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 ganglia, thalami, and cerebral gray–white matter junctions) are affected in CPM (e.g., Chen et al. 1996; Graff-Radford et al. 2011; Hagiwara et al. 2008; Harlan et al. 1988; Price et al. 1987; Waragai and Satoh 1998), despite suggestions that pathology in these other regions may not strictly represent demyelination (Kleinschmidt-Demasters et al. 2006; Kumar et al. 2006). Because a postmortem study of 112 autopsy cases of CPM patients reported that 28 percent could also be diagnosed with WE (Goebel and Herman-Ben Zur 1976), pontine dysfunction should be regarded as a cardinal clinical sign of CPM.
