Tiagabine exerts its antiepileptic drug (AED) activity by selectively inhib
iting the uptake of gamma-aminobutyric acid (GABA) onto the transporter mol
ecules, and thus, increasing extracellular concentrations of GABA in the br
ain. The absorption and elimination of tiagabine follow linear pharmacokine
tics. Tiagabine is metabolized by hepatic cytochrome P450 enzymes and enzym
e-inducing AEDs increase tiagabine clearance by 50-65%. Tiagabine has shown
no clinically important interactions with other drugs, including oral cont
raceptives. In the perforant pathway stimulation model of status epilepticu
s, tiagabine reduced the seizure number and severity, and also prevented th
e loss of pyramidal cells in the hippocampus as well as alleviated impairme
nt of the spatial memory impairment associated with hippocampal damage. Tia
gabine has both antiepileptogenic and anticonvulsant effects in the kindlin
g model of epilepsy. Based on the data from the short- and long-term add-on
studies, tiagabine is effective adjunctive therapy for all partial seizure
types in adolescents and adults. Conversion to tiagabine monotherapy has b
een also possible in substantial amount of patients with partial seizures i
n three trials. Tiagabine is generally well-tolerated. The most common adve
rse events in controlled studies involve the central nervous system; for ex
ample, dizziness, asthenia, nervousness, tremor, depressed mood and emotion
al lability. Special safety analyses with formal neuropsychological testing
suggest that tiagabine does not adversely affect cognition or mood. Tiagab
ine represents an important new therapeutic option for patients with treatm
ent-refractory partial seizures. The role of tiagabine in the management of
partial epilepsy of patients with intellectual disability is especially em
phasized since tiagabine has a low side-effect profile in the cognitive are
a.