Hyperintensity in Bilateral Posterior Limbs of Internal Capsule Due to Hypernatremia

Osmotic demyelination syndrome is usually caused by rapid correction of hyponatremia but sometimes develops from acute severe hypernatremia. Studies suggested that serum sodium increasing at the rate of less than 6~8 mmol/L in 24 hours has a low risk of osmotic demyelination syndrome, but sometimes exceptions present. Aside from the classical sites of involvement, such as pons and basal ganglia, internal capsules are rarely affected. We report a case with acute paraparesis caused by acute hypernatremia-induced extrapontine myelinolysis involving the posterior limbs of bilateral internal capsules.

A 54-year-old man was admitted for aseptic encephalitis and moved to the intensive care unit due to poor consciousness and respiratory failure. Although cerebrospinal fluid pleocytosis was improved later, acute hypernatremia due to partial diabetes insipidus developed. He presented acute paraplegia two days later with a negative result on the whole spine MRI. Although the increasing rate of serum sodium did not exceed the recommended safety range, the extrapontine myelinolysis involving posterior limbs of the bilateral internal capsule, as long as the corpus callosum, still developed. The patient regained partial walking ability after one year.

This case report extends the spectrum of classical osmotic demyelination in clinical manifestations, image findings, and the causal range of electrolyte derangements.