Epilepsy is one of the most prevalent neurological syndromes in the world today. 
Epilepsy describes a group of brain disorders whose symptoms and causes are 
diverse and complicated, but all share a common behavioural manifestation: the 
seizure. Seizures result from the abnormal discharge of groups of neurons within 
the brain, usually within a focal point, that can result in the recruitment of 
large brain regions into epileptiform activity. Although the range of 
explanations for the development of seizures can be as varied as genetic 
composition to acute head trauma, the net result is often similar. The 
excitability of neurons is governed by the input they receive from their 
neighbours and the intrinsic excitability of the neuron. In this review we focus 
on elements that are crucial to determining the intrinsic excitability of 
neurons in the CNS, the voltage gated ion channels (VGICs). VGICs as well as 
being important for physiological function are critical in producing 
hyperexcitability such as that associated with seizure discharges. Many drugs 
routinely used in the clinical setting, as well as several novel experimental 
drugs, have shown interactions with VGICs that underpin, at least in part, their 
anticonvulsant action. We review the physiological roles of voltage gated ion 
channels that are selective for sodium, potassium and calcium conductance and 
attempt to highlight their role in the pathology of epilepsy. This is 
supplemented by the mechanisms of drug action at these important anticonvulsant 
targets for classical and clinically relevant compounds (e.g. phenytoin, 
ethosuximide) as well as some important second generation drugs (e.g. 
gabapentin, levetiracetam) and novel experimental agents (e.g. retigabine, 
losigamone, safinamide). We also briefly discuss the urgent need for new drugs 
in this arena and the potential of combinatorial methods and recombinant 
screening to identify leads.