Antiepileptic drugs (AEDs) have measurable effects on neuronal membran
e and synaptic function. These mechanisms of action partially predict
effectiveness in animal models of epilepsy and in human epilepsy. Carb
amazepine, phenytoin, lamotrigine, oxcarbazepine and valproic acid (so
dium valproate) block voltage-dependent sodium channels. Ethosuximide
reduces T-type calcium currents. Phenobarbital (phenobarbitone), benzo
diazepines, gabapentin, vigabatrin, tiagabine, valproic acid and felba
mate enhance the neuronal inhibition induced by gamma-aminobutyric aci
d (GABA). Felbamate also decreases the activity of excitatory neurotra
nsmitters. AEDs with known mechanisms of action will further increase
the range of options for patients with epilepsy. A rational approach t
o 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 considerat
ion given to mechanisms of action, will enable the large majority of p
atients with epilepsy to achieve the best possible control of their se
izures within the limits of current therapy.