Antiepileptic Drugs and Neurodevelopment: An Update

Palac, Susan; Meador, Kimford J.

doi:10.1007/s11910-011-0194-y

Cited by 30 publications

(15 citation statements)

References 48 publications

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“…This can led to cortical dysplasias and reduced brain volume. In children exposed in utero to AEDs, the neurotransmitter changes and resultant cellular changes may account for impaired cognition [36]. …”

Section: Animal Studiesmentioning

confidence: 99%

Neurodevelopmental Effects of Fetal Antiepileptic Drug Exposure

Velez‐Ruiz

Meador

2015

Drug Saf

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Many studies investigating cognitive outcomes in children of women with epilepsy report an increased risk of mental impairment. Verbal scores on neuropsychometric measures may be selectively more involved. While a variety of factors contribute to the cognitive problems of children of women with epilepsy, antiepileptic drugs (AEDs) appear to play a major role. The mechanisms by which AEDs affect neurodevelopmental outcomes remain poorly defined. Animal models suggest that AED-induced apoptosis, altered neurotransmitter environment, and impaired synaptogenesis are some of the mechanisms responsible for cognitive and behavioral teratogenesis. AEDs that are known to induce apoptosis, such as valproate, appear to affect children’s neurodevelopment in a more severe fashion. Fetal valproate exposure has dose-dependent associations with reduced cognitive abilities across a range of domains, and these appear to persist at least until the age of 6. Some studies have shown neurodevelopmental deficiencies associated to the use of phenobarbital and possibly phenytoin. So far, most of the investigations available suggest that fetal exposures to lamotrigine or levetiracetam are safer with regards to cognition when compared to other AEDs. Studies on carbamazepine show contradictory results, but most information available suggests that major poor cognitive outcomes should not be attributed to this medication. Overall, children exposed to polytherapy prenatally appear to have worse cognitive and behavioral outcomes compared with children exposed to monotherapy, and with the unexposed. There is an increase risk of neurodevelopmental deficits when polytherapy involves the use of valproate versus other agents.

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Section: Animal Studiesmentioning

confidence: 99%

Neurodevelopmental Effects of Fetal Antiepileptic Drug Exposure

Velez‐Ruiz

Meador

2015

Drug Saf

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“…There seems reasonably good evidence that certain maternal anticonvulsants such as carbamazepine, valproic acid, and perhaps other anticonvulsants increase risk for ASD (Palac and Meador 2011). Other putative environmental risk factors that may have been more common in earlier decades such as congenital rubella have now virtually disappeared.…”

Section: Nongenetic Contributionsmentioning

confidence: 99%

Life Course Health Development in Autism Spectrum Disorders

Drmic

Szatmári

Volkmar

2017

Handbook of Life Course Health Development

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Life course health development (LCHD) incorporates theories and empirical evidence from the biological, physical, and social sciences to formulate a framework that explains how health develops over the life course. The life course health development conceptual framework can be applied to autism spectrum disorders (ASD) to help prioritize a research agenda and improve health development across the lifespan for individuals with ASD, their families, and communities. The following chapter highlights some issues and findings that are pertinent to an understanding of ASD using the lens of the life course health development principles. The chapter begins with a description of the clinical phenotype, followed by epidemiology of the disorder, and reviews changes in classification and diagnosis over time. Pathogenesis of the disorder is discussed, including information pertaining to hereditability, genetic and nongenetic factors, epigenetics, biomarkers, and genotype-phenotype correlations. Long-term follow-up outcome studies of adult independence and quality of life are reviewed, including examination of predictors of outcome, as well as stability of the diagnosis, symptom presentation, and cognitive functioning over time. Areas of key transitions over the life course are discussed from childhood to later adulthood. In addition, the importance of mental health status and care are highlighted. Finally, a number of research, data/methods, and translational priorities are offered that may help lead to a better understanding of life course health development in ASD.

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“…The cognitive impact of in utero exposure to AEDs over the course of early development (up to 6 years of age) has recently been documented in a series of publications derived from two large-scale prospective studies: the Neurodevelopmental Effects of Antiepileptic Drugs (NEAD) study and the Liverpool and Manchester Neurodevelopmental Group (LMNDG). After controlling for relevant covariates, results suggest an increased risk for cognitive impairment in children exposed to valproate or AED polytherapy [25–31]. Children exposed to valproate in utero are also at higher risk for neurodevelopmental disorders, including autism spectrum disorders and ADHD, and show poorer adaptive functioning [32–35].…”

Section: What Have Been the Developments Since Publication?mentioning

confidence: 99%

Comments on Motamedi G, Meador K. Epilepsy and cognition. Epilepsy & Behavior 2003;4:S25–S28.

Busch

2014

Epilepsy & Behavior

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Antiepileptic Drugs and Neurodevelopment: An Update

Cited by 30 publications

References 48 publications

Neurodevelopmental Effects of Fetal Antiepileptic Drug Exposure

Neurodevelopmental Effects of Fetal Antiepileptic Drug Exposure

Life Course Health Development in Autism Spectrum Disorders

Comments on Motamedi G, Meador K. Epilepsy and cognition. Epilepsy & Behavior 2003;4:S25–S28.

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