Epilepsy is one of the most wide spread and serious paroxysmal disorders as well as 30% cases of resistant epilepsy. Topiramate (TPM) is one of many drugs of the second generation. Topiramate, a sulfonatesubstituted derivative of the monosacharide D-fructose, has been associated with a broad spectrum of antiepileptic activity. The precise mechanism of TPM is unknown, is considered that TPM produce antiepileptic effects through enhancement of GABA-erge activity, inhibition of kainate/AMAP glutamate receptors, inhibition of voltage- sensitivite sodium and calcium channel, increases in potasium conductance and inhibition of carbonic anhydrase. Oral TPM is rapidly absorbed in patients with epilepsy with a relative bioavailability of near 80%. In many clinical trials, appeareddosages (i.e. 200 mg b.d.) of topiramate as monotherapy or adjunctive therapy were effective in reducing the frequency of seizures in patients with primary generalised tonic-clonic seizures, partial seizures. The cost-utility analysis included direct medical and social services cost in the UK, TPM was predicted to be cost-effective relative to standard treatment with valproic acid in adults with generalised or unclassified epilepsy cross a range of thresholds for the cost per quality-adjusted life-year (QALY) gained as was preferred over lamotrigine. However, in adults with partial epilepsy, lamotrigine appeared to be cost-effective relative to standard treatment with carbamazepine over gabapentin and topiramate. Treatment with topiramate is commonly associated with adverse events, among others especially with weight-loss and cognitive dysfunction. The carbonic anhydrase inhibitory effects of TPM may result in metabolic acidosis, renal calculi and hypohidrosis.

epilepsy, topiramate, pharmacokinetic properties, therapeutic efficacy, adverse events