Appearance of reciprocal facilitation of ankle extensors from ankle flexors in patients with stroke or spinal cord injury.

The purpose of the present study was to investigate the pathophysiological role of reciprocal facilitation between antagonistic motoneuron pools in spasticity. The soleus H-reflex was conditioned by prior stimulation of the peroneal nerve in 15 healthy subjects, six hemiplegic patients and 11 spinal cord injured (SCI) patients. The hemiplegic patients were tested from soon after the onset of hemiplegia and up to 2 years later. Whereas stimulation of the peroneal nerve produced short-latency inhibition of the soleus H-reflex in healthy subjects, it produced facilitation in spastic SCI and hemiplegic patients. This facilitation was demonstrated to have a low threshold compatible with activation of group I afferents and was most likely mediated by an oligosynaptic (reciprocal) excitatory pathway. The facilitation appeared in parallel with the development of hyperactive Achilles tendon reflexes, which was the only clinical finding that could be correlated positively with the facilitation. It is suggested that the appearance of reciprocal excitation plays a role in the pathophysiology of spasticity.

Amplitude of the maximum motor response (Mmax) in human muscles typically decreases during the course of an experiment.

It was shown that the amplitude of the soleus Mmax and Hmax responses decreases in the course of long-lasting H-reflex studies. The peak-to-peak amplitudes of the Mmax and Hmax responses in the soleus muscle (and the Mmax in the tibialis anterior muscle and small hand muscles) were measured repeatedly for 1-3 h in 20 subjects. 3-5 Mmax responses and 5-10 Hmax responses were elicited about every 3 min while the subject was at rest. Decreases in the soleus Mmax response of up to 50.5% (mean 20.5% SEM 2.2) and of the soleus Hmax of up to 49.7% (mean 19.1% SEM 3.7) in relation to the amplitudes measured at the beginning of the experiment were seen in 17 subjects. In 3 subjects no Mmax amplitude decrease was seen. The maximum decrease was reached between 10 and 100 min (mean 44.2 min SEM 4.3). An Mmax amplitude decrease was also seen in the tibialis anterior muscle and in two small hand muscles. In some subjects the decrease of the Mmax response seemed to be initiated by the infrequent supramaximal stimulations. The possible causes for this amplitude reduction, as well as the methodological consequences of these findings for H-reflex studies and fatigue studies, are briefly discussed.