Pharmacology: Pharmacological Effects and Mechanism of Action: Levetiracetam exhibits a novel pharmacological profile insofar as it inhibits partial and secondarily generalized tonic-clonic seizures in the kindling model, yet is ineffective against maximum electroshock- and pentylenetetrazol induced seizures, findings consistent with clinical effectiveness against partial and secondarily generalized tonic-clonic seizures. The mechanism by which levetiracetam exerts these antiseizure effects is unknown. No evidence for an action on voltage-gated Na+ channels or either GABA- or glutamate-mediated synaptic transmission has emerged. A stereoselective binding site has been identified in rat brain membranes and the synaptic vesicle protein SVZA has been shown to be a brain-binding target of levetiracetam.
Pharmacokinetics: Levetiracetam is readily absorbed from the gastrointestinal tract with a bioavailability of almost 100%; peak plasma concentrations are usually achieved within 1.3 hours of oral doses and steady state achieved after 2 days. Plasma protein binding is minimal at less than 10%. Levetiracetam is not extensively metabolised; about 25% of a dose is metabolised by hydroxylation to inactive metabolites. Around 95% of a dose is excreted as unchanged drug in the urine.
The plasma elimination half-life has been reported to be about 7 hours in adults and children aged 12 years and over, the half-life may be shorter in younger children.
Levetiracetam is distributed into breast milk.