On the effect of chemically activated fine muscle afferents on interneurones mediating group I non-reciprocal inhibition of extensor ankle and knee muscles in humans.

In a previous paper it was shown that muscle nociceptive discharge depressed the activity of interneurones mediating group I non-reciprocal inhibition (or Ib interneurones) in humans [A. Rossi, B. Decchi, Changes in Ib heteronymous inhibition to soleus motoneurons during cutaneous and muscle nociceptive stimulation in humans, Brain Res. 774 (1997) 55-61.]. However, since nociceptive discharge depressed the size of the soleus H-reflex (by which Ib inhibition was tested) the question arises as to whether modification of motoneurone membrane conductance per se could depress the size of Ib inhibitory post-synaptic potentials. The results of the present study suggest that the contribution of motoneurone hyperpolarization to Ib disinhibition is negligible and that muscle nociceptive discharge actually depresses the activity of these pathways.

Interactions between nociceptive and non-nociceptive afferent projections to cerebral cortex in humans.

We investigated the effect of a tonic discharge of muscle nociceptive afferents on somatosensory evoked potentials (SEPs) in humans in response to stimulation of non-nociceptive afferents arising from the same muscle. Conditioning nociceptive muscle stimulation was achieved by local injection of 50 mg levo-ascorbic acid (in a volume of 0.3 ml) in the body of the extensor digitorum brevis muscle (EDB). The test stimulus for SEPs was an electrical pulse applied to the EDB nerve at an intensity below the motor threshold. The main finding was that tonic muscle nociceptive stimulation strongly depressed the middle-latency P60-N75 complex without modifying the size of the early P40-N50 complex of SEPs. Depression of the P60-N75 complex was correlated with the pain-induced loss of proprioception of the foot, making it plausible that this cortical complex reflects neuronal processes leading to perception.