• David Andrew Rice, Thomas Graven-Nielsen, Gwyn Nancy Lewis, Peter John McNair, and Nicola Dalbeth.
• Health and Rehabilitation Research Institute, Auckland University of Technology, 55 Wellesley Street East, Auckland, 1010, New Zealand. david.rice@aut.ac.nz.
• Arthritis Res. Ther. 2015 Aug 12; 17: 204.

IntroductionNotable weakness of the quadriceps muscles is typically observed as a consequence of knee joint arthritis, knee surgery and knee injury. 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). To investigate the mechanisms underlying AMI, this study explored the effects of experimental knee pain on lower limb corticospinal and motor cortex excitability.MethodsTwenty-four healthy volunteers participated in this study. In experiment 1, experimental knee pain was induced by the injection of hypertonic saline into the infrapatellar fat pad (n = 18). In experiment 2, isotonic saline was injected into the fat pad as a non-painful control (n = 8). Pain intensity was measured on a 10-cm electronic visual analogue scale. Transcranial magnetic stimulation and electromyography were used to measure lower limb motor-evoked potential amplitude and short-interval intracortical inhibition before and after the injection.ResultsThe peak VAS score following hypertonic saline (5.0 ± 0.5 cm) was higher than after isotonic saline (p <0.001). Compared with baseline, there was a significant increase in vastus lateralis (p = 0.02) and vastus medialis motor-evoked potential amplitude (p = 0.02) during experimental knee pain that was not apparent during the control condition. Biceps femoris and tibialis anterior motor-evoked potential amplitude did not change following injection (all p >0.05). There was no change in short-interval intracortical inhibition measured from vastus lateralis following injection (both p >0.05).ConclusionsQuadriceps corticospinal excitability increases during experimental knee pain, providing no evidence for a supraspinal contribution to quadriceps AMI.

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