Abstract
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.
Highlights
Notable weakness of the quadriceps muscles is typically observed as a consequence of knee joint arthritis, knee surgery and knee injury
These findings show that nociception alone is sufficient to induce quadriceps arthrogenic muscle inhibition (AMI) and suggest that articular nociception inhibits the activation of other muscles around the joint
motor-evoked potential (MEP) amplitude There was a significant change in vastus lateralis (VL) (Friedman: χ2 = 8.44, p = 0.01; Fig. 1) and vastus medialis (VM) (Friedman: χ2 = 10.33, p = 0.006; Fig. 1) MEP amplitude over time following hypertonic saline injection
Summary
Notable 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). Marked and sustained weakness of the quadriceps muscle is often observed in response to knee joint injury, surgery and pathology This weakness is partly due to an ongoing muscle activation deficit characterised by an inability of supraspinal pathways to voluntarily drive the quadriceps muscle, known as arthrogenic muscle inhibition (AMI) (for a review see [1]). A significant association was observed between knee pain intensity and the subsequent change in muscle strength [23] These findings show that nociception alone is sufficient to induce quadriceps AMI and suggest that articular nociception inhibits the activation of other muscles around the joint
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