Osmotic
demyelination syndrome is a devastating
neurologic disorder often seen after the rapid correction of chronic
hyponatremia. The permeability of the blood-brain barrier is increased in experimental osmotic
demyelination, and some have suggested that
corticosteroids protect against this disorder by keeping the permeability of the blood-brain barrier low. We previously reported that re-lowering of the serum
sodium after rapid correction of chronic
hyponatremia was beneficial if performed early in the course (12 to 24 h). Here we compared mortality, blood-brain barrier permeability, and microglial activation in rats after the rapid correction of chronic
hyponatremia. We studied three groups of rats after correction of chronic
hyponatremia: and treated them with
sodium chloride, with or without
dexamethasone; or with
sodium chloride followed by re-induction of
hyponatremia. We found that treatment with
dexamethasone or re-induction of
hyponatremia effectively prevented the opening of the blood-brain barrier, reduced
neurological manifestations, and decreased microglial activation; however, only re-induction of
hyponatremia resulted in a significant decrease in mortality 5 days after the correction of chronic
hyponatremia. Restoring the permeability of the blood-brain barrier to normal levels did not decrease mortality. Our results suggest that after inadvertent rapid correction of
hyponatremia, treatment options should favor re-lowering serum
sodium. The increased permeability of blood-brain barrier seen in osmotic
demyelination syndrome may not be a primary pathophysiologic insult of this syndrome.