| Although spinal cord stimulation (SCS) is currently widely used for treatment of different forms of neuropathic pain, the physiological mechanisms involved are largely unknown. The gradual onset of the effect and the prolonged pain relief following the cessation of stimulation have been interpreted as evidence against a mere conduction block and regarded as indicative of the involvement of long-lasting neurohumoral mechanism.The neurochemical effects of SCS are primarily attribute to antidromic activation of dorsal horn collaterals, but an effect on descending modulation systems by orthodromic activation of supraspinal structures is also implicated. Microdialysis studies in animals indicate that SCS can induce the release of serotonin, substance P, glycine in the spinal cord. However, these studies were conducted in normal animals. Because marked changes of spinal neurotransmitterlevels and function can be detected during the development of neuropathic pain after axonal damage, data obtained in normal animals might not be relevant for the SCS-mediated suppression of neuropathic signs. Thus, the SCS activation effect on descending modulatory system in neuropathic pain status has not been verified.Numerous animal models of peripheral neuropathy have been developed; most of them involve injury to the main trunk of the sciatic nerve. Recently, the SNI model has been reported to yield a very high incidence of robust, long lasting signs of neuropathy, and it has also been used in studies of neuropathic pain mechanisms and for testing of drugs and electrical CNS stimulation. Therefore, we performed a few pilot SCS experiments in this model. However, it appeared that these animals rarely responded with the expected "allodynia" suppression. Since more than 80% of the sciatic nerve fibers have been injured in SNI model, which caused severe allodynia symptom, these may also results in marked neurotransmitters disturbance and central sensitization which maybe more difficult to for the treatment. But, the relationship of SCS effect and the degree of nerve injury has not been well studied.The present study was undertaken with the aim to explore whether variants of the SNI model are more likely to respond to SCS. A further aim was to examine a possible relationship between the extent of nerve lesion, magnitude of allodynia and the effect of SCS. In the variant neuropathic pain model, which is responsive to SCS, will be used to explore of SCS effect on descending modulatory system by spinal cord microdialysis technique.The main results were as follows:2. The general incidence of mechanical allodynia to von Frey filament stimulation was about 60% ( 45-73% ) in all variant models and SNI model. Although there were no statistically significant differences between the groups but there was a tendency that TA and TL produced a somewhat higher incidence of allodynia (68-73%).3. There wee significant different in allodynia lasting time in different models: the allodynia symptom in SNI and TA model persisted until the end of testing (up to 10 weeks); TL model persisted 7 weeks after nerve injury, and some of them up to 10 weeks; PA model was about 6 weeks; but PTL model did not last for more than three weeks (p< 0.05).4. With the exception of the PTL model, all rats that presented with mechanical allodynia also showed marked cold allodynia (grade 3-4). The cold allodynia was present 4-7 days after surgery and lasted from about three (in the PA model) to six weeks (in the SNI, TA and TL models), which was short than tactile allodynia. The correlations between the two forms of hypersensitivity in the SNI, TA, TL and PTL groups were highly significant (PO.0001).5. The incidence of SCS responders in the TA, TL, PTL groups was much higher (42-50%) than SNI model (0.8%) (P<0.05). But there were no statistical difference between these variant SNI modelsAvere all of the same... |
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