Interaction of nociceptive and non-nociceptive cutaneous afferents from foot sole in common reflex pathways to tibialis anterior motoneurones in humans.

In six healthy subjects, the reflex responses of the tibialis anterior muscle (TA) to stimulation of the cutaneous afferents arising from plantar foot, were studied at rest and during different levels of steady voluntary contraction of the TA. At rest, the threshold of the response and the threshold of subjective pain sensation coincided. The mean latency of this TA nociceptive response was 84.7 ms. Steady voluntary contractions of the TA, which was increased progressively from 3% to 15% of the maximum voluntary contraction, produced a significant and parallel reduction in the threshold and latency of the response: at 15%, the mean latency was about 26 ms shorter than at rest and its threshold was about half (i.e. below the pain threshold). The conduction velocity of the afferents responsible for TA response at rest was within the range of A-delta pain afferents (mean 27.4 m/s), whereas during voluntary contraction it was within the A-beta fibre range (mean 45.1 m/s). This suggests that descending command makes the discharge of low-threshold, fast-conducting fibres sufficient for reflex activation of TA motoneurones (MNs). Central delay (about 4 ms) and MN recruitment order (according to the size principle) were found to be the same for both nociceptive and non-nociceptive TA reflex responses. Finally, experiments of spatial summation revealed an interaction between nociceptive and non-nociceptive inputs at a premotoneuronal level. It is therefore proposed that nociceptive and non-nociceptive cutaneous afferents arising from the foot sole use the same short-latency spinal pathway to contact TA MNs and that their relative contribution to its segmental activation is contingent upon descending command

Heteronymous recurrent inhibition from gastrocnemius muscle to soleus motoneurones in humans.

Presence of heteronymous recurrent inhibition in motoneurones (Mns) innervating the soleus muscle (Sol) was investigated following electrical stimulation of the nerve of gastrocnemius medialis muscle (GM). Sub-threshold electrical stimulation for alpha Mns produced short-lasting inhibition of the Sol, reflecting non-reciprocal group I inhibition. After increasing the intensity of stimulation above the motor threshold, a short-latency, long-lasting inhibition appeared superimposed on the group I inhibition. Its amount increased with the size of the conditioning motor response and after acute administration of L-acetylcarnitine. It is concluded that this long-lasting inhibition of the Sol Mns is due to the heteronymous activity of the GM-coupled Renshaw cells

Group Ia non-reciprocal inhibition from wrist extensor to flexor motoneurones in humans.

Interneurones mediating disynaptic inhibition from extensor to flexor carpi radialis muscles were characterized by pharmacological stimulation of Renshaw cells. It is, indeed, known that only Ia interneurones are blocked by recurrent inhibition. Renshaw cell potentiation, induced by intravenous administration of 2 g levo-acetylcarnitine, blocked Ia reciprocal inhibition from triceps to biceps muscles but not disynaptic inhibition from extensor to flexor carpi radialis muscles. It is concluded that the interneurones mediating this latter inhibition are not Ia interneurones. This kind of inhibition could be an example of a Ia non-reciprocal inhibitory pathway

Carpal tunnel syndrome in amyotrophic lateral sclerosis and late onset cerebellar ataxia.

We report on clinical and electrophysiological findings and management in nine patients who developed carpal tunnel syndrome during the course of amyotrophic lateral sclerosis and late onset cerebellar ataxia, two neurodegenerative diseases. The patients were treated with surgical decompression (five cases) and local steroid injections (four cases). Only one showed lasting relief of symptoms and significantly improved distal conduction in the median nerve at follow-up after 2 to 3 months. The symptoms and conduction data remained unchanged in three patients who could be followed for more than 1 year. We think that axonal neuropathy plays an important role in the development of carpal tunnel syndrome in these patients and accounts for the failure of the standard treatments