Idiopathic/genetic epilepsies (IGE/GGE) represent a large group among epilepsies of childhood and adolescence. The typical subtypes, childhood and juvenile absence epilepsy, juvenile myoclonic epilepsy, and epilepsy with generalized tonic–clonic seizures on awakening, showed a favourable psychosocial outcome in the majority of cases. They can be treated with valproic acid and ethosuximide as first-line medication, and levetiracetam, lamotrigine, topiramate and perampanel. Each subtype of IGE/GGE is defined by its specific age of onset (childhood or adolescence) and type of generalized seizures, typical findings on the EEG, a normal cerebral MRI and often normal psychomotor development. In the underlying cause of these epilepsies complex genetic defects are believed to play a major role, namely structural genetic variation. For example, copy number variations in loci 15q13.3, 15q11 and 16p13 could be identified as one risk factor. Mutations in calcium channel genes (namely T-type calcium channel, CACNA1H, and P/Q-type calcium channel, CACNAB4 and CACNA1A) seem to take part in the pathomechanism of IGE. Monogenetic defects are seldom found to be the main cause of epilepsy. These monogenetic defects, mainly in the GABAA-receptor- and GLUT1 genes (SLC2A1), are often associated with other symptoms such as ataxia, movement disorders and mental retardation.
Photosensitivity is often seen in IGE, but can also occur without IGE. A genetic cause is also assumed; one of the most important candidate genes is CHD2.