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The present experiments were made in man with the aim of studying the possible influences of different head-body tilts on the activity of the interneurons Ia, Ib and the Renshaw cells functionally coupled to the soleus alpha-motoneurons. Subjects were seated on a chair, rotable with respect to the vertical axis, and were studied at 80 degrees and 40 degrees to the horizontal. The excitability of the soleus alpha-motoneurons slightly decreased when the body was placed at 40 degrees of backward inclination whereas the Renshaw cell activity showed a reinforcement of inhibition on the same motoneurons. The reciprocal inhibition from the anterior tibial to the soleus muscle increased at 40 degrees of backward inclination with respect to the control values at 80 degrees. Finally, short-latency homonymous facilitation and inhibition showed no significant change in relation to body position. The results indicate that different head-body positions are able to modify the bias of spinal interneurons in man. We discuss the hypothetical role of the vestibular system in producing the effects seen.

Experiments involving the acute administration of a central cholinergic substance ( l -acetylcarnitine) were performed on 6 healthy subjects to obtain additional evidence that the electrophysiological method developed by Bussel and Pierrot-Deseilligny in 1977 does actually assess recurrent inhibition in man. In all the subjects, the drug further decreased the amplitude of a test H reflex (H′) following a conditioning H reflex (H1). The amount of this supplementary inhibition was found to be related to the size of H1 reflex. Experimental evidence is also presented that H′ reflex supplementary depression is not contaminated by homonymous Ib effects. It is concluded that the method effectively tests the excitability of Renshaw cells in man.

The influence of static head-body tilts in the sagittal plane on the activity of Renshaw cells coupled to the soleus extensor alpha-motoneurons was studied in eight human subjects. Head-body rotation was carried out using a tilting seat and its effect was evaluated at 80 degrees (normal sitting position) and at 40 degrees of backward inclination (nose-up). Renshaw cell activity was assessed through a specially designed method of paired H-reflexes first described by Bussel and Pierrot-Deseilligny. alpha-Motoneuron excitability was also independently studied by mapping a reference H-reflex amplitude as a function of static head-body displacements. In almost all subjects Renshaw cell activity was increased at 40 degrees backward inclination with respect to control values at 80 degrees. These changes were attributed to the tonic labyrinthine reflexes capable of decoupling Renshaw cell activity from their motoneurons when the body was tilted backward from the upright position. We discuss the hypothetical functional modalities of the recurrent inhibitory circuit during postural adjustments elicited by labyrinthine input.

Renshaw cells, which mediate the recurrent inhibition of spinal a-motoneurones, are activated by acetylcholine, both through motoneurone collaterals and the reticulo-spinal system. Since it is known that L-acetylcarnitine (L-AC) has central cholinergic effects, we tested in ten normal subjects and three spastic patients the ability of L-AC to induce changes in excitability of the Renshaw cells. These were activated by a conditioning monosynaptic reflex of the soleus muscle, evoked by electrical stimulation of the tibial nerve, and the resulting recurrent inhibition of the motoneurones was assessed by a subsequent monosynaptic reflex (H'). Recurrent inhibition was tested prior to, during and after an intravenous administration of a solution containing 2000 mg of L-AC. L-AC administration proved to be able to induce in all subjects a decrease in the H'-reflex. This effect ensued approximately 30 min after onset of L-AC administration, reached the peak after 40 min and vanished in about one hour. The extent of the decrease in H' varied among subjects, being on the average 22% of the control values. A relationship was found between duration of L-AC administration and time for reaching the maximal effect. These results show that L-AC is able to decrease a-motoneurone excitability by increasing Renshaw cell activity, both in normal and spastic subjects.

The recovery curve of the soleus H reflex, evoked by stimulation of the tibial nerve in the popliteal fossa, was studied by applying an electrical conditioning stimulus to the inferior soleus nerve. Under these conditions a long-latency facilitatory phase could be superimposed on a long-lasting inhibition, the excitability cycle being therefore similar to that obtained by means of a paired shock to the tibial nerve. In order to identify the afferent fibres responsible for the effects observed, various conditioning stimulus strengths and nerve compression were used. A low-intensity stimulus induced only a facilitatory phase, while the inhibition promptly ensued on increasing stimulus strength, which remained however subliminal for activation of group II fibres. During calf compression exerted by a sphygmomanometer cuff placed between the conditioning and test stimuli, the facilitatory effects disappeared within 10 to 15 min, and the inhibitory ones disappeared within 25 to 30 min from the onset of compression. Tonic voluntary contraction enhanced both the inhibition and the facilitation. In a subject with complete spinal section, both inhibitory and facilitatory phases could be demonstrated on low-intensity stimulation. The present data, and previous results of ours, allow the following conclusions. (1) Facilitation and inhibition are produced by fibres likely belonging to group Ia spindle afferents. (2) Both effects are of spinal origin. (3) The spinal circuits mediating the effects may be modulated by descending commands. (4) The facilitation is sustained by tonic supraspinal influences while the inhibition is independent of it. Arguments are proposed against the hypotheses that the inhibition be due to transmitter depletion or to presynaptic mechanisms.

Experiments were conducted in man to evaluate the changes in Ia inhibitory interneurons activated from the anterior tibial muscle and projecting to the soleus alpha-motoneurons in relation to different static body positions. Subjects were fixed to a tilting chair and the effects of body rotation were evaluated at 80 degrees (normal sitting position) and 40 degrees of backward inclination (head supine, nose-up). A test H-reflex was used to assess changes in excitability of the soleus alpha-motoneurons after a conditioning stimulus applied to the deep peroneal nerve. In 5 out of 6 subjects, we observed a significant increase in the reciprocal inhibition after backward inclination of the body (40 degrees) with respect to the control position (80 degrees). Such increase was attributed to facilitation of the Ia inhibitory interneurons projecting to the soleus motoneurons. We consider the possibility that the observed increment in reciprocal inhibition after backward inclination be sustained by variations of tonic vestibular activity.

Movements of the paretic hand in patients with chronic subcortical stroke are associated with high interhemispheric inhibition (IHI) targeting the motor cortex in the lesioned hemisphere relative to healthy controls. The purpose of this investigation was to determine whether this abnormality also involves IHI operating during movements of the non-paretic hand. Here, we studied IHI in the process of generation of voluntary index finger movements by the paretic and non-paretic hands in a simple reaction time paradigm in a group of patients with chronic subcortical stroke. With movements of the non-paretic index finger, IHI targeting the contralateral primary motor cortex ((c)M1) decreased progressively to turn into facilitation at around movement onset, similar to healthy controls. In contrast, movements of the paretic index finger resulted in significantly deeper inhibition at all premovement timings relative to the non-paretic hand. In conclusion, these results document a deeper premovement IHI with paretic than non-paretic hand movements of patients with chronic subcortical stroke, a possible mechanism underlying deficits in motor control.

Active immunisation with rubella vaccine has not been commonly associated with neurological complications. We report the case of a 23-year-old woman who developed a mild, distal demyelinating neuropathy after immunisation with the live attenuated RA 27/3 rubella strain. Post-immunisation immunologic studies carried over 24 months showed the presence of antibodies to the RV proteins, particularly to the capsid antigen, and to the myelin basic protein (MBP). A similarity between a C antigen motif and a sequence of the MBP was found by computer analysis. The cross-reactivity was confirmed by immunising mice with a synthetic peptide derived from the MBP, which developed a strong humoral response to RV and MBP. This finding raises the possibility that a virus-induced immune response could lead to an autoaggressive reaction responsible for demyelination.