In the late 1990’s Caine and colleagues noted that neuropathological signs associated with WE were observed upon autopsy in alcoholics who had not been diagnosed in life with WE (Caine, Halliday, Kril, & Harper, 1997). The result was a modification of the historical triad used in clinical settings to diagnosis WE by adding a dietary deficiency criterion and suggested that individuals need only to meet 2 of the 4 criteria to be classified as showing signs of Wernicke’s encephalopathy. A study that examined the utility of antemortem Caine criteria (Pitel et al., 2011) reported graded deficits in the alcohol groups categorized by number of criteria met. The most pronounced deficits occurred in the group of alcoholics who met 2 or more Caine criteria. Further, Pitel and colleagues reported that lower thiamine levels were selectively associated with lower memory scores. Additionally, a recent study (Ritz et al., 2016) reported that malnutrition, liver dysfunction, and thiamine metabolism partially explained the heterogeneity of alcohol-related neuropsychological impairments observed in a group of 30 alcoholics, with the most severe cognitive impairments associated with malnutrition, defined as “at least 30-missed meal days” over the lifetime concurrent with heavy drinking.
