Uva Clinical Critical Care | Central Pontine Myelinolysis 1 Unlocking the Mysteries of Central Pontine Myelinolysis: Current Strategies and Prognosis Indunil Karunarathna 1 , S Rajapaksha 1 , Kapila De Alvis 1 , S Gunathilake 1 , U Ekanayake 1 , P Gunasena 1 , C Fernando 1 , T Hapuarachchi 1 , P Aluthge 1 , N Perera 1 , Asoka Jayawardana 1 , Sau Bandara 1 , A Warnakulasooriya 1 , K Gunawardana 1 , 1. Ministry of Health / Teaching Hospital Badulla / University of Colombo. Abstract: Central pontine myelinolysis (CPM) is a neurologic disorder that primarily affects the central pons, often as a result of rapid correction of hyponatremia. Once associated with high mortality, CPM is now better understood, with improved survival rates due to advancements in early diagnosis and management. This review explores the pathophysiology of CPM, its histopathological characteristics, clinical presentation, and the importance of cautious sodium correction to prevent its occurrence. Current recommendations emphasize limiting sodium correction to 8-12 mEq/L per 24 hours, with stricter limits for chronic hyponatremia. Diagnostic evaluation includes clinical assessment and MRI imaging, with supportive care and experimental treatments such as desmopressin and plasmapheresis being potential therapeutic options. Prevention and management involve coordinated interprofessional care, including regular monitoring of serum sodium levels. Despite improvements in survival, complications like locked-in syndrome and secondary infections can severely impact patient outcomes. Key Words: Central pontine myelinolysis, hyponatremia, osmotic demyelination syndrome, rapid sodium correction, locked-in syndrome, desmopressin, plasmapheresis, MRI, neurorehabilitation, neurologic complications. Key Points CPM Etiology: Central pontine myelinolysis (CPM) is predominantly caused by the rapid correction of hyponatremia, especially in patients with chronic or severe hyponatremia. Clinical Presentation: Symptoms typically appear 1 to 14 days after sodium correction and may include encephalopathy, quadriparesis, dysarthria, and in severe cases, locked-in syndrome and coma. Prevention: The key to preventing CPM is limiting the rate of sodium correction to 8-12 mEq/L per 24 hours, with more stringent limits in patients with chronic hyponatremia. Management: Desmopressin and hypertonic saline are useful in managing sodium correction, while supportive care measures, including ventilator support and physiotherapy, are essential for recovery. Prognosis: Survival rates have improved to 94%, but 25- 30% of patients may remain incapacitated. Early recognition and prevention are vital to improving outcomes. Interprofessional Collaboration: Effective management requires coordinated care involving intensivists, neurologists, critical care nurses, and pharmacists, with a focus on careful monitoring and prevention. Introduction Central pontine myelinolysis (CPM), a key component of osmotic demyelination syndrome (ODS), involves damage to brain regions, primarily the white matter tracts in the pons, following the rapid correction of metabolic imbalances like hyponatremia. First described in 1959 by Adams and colleagues in patients with pseudobulbar palsy and quadriplegia, initial cases were seen in individuals with alcohol use disorder and malnutrition. By the 1970s, a link between CPM and the rapid correction of sodium levels became evident. Since then, CPM has been observed in patients with conditions such as severe burns, liver transplants, anorexia nervosa, hyperemesis gravidarum, and hyperglycemia. The onset of clinical features typically occurs within days of rapidly correcting hyponatremia and can range from encephalopathy to coma or death. Though rare,