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A comparative study of the effects of carbamazepine and the NMDA receptor antagonist remacemide on road tracking and car-following performance in actual traffic

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Abstract

Rationale: Antiepileptic drugs are known to produce side effects which may impair driving performance. Performance effects, however, may differ substantially between individual antiepileptic drugs. Objective: To compare the effects of carbamazepine, remacemide, and placebo on actual driving performance during a 12-day incremental dosing regimen. Methods: Twenty-two healthy volunteers participated in a three-way, double-blind, cross-over driving study. Treatment effects were assessed in two actual driving tests carried out on days 8, 10, and 12 of each treatment period. The Road Tracking Test involved driving an instrumented vehicle at a constant speed and steady lateral position between the delineated lane boundaries. Standard deviation of lateral position (SDLP) was measured to indicate precision of road tracking control. The Car-Following Test involved driving the same vehicle behind a leading car and maintaining that distance while the latter executed a series of deceleration/acceleration maneuvers. Time to speed adaptation (TSA) and brake reaction time were the primary measures. Results: Remacemide did not affect the subjects' driving performance. Carbamazepine increased SDLP throughout treatment and lengthened TSA on day 8. Changes in SDLP relative to placebo were comparable to those previously seen in drivers conducting the same test with blood alcohol concentrations of 0.05 g/dl. Conclusion: Remacemide, at the given dose regimen, does not affect driving performance. Carbamazepine, at the given dose regimen, can produce mild but sufficient impairment to put epileptic patients at risk when driving, at least during initiation therapy.

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Ramaekers, J., Lamers, C., Verhey, F. et al. A comparative study of the effects of carbamazepine and the NMDA receptor antagonist remacemide on road tracking and car-following performance in actual traffic. Psychopharmacology 159, 203–210 (2002). https://doi.org/10.1007/s002130100898

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  • DOI: https://doi.org/10.1007/s002130100898

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