Myoclonic Epilepsy Beginning in Infancy or Early Childhood Medication

Updated: Jun 28, 2018
  • Author: Michael C Kruer, MD; Chief Editor: Amy Kao, MD  more...
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Medication Summary

The long-term goals of pharmacotherapy are to reduce morbidity and prevent complications.

Go to Antiepileptic Drugs for complete information on this topic.


Antiepileptic Drugs

Class Summary

These agents prevent seizure recurrence and terminate clinical and electrographic seizure activity. Patients with the benign form of myoclonic epilepsy often respond very well to first-line AEDs.

Valproic acid (Depakote, Depakene, Depacon, Stavzor)

Valproic acid is chemically unrelated to other drugs that treat seizure disorders. Although its mechanism of action not established, its activity may be related to increased brain levels of gamma-aminobutyric acid (GABA), or enhanced GABA action. Valproate also may potentiate postsynaptic GABA responses, affect potassium channels, or have direct membrane-stabilizing effect.

The use of valproic acid in young children (younger than 2 y) is associated with an increased risk of hepatotoxicity. Hepatotoxicity is estimated to occur in fewer than 1 in 250 children treated.

Clonazepam (Klonopin)

Clonazepam facilitates inhibitory GABA neurotransmission and other inhibitory transmitters. It is useful in immediate control of seizures, but it may be associated with relatively rapid loss of efficacy against seizures.

Ethosuximide (Zarontin)

The mechanism of action of ethosuximide is based on reducing current in T-type calcium channels found on thalamic neurons. Spike-and-wave patterns during petit mal seizures are thought to be initiated in thalamocortical relays by activation of these channels. Ethosuximide is used as adjunctive medication to valproic acid if that medication has failed to control seizures.

Cannabidiol (Epidiolex)

Purified formulation of cannabidiol indicated for treatment of seizures associated with Lennox-Gastaut syndrome (LGS) or Dravet syndrome (DS) in patients aged 2 years or older. Cannabidiol is a structurally novel anticonvulsant and the exact mechanism by which it produces anticonvulsant effects is unknown. It does not appear to exert its anticonvulsant effects through CB1 receptors, nor through voltage-gated sodium channels.