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Reflex inhibition of the human quadriceps in the presence of knee joint damage

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Stokes, Maria (1984) Reflex inhibition of the human quadriceps in the presence of knee joint damage. Doctoral thesis, Polytechnic of North London.

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Abstract

Quadriceps weakness can occur by atrophy and by reflex inhibition due to stimuli from a damaged knee joint. The mechanisms by which quadriceps weakness occurs are not understood enough to allow weakness to be prevented.

The nature of reflex inhibition has been studied in patients undergoing arthrotomy and meniscectomy in order to find ways of preventing inhibition. The maximal voluntary activation (MVA) of quadriceps was recorded, using surface integrated electromyography, during straight leg isometric contractions before end after surgery. Post-operative inhibition was expressed as the percentage reduction from the pre-operative MVA. Knee pain experienced during each contraction was recorded on a linear analogue scale.

Post-meniscectomy reflex inhibition of quadriceps is severe (70-80% during the first 3 days), prolonged (35-40% at 2 weeks) and is not related to pain after 24 hours. Inhibition can be temporarily prevented by per-operative infiltration of the knee with a local anaesthetic (Chapter 3). Prolonged voluntary tourniquet ischaemia in normal subjects did not alter subsequent quadriceps function, indicating that the reduced NVA observed in the meniscectomy patients was not due to ischaemia (Chapter 4). Isometric quadriceps contractions are inhibited less with the knee flexed than extended (Chapter 5). Transcutaneous nerve stimulation (TNS) had only a small effect on inhibition, and pain relief was similar in both the treatment and the control groups (Chapter 6). In patients who developed knee joint effusions post-operatively, aspiration always reduced inhibition but did not abolish it (Chapter 7).

The effect of knee joint afferent activity on quadriceps activation was studied in normal subjects with knee joint infusions. Intra-articular pressure/volume relationships at rest were similar to results reported by other authors, and during contraction the pressures were higher at each volume (Chapter 8). Inhibition of reflex activation of quadriceps was examined by measuring quadriceps H-reflex (Chapters 9,10 and 11). The central neural pathway of the joint afferent stimuli was investigated by testing for spatial facilitation between joint stimulation (by infusion) and known pathways of quadriceps H-reflex inhibition (by stimulating various nerves). The results suggest that the joint afferents have connections with Ib and cutaneous flexor reflex afferent (FRA) inhibitory pathways, but results for reciprocal inhibition were equivocal.

The present investigations have quantified the severity and duration of post-meniscectomy quadriceps inhibition, and have confirmed that the inhibition occurs by a reflex mechanism originating from the knee joint and that it is possible to block the inhibitory stimuli. Investigation of the pathway of the afferent stimuli suggested convergence of joint afferents with Ib pathways and with cutaneous FRA pathways.

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