Wernicke’s encephalopathy (WE), which arises from thiamine (vitamin B1) deficiency associated with chronic alcohol consumption (but see, Berger & Singhal, 2014), may, if left untreated, progress to Korsakoff’s syndrome (KS), a severe neurological disorder characterized by anterograde and retrograde amnesia (Kopelman, Thomson, Guerrini, & Marshall, 2009; Zahr, Kaufman, & Harper, 2011). WE symptomatology constitutes visual, gait, and mental disturbances, including memory loss and emotional changes (Thomson et al., 2008). On T2 images, individuals with WE show symmetrical hyperintensities (bright spots) in midbrain gray matter surrounding the cerebral aqueduct, mammillary bodies, and third ventricle (Figure 1A) (Lenz et al., 2002; Sullivan & Pfefferbaum, 2009). Hyperintensities are thought to be caused by altered interstitial fluid mobility and water content, which may indicate demyelination or axonal damage (Wardlaw, Valdes Hernandez, & Munoz-Maniega, 2015). Brain regions affected (e.g., volume loss) by WE include the thalamus, cerebellum (vermis, dentate nuclei), pons, medulla, tectal plates, olivary bodies, and midbrain (red nuclei, substantia nigra) (Ha, Weon, Jang, Kang, & Choi, 2012; Kalidass, Sunnathkal, Rangashamanna, & Paraswani, 2012; Kang, Kang, Choi, & Choi, 2005; Liou, Kuo, & Chen,
