Sodium is the most important cation contributing to extracellular osmolality. Except for transient changes, the extracellular fluid and intracellular fluid are in osmotic equilibrium. Hypernatremia leads to increase in the volume of extracellular water with cerebral dehydration. Over distension of cerebral vessels leads to distension of cerebral vessels leading to subdural, subarachnoid and intracerebral hemorrhage. As a protective mechanism, the brain appears to generate new intracellular solute called as idiogenic osmoles. Intracellular osmolality is thereby increased, minimizing the loss of intracellular brain water. Rapid correction of such a hyperosmolar state may lead to excess movement of water into the cerebral cells due to the idiogenic osmoles leading to cerebral edema. Occasionally, this cerebral edema may be irreversible and fatal. Thus, a rapid rise or rapid fall in the serum sodium levels induces osmotic stress against a background of metabolic imbalance with osmotic opening of the blood-brain barrier or osmotic vascular injury. This results in cerebral edema and/or release of myelinotoxic factors which in turn may lead to demyelination and cellular injury. In adults, the osmotic vascular injury and cytotoxic edema is principally derived from the highly vascular grey matter which affects the adjacent myelinated white matter leading to demyelination of all regions in the brain, the pons has the greatest degree of grey-white apposition. Areas such as the striatum, thalamus, geniculate bodies and cerebral cortex-white matter junctions also have apposition of grey and white matter thus leading to central pontine myelinolysis (CPM)