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The Journal of Neurophysiology Vol. 87 No. 4 April 2002, pp. 1763-1771
Copyright ©2002 by the American Physiological Society
Department of Cell Biology, Physiology and Immunology, Universitat Autònoma de Barcelona, E-08193 Bellaterra, Spain
Valero-Cabré, Antoni and
Xavier Navarro.
Changes in Crossed Spinal Reflexes After Peripheral Nerve
Injury and Repair. J. Neurophysiol. 87: 1763-1771, 2002. We investigated the changes induced in crossed extensor
reflex responses after peripheral nerve injury and repair in the rat. Adults rats were submitted to non repaired sciatic nerve crush (CRH,
n = 9), section repaired by either aligned epineurial
suture (CS, n = 11) or silicone tube (SIL4,
n = 13), and 8 mm resection repaired by tubulization
(SIL8, n = 12). To assess reinnervation, the sciatic
nerve was stimulated proximal to the injury site, and the evoked
compound muscle action potential (M and H waves) from tibialis anterior
and plantar muscles and nerve action potential (CNAP) from the tibial
nerve and the 4th digital nerve were recorded at monthly intervals for
3 mo postoperation. Nociceptive reinnervation to the hindpaw was also
assessed by plantar algesimetry. Crossed extensor reflexes were evoked
by stimulation of the tibial nerve at the ankle and recorded from the
contralateral tibialis anterior muscle. Reinnervation of the hindpaw
increased progressively with time during the 3 mo after lesion. The
degree of muscle and sensory target reinnervation was dependent on the
severity of the injury and the nerve gap created. The crossed extensor
reflex consisted of three bursts of activity (C1, C2, and C3) of
gradually longer latency, lower amplitude, and higher threshold in
control rats. During follow-up after sciatic nerve injury, all animals
in the operated groups showed recovery of components C1 and C2 and of the reflex H wave, whereas component C3 was detected in a significantly lower proportion of animals in groups with tube repair. The maximal amplitude of components C1 and C2 recovered to values higher than preoperative values, reaching final levels between 150 and 245% at the
end of the follow-up in groups CRH, CS, and SIL4. When reflex amplitude
was normalized by the CNAP amplitude of the regenerated tibial nerve,
components C1 (300-400%) and C2 (150-350%) showed highly increased
responses, while C3 was similar to baseline levels. In conclusion,
reflexes mediated by myelinated sensory afferents showed, after nerve
injuries, a higher degree of facilitation than those mediated by
unmyelinated fibers. These changes tended to decline toward baseline
values with progressive reinnervation but still remained significant 3 mo after injury.
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