Answer
Answer
Adams et al described central pontine myelinolysis (CPM) as a unique clinical entity. They published their findings in 1958, observing that patients who suffered from alcoholism or malnutrition developed spastic quadriplegia, pseudobulbar palsy, and varying degrees of encephalopathy or coma from acute, noninflammatory demyelination that centered within the basis pontis. [1]
Physicians currently recognize that central pontine myelinolysis occurs inconsistently as a complication of severe and prolonged hyponatremia, particularly when corrected too rapidly. [2] Standard of care requires judicious treatment of electrolyte disturbances to reduce the incidence of osmotic myelinolysis. [3]
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Media Gallery
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T2-weighted MRI scan of the brain demonstrating patchy areas of signal change within the pons that are consistent with demyelination or central pontine myelinolysis. Courtesy of Dr Andrew Waclawik, Department of Neurology, University of Wisconsin, Madison.
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