| Central post-stroke pain(central post-stroke pain,CPSP)is an intractable neuropathic pain syndrome that occurs after ischemic or hemorrhagic stroke and seriously affects the patients’ life quality.So far,the pathogenesis of CPSP is not fully understood,and the clinical treatment of CPSP has not achieved good results.Our previous study found that thalamic MD and VM nuclei may act as mechanical and thermal ‘nociceptive discriminators’ in precisely distinguishing the incoming noxious information per se,and in turn generating the descending facilitatory and inhibitory activities,respectively.Studies showed that sympathetic nerve system(sympathetic nerve system,SNS)was involved in regulation of acute and chronic pain,and sympathetic nerve block can relieve chronic and intactable pain.In this study,paw withdrawal reflexes induced by mechanical and heat stimulation were observed,changes in endogenous descending modulation on pain were explored in thalamic hemorrhage model rats.Effects of stellate/superior cervical ganglion block on central pain after hemorrhagic stroke were observed.This study intends to provide a new idea and therapeutic target for the treatment of clinical CPSP patients.Purposes:1.To establish a model of hemorrhagic stroke in rats,and explore the changes in endonenous descending modulation of pain after thalamic hemorrhagic stroke in rats2.To explore the effects of stellate/superior cervical ganglion block 4 hours after cerebral hemorrhage on CPSP in a rat model of thalamic hemorrhage.3.To explore the effects of stellate/superior cervical ganglion block 7 days after cerebral hemorrhage on CPSP in a rat model of thalamic hemorrhage.Methods:1.Establishment of a model of hemorrhagic stroke in rats10μl,20μl and 30μl of autologous blood was unilaterally injectied into thalamic MD nucleus in female SD rats.2.Stellate/superior cervical ganglion block0.2ml of 2% lidocaine was injected into the superior cervical/stellate ganglion.Observed indicators:1.Paw withdrawal mechanical threshold and paw withdrawal thermal latency of bilateral hind limbs were observed 1-4 hours and 1-14 days after hemorrhagic stroke modeling.2.4 hours or 7 days after injection of 30 μl autologous blood into thalamic MD nucleus,blockage of stellate or superior cervical ganglia was performed,bilateral paw withdrawal mechanical threshold and paw withdrawal thermal latency were observed before,1-4 hours and 1-7 days after sympathetic ganglia block.Experimental results:1.In rats with 10μl and 20μl autologous blood injection,bilateral mechanical hyperalgesia was found 10-12 days and 10-13 days respectively after modeling(P <0.05).In rats with 30μl autologous blood injection,bilateral mechanical hyperalgesia was found 1 hour after modeling and lated for 14 days(P < 0.001).No significant changes in paw withdrawal thermal latency were found in all groups2.In rats with 30μl autologous blood injection,stellate/superior cervical ganglion blockage was applyed 4 hours after modeling.Increased bilateral paw withdrawal mechanical thresholds were found 1 hour after the blockage and lasted for 7 days(P <0.001),paw withdrawal mechanical thresholds were significantly higher in rats 2hours to 6 days after superior cervical ganglion blockage than that of the stellate ganglion blockage(P < 0.05).Bilateral paw withdrawal thermal latency in both groups began to rise 1 hour after treatment and lasted for 7 days,paw withdrawal thermal latencies were significantly higher in rats 1-4 days after superior cervical ganglion blockage than that of the stellate ganglion blockage(P < 0.05).3.In rats treated by a bolus of 30μl autologous blood injection,stellate/superior cervical ganglion blockage was applyed 7 days after the modeling.Increased bilateral paw withdrawal mechanical thresholds in both groups were found 1 hour after the block and lasted for 7 days(P < 0.001),paw withdrawal mechanical thresholds were significantly higher in rats with superior cervical ganglion blockage than that of the stellate ganglion blockage 1 to 2 days after blockage(P < 0.05).Increased bilateral paw withdrawal thermal latency in both groups were found 1 hour after blokage and lasted for 3 days(P < 0.05).Conclusions:1.A stable hemorrhagic post-stroke central pain model(CPSP model)can be successfully induced by microinjection of autologous blood into the thalamic MD nucleus,endogenous descending facilitation enhanced in thalamic hemorrhage model rats.2.The effect of superior cervical ganglion blockage on CPSP is better than that of stellate ganglion blockage,and early treatment after stroke is more effective.3.The enhanced endogenous descending facilitation in thalamic hemorrhage model rats is closely related to hyperactivity of sympathetic nervous system. |
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