TIAGABINE

Tiagabine inhibits gamma-aminobutyric acid uptake into neurons and gli a. This mechanism of action is specific and unique among the antiepile ptic drugs (AEDs). Tiagabine is efficacious in animal seizure models a t subtoxic doses. There is no evidence of clinically important teratog enicity, carcinogenicity or mutagenicity in animals treated acutely or chronically with tiagabine. Tiagabine has no clinically relevant effe ct on hepatic metabolism or serum levels of other AEDs, has no clinica lly significant effects on laboratory values and has not been shown to have any clinically important interactions with common non-AEDs. Tiag abine has linear, predictable pharmacokinetics that do not vary signif icantly with age. Adverse effects are usually mild to moderate in seve rity and almost always resolve without medical intervention. The most common adverse events in controlled studies are dizziness, asthenia, s omnolence, accidental injury, infection, headache, nausea and nervousn ess. Tiagabine is effective as add-on therapy for partial seizures in patients with medically refractory epilepsy in doses ranging from 32-5 6 mg daily. Despite its short half-life of 2-3 hours in patients on en zyme-inducing AEDs, tiagabine is effective when dosed 2-3 times a day Conversion to tiagabine monotherapy can be achieved in patients with m edically refractory epilepsy, though additional studies are needed to establish the effective dosage range. The introduction of drugs like t iagabine that have known mechanisms of action which differ from existi ng treatments further increases the range of options for patients with epilepsy.