| 1. |
- Laegreid, Liv, et al.
(författare)
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Benzodiazepine amplification of valproate teratogenic effects in children of mothers with absence epilepsy.
- 1993
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Ingår i: Neuropediatrics. - : Georg Thieme Verlag KG. - 0174-304X .- 1439-1899. ; 24:2, s. 88-92
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Tidskriftsartikel (refereegranskat)abstract
- Valproate (VPA) is one of the most frequently used antiepileptic drugs (AEDs). Concern has recently been raised regarding VPA medication during pregnancy and teratogenic effects in the offspring. Both neural tube defects (5, 18, 34) and a constellation of signs termed the fetal valproate syndrome (1, 12) have been reported. Benzodiazepines (BZDs) are also widely used and sometimes as effective adjunctives in AED therapy. Both VPA and BZD have close connections to GABA transmission. Recently, clinical and epidemiological human studies (26, 27, 37, 39), supported by animal studies (17, 24, 40), have indicated that BZDs may act as human teratogens. We report on 7 children with congenital malformations, dysmorphism and abnormal neurological signs from birth. The mothers had well controlled primary generalized absence epilepsy without major seizures during pregnancy. Five children had been exposed to VPA monotherapy and two children to VPA and BZD combined during the first trimester. Those two infants had myelomeningoceles and the most pronounced dysmorphism in the group. We propose that these observations indicate a possible amplifying action of BZDs on VPA teratogenicity. Unrecognized BZD use during pregnancies exposed to VPA may be of importance when estimating the teratogenic risks of VPA therapy.
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| 2. |
- Viggedal, Gerd, 1950, et al.
(författare)
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Mental development in late infancy after prenatal exposure to benzodiazepines--a prospective study.
- 1993
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Ingår i: Journal of Child Psychology and Psychiatry, and Allied Disciplines. - 0021-9630. ; 34:3, s. 295-305
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Tidskriftsartikel (refereegranskat)abstract
- Seventeen infants born to mothers who used benzodiazepines (BZD) throughout pregnancy were followed prospectively and compared with 29 infants born to mothers who had not used psychoactive substances. On the Griffiths' Developmental Scale, the BZD-exposed infants demonstrated consistently lower mean GQs and DQs for all subscales at 5, 10 and 18 months of age. The differences in GQ reached statistical significance at 10 and 18 months. The DQs differed significantly for all subscales at 10 months and for the personal-social behaviour and hearing and speech subscales at 18 months of age. We suggest that prenatal exposure to BZD may cause a general delay in mental development up to 18 months of age.
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