As an equally consumed intoxicant among adolescents, comorbid alcohol use is common among chronic marijuana users (Medina et al., 2007c). 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; Pfefferbaum et al., 2006b; Pfefferbaum and Sullivan, 2005) and similar sequelae are implicated in adolescent users. Prefrontal white matter volumes appear smaller in heavy alcohol using adolescents (De Bellis et al., 2005; Medina et al., 2008). In addition, atypical brain response during spatial working memory (Tapert et al., 2004), and deficits on neuropsychological measures of attention (Tapert and Brown, 1999), retrieval (Brown et al., 2000), and visuospatial functioning (Tapert et al., 2002) suggest functional consequences of adolescent heavy drinking with sustained effects through adulthood (Brown et al., 2008). A detailed characterization of white matter is thus essential for understanding the influence of combined marijuana and alcohol use on the developing adolescent brain.
