BEHAVIORAL PAIN-RELATED DISORDERS AND CONTRIBUTION OF THE SAPHENOUS NERVE IN CRUSH AND CHRONIC CONSTRICTION INJURY OF THE RAT SCIATIC-NERVE

Citation
N. Attal et al., BEHAVIORAL PAIN-RELATED DISORDERS AND CONTRIBUTION OF THE SAPHENOUS NERVE IN CRUSH AND CHRONIC CONSTRICTION INJURY OF THE RAT SCIATIC-NERVE, Pain, 59(2), 1994, pp. 301-312
Citations number
41
Categorie Soggetti
Neurosciences
Journal title
PainACNP
ISSN journal
03043959
Volume
59
Issue
2
Year of publication
1994
Pages
301 - 312
Database
ISI
SICI code
0304-3959(1994)59:2<301:BPDACO>2.0.ZU;2-6
Abstract
This study evaluated the pain-related behaviours induced by 2 models o f peripheral sciatic nerve injuries in the rat: transient nerve crush and chronic constriction injury (CCI). Various lesions of the saphenou s nerve were performed in order to investigate the role of saphenous i nnervation in behavioural disorders induced by these nerve injuries. B ehavioural testing included assessment of responses to phasic stimulat ion (mechanical and thermal) and observation of 'spontaneous' pain-rel ated behaviour. Results confirmed that the model of CCI induces marked and prolonged phasic and spontaneous pain-related disorders (up to we ek 7). Rats with crush injury exhibited moderate and transient hyperal gesia and allodynia to mechanical and thermal stimulation on the lesio ned side (with a maximum at day 3 and a recovery by week 1). Section p lus ligation of the ipsilateral saphenous nerve on the day of surgery prevented nociceptive behaviours and induced persistent mechanical and thermal anaesthesia or hypoesthesia of the lesioned paw in both model s (lasting up to 3-4 weeks). Section without ligation of the saphenous nerve induced comparable results in rats with sciatic crush, but did not Significantly modify nociceptive behaviours in rats with CCI. Thes e data emphasise the role of adjacent saphenous nerve in the mechanism s of pain-related disorders induced by these peripheral nerve lesions. On the contralateral paw, pain-related modifications were also observ ed in both models, suggesting that unilateral nerve lesions induce rem ote modifications extending beyond the site of the injured nerve.