Abstract: Objective To study the changes of mechanical allodynia and temperature hyperalgesia, as well as the expression of the spinal macrophage colony stimulating factor (M-CSF) and its receptor CSF-1R during the development of complicated regional pain symptomⅠ(CRPSⅠ). Methods The animal model of CRPSⅠ was established using prolonged ischemia-reperfusion injury of rodent left hindpaw. The mechanical allodynia and temperature hyperalgesia of ipsilateral hindpaw were continuously measured for 14 d after reperfusion, and the expressions of spinal M-CSF and CSF-1R in ipsilateral spinal cord horn were measured with immunofluorescence technique on day 3, day 7 and day 14 after reperfusion. Results The thresholds of mechanical allodynia and temperature hyperalgesia of ipsilateral hindpaw were significantly decreased (P<0.05). M-CSF was secreted by the astrocytes. CSF-1R was primarily distributed on the microglia. The immunofluorescence intensities of M-CSF and CSF-1R in ipsilateral spinal cord horn were significantly increased on day 7 and day 14 after reperfusion (P<0.05). Conclusion The ischemia-reperfusion injury simulated pain syndrome in CRPSⅠand increased the expressions of spinal M-CSF and CSF-1R.