In 1949, Victor and Adams observed an alcoholic patient who developed quadriplegia and pseudobulbar palsy, and inability to chew, talk or swallow. A post-mortem confirmed their suspicion of 'a large, symmetrical, essentially demyelinative lesion occupying the greater part of the basis pontis.' This paper follows the historical evolution of central pontine myelinolysis and the changing concepts of its metabolic aetiology. Too rapid a rate of correction of hyponatraemia is the most common, but not invariable aetiology.
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