institute, Auckland University of Technology, Private Bag 92006, Auckland, 1142 New Zealand ;.Waitemata Pain Services, Department of Anaesthesiology and Perioperative Medicine, North Shore Hospital, 124 Shakespeare Road, Milford, Auckland, 0622 New Zealand ;.Department of Medicine, University of Auckland, 143 Park Road, Auckland, 1023 New Zealand
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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