Exteroceptive Reflexes to Stimulation of the Sural Nerve in Normal Man

Author(s):  
M. Hugon
NeuroImage ◽  
2007 ◽  
Vol 34 (2) ◽  
pp. 743-763 ◽  
Author(s):  
R. Dowman ◽  
T. Darcey ◽  
H. Barkan ◽  
V. Thadani ◽  
D. Roberts

1985 ◽  
Vol 53 (2) ◽  
pp. 497-517 ◽  
Author(s):  
R. K. Powers ◽  
M. D. Binder

To characterize the oligosynaptic group I afferent input to the cat medial gastrocneumius (MG) motoneuron pool, the medial branch of the tibial nerve (MTIB: flexor digitorum and hallucis longus, popliteus, tibialis posterior and interosseous nerves), the nerves to flexor digitorum and hallucis longus (FDHL), or the nerves to the quadriceps muscles (QUAD) were stimulated at submaximal group I strength while recording intracellularly from MG motoneurons. Since previous work indicates that stimulation of these nerves at group I strength produces no significant monosynaptic Ia excitation or Renshaw inhibition of MG motoneurons, group I effects were assumed to be predominantly, though not exclusively, due to the action of Ib-fibers. Evidence supporting this assumption is presented in the following paper. MTIB, FDHL, and QUAD postsynaptic potentials (PSPs) were most commonly inhibitory. Since the MTIB, FDHL, and QUAD nerves are composed predominantly of fibers innervating muscles with extensor action, their inhibitory effect on MG motoneurons is consistent with previous findings that stimulation of Ib-afferents in nerves to extensor muscles produces di- and trisynaptic inhibition of extensor motoneurons. However, excitatory effects were observed in about one third of the motoneurons, indicating that oligosynaptic group I input is not homogeneously distributed within the MG motoneuron pool. Variations in QUAD, FDHL, and MTIB PSP pattern and amplitude were correlated with variations in the PSP pattern evoked by stimulation of the sural nerve: excitatory oligosynaptic group I PSPs generally appeared in motoneurons receiving excitatory cutaneous (sural nerve) input, whereas inhibitory PSPs generally appeared in motoneurons receiving some inhibitory cutaneous input and were largest in motoneurons receiving predominantly inhibition from the sural nerve. These variations in QUAD, FDHL, and MTIB PSP pattern and amplitude were not due to variations in resting potential and were only partly due to variations in intrinsic motoneuron properties or motoneuron "type." Our results indicate that activation of these cutaneous and group I muscle afferents can exert similar effects on the MG motoneuron pool. Moreover, the presence of a strong correlation between the distributions of cutaneous and oligosynaptic group I PSPs within a single motoneuron pool is consistent with the results of previous studies that have shown that some of the input to motoneurons from these peripheral afferents is mediated through common interneurons.


Acute Pain ◽  
2007 ◽  
Vol 9 (1) ◽  
pp. 47
Author(s):  
R. Dowman ◽  
T. Darcey ◽  
H. Barkan ◽  
V. Thadani ◽  
D. Roberts

1997 ◽  
Vol 87 (4) ◽  
pp. 785-794 ◽  
Author(s):  
Michele Curatolo ◽  
Steen Petersen-Felix ◽  
Lars Arendt-Nielsen ◽  
Alex M. Zbinden

Background It is not known whether epidural epinephrine has an analgesic effect per se. The segmental distribution of clonidine epidural analgesia and its effects on temporal summation and different types of noxious stimuli are unknown. The aim of this study was to clarify these issues. Methods Fifteen healthy volunteers received epidurally (L2-L3 or L3-L4) 20 ml of either epinephrine, 100 microg, in saline; clonidine, 8 microg/kg, in saline; or saline, 0.9%, alone, on three different days in a randomized, double-blind, cross-over fashion. Pain rating after electrical stimulation, pinprick, and cold perception were recorded on the dermatomes S1, L4, L1, T9, T6, T1, and forehead. Pressure pain tolerance threshold was recorded at S1, T6, and ear. Pain thresholds to single and repeated (temporal summation) electrical stimulation of the sural nerve were determined. Results Epinephrine significantly reduced sensitivity to pinprick at L1-L4-S1. Clonidine significantly decreased pain rating after electrical stimulation at L1-L4 and sensitivity to pinprick and cold at L1-L4-S1, increased pressure pain tolerance threshold at S1, and increased thresholds after single and repeated stimulation of the sural nerve. Conclusions Epidural epinephrine and clonidine produce segmental hypoalgesia. Clonidine bolus should be administered at a spinal level corresponding to the painful area. Clonidine inhibits temporal summation elicited by repeated electrical stimulation and may therefore attenuate spinal cord hyperexcitability.


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