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The seizures of childhood absence epilepsy (CAE) are usually staring spells during which the child is not aware or responsive. The child's eyes may roll up briefly. Each spell lasts about 10 seconds and ends abruptly. The child often is not even aware that anything has happened. These episodes can occur 1 to 50 times per day, often during exercise. Tonic-clonic (grand mal) seizures, with or without fever, may occur for a while before absence seizures develop and may occur from time to time thereafter.
CAE accounts for 2% to 8% of patients with epilepsy. The absence seizures usually begin between the ages of 4 and 8 years in children who have normal intelligence and neurologic function.
The cause is predominantly genetic. About one-third of the families of children with CAE report a family history of similar seizures. The brothers and sisters of children with CAE have about a 10% chance of developing epilepsy.
The EEG shows spike and wave discharges at 1.5 to 4.0 Hz (cycles per second) that are the same on both sides of the brain. CT and MRI scans of the brain are normal, so they may not be recommended.
Either Zarontin (ethosuximide) or Depakote (valproate) can be used to treat CAE. The advantage of using Depakote is that it treats both absence and tonic-clonic seizures. If the absences are persistent, Depakote and Zarontin should be tried one at a time and then in combination. Lamictal (lamotrigine) has been shown to be effective in treating CAE. Some of the newer antiepileptic drugs show promise in CAE but have not undergone controlled studies. These include Keppra (leviteracetam), Topamax (topiramae), and Zonegram (zonisamide).
Childhood absence epilepsy is considered to be one of the relatively benign childhood epilepsies. For 65% of these children, the seizures respond to treatment and disappear by mid-adolescence. Absence seizures persisting into adult life are rare, but it happens occasionally.
CAE accounts for 2% to 8% of patients with epilepsy. The absence seizures usually begin between the ages of 4 and 8 years in children who have normal intelligence and neurologic function.
The cause is predominantly genetic. About one-third of the families of children with CAE report a family history of similar seizures. The brothers and sisters of children with CAE have about a 10% chance of developing epilepsy.
The EEG shows spike and wave discharges at 1.5 to 4.0 Hz (cycles per second) that are the same on both sides of the brain. CT and MRI scans of the brain are normal, so they may not be recommended.
Either Zarontin (ethosuximide) or Depakote (valproate) can be used to treat CAE. The advantage of using Depakote is that it treats both absence and tonic-clonic seizures. If the absences are persistent, Depakote and Zarontin should be tried one at a time and then in combination. Lamictal (lamotrigine) has been shown to be effective in treating CAE. Some of the newer antiepileptic drugs show promise in CAE but have not undergone controlled studies. These include Keppra (leviteracetam), Topamax (topiramae), and Zonegram (zonisamide).
Childhood absence epilepsy is considered to be one of the relatively benign childhood epilepsies. For 65% of these children, the seizures respond to treatment and disappear by mid-adolescence. Absence seizures persisting into adult life are rare, but it happens occasionally.
