Abstract
To review the pharmacology, pharmacokinetics, efficacy, and safety of rufinamide in the treatment of epileptic seizures and describe its potential place in therapy. MEDLINE (1966-January 2010) and PubMed (1966-January 2010) literature searches were conducted to identify primary literature investigating rufinamide. References from selected publications discussing rufinamide, as well as the package insert, were reviewed. Published controlled trials describing the efficacy and safety of rufinamide were given preference. Available abstracts were also reviewed. Four published trials were identified and included and a retrospective review of the clinical use of rufinamide was also analyzed. The remainder of the information described is from 4 abstracts. Rufinamide is a new antiepileptic agent that differs structurally from other antiepileptic drugs and is approved as adjunctive therapy for Lennox-Gastaut syndrome (LGS). It presumably provides its antiseizure activity by prolonging sodium channel inactivity, stabilizing cell membranes. It is absorbed and metabolized extensively, then excreted renally as an inactive metabolite. Clinical trials show that adjunctive rufinamide is effective at reducing seizure frequency in patients with LGS and refractory partial seizures. Rufinamide showed no effect on cognitive function in patients with refractory partial seizures. Short-term adverse event rates were similar to those of placebo. Safety data from long-term studies show that rufinamide is well tolerated, causing headache, dizziness, and fatigue at rates of >10%. Rufinamide has few clinically relevant drug interactions, although it does increase phenytoin serum concentrations, while valproate increases rufinamide serum concentrations. Data show that rufinamide is safe and effective as an adjunctive agent for LGS and may be used to treat partial seizures. The benefits of rufinamide include its pharmacokinetics, limited drug interactions, and lack of effect on cognitive function, but its use is limited by the rarity of LGS and the lack of comparative data with other antiepileptic agents.
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