Postnatal concerns in children born to women with epilepsy

Thomas Jefferson University, Filadelfia, Pennsylvania, United States
Epilepsy & Behavior (Impact Factor: 2.26). 12/2007; 11(3):270-6. DOI: 10.1016/j.yebeh.2007.08.022
Source: PubMed


Infants born to mothers with epilepsy are at substantial risk for neurocognitive and behavioral disorders. Although exposure of the child to antiepileptic drugs (AEDs) during pregnancy and postnatally through breast milk has been implicated in disorders of higher cortical function, there have been relatively few clinical or animal studies examining the long-term effects of AEDs on cognition in the developing brain. In the limited animal studies done thus far, drug-specific effects on cognitive function have been identified. Phenobarbital, in particular, has been found to lead to adverse cognitive outcomes, whereas the newer AEDs have generally had more favorable outcomes. Although the pathophysiological mechanisms responsible for these deficits remain largely unknown, there is evidence that AEDs can adversely effect neuronal proliferation and migration, and increase apoptosis. While animal studies can provide valuable information regarding mechanism of AED-induced developmental pathology, they do not provide insight into cortical functions unique to humans, such as speech and language. Understanding the full spectrum of AED-induced effects on the developing brain will require both rigorous basic science and clinical studies.

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    • "all perturbation would break it . Several observations could indeed indicate that network dynamics in the developing neocortex can rapidly switch to a pathological state . Maybe the most striking one is the fact that the neocortex is exceptionally prone to seizures at early developmental stages ( Ben - Ari & Holmes , 2006 ; Bender & Baram , 2007 ; Holmes et al . 2007 ; Scantlebury et al . 2007 ) . For example , it was recently shown that GDPs in that region rapidly evolve towards interictal and ictal - like seizures if synaptic activity levels are pharmacologically increased ( Rheims et al . 2008b ) . Likewise , the blockade of excitatory amino acid transporters ( EAAT ) that remove glutamate from t"
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