Childhood absence epilepsy is a fairly common disorder with a prevalence of 1 in 1000 people.

For example, children with childhood absence epilepsy may be susceptible to hyperventilation.

Childhood absence epilepsy develops between ages 4 and 10.

One in eight children that are diagnosed with childhood absence epilepsy will eventually evolve into JME.

Studies suggest certain mutations in this gene lead to childhood absence epilepsy (CAE).

Childhood absence epilepsy (pyknolepsy)

Also known as pyknolepsy, childhood absence epilepsy (CAE) represents up to 10% of all childhood epilepsies.

These are childhood absence epilepsy, epilepsy with myoclonic absences and juvenile myoclonic epilepsy.

These include benign focal childhood epilepsy, childhood absence epilepsy, and juvenile myoclonic epilepsy, which have no other known cause.

Childhood absence epilepsy (CAE), also known as pyknolepsy, is an idiopathic generalized epilepsy which occurs in otherwise normal children.

Some forms of this condition that may be outgrown, as is the case with childhood absence epilepsy and a large number of patients with juvenile myoclonic epilepsy.

Childhood absence epilepsy (CAE) is an idiopathic generalized epilepsy that affects children between the ages of 4 and 12 years of age, although peak onset is around five to six years old.

This view has been recently confirmed by Glauser et al. (2010) who performed a double-blind, randomized, controlled clinical trial, to compare the efficacy, tolerability, and neuropsychological effects of ethosuximide, valproic acid, and lamotrigine in children with newly diagnosed childhood absence epilepsy.