Unstable pain in the oral and maxillofacial region has often been treated with imipramine, a tricyclic antidepressant. Trigeminal neuralgia has been treated with carbamazepine. Although these drugs have been effective in a number of cases, their mechanism of analgesic effect has not been thoroughly clarified. In the present study, visual analogue pain scale (VAS) was used to evaluate subjective pain. To evaluate objective pain, the somatosensory evoked potential (SEP) of the cerebral evoked

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... ntial (CEP), which was induced by electric dental stimulation, was enployed. In this way, the analgesic effect of the study drugs was analyzed. Moreover, to study the effect of drugs on the CNS and information processing, auditory evoked potential was assessed by the right-left discriminatory response task. Event related potential (ERP) representing the wave of target stimuli was studied. Reaction time (RT) was also determined stimultaneously with SEP and ERP. For comparison, diclofenac sodium (an analgesic) and placebo were similarly evaluated. In the SEP wave, peak latency of the late component was prolonged by the administration of imipramine and carbamazepine. The N2-P2 amplitude involved in algesthesia was reduced by the administration of imipramine (p <0. 05), carbamazepine (p <0. 025), and diclofenac sodium (p <0. 01). Values determined with the VAS declined after the administration of imipramine, carbamazepine (for both, p <0. 01) and diclofenac sodium (p <0. 05). In the ERP wave, P3-peak latency alone was prolonged by the administration of imipramine and carbamazepine (p <0. 05). N2-P3 amplitude was reduced by imipramine (p <0. 05) and carbamazepine (p <0. 001). No significant change was seen after administering placebo, and no significant difference in the mode of ERP was observed after the administration of diclofenac sodium. The results of this study of CEP suggest that imipramine and carbamazepine suppress the high CNS, secondarily inducing an analgesic effect.