Abstract
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.
Keywords
Epilepsy - antiepileptic drugs - cognition - hippocampal plasticity
