The implications of heavy prenatal exposure to alcohol are long-term and pervasive, affecting the individual’s emotional and behavioral functioning throughout the lifespan ( Crocker et al., 2009 Fryer et al., 2007 Streissguth et al., 2004). Cognitive deficits have been documented in neuropsychological domains of executive functioning, learning, memory, language, attention, and social abilities (for review, see ( Mattson et al., 2011). Children who have histories of AE, with and without the characteristic facial dysmorphology associated with FAS, have impaired intellectual functioning and display similar cognitive and behavioral impairments ( Mattson and Riley, 1998 Mattson and Riley, 2000). and many Western European countries ( May et al., 2009). Although FAS is estimated to occur in 2 to 7 cases per 1,000 live births ( May et al., 2009 Sampson et al., 1997), FASDs are more prevalent, and may occur in as many as 2–5% of the population in the U.S. Fetal alcohol syndrome (FAS) is on the most extreme end of the spectrum and is diagnosed in the presence of central nervous system (CNS) dysfunction, pre- and post-natal growth deficiencies, and characteristic craniofacial anomalies (i.e., smooth philtrum, thin vermillion border, and small palpebral fissures) ( Bertrand et al., 2004 Hoyme et al., 2005 Jones et al., 1973). The deleterious effects of prenatal alcohol exposure (AE) include a range of neuropsychological and behavioral deficits that fall under the non-diagnostic umbrella term fetal alcohol spectrum disorders (FASD ( Bertrand et al., 2004).
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