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Chapter: Basic & Clinical Pharmacology : Antiseizure Drugs

Levetiracetam

Levetiracetam is a piracetam analog that is ineffective against sei-zures induced by maximum electroshock or pentylenetetrazol but has prominent activity in the kindling model.

LEVETIRACETAM

Levetiracetam is a piracetam analog that is ineffective against sei-zures induced by maximum electroshock or pentylenetetrazol but has prominent activity in the kindling model. This is the first major drug with this unusual preclinical profile that is effective against partial seizures.


Mechanism of Action

Levetiracetam binds selectively to the synaptic vesicular protein SV2A. The function of this protein is not understood but it is likely that levetiracetam modifies the synaptic release of glutamate and GABA through an action on vesicular function.

Clinical Uses

Levetiracetam is marketed for the adjunctive treatment of partial seizures in adults and children for primary generalized tonic-clonic seizures and for the myoclonic seizures of juvenile myoclonic epi-lepsy. Adult dosing can begin with 500 or 1000 mg/d. The dosage can be increased every 2–4 weeks by 1000 mg to a maximum dosage of 3000 mg/d. The drug is dosed twice daily. Adverse effects include somnolence, asthenia, ataxia, and dizziness. Less common but more serious are mood and behavioral changes; psychotic reactions are rare. Drug interactions are minimal; levetiracetam is not metabo-lized by cytochrome P450. Oral formulations include extended-release tablets; an intravenous preparation is also available.

Pharmacokinetics

Oral absorption of levetiracetam is nearly complete; it is rapid and unaffected by food, with peak plasma concentrations in 1.3 hours. Kinetics are linear. Protein binding is less than 10%. The plasma half-life is 6–8 hours, but may be longer in the elderly. Two thirds of the drug is excreted unchanged in the urine; the drug has no known active metabolites.


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