Central pontine myelinolysis (CPM), now more accurately termed osmotic demyelination syndrome (ODS), results from overly rapid correction of chronic hyponatremia. In chronic hyponatremia (> 48 hours), brain cells adapt by extruding organic osmolytes (glutamate, taurine, myo-inositol, glycerophosphocholine) to prevent cerebral edema. When serum sodium is corrected too rapidly, the extracellular osmolality rises faster than brain cells can re-accumulate osmolytes, creating an osmotic gradient that draws water out of brain cells. Oligodendrocytes are particularly vulnerable to this osmotic stress, causing apoptosis and demyelination. The pons is most commonly affected (dense fiber tracts, watershed vascular zone), but extrapontine sites (basal ganglia, thalamus, cerebral white matter) occur in up to 50% of cases — hence the term ODS. Symptoms typically appear 2-6 days after sodium correction: initial improvement from hyponatremia correction is followed by new neurological deterioration (biphasic clinical course).