Article

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: 4.59). 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.

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    • "Investigators have increasingly sought to document correlations between the functional deficits reported in children who have been exposed to alcohol in utero and underlying neurobiology. These endeavors have been given added impetus by the observation of functional deficits associated with PAE, even in cases where children do not exhibit the facial features required for a diagnosis of fetal alcohol syndrome (FAS) (Riley et al., 2011). The wide range of physical, behavioral , and developmental abnormalities in children exposed to alcohol in utero is recognized by their inclusion in the umbrella term fetal alcohol spectrum disorders (FASD). "
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    ABSTRACT: Background: Children exposed to alcohol in utero demonstrate reduced white matter microstructural integrity. While early evidence suggests altered functional brain connectivity in the lateralization of motor networks in school-age children with prenatal alcohol exposure (PAE), the specific effects of alcohol exposure on the establishment of intrinsic connectivity in early infancy have not been explored. Methods: Sixty subjects received functional imaging at 2 to 4 weeks of age for 6 to 8 minutes during quiet natural sleep. Thirteen alcohol-exposed (PAE) and 14 age-matched control (CTRL) participants with usable data were included in a multivariate model of connectivity between sensorimotor intrinsic functional connectivity networks. Seed-based analyses of group differences in interhemispheric connectivity of intrinsic motor networks were also conducted. The Dubowitz neurological assessment was performed at the imaging visit. Results: Alcohol exposure was associated with significant increases in connectivity between somatosensory, motor networks, brainstem/thalamic, and striatal intrinsic networks. Reductions in interhemispheric connectivity of motor and somatosensory networks did not reach significance. Conclusions: Although results are preliminary, findings suggest PAE may disrupt the temporal coherence in blood oxygenation utilization in intrinsic networks underlying motor performance in newborn infants. Studies that employ longitudinal designs to investigate the effects of in utero alcohol exposure on the evolving resting-state networks will be key in establishing the distribution and timing of connectivity disturbances already described in older children.
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    • "Neuroimaging reports to date, however, have focused largely on ages 5 years through to young adulthood with the majority in late childhood or adolescence (Lebel et al. 2012; Treit et al. 2013). There is a paucity of neuroimaging data in children with prenatally alcohol-exposure during the first years of life, a period during which the most rapid brain growth occurs (Moore et al. 2014; Riley et al. 2011). Nevertheless, a small study reporting changes in white matter microstructure in the association tracts (Donald et al. 2015a) and one reporting alterations in structural connectivity (Taylor et al. 2015) provide emerging evidence that the effects of prenatal alcohol exposure can be identified using quantitative neuroimaging techniques . "
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    ABSTRACT: Neuroimaging studies have indicated that prenatal alcohol exposure is associated with alterations in the structure of specific brain regions. However, the temporal specificity of such changes and their behavioral consequences are less known. Here we explore the brain structure of infants with in utero exposure to alcohol shortly after birth. T2 structural MRI images were acquired from 28 alcohol-exposed infants and 45 demographically matched healthy controls at 2-4 weeks of age on a 3T Siemens Allegra system as part of large birth cohort study, the Drakenstein Child Health Study (DCHS). Neonatal neurobehavior was assessed at this visit; early developmental outcome assessed on the Bayley Scales of Infant Development III at 6 months of age. Volumes of gray matter regions were estimated based on the segmentations of the University of North Carolina neonatal atlas. Significantly decreased total gray matter volume was demonstrated for the alcohol-exposed cohort compared to healthy control infants (p < 0.001). Subcortical gray matter regions that were significantly different between groups after correcting for overall gray matter volume included left hippocampus, bilateral amygdala and left thalamus (p < 0.01). These findings persisted even when correcting for infant age, gender, ethnicity and maternal smoking status. Both early neurobehavioral and developmental adverse outcomes at 6 months across multiple domains were significantly associated with regional volumes primarily in the temporal and frontal lobes in infants with prenatal alcohol exposure. Alcohol exposure during the prenatal period has potentially enduring neurobiological consequences for exposed children. These findings suggest the effects of prenatal alcohol exposure on brain growth is present very early in the first year of life, a period during which the most rapid growth and maturation occurs.
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    • "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. "
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    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.
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