Osmotic demyelination syndrome

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It has been suggested that this article or section be merged with Central pontine myelinolysis. (Discuss)

Osmotic Demyelination Syndrome occurs with rapid correction of Hyponatremia. It is characterized by acute paralysis, dysarthria, dysphagia and other neurological symptoms.

[edit] Pathology

The currently accepted theory states that the brain cells adjust their osmolarities by changing levels of certain Osmolytes like Inositol, Betaine, Glutamine etc. In hyponatremia the levels of these osmolytes fall, preventing entry of free-water into cells. The reverse is true for hypernatremia. So rapid correction of Sodium in hyponatremia would cause the extra cellular fluid to be relatively hypertonic. Free-water would then move out of the cells. This leads to a central pontine myelinolysis, manifesting as the paralyses. Rapid correction of hypernatremia causes water to move into cells, leading to multiple cerebral hemorrhages, equally catastrophic as Osmotic Demyelination.

[edit] Management

There is no specific treatment and the syndrome is associated with high mortality and morbidity. This being a potentially avoidable disaster, following recommendations may be adhered to while maintaining sodium levels:

Hyponatremia: Correction rate=0.5-1.0meq/L/hr, with not more than 12meq/l correction in 24 hrs. If the patient has seizures (or [Na⁺]<115), correction can be attempted at up to 2meq/L/hr, but only till seizure activity lasts and [Na⁺] reaches above 125-130 meq/L.

Hypernatremia: Correct at 0.5meq/L/hr. Not more than 12 meq/L/24hrs.

Animal studies suggest inositol reduces the severity of osmotic demyelination syndrome if given prior to rapid correction of chronic hyponatraemia.^[1] Further study is required prior to its application in humans for this indication.