Neurodevelopmental functioning in children with FAS, pFAS, and ARND.
ABSTRACT The purpose of this article is to compare the neurodevelopmental profiles of 78 foster and adopted children with fetal alcohol syndrome (FAS), partial FAS (pFAS), or alcohol-related neurodevelopmental disorder (ARND).
Seventy-eight foster and adopted children underwent a comprehensive diagnostic evaluation. By using criteria more stringent than those required by current guidelines, the children were placed in 1 of 3 diagnostic categories: FAS, pFAS, or ARND. Each child was evaluated across the domains of neuropsychological functioning most frequently affected by prenatal exposure to alcohol. Multivariate analyses of variance were conducted to examine differences in neuropsychological functioning between the 3 diagnostic groups. Descriptive discriminant analyses were performed in follow-up to the multivariate analyses of variance.
The children in the 3 diagnostic categories were similar for descriptive and child welfare variables. Children with FAS had significantly decreased mean weight, height, and head circumference. Children with FAS exhibited the most impaired level of general intelligence, significantly worse language-based memory compared with children with ARND, and significantly poorer functional communication skills than children with pFAS. On executive functioning, the FAS group of children performed significantly worse on sequencing and shift than either the pFAS or ARND groups. Children with pFAS and ARND were similar in all neurodevelopmental domains that were tested.
The children who met tightly defined physical criteria for a diagnosis of FAS demonstrated significantly poorer neurodevelopmental functioning than children with pFAS and ARND. Children in these latter 2 groups were similar in all neurodevelopmental domains that were tested.
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ABSTRACT: Maternal drinking during pregnancy can result in a wide spectrum of cognitive and behavioral abnormalities termed fetal alcohol spectrum disorders (FASD). The heterogeneity observed in FASD-related phenotypes can be attributed to a number of environmental and genetic factors; however, ethanol dose and timing of exposure may have significant influences. Here, we report the behavioral effects of acute, binge-like ethanol exposure at three neurodevelopmental times corresponding to the first, second, and third trimester of human development in C57BL/6J mice. Results show that developmental ethanol exposure consistently delays the development of basic motor skill reflexes and coordination as well as impairs spatial learning and memory. Observed changes in activity and anxiety-related behaviors, however, appear to be dependent on timing of alcohol exposure. The variability in behaviors between different treatment models suggests that these may be useful in evaluating the mechanisms disrupted by ethanol at specific neurodevelopmental times. The results provide further evidence that, regardless of developmental stage, the developing brain is acutely sen-sitive to alcohol exposure.Journal of Behavioral and Brain Science 02/2013; 3(01):85-99. DOI:10.4236/jbbs.2013.31009
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ABSTRACT: The purpose of this article is to assess the rate of misdiagnosis and missed diagnoses of fetal alcohol spectrum disorders (FASD) among a population of foster and adopted youth referred to a children's mental health center. Data were collected from a sample of 547 children who underwent a comprehensive multidisciplinary diagnostic evaluation. Utilizing current diagnostic criteria, children were diagnosed, as appropriate, with fetal alcohol syndrome, partial fetal alcohol syndrome, alcohol-related neurodevelopmental disorder, or alcohol-related birth defects. Changes in rates of alcohol exposure-related diagnoses and cooccurring mental health disorders pre- and postassessment were analyzed by using McNemar's test for dependent proportions. Among 156 children and adolescents who met criteria for a diagnosis within the fetal alcohol spectrum, 125 had never been diagnosed as affected by prenatal alcohol exposure, a missed diagnosis rate of 80.1%. Of the 31 who had been recognized before referral as affected by prenatal alcohol exposure, 10 children's FASD diagnoses were changed within the spectrum, representing a misdiagnosis rate of 6.4%. The remaining 21 (13.5%) children's diagnoses stayed the same. There also were significant changes in the rate of mental health diagnosis, and learning disorders, communication disorders, and intellectual disability, objective signs of neurocognitive damage, were not recognized in a significant number of children with FASD. Within this clinical sample, 86.5% of youth with FASD had never been previously diagnosed or had been misdiagnosed. These high rates of missed diagnoses and misdiagnosis have significant implications for intervention and therapeutic services. Copyright © 2015 by the American Academy of Pediatrics.Pediatrics 01/2015; 135(2). DOI:10.1542/peds.2014-2171 · 5.30 Impact Factor
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ABSTRACT: Prenatal exposure to alcohol affects the expression and function of glutamatergic neurotransmitter receptors in diverse brain regions. The present study was undertaken to fill a current gap in knowledge regarding the regional specificity of ethanol-related alterations in glutamatergic receptors in the frontal cortex. We quantified subregional expression and function of glutamatergic neurotransmitter receptors (AMPARs, NMDARs, GluN2B-containing NMDARs, mGluR1s, and mGluR5s) by radioligand binding in the agranular insular cortex (AID), lateral orbital area (LO), prelimbic cortex (PrL) and primary motor cortex (M1) of adult rats exposed to moderate levels of ethanol during prenatal development. Increased expression of GluN2B-containing NMDARs was observed in AID of ethanol-exposed rats compared to modest reductions in other regions. We subsequently performed slice electrophysiology measurements in a whole-cell patch-clamp preparation to quantify the sensitivity of evoked NMDAR-mediated excitatory postsynaptic currents (EPSCs) in layer II/III pyramidal neurons of AID to the GluN2B negative allosteric modulator ifenprodil. Consistent with increased GluN2B expression, ifenprodil caused a greater reduction in NMDAR-mediated EPSCs from prenatal alcohol-exposed rats than saccharin-exposed control animals. No alterations in AMPAR-mediated EPSCs or the ratio of AMPARs/NMDARs were observed. Together, these data indicate that moderate prenatal alcohol exposure has a significant and lasting impact on GluN2B-containing receptors in AID, which could help to explain ethanol-related alterations in learning and behaviors that depend on this region.PLoS ONE 03/2015; 10(3):e0118721. DOI:10.1371/journal.pone.0118721 · 3.53 Impact Factor