Intelligence of children of epileptic mothers

Gally, Eija; Kantola-Sorsa, Elisa; Granström, Marja‐Liisa

doi:10.1016/s0022-3476(88)80377-9

Cited by 129 publications

(82 citation statements)

References 20 publications

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“…A cohort study by Hanson et al [64] estimated that 11% of phenytoin-exposed children showed enough unusual features to justify the diagnosis of the syndrome. In contrast, a prospective, controlled, exposure-blinded, population-based study found low intelligence (<85), an important feature of the syndrome, in only 2 of 103 phenytoin-exposed children (1.9%) [55].…”

Section: Phenytoinmentioning

confidence: 82%

“…Comparison groups included 40 nonexposed children of WWE and more than 27,000 control children of mothers without epilepsy. Phenytoin doses were not reported, but maternal phenytoin levels during pregnancy were available in the study by Gaily et al [55]. Both studies reported lower IQ values in children of WWE compared with controls, but no significant associations were observed to phenytoin or other drug exposure.…”

Section: Phenytoinmentioning

confidence: 99%

“…Pooled data from two prospective population-based studies [55,56] showed a 1.9% (2/105) incidence of mental deficiency in carbamazepine monotherapy-exposed children of WWE. One of the two children had West syndrome in infancy as a possible etiology.…”

Section: Carbamazepinementioning

confidence: 99%

“…Prospective data on IQ scores after prenatal phenytoin exposure have been reported from two controlled population-based studies [55,59] with blinded evaluation of outcome. The results were controlled for socioeconomic class or maternal educational level.…”

Section: Phenytoinmentioning

confidence: 99%

“…Their mean IQ did not differ from that of other children of WWE. Pooled data from two prospective population-based studies [55,56] showed mental deficiency in 1 of 84 (1.2%) polytherapyexposed children. The child had been exposed to phenytoin, carbamazepine, and alcohol.…”

Section: Polytherapymentioning

confidence: 99%

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Cognitive/behavioral teratogenetic effects of antiepileptic drugs

Meador

Baker

Cohen

et al. 2007

Epilepsy & Behavior

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The majority of children of mothers with epilepsy are normal, but they are at increased risk for developmental delay. Antiepileptic drugs (AEDs) appear to play a role. Our current knowledge is reviewed, including research design issues and recommendations for future research. In animals, exposure of the immature brain to some AEDs can produce widespread neuronal apoptosis and behavioral deficits. The risks of AEDs in humans are less clear, but recent studies raise concerns, especially for valproate. There is a critical need for well-designed systematic research to improve our understanding of AED effects on the fetal brain. KeywordsAntiepileptic drugs; Anticonvulsant drugs; Pregnancy; Teratogenesis; Development; Cognition; Behavior Animal studies on behavioral effects of in utero AED exposureAnimal studies have demonstrated that in utero antiepileptic drug (AED) exposure can produce behavioral as well as anatomical defects, which can occur at dosages lower than those required to produce somatic malformations [1,2]. Gestational or neonatal exposure to benzodiazepines can affect brain chemistry and behavior causing hyperactivity or learning deficits [3,4]. Despite the common use of carbamazepine in humans, very few neurobehavioral studies in animals have been conducted with this AED. In utero carbamazepine exposure did not produce hyperexcitability in primates [5]. Perinatal phenobarbital exposure in rats reduces brain weight [6]. Mice exposed prenatally to phenobarbital have neuronal deficits, reduced brain weight, and impaired development of reflexes, open-field activity, schedule-controlled behavior, spatial learning, and cate-cholamine brain levels [7][8][9][10][11][12]. Gestational or neonatal exposure to phenytoin reduces brain weight [13,14], alters neuronal membranes in the hippocampus [15], delays neurodevelopment [16], and impairs spatial learning and motor coordination [17][18][19][20][21][22][23][24][25]. Hyperactivity has been observed in rats and primates following prenatal exposure to phenytoin [5,23,25]. Gestational primidone in rats produces learning deficits and reduces open-field activity [26]. In utero valproate exposure can alter neuronal membranes [27], decrease brain weight in mice [28], and result in adverse neurobehavioral effects [29,30].

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Section: Phenytoinmentioning

confidence: 82%

Section: Phenytoinmentioning

confidence: 99%

Section: Carbamazepinementioning

confidence: 99%

Section: Phenytoinmentioning

confidence: 99%

Section: Polytherapymentioning

confidence: 99%

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