Behavioral issues may also be present and their occurrence might be associated with significantly worse cognitive development. Some evidence suggest that  are impairment is more prominent in verbal rather than non-verbal capacities of children with CAE  or are even limited to few areas of verbal expression as phonological and category fluency. Attention deficit disorder and specific learning disorders are also frequently found in the CAE and can interfere with academic performance as well as with day to day activities of the children. Causes
CAE is considered as a complex polygenic disorder. This fact is supported by the high occurrence (up to 20%) of generalized epilepsies or febrile seizures in family members of children with CAE. In cases with early onset or accompanying features, Glut-1 deficiency (a metabolic disorder responding well to ketogenic diet) could be the cause of the absence seizures. Genetic mutations have been identified in recent years involving mainly GABA receptors and calcium channel modulator genes. Pathophysiology
Pathophysiology of absence seizures has been widely studied in animal models but is not fully decoded to date. There is however solid evidence for the involvement of bilateral cortical and subcortical networks which are part of the default state system. Pathophysiology when genetic mutations are present is further discussed below. Particularly in the Han Chinese population, there is an association between mutations in the calcium channel, voltage-dependent, T type, alpha 1H subunit (CACNA1H), and childhood absence epilepsy. These mutations cause increased channel activity and associated increased neuronal excitability.
They involve abrupt impairment of consciousness with loss of awareness and responsiveness, behavioral arrest, and arrest of the activity that may vary from complete arrest to continuing the activity with an altered status. Other seizure features include starring, eyelid movement or eye-opening and pallor. Mild automatisms and mild movements at the beginning of the seizures are frequent, but major motor involvement, as atonic falls, early in the course of the disease excludes this diagnosis.The International League Against Epilepsy commission defined absence seizure as “of sudden onset, interruption of ongoing activities, staring, possible upwards version of eyes with few seconds duration, associated with symmetrical 2–4 Hz, mainly 3 Hz spike-wave complexes, normal background activity. Absence seizure was divided into two subgroups (Penry et al. 1975), first with consciousness impairment, and others were associated with the other clinical component, namely clonic, atonic, tonic, autonomic, and with automatisms. Though CAE usually occurs in children with normal neurodevelopment and are sensitive to antiepileptic treatments children with CAE have a risk of academic failure and high rates of attention deficits. Neuropsychological impairment
Neuropsychological impairment in children with CAE is frequent and includes executive dysfunction, attention problems, learning disabilities, and language problems. These problems even persist after seizures are treated. Monitoring with validated cognition scales should be performed. Many existing data illustrate that children with CAE have an average IQ but present subtle cognitive difficulties. In cases with lower IQ, significant social difficulties can be often seen.