Carbamazepine is the drug of first choice in the treatment of simple and complex partial seizures and trigeminal and glossopharyngeal neuralgias. It is usually preferred to phenobarbitone or phenytoin because of its powerful antiepileptic activity combined with a relative lack of adverse effects. In this article the mechanisms of action and pharmacological properties of carbamazepine are outlined in order to explain the pathogenesis of most side and toxic effects. Most of these effects, namely those affecting the nervous or cardiovascular systems, correlate well with an increased concentration of the drug in plasma and disappear spontaneously upon discontinuation of therapy. Other, less frequent toxic effects, namely aplastic anaemia or fatal hepatitis, may be ascribed to unforeseeable idiosyncratic reactions. Carbamazepine poisoning, usually accidental and sometimes secondary to the coadministration of other drugs, yields a clinical picture with neurological and cardiovascular signs. The outcome is usually favourable, sometimes with spontaneous improvement, and death is a distinct rarity. No specific antidotes are available. The oral administration of activated charcoal has been shown to be an effective therapeutic measure significantly reducing the plasma half-life of the drug.