ABSTRACT
Concurrent tiagabine pharmacotherapy and pharmacotherapy with opiate analgesics, sedative-hypnotics, or other drugs that produce CNS depression may result in additive CNS depression. Tiagabine pharmacotherapy commonly has been associated with abnormal thinking, asthenia, dizziness, nervousness, somnolence, and tremor. Signs and symptoms of tiagabine overdosage include agitation, confusion, hostility, impaired consciousness, myoclonus, somnolence, speech impairment, and weakness. Tiagabine is extensively metabolized by the process of oxidation and glucuronidation in the liver by the hepatic cytochrome P450 isoenzyme CYP-3A. Tiagabine overdosage requires emergency symptomatic medical support of body systems with attention to increasing tiagabine elimination. Concurrent alcohol use may increase the CNS depressant action of tiagabine. Advise patients to avoid, or limit, their use of alcohol while receiving tiagabine pharmacotherapy. Tiagabine selectively and reversibly inhibits the re-uptake of GABA into presynaptic neurons and glial cells following synaptic release. Thus, synaptic concentrations of GABA are increased, GABAergic transmission is enhanced, and seizure activity is reduced.
