Antiepileptic drugs (AEDs) have measurable effects on neuronal membrane and synaptic function. These mechanisms of action partially predict effectiveness in animal models of epilepsy and in human epilepsy. Carbamazepine, phenytoin, lamotrigine, oxcarbazepine and valproic acid (sodium valproate) block voltagedependent sodium channels. Ethosuximide reduces T-type calcium currents. Phenobarbital (phenobarbitone), benzodiazepines, gabapentin, vigabatrin, tiagabine, valproic acid and felbamate enhance the neuronal inhibition induced by &ggr;-aminobutyric acid (GABA). Felbamate also decreases the activity of excitatory neurotransmitters.AEDs with known mechanisms of action will further increase the range of options for patients with epilepsy. A rational approach to polytherapy may emerge in the near future, in which medications with complementary, synergistic mechanisms of action are used. Until then, cautious use of medications alone and in combination, with consideration given to mechanisms of action, will enable the large majority of patients with epilepsy to achieve the best possible control of their seizures within the limits of current therapy.