Several genes associated with childhood absence epilepsy provide instructions for making pieces (subunits) of the GABA A receptor protein. Each genetic change appears to play a role in some populations but not others. Most genetic changes associated with childhood absence epilepsy are rare, having been found in only a small number of affected individuals. It is thought that multiple genetic changes or a combination of genetic and environmental factors contribute to development of the condition. The genetics of childhood absence epilepsy are complex and not completely understood. However, some affected individuals continue to have absence seizures into adulthood, or they may develop generalized tonic-clonic seizures, which cause muscle rigidity, convulsions, and loss of consciousness, or myoclonic seizures, which are characterized by rapid, uncontrolled muscle jerks. In most people with childhood absence epilepsy, the absence seizures disappear in adolescence. Febrile seizures are involuntary muscle contractions (convulsions) brought on by a high body temperature (fever). Some affected individuals have febrile seizures before they develop childhood absence epilepsy. The seizures usually last several seconds and they occur often, up to 200 times each day. During seizures, children are not aware of and do not respond to people or activities around them. Affected children have absence seizures (also known as petit mal seizures), which are brief episodes of impaired consciousness that look like staring spells. This condition begins in childhood, usually between ages 3 and 8. Childhood absence epilepsy is a condition characterized by recurrent seizures (epilepsy).

Absence seizure eeg