Childhood and juvenile absence epilepsies

Childhood and juvenile absence epilepsies are genetic (idiopathic) generalised epilepsies.

The usual age of onset for childhood absence epilepsy (formerly known as petit mal epilepsy) is 4 to 9 years, and for juvenile absence epilepsy is 10 to 15 years. Ethosuximide and sodium valproate are equally effective, but ethosuximide is better tolerated and therefore is the drug of first choice. Unlike sodium valproate, ethosuximide does not protect against associated generalised tonic-clonic seizures—these occur later in about 25% of patients, especially those with juvenile absence epilepsy. Lamotrigine is not as effective as ethosuximide and sodium valproate. Absence epilepsy can be aggravated by carbamazepine, oxcarbazepine and phenytoin.

If possible, avoid sodium valproate in females of childbearing potential. If the drug is needed, have an informed discussion with the patient and parents about its harms and benefits before starting therapy, see Planning for pregnancy in patients with epilepsy and Teratogenic and neurodevelopmental effects of antiepileptic drugs. Ensure that the girl has reliable contraception.

If considering starting sodium valproate in males of reproductive potential, see Sodium valproate use in males of reproductive potential; a discussion about the potential risk of neurodevelopmental disorders in children born to males taking sodium valproate may be appropriate.

Use:

1 ethosuximide 5 mg/kg (up to 250 mg) orally, twice daily for 4 to 7 days, then increase to 10 mg/kg twice daily; usual maintenance dose 10 to 20 mg/kg (up to 750 mg) twice daily epilepsy, childhood and juvenile absence ethosuximide    

OR

2 sodium valproate , child older than 2 years, 5 mg/kg orally, twice daily for 5 days, then increase to 10 mg/kg twice daily; usual maintenance dose 10 to 20 mg/kg (up to 1250 mg) twice daily. epilepsy, childhood and juvenile absence sodium valproate    

Continue treatment until the electroencephalogram (EEG) stops showing 3 per second spike-wave activity and seizures have not occurred for 2 years. If an epileptiform abnormality persists in the EEG, this does not necessarily contraindicate stopping treatment. See advice on stopping treatment.