Cutaneous nociceptive facilitation of Ib heteronymous pathways to lower limb motoneurones in humans.

The effects of tonic pain stimulation on heteronymous Ib pathways from the gastrocnemius medialis (GM) to the soleus (Sol) and to the quadriceps (Q) muscles were investigated in four healthy human subjects. Tonic pain stimulation was performed by subcutaneous injection of 0.5 mg levo-ascorbic acid or vitamin C (L-LAS) in a volume of 0.5 ml on the dorsal surface of the ipsilateral foot. The mean curve of L-AS-induced pain sensation showed a steep rising phase reaching maximum intensity at 2-3 min, followed by a slow decay phase lasting about 15-20 min. Between about 5 and 20 min after injection, there was evidence of pure pain stimulation due to chemical activation of free nerve endings. During this interval, significant potentiation of Ib inhibition from GM to both Sol and Q motoneurones was observed. The time-course of these Ib heteronymous changes paralleled that of subjective pain sensation. These findings demonstrate that nociceptive discharge modifies the gain of Ib heteronymous effects in humans. Since the man function of these Ib pathways is to coordinate activity of muscles operating at different joints, it is suggested that nociceptive input may change muscle synergies by selecting specific subpopulations of Ib interneurones, thus contributing to establish appropriate adaptive motor strategies

Changes in Ib heteronymous inhibition to soleus motoneurones during cutaneous and muscle nociceptive stimulation in humans.

The effects of selective tonic cutaneous and muscle pain stimulation on heteronymous Ib pathways from the gastrocnemius medialis to the soleus motoneurones were studied in five healthy human subjects. Tonic pain stimulation, monitored by a psychophysical method, was obtained by local injection of 60 mg levo-ascorbic acid (L-AS) in a volume of 0.3 ml. Nociceptive cutaneous and muscle stimulation of the dorsal foot produced opposite, long-lasting changes in heteronymous Ib pathways to soleus motoneurones: Ib facilitation during cutaneous stimulation was reversed by disinhibition during muscle stimulation. The time-course of these Ib changes strictly paralleled that of subjective pain sensation. On the contrary, when the same nociceptive stimuli were applied to the leg (at pretibial level), the differences between cutaneous and muscle pain disappeared and similar short-lasting phases of facilitation and inhibition of Ib activity were observed. It is concluded that tonic discharge of cutaneous and muscle nociceptive afferents arising from the foot have specific and opposite effects on Ib inhibitory pathways to ankle extensor motoneurones. These interactions between muscle and cutaneous nociceptive and Ib pathways may be used to change muscle synergies, thus contributing to the establishment of appropriate adaptive locomotor strategies during pain

Effect of chemically activated fine muscle afferents on spinal recurrent inhibition in humans.

Abstract OBJECTIVE: To test the hypothesis that 'metabolites released during fatiguing muscle contractions excite group III-IV muscle nociceptive afferents, inhibiting homonymous motoneurones via Renshaw cells,' by recording changes in recurrent inhibition of soleus motoneurones when high-threshold, small-diameter afferents (group III-IV fibres) from the same muscle were tonically activated. METHODS: Experiments were performed in 7 healthy subjects at rest and during weak isometric voluntary contraction of the soleus muscle. Muscle nociceptive afferents were activated by local standardized injection of levo-ascorbic acid. Renshaw cells were orthodromically activated by a conditioning H reflex and the resulting recurrent inhibition of the soleus motoneurones was assessed by a subsequent test H reflex. An additional H reflex of the same size as the test reflex was used to assess motoneurone excitability. RESULTS: At rest, muscle nociceptive stimulation produced transient facilitation of both test H and reference H reflexes. Under weak voluntary contraction, muscle nociceptive stimulation produced long-lasting extra-inhibition and extra-facilitation of the test reflex and reference reflex respectively, the time course of which closely resembled that of the subjective muscle pain curve. CONCLUSIONS: Discharge of putative group III-IV muscle afferents facilitated homonymous recurrent inhibition. The filtering property of recurrent inhibition may contribute to limit motoneurone activity during muscle pain and/or adapt motoneurone firing rate to the modified contractile properties of motor units as muscle fatigue developed

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

Supraspinal influences on recurrent inhibition in humans. Paralysis of descending control of Renshaw cells in patients with mental retardation.

The recurrent inhibition of alpha motoneurons was studied in 8 mentally retarded subjects (age 16-35 years), six of whom also had non-pyramidal or extrapyramidal motor alterations, manifesting as rigid and inflexible voluntary and/or postural movements. Despite a similar degree of mental retardation (Raven spatial general intelligence test), the other 2 cases showed much more modest changes in motor behavior. At rest, recurrent inhibition on soleus motoneurons was normal in all patients. In the 6 cases exhibiting more severe motor abnormality, the changes in Renshaw cell excitability, which occur during postural or voluntary contractions in normal subjects, were not found. This expressed the lack of supraspinal influences on Renshaw cells in these patients. On the other hand, supraspinal modulating influences on Renshaw cells were virtually normal in the remaining 2 patients. The absence of excitability changes of recurrent inhibition to postural or voluntary movements is discussed in relation to the abnormality of motor behavior observed in these patients. In addition, since paralysis of adaptive changes of recurrent inhibition has so far only been described in spastic subjects, the present study demonstrates that the descending pathways, which control recurrent inhibition gain, are different from those which, when damaged, lead to spasticity. Finally, our results indicate that the changes in motor behavior often associated with mental retardation cannot be regarded merely as the consequence of defective motor learning

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

Nerve conduction study, electromyography and somatosensory evoked potentials in non-Friedreich early onset cerebellar ataxia. A comparative study with Friedreich's ataxia and late onset cerebellar ataxia.

Electrophysiological findings in 14 patients with non-Friedreich early onset cerebellar ataxia are reported. Nerve conduction studies showed reduction of sensory action potential amplitudes in 7 cases associated in 3 with a decrease of sensory conduction velocities. Six subjects also exhibited a chronic neurogenic pattern to standard needle electromyography. Motor conduction velocities were normal in all cases; only two cases showed an increase in distal motor latencies. Short-latency somatosensory evoked potentials following median nerve stimulation revealed a prolonged central conduction time (N13-N20 interpeak latency) in 7 cases, compatible with supraspinal damage of the somatosensory pathways. These electrophysiological data are compared with those obtained in two reference groups of patients, respectively affected by Friedreich's ataxia and olivo-ponto-cerebellar atrophy