Neuroprotection: A new therapeutic option in the treatment of epilepsy?

The primary aim in treating patients with epilepsy is the suppression of se izures. Apart from this symptomatic treatment so far no pharmacological app roach exists to alter the natural course of the disease ("disease modificat ion"). There is clinical, as well as pre-clinical evidence that neuronal da mage and an impairment of cognitive function frequently occurs during the c ourse of epilepsy. It seems logical to investigate the feasibility of new t herapeutic approaches in which neuroprotection plays a major role. The prev ention of neuronal damage induced either by the pathophysiological cellular alterations generated by the disease itself, by repetetive seizures, or a status epilepticus is of major interest. Unfortunately so far data concerni ng the neuroprotective potential of anticonvulsive drugs is only available in preclinical studies. The four basic mechanisms by which neuronal damage usually occurs are (1) increased Na+-influx, (2) increased Ca2+-influx, (3) diminished GABA-ergic activity and (4) increased glutamatergic excitotoxic ity through massive stimulation of ionotropic Glutamat-receptors (especiall y non-NMDA-receptors). This review reflects the current literature regardin g the protective effects of anticonvulsive drugs.