Lamotrigine, a sodium channel blocker that selectively inhibits the neuronal release of glutamate, has been shown to produce analgesia in acute and chronic pain models in rats without causing noticeable sedation. After oral administration it also reduces pain scores, as assessed by the cold pain test, in volunteers. The purpose of this study was to determine the analgesic effect of lamotrigine given by mouth to healthy volunteers as evidenced by alterations in chemoβsomatosensory evoked potentials. The following factors were measured: latency to N~1~ and P~100~ peak (ms); amplitude between the N~1~ and P~100~ peak (ΞΌV); visual analogue pain intensity scores. A doubleβblind, randomised and crossover design was used in which 12 volunteers received either placebo or lamotrigine 300βmg on separate occasions as determined by the randomisation schedule. Volunteers were tested before and 2βh after the treatment. The plasma lamotrigine concentration was measured immediately after the end of the experimental sessions. Lamotrigine produced a significantly higher latency to P~100~ values at 2βh postdrug than placebo (pβ<β0.05) but had no significant effects on the other factors. Although plasma concentrations were similar to those observed in the cold pain test, we conclude that lamotrigine 300βmg by mouth had no analgesic effect in this acute pain model.