non-exposed sample, those with ADHD were more impaired than controls, suggesting that these executive function deficits in exposed children are due to different underlying mechanisms of impairment (Glass et al., 2013). A unique etiological origin of ADHD in those with PAE could also account for differential response to ADHD pharmaceutical treatment (Frankel, Paley, Marquardt, & O’Connor, 2006; Koren, 2015; Murawski, Moore, Thomas, & Riley, 2015; O’Malley, Koplin, & Dohner, 2000; Peadon & Elliott, 2010). This highlights an important distinction in individuals with a traditional ADHD diagnosis, i.e., differences in etiological origin are responsible for the differing ADHD characteristics in PAE individuals compared to ADHD characteristics in non-PAE individuals. The distinction in putative etiology and differential response to therapeutics may be underappreciated, given that most PAE studies do not ascertain whether the mother is alcohol dependent and most COA studies do not ascertain whether the alcohol-dependent mother drank while pregnant.
