Vigabatrin, a structural analogue of GABA, increases the brain concentration of GABA (an inhibitory neurotransmitter) through irreversible inhibition of GABA transaminase. It is reserved for the treatment of epilepsy that is unsatisfactorily controlled by more established drugs. Lower doses should be used in the elderly and in those with impaired renal function. Vigabatrin should be avoided in those with a psychiatric history.
Adverse effects
• The most common reported adverse event (up to 30%) is drowsiness.• Fatigue, irritability, dizziness, confusion and weight gain have all been reported.
• Behavioural side effects (e.g. ill temper) may occur.
• Psychotic reactions, including hallucinations and paranoia, are common.
• Nystagmus, ataxia, tremor, paraesthesia, retinal disorders, visual-field defects and photophobia. Regular testing of visual fields is recommended. The patient should be warned to report any visual symptoms and an urgent ophthalmological opinion should be sought if visual-field loss is suspected.
Pharmacokinetics
Absorption is not influenced by food and peak plasma concentrations occur within two hours of an oral dose. In contrast to most other anticonvulsants, vigabatrin is not metabolized in the liver, but is excreted unchanged by the kidney and has a plasma half-life of about five hours. Its efficacy does not correlate with the plasma concentration and its duration of action is prolonged due to irreversible binding to GABA transaminase.
