Fetal alcohol spectrum disorders: An overview

Department of Psychology, Center for Behavioral Teratology, San Diego State University, San Diego, CA 92120, USA.
Neuropsychology Review (Impact Factor: 5.4). 06/2011; 21(2):73-80. DOI: 10.1007/s11065-011-9166-x
Source: PubMed

ABSTRACT When fetal alcohol syndrome (FAS) was initially described, diagnosis was based upon physical parameters including facial anomalies and growth retardation, with evidence of developmental delay or mental deficiency. Forty years of research has shown that FAS lies towards the extreme end of what are now termed fetal alcohol spectrum disorders (FASD). The most profound effects of prenatal alcohol exposure are on the developing brain and the cognitive and behavioral effects that ensue. Alcohol exposure affects brain development via numerous pathways at all stages from neurogenesis to myelination. For example, the same processes that give rise to the facial characteristics of FAS also cause abnormal brain development. Behaviors as diverse as executive functioning to motor control are affected. This special issue of Neuropsychology Review addresses these changes in brain and behavior highlighting the relationship between the two. A diagnostic goal is to recognize FAS as a disorder of brain rather than one of physical characteristics.

  • Source
    • "These cases are referred to as alcoholrelated neurodevelopmental disorders (ARND) and are often difficult to identify because they lack the characteristic facial features and growth retardation seen in FAS. In fact, an ARND diagnosis requires confirmation of prenatal alcohol exposure, which often is unavailable or unreliable (see Riley et al. 2011 for a comparison of various diagnostic schemas for FAS and ARND). Finding novel ways to identify at-risk individuals for disabilities along the spectrum is critical, as is identifying effective interventions to mitigate these cognitive and behavioral effects. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Prenatal alcohol exposure can cause a number of physical, behavioral, cognitive, and neural impairments, collectively known as fetal alcohol spectrum disorders (FASD). This article examines basic research that has been or could be translated into practical applications for the diagnosis or treatment of FASD. Diagnosing FASD continues to be a challenge, but advances are being made at both basic science and clinical levels. These include identification of biomarkers, recognition of subtle facial characteristics of exposure, and examination of the relation between face, brain, and behavior. Basic research also is pointing toward potential new interventions for FASD involving pharmacotherapies, nutritional therapies, and exercise interventions. Although researchers have assessed the majority of these treatments in animal models of FASD, a limited number of recent clinical studies exist. An assessment of this literature suggests that targeted interventions can improve some impairments resulting from developmental alcohol exposure. However, combining interventions may prove more efficacious. Ultimately, advances in basic and clinical sciences may translate to clinical care, improving both diagnosis and treatment.
    09/2015; 37(1):97-108.
  • Source
    • "Prenatal alcohol exposure may lead to a range of physical and cognitive abnormalities in children that persist into adulthood ( Mattson et al., 2011 ; Riley et al., 2011 ). The range of deficiencies observed in affected individuals is collectively described as fetal alcohol spectrum disorders (FASD) ( Sampson et al., 1997 ), with fetal alcohol syndrome (FAS) representing the most severe form. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Prenatal alcohol exposure can cause a wide range of deficits in executive function that persist throughout life, but little is known about how changes in brain structure relate to cognition in affected individuals. In the current study, we predicted that the rate of white matter volumetric development would be atypical in children with fetal alcohol spectrum disorders (FASD) when compared to typically developing children, and that the rate of change in cognitive function would relate to differential white matter development between groups. Data were available for 103 subjects [49 with FASD, 54 controls, age range 6-17, mean age = 11.83] with 153 total observations. Groups were age-matched. Participants underwent structural magnetic resonance imaging (MRI) and an executive function (EF) battery. Using white matter volumes measured bilaterally for frontal and parietal regions and the corpus callosum, change was predicted by modeling the effects of age, intracranial volume, sex, and interactions with exposure status and EF measures. While both groups showed regional increases in white matter volumes and improvement in cognitive performance over time, there were significant effects of exposure status on age-related relationships between white matter increases and EF measures. Specifically, individuals with FASD consistently showed a positive relationship between improved cognitive function and increased white matter volume over time, while no such relationships were seen in controls. These novel results relating improved cognitive function with increased white matter volume in FASD suggest that better cognitive outcomes could be possible for FASD subjects through interventions that enhance white matter plasticity.
    Clinical neuroimaging 06/2014; 5:19-27. DOI:10.1016/j.nicl.2014.05.010 · 2.53 Impact Factor
  • Source
    • "While moderate alcohol consumption by adults has proven health benefits (French and Zavala, 2007; Gunzerath et al., 2004), excessive alcohol consumption has numerous detrimental effects, making it the 3rd leading cause of the global burden of injury and disease (Lim et al., 2012). Moreover, even moderate alcohol consumption during pregnancy is known to cause fetal alcohol spectrum disorders (FASDs), collectively the largest preventable set of birth defects (May et al., 2009; Riley et al., 2011). FASDs are characterized by prenatal and postnatal growth restriction, craniofacial dysmorphology, and structural/functional abnormalities of the central nervous system (CNS) (Hoyme et al., 2005). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Stem cells, especially human embryonic stem cells (hESCs), are useful models to study molecular mechanisms of human disorders that originate during gestation. Alcohol (ethanol, EtOH) consumption during pregnancy causes a variety of prenatal and postnatal disorders collectively referred to as fetal alcohol spectrum disorders (FASDs). To better understand the molecular events leading to FASDs, we performed a genome-wide analysis of EtOH's effects on the maintenance and differentiation of hESCs in culture. Gene Co-expression Network Analysis showed significant alterations in gene profiles of EtOH-treated differentiated or undifferentiated hESCs, particularly those associated with molecular pathways for metabolic processes, oxidative stress, and neuronal properties of stem cells. A genome-wide DNA methylome analysis revealed widespread EtOH-induced alterations with significant hypermethylation of many regions of chromosomes. Undifferentiated hESCs were more vulnerable to EtOH's effect than their differentiated counterparts, with methylation on the promoter regions of chromosomes 2, 16 and 18 in undifferentiated hESCs most affected by EtOH exposure. Combined transcriptomic and DNA methylomic analysis produced a list of differentiation-related genes dysregulated by EtOH-induced DNA methylation changes, which likely play a role in EtOH-induced decreases in hESC pluripotency. DNA sequence motif analysis of genes epigenetically altered by EtOH identified major motifs representing potential binding sites for transcription factors. These findings should help in deciphering the precise mechanisms of alcohol-induced teratogenesis.
    Stem Cell Research 04/2014; 12(3):791-806. DOI:10.1016/j.scr.2014.03.009 · 3.91 Impact Factor
Show more


Available from