| Pain is a common syndrome and it brings serious misery to the patients. Sustained pain and hyperalgesia can be evoked when continuous noxious stimulus acts on body, in which condition non-noxious stimulus can induce pain and noxious stimulus can evoke strong feelings of pain. Pain is one kind of somatosensory and the development and maintenance of pain are correlated with the activity of many parts of the central and peripheral nerve systems. Many studies have showed that nociceptive afferences can evoke the sensitization of the correlated peripheral and spinal regions and this will lead to hyperalgesia. But it has not been reported if the noxious stimulus effects on the excitation and transmission of the whole somatosensory pathway. It also remains to be elucidated the effect of sustained pain and hyperalgesia on excitation and transmission of the auditory system.To investigate the effect of sustained pain and hyperalgesia on the somatosensory and auditory brain-stem pathway, the present study was designed to observe changes of somatosensory evoked potentials (SEPs) and brainstem auditory evoked potentials (BAEPs) in sustained pain and hyperalgesic rats induced by formalin using computer averaging technique.1 The change of SEPs in formalin-induced sustained pain and hyperalgesic ratsThe SEPs of 17 Wister rats were recorded in the quiet shielding room. A negative SEP component could be recorded on the C3 region of the calveria of Wister rats when the second and third fingers of the left hand were stimulated by a series of electric pulse. The onset latency, peak latency, and amplitude were 33.30±6.90 ms, 54.00±9.80 ms, 17.28±9.65 μV, respectively. The amplitude of the component increased to 19.79±4.30 μV significantly(p<0.05) 30 min after intraperitoneal injection of alphachloralose. This suggested that the compontent was the main component of the cardinal cortex reaction. The rats exhibited clear pain behavior response such as shaked, trembled frequently and lifted of the injected leg when 5% formalin was injected into the hind paw. Correlative inflammatory reaction appeared after the injection of formalin. The onset and peak latencies shortened, and the amplitude of them hightened with the prolongation of time after injection. The onset latency shortened significantly 5 minutes after the injection (p<0.05), and most of them were shorter than 30 ms. The shortened level became more significant with the prolongation after the injection and it was 14.20±4.71 ms at 60 minute. It showed statistical significant difference between the every time points of onset latency with the injection of formalin. The change in the peak latency is similar to that of onset latency. It shortened with the injection of formalin in 5 minutes but it showed no significant difference. Compared with that before the injection, the shortened level of peak latency became more significant with the duration of the injection of formalin. Peak latency was 46.61±9.47ms at 30 minute and it showed significant difference with that before the injection (p<0.05). The peak latency still showed shortened trend after this time point and became to 40.30±8.46 ms at 60 minute after the injection. It showed significant difference between the every 2 time points. The change of amplitude showed the rising trend after the injection of formalin, but this change was not significant in 10 minutes. It showed significant change at 20 minute and attained to the maximum point at 60 minute. The amplitude 20 minutes after the injection was higher than 30μV and this showed significant difference with normal condition (p<0.05).2 The change of BAEPs in formalin-induced sustained pain and hyperalgesic rats BAEPs of 10 Wister rats were recorded in the quiet shielding room. Seven negative waves were recorded on the calveria of the rats when they were stimulated with tone burst. 60% of wave VI and 48% of wave VII were detected and the other waves were detected all. We recorded and analysed the change of BAEPs at 5,15,30,and 60 minute after the in...
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