The aim of the study was to investigate whether impaired inhibition decreased in the healthy subjects, but because only weak inhibition was observed at rest in the patients control of transmission in spinal inhibitory pathways contributes to the functional disability of patients with it was not possible to determine whether a similar decrease occurred in this group. There were no differences in the spasticity. To this end, transmission in the pathways mediating disynaptic reciprocal Ia inhibition and modulation of inhibition during tonic plantar flexion and dorsiflexion in the two populations. Presynaptic inhibition presynaptic inhibition was investigated in 23 healthy subjects and 20 patients with spastic multiple sclerosis of Ia afferents terminating on soleus motor neurones was evaluated from the monosynaptic Ia facilitation of the during ankle dorsiflexion and plantar flexion. In healthy subjects, but not in spastic patients, the soleus H reflex soleus H reflex evoked by femoral nerve stimulation. Femoral nerve facilitation was decreased at the onset of was depressed at the onset of dorsiflexion (300 ms rise time, 20% of maximal voluntary effort). At the onset of dorsiflexion and increased at the onset of plantar flexion in the healthy subjects and patients, but the changes were plantar flexion, the soleus H reflex was more facilitated in the healthy subjects than in the patients. The H reflex significantly greater in the healthy subjects. There was no difference between the two populations in the increased more with increasing level of tonic plantar flexion and decreased more with dorsiflexion in the healthy modulation of presynaptic inhibition during tonic plantar flexion and dorsiflexion. It is suggested that the abnormal subjects than in the spastic patients. Transmission in the disynaptic Ia reciprocal inhibitory pathway from ankle regulation of disynaptic reciprocal inhibition and presynaptic inhibition in patients with spasticity is dorsiflexors to plantar flexors was investigated by con-ditioning the soleus H reflex by previous stimulation of responsible for the abnormal modulation of stretch reflexes in relation to voluntary movement in these the common peroneal nerve (conditioning-test interval 2– 3 ms; stimulation intensity 1.05 times the motor response patients. Lack of an increase in reciprocal inhibition and presynaptic inhibition at the onset of dorsiflexion may be threshold). At the onset of dorsiflexion, stimulation of the common peroneal nerve evoked a significantly larger responsible for the tendency to elicitation of unwanted stretch reflex activity and co-contraction of antagonistic inhibition than at rest in the healthy subjects but not in the spastic patients. At the onset of plantar flexion the muscles in patients with spasticity.
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