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Tiagabine in the Management of Epilepsy
Author(s) -
Brodie Martin J.
Publication year - 1997
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1997.tb04528.x
Subject(s) - tiagabine , epilepsy , adverse effect , medicine , anticonvulsant , somnolence , pharmacology , anesthesia , vigabatrin , central nervous system , psychiatry
Summary: Tiagabine (TGB) is a new antiepileptic drug (AED) that uniquely reduces the uptake of the inhibitory neurotransmitter ‐γ‐aminobutyric acid into presynaptic neuronal and glial cells. It is metabolized in the liver with an elimination half‐life of approximately 7 to 9 h. Although TGB does not induce or inhibit hepatic metabolic processes, it does provide a target for other enzyme‐inducing AEDs. TGB has proved effective as add‐on treatment for partial seizures, with or without becoming secondarily generalized, as demonstrated in five placebo‐controlled trials and six long‐term open studies. Preliminary results with TGB in children with refractory epilepsy and as monotherapy are promising. Few patients withdrew from these trials because of adverse events. The most common side effects with TGB involved the central nervous system, i.e., dizziness, asthenia, somnolence, nervousness, headache, and tremor. Most adverse events occurred during dosage titration, were often transient, and were usually of mild to moderate severity. The recommended maintenance dose for TGB, when combined with enzyme‐inducing drugs as add‐on therapy, is 30 to 50 mg/day. Trials are under way in patients with primarily generalized seizures and in newly diagnosed epilepsy. TGB is a well‐tolerated and effective novel AED that will find an enduring place in the management of epilepsy.