Evidence from animal models and clinical studies confirm that PAE often results in some degree of insult to the developing fetal brain that can affect many neural systems (Patten, Fontaine, & Christie, 2014). In particular, the prefrontal cortex (PFC) is directly affected by prenatal alcohol exposure in humans (Moore, Migliorini, Infante, & Riley, 2014). Several animal model studies have also documented that fetal alcohol exposure damages the medial PFC, with effects including neuronal cell loss (Mihalick, Crandall, Langlois, Krienke, & Dube, 2001), reduction in dendritic branching and density (Hamilton, Whitcher, & Klintsova, 2010; Lawrence, Otero, & Kelly, 2012), and reduction of presynaptic proteins involved in synaptic transmission and implicated in cognitive function (Barr, Hofmann, Phillips, Weinberg, & Honer, 2005). The PFC is necessary in executive function tasks including regulation of attention to relevant stimuli and response inhibition (Talpos & Shoaib, 2015). Consistent with this, response inhibition and overall executive function are frequently compromised in individuals with PAE (Kodituwakku, 2007; Mattson et al., 2011). Impairment of executive functioning is associated with externalizing disorders including attention deficit hyperactive disorder (ADHD) (Sun & Buys, 2012), conduct disorder (CD) (Johnson, 2015), and oppositional defiant disorder (ODD) (Matthys, Vanderschuren, & Schutter, 2013).
