Table 1: Antiepileptic drugs grouped by their main mechanism of action.

Phenytoin, Carbamazepine Block voltage-dependent sodium channels at high firing frequencies
Barbiturates Prolong GABA-mediated chloride channel openings
Some blockade of voltage-dependent sodium channels
Benzodiazepines Increase frequency of GABA-mediated chloride channel openings
Felbamate May block voltage-dependent sodium channels at high firing frequencies
May modulate NMDA receptor via strychnine-insensitive glycine receptor
Gabapentin Increases neuronal GABA concentration
Enhances GABA mediated inhibition
Topiramate
               • Blocks voltage-dependent sodium channels at high firing frequencies
               • Increases frequency at which GABA opens Cl- channels (different site than benzodiazepines)
               • Antagonizes glutamate action at AMPA/kainate receptor subtype
               • Inhibition of carbonic anydrase
Lamotrigine Blocks voltage-dependent sodium channels at high firing frequencies
May interfere with pathologic glutamate release
Ethosuximide Blocks low threshold, “transient” (T-type) calcium channels in thalamic neurons
Valproate May enhance GABA transmission in specific circuits
Blocks voltage-dependent sodium channels
Vigabatrin Irreversibly inhibits GABA-transaminase
Tiagabine Interferes with GABA re-uptake
Levetiracetam

Binding of reversible saturable specific binding site
Reduces high-voltsge- activated Ca2+ currents
Reverses inhibition of GABA and glycine gated currents induced by negative allosteric modulators
Oxcarbazepine Blocks voltage-dependent sodium channels at high firing frequencies
Exerts effect on K+ channels
Zonisamide
Blocks voltage-dependent sodium channels and
T-type calcium channels