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Types and mechanisms of cognitive deficits in childhood epilepsy
24 August 2010
06 February 2011
17 July 2015 (online)
Many human studies on cognition have focused on infants, preschool, and school age children. This period is characterized by peak hippocampal and cortical regional development, as well as myelinogenesis, dendritogenesis, and synaptogenesis. The presence of epilepsy and its treatment during the period of maximal white-matter growth might result in impairment in spatial learning, memory processes and other aspects of cognition. Several variables are associated with cognitive impairment in epilepsy, which includes maternal-related, seizure-related and medication-related variables. Paroxysmal seizures and electroencephalography epileptic discharges may cause transient, persistent or progressive cognitive impairment. Transient disruption of cognitive processing may occur with paroxysmal epileptic activity. Repeated seizure activity selectively impairs myelin accumulation, consumes, and reduces hippocampal plasticity available for information processing. High doses of antiepileptic drugs (AEDs) and polypharmacy are also significant risks for cognitive impairment with AEDs. AEDs produce global changes in the excitation levels in the central nervous system and often lead to cognitive deficits. In utero exposure to AEDs may cause defects in neuronal proliferation and migration and increase apoptosis. Although the immature brain has increased vulnerability to seizures but appears to be more “resistant” to the damaging affect of epilepsy than does the mature brain, however, if sufficiently long, a seizure can result in damage at any age. Cognitive impairment even if trivial may adversely affect the child's psychosocial functioning in daily life by interference with educational skills and learning tasks. To conclude, understanding the mechanisms underlying cognitive impairment with epilepsy and AEDs raise important clinical and research implications and recommendations.