AN INTERESTING CASE OF NORMONATREMIC EXTRAPONTINE MYELINOLYSIS IN AN ALCOHOLIC

The clinical presentation of Osmotic Demyelination Syndrome (ODS), bifurcated into Central Pontine Myelinolysis (CPM) and Extrapontine Myelinolysis (EPM), has long been tethered to the dogma of rapid hyponatremia correction. However, contemporary neurology increasingly recognizes a phenotype of the disorder that defies this established etiology, occurring in normonatremic patients particularly within the context of chronic alcohol use disorder.[1] This report presents the comprehensive case analysis of a 35-year-old male with a significant history of alcohol dependence, who presented with acute encephalopathy and a constellation of laboratory findings—severe bicytopenia, massive lactate dehydrogenase elevation, and hypocomplementemia—that strongly mimicked a catastrophic autoimmune event such as Evans Syndrome or Systemic Lupus Erythematosus. Through rigorous exclusion of autoimmune pathologies via specific serological profiling and the subsequent identification of characteristic lesions in the basal ganglia and subcortical white matter on magnetic resonance imaging, a diagnosis of Extrapontine Myelinolysis was established. Crucially, this occurred in the absence of documented hyponatremia, challenging the conventional osmotic gradient hypothesis. This paper provides an exhaustive examination of the betraying cues in alcoholic EPM, dissecting the pathophysiology of alcohol-induced blood-brain barrier dysfunction, the mechanisms of hematological and immunological mimicry in alcoholic liver disease, and the prognostic implications of EPM when detached from its classic precipitant. The favorable response to corticosteroid therapy in this case supports emerging theories regarding the predominance of vasogenic over cytotoxic edema in alcohol-associated myelinolysis, suggesting a wider therapeutic window than previously assumed.