A significant proportion of CPM cases (Goebel and Herman-Ben Zur 1976; Messert et al. 1979) include a history of alcoholism. People with CPM, which is associated with electrolyte disturbances and specifically with aggressive correction of low sodium levels in the blood (i.e., hyponatraemia) (Chua et al. 2002), may have symptoms such as the inability to control facial movements, decreased voluntary muscle control (i.e., ataxia), and acute changes in consciousness (Kumar et al. 2006; Pfister et al. 1985). Classically, CPM was characterized by the presence of a symmetric triangular or “bat-wing” lesion in the pons (DeWitt et al. 1984; Gerard et al. 1987), with hypointense T1-weighted (Kleinschmidt-Demasters et al. 2006; Martin and Young 1995) and hyperintense T2-weighted (Buis and Wijdicks 2002; Kleinschmidt-Demasters et al. 2006; Pfister et al. 1985; Martin and Young 1995) images (see figure 4) reflecting damage to the protective covering of nerve cells (i.e., demyelination) as noted postmortem (Goldman and Horoupian 1981). The term osmotic myelinolysis (e.g., Chua et al. 2002; de Souza and Desai 2012) was coined to reflect the fact that other brain regions (e.g., basal
