Disynaptic Ia Reciprocal Inhibition in Stroke Patients before and after Therapeutic Electrical Stimulation

• Published in: Rihabiritēshon igaku Vol. 37; no. 7; pp. 453 - 458
• Main Authors: FUJIWARA, Toshiyuki, MURAOKA, Yoshihiro, MASAKADO, Yoshihisa, TOMITA, Yutaka
• Format: Journal Article
• Language: English
• Published: The Japanese Association of Rehabilitation Medicine 2000
• Subjects: H-wave; reciprocal inhibition; spasticity; stroke; therapeutic electrical stimulation
• ISSN: 0034-351X; 1880-778X
• DOI: 10.2490/jjrm1963.37.453

We studied disynaptic Ia reciprocal inhibition between the soleus muscle and the tibialis anterior (TA) muscle before and after therapeutic electrical stimulation (TES) to the TA muscle with surface electrodes in fifteen stroke hemiplegic patients. The stimulation parameters were held at fixed values as follows: frequency at 20Hz, monophasic rectangular waveform, pulse width at 0.3ms, and full contraction intensity. A 5-second stimulation followed by 15-second rest was repeated for 15min. The amount of disynaptic Ia reciprocal inhibition was determined by the short latency suppression of the soleus or TA muscle H waves by conditioning stimulation of the antagonistic muscle nerves. Disynaptic Ia reciprocal inhibition from the peroneal nerve afferents to the soleus muscle was significantly increased after TES in 6 hemiplegic patients. On the other hand, the disynaptic Ia inhibition of the TA muscle by group Ia volleys from the tibial nerve was decreased in all subjects of 3 patients in whom H waves were detected in the TA muscle. TES might change transmission efficiency of two synapses originated from disynaptic Ia inhibitory interneurons of the TA muscle: one was the synapse to α-motoneuron of the soleus muscle and the other was the synapse to Ia inhibitory interneurons of the soleus muscle. We suggested that the facilitation of voluntary contraction in the agonist muscle and the reduction of the spasticity in the antagonist muscle by TES might result from enhancement of the synaptic transmission efficiency in reciprocal Ia inhibitory pathways.