Medium-latency reflex response of soleus elicited by peroneal nerve stimulation

UYSAL H., Larsson L., Efendi H., Burke D., Ertekin C.

EXPERIMENTAL BRAIN RESEARCH, vol.193, no.2, pp.275-286, 2009 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 193 Issue: 2
  • Publication Date: 2009
  • Doi Number: 10.1007/s00221-008-1621-4
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.275-286
  • Kocaeli University Affiliated: No


A medium-latency response (MLR) has been recorded from soleus during stance and walking, and has been attributed to stretch-evoked volleys in group II afferents. The present paper describes a MLR in soleus evoked by stimulating the deep peroneal nerve, documents its characteristics and addresses its likely origin. The MLR of soleus was recorded in healthy subjects and hemiplegic patients, following electrical stimulation of the deep peroneal nerve at the fibula at rest, during voluntary dorsiflexion, during plantar flexion, during external restraint to the ankle dorsiflexion movement, during limb cooling, during limb ischaemia and 1 h after the ingestion of tizanidine. The dorsiflexion movement of the foot was measured using an accelerometer. During cooling, ischaemia and after tizanidine, changes in the MLR were compared with changes in the soleus H reflex, Achilles tendon reflex and, during cooling, F waves of abductor hallucis. The MLR was facilitated by voluntary dorsiflexion, was suppressed during plantar flexion, disappeared when ankle movement was prevented, and was enhanced in patients with spastic hemiplegia. Cooling delayed the MLR significantly more than the Achilles tendon reflex and the abductor hallucis F wave. During ischaemia the response was significantly less affected than the Achilles tendon reflex and the soleus H reflex. Tizanidine suppressed the MLR, but not the soleus H and tendon reflexes. The latencies and the experiments using cooling, ischaemia and tizanidine implicate soleus group II afferents in the genesis of this response.