| Summary: | 碩士 === 國立臺灣大學 === 動物學研究所 === 100 === Neuropathic pain is triggered by lesions in the somatosensory nervous system. Pain occurs spontaneously and responses to noxious and innocuous stimuli are pathologically amplified. Neural activity in supraspinal centers play an important role in the modulation of pain behavior in neuropathic pain, but the precise mechanism underlying are not fully understood. In this study, we combined behavioural test with positron emission tomography (PET), using 18- fluorode-oxyglucose (18-FDG) as a tracer, to investigate the change of brain glucose metabolic activity in the spared nerve injury (SNI) model of neuropathic pain of the rat. Two major branches of the sciatic nerve were transected under anesthesia condition. After SNI surgery, the rats displayed spontaneous pain behavior, mechanical allodynia and thermal hyperalgesia behavior lasting at least 4 weeks. In PET study of spontaneous paw lifting, glucose metabolic activity in SNI condition was significantly increased in contralateral posterior insular cortex (PIC) compared to pre-surgery control, and significantly increased in septum and paraventricular thalamic nucleus (PVA) compared to sham control. And the glucose metabolic activity of insular cortex correlated linearly with the magnitude of spontaneous paw lifting. In PET study of allodynia, 6 g vonFrey hair was used to stimulus the paw pad of the affected hindlimb. Glucose metabolic activity change in SNI condition was significantly increased in bilateral primary sensory cortex (S1), contralateral secondary sensory cortex (S2), contralateral primary motor cortex (M1), ipsilateral secondary motor cortex (M2), contralateral rostral agranular insular cortex (RAIC)，posterior insular cortex (PIC), hypothalamus, mediodorsal nucleus (MD) of thalamus and cerebellum compared to pre-surgery control. The data suggest that there are many brain areas involved in neuropathic pain, and insular cortex may play an important role in spontaneous pain condition.
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