Heavy alcohol use is associated with a wide range of neural consequences in adults (Estruch et al. 1997; Nicolas et al. 2000; Pfefferbaum et al. 2006a, b; Pfefferbaum and Sullivan 2005) and similar sequelae are implicated in adolescent users. Hippocampal (De Bellis et al. 2000; Nagel et al. 2005) and prefrontal white matter volumes appear smaller in heavy alcohol using adolescents (De Bellis et al. 2005; Medina et al. 2008). Alterations in anisotropy in the genu and isthmus of the corpus callosum in alcohol-using teens (De Bellis et al. 2008) and in frontal, cerebellar, temporal, and parietal regions in adolescent binge-drinkers (McQueeny et al. 2009) lends further support to atypical developmental trajectories. White matter quality appears to relate to drinking in a dose dependent manner, where higher blood alcohol concentrations are associated with poorer tissue integrity in the corpus callosum, internal and external capsules, and superior corona radiata (see Fig. 2) (McQueeny et al. 2009). Functional consequences of adolescent heavy drinking are seen in attenuated frontal cortex response during spatial working memory (Tapert et al. 2004), and deficits on neuropsychological
