Osmotic Demyelination Syndrome in a Patient With Schizophrenia: A Case Report

Primary polydipsia affects approximately 11%-20% of patients with chronic schizophrenia, and up to one-third develop symptomatic hyponatremia. Rapid correction of hyponatremia can precipitate osmotic demyelination syndrome (ODS), involving demyelination in the central pons and extrapontine regions. ODS presenting with severe extrapyramidal symptoms (EPS) in schizophrenia has not been previously documented.

A 34-year-old man with chronic schizophrenia, maintained on oral olanzapine and monthly flupentixol decanoate, developed polydipsia-induced hyponatremia. His serum sodium was corrected at 9 mEq/L/day at a local hospital. Ten days later, he presented with fever, cough, dysarthria, dysphagia, and lead-pipe rigidity. Laboratory tests revealed leukocytosis and rhabdomyolysis without delirium or autonomic instability. Dysarthria and dysphagia were consistent with pseudobulbar palsy. Brain MRI showed T2-weighted and FLAIR hyperintensities in the bilateral basal ganglia and central pons, confirming ODS. The patient had a favorable clinical course with supportive treatment and regained independent mobility without the need for empirical immunotherapy.

This case highlights ODS as a rare but critical differential diagnosis for severe EPS in schizophrenia, particularly when presenting with lead-pipe rigidity and pseudobulbar palsy. Greater awareness of this presentation can facilitate timely diagnosis and appropriate management, avoiding misattribution to antipsychotic-induced side effects that may result in long-term morbidity or mortality.