Pain is an unpleasant sensory experience which involves detection of potential or actual harms to functional integrity of the organism, and transmission of these neuronal signals to central nervous system and perception with relation to experience, and thereby significantly contributes to homeostasis. WAG/Rij rats are established absence epilepsy animal model in which age-dependent absence epilepsy develops. The aim of this study was to assess possible effect of LEV on pain sensitivity in WAG/Rij rats. The effects of levetiracetam were evaluated in adult WAG/Rij epileptic rats (male, 250-350g, n=11) by “thermal plantar (heat-induced)” test. Different doses of LEV (60 mg/kg and 120 mg/kg, both i.p.) were tested in the same group of rats by 1 week apart. Effect on acute pain was evaluated at interictal period (confirmed by simultaneous electroencephalography through epiduraly implanted electrodes) at 10, 30 and 60 minutes after LEV administration and pain threshold responses were compared to their basal pain threshold values. The determined pain threshold values were analyzed by Friedman repeated measures analysis of variances (ANOVA) followed by a pair wise comparison using a Conover test on the ranked data. P<0.05 value was accepted statistically significant. The protocol of this study was approved by the local Ethic Committee. Administration of LEV caused dose-dependent increase in pain sensitivity in thermal plantar test. Low dose of (60 mg/kg) LEV did not cause any significant change in thermal stimulated pain latencies which was 3±1.0 sec before and 2.5±0.5 sec, 2.4±0.6 sec and 2.3±0.9 sec 10, 30 and 60 minutes after 60 mg/kg LEV (p>0.05 for all) (n=11, p>0.05 for all) administration. 120 mg/kg LEV significantly reduced thermal stimulated pain latencies which were 2.9±0.6 sec before and 2.1±0.4 sec (p<0.05), 2±0.4 sec (p<0.05), 30 and 60 minutes after (n=11 for all). Results from this study demonstrate that LEV caused a pro-algesic effect in these epileptic rats. This is contradictory to effects of LEV on healthy rats and we have no clear evidence for underlying mechanism for this proalgesic effect. It was evident that the higher dose used (120 mg/kg) caused a significant decrease in seizures the WAG Rij experienced, and the cessation of seizures by LEV might have caused alteration in endogenous pain modulation in these animals and proalgesia was resulted.