Premium
Effects of lamotrigine on pain‐induced chemo‐somatosensory evoked potentials
Author(s) -
Klamt J. G.,
Posner J.
Publication year - 1999
Publication title -
anaesthesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.839
H-Index - 117
eISSN - 1365-2044
pISSN - 0003-2409
DOI - 10.1046/j.1365-2044.1999.00959.x
Subject(s) - lamotrigine , medicine , anesthesia , placebo , analgesic , crossover study , anticonvulsant , sodium channel blocker , pharmacology , epilepsy , sodium channel , sodium , chemistry , alternative medicine , pathology , psychiatry , organic chemistry
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 chemo‐somatosensory 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 (μV); visual analogue pain intensity scores. A double‐blind, randomised and crossover design was used in which 12 volunteers received either placebo or lamotrigine 300 mg on separate occasions as determined by the randomisation schedule. Volunteers were tested before and 2 h 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 2 h postdrug than placebo (p < 0.05) 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 300 mg by mouth had no analgesic effect in this acute pain model.