Abstract
Central pontine myelinolysis (CPM) was first described in 1959 s a complication seen in alcoholic malnourished patients [1]. It efers to a demyelinating lesion of the central pons, thought to arise econdary to osmotic stress and be part of an osmotic demyelinaion syndrome (ODS) that can affect areas outside of the brain stem ike axons in the putamina, caudate nuclei, thalami, cerebellum, plenium of the corpus callosum, and subcortical white matter [2]. utative pathomechanisms, in conjunction with osmotic dysreguation may include break down of the blood brain barrier and an ctive demyelination process involving activated glial and inflamatory cells. Here we present a case of a patient who developed PM in the setting of acute hypoglycemia and Levofloxacin adminstration.
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