Neuroscientific models of alcohol use disorders (AUDs) posit dysfunction of networks involved in self-regulation, motivation, and reward, leading to impaired insight and loss of control over drinking behavior (Koob and Volkow, 2010). Inquiry into the neural substrates of AUDs has been facilitated by rapid development of in vivo neuroimaging technology, particularly magnetic resonance imaging (MRI). White matter (WM) networks, which form the connective structure enabling communication among neurons, are a critical element in neuroscientific conceptualization of AUDs. WM is highly involved in cognition and emotion in general (Filley, 2010), and WM health has been linked to memory and visuospatial functioning in AUDs (Müller-Oehring et al., 2009; Sullivan et al., 2000). Experts have reached consensus that WM atrophy is a hallmark injury of AUDs (Kril and Halliday, 1999; Oscar-Berman and Marinković, 2007; Sullivan, 2000; Sullivan and Pfefferbaum, 2005), but the nature, magnitude, and moderators of WM reduction are complex and poorly understood. Given the broad functional significance of WM, characterizing the extent of atrophy is key to understanding the pathophysiology of AUDs. By combining effect sizes (ES) from MRI studies comparing
