Prenatal alcohol exposure (AE) is a leading preventable cause of birth defects, developmental disorders, and mental retardation (American Academy of Pediatrics Committee on Substance Abuse and Committee on Children With Disabilities, 2000). A subset of children with histories of heavy prenatal alcohol exposure meet the diagnostic criteria for fetal alcohol syndrome (FAS), which consist of craniofacial dysmorphology, growth deficiency, and evidence of central nervous system involvement (Hoyme et al., 2005, Stratton et al., 1996, Bertrand et al., 2005, Jones and Smith, 1973). While the diagnostic criteria for FAS serve as an avenue for identification of some children with AE, the majority of children affected by such exposure do not exhibit enough of the characteristic physical features to receive an FAS diagnosis (Bertrand et al., 2005, Sampson et al., 1997). Even in the absence of FAS, however, they exhibit similar neurobehavioral impairments as children with FAS (e.g., Mattson et al., 1997, Mattson and Riley, 1998, Mattson et al., 1998, Mattson et al., 2011).
