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Myelinolysis after Correction of Hyponatremia

Robert Laureno, MD; and Barbara Illowsky Karp, MD
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From the Washington Hospital Center, Washington, D.C.; and the National Institutes of Health, Bethesda, Maryland. Requests for Reprints: Robert Laureno, MD, Washington Hospital Center, Room 2A44, 110 Irving Street, NW, Washington, DC 20010. Current Author Addresses: Dr. Laureno: Washington Hospital Center, Room 2A44, 110 Irving Street, NW, Washington, DC 20010. Dr. Karp: Building 10, Room 5N-226, Office of the Clinical Director, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1997;126(1):57-62. doi:10.7326/0003-4819-126-1-199701010-00008
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Myelinolysis is a neurologic disorder that can occur after rapid correction of hyponatremia.Initially named “central pontine myelinolysis,” this disease is now known to also affect extrapontine brain areas. Manifestations of myelinolysis usually evolve several days after correction of hyponatremia. Typical features are disorders of upper motor neurons, spastic quadriparesis and pseudobulbar palsy, and mental disorders ranging from mild confusion to coma. Death may occur. The motor and localizing signs of myelinolysis differ from the generalized encephalopathy that is caused by untreated hyponatremia.

Experiments have duplicated the clinical and pathologic features of myelinolysis by rapidly reversing hyponatremia in animals.Myelinolysis is more likely to occur after the treatment of chronic rather than acute hyponatremia and is more likely to occur with a rapid rate of correction. The exact pathogenesis of myelinolysis has not been determined.

Optimal management of hyponatremic patients involves weighing the risk for illness and death from untreated hyponatremia against the risk for myelinolysis due to correction of hyponatremia.Experiments in animals and clinical experience suggest that correction of chronic hyponatremia should be kept at a rate less than 10 mmol/L in any 24-hour period.


Grahic Jump Location
Figure 1.
T2-weighted magnetic resonance imaging scan showing a symmetrical area of increased signal in the center of the pons consistent with central pontine myelinolysis.
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Grahic Jump Location
Figure 2.
Section of pons with central pontine myelinolysis.
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Grahic Jump Location
Figure 3.
Comparison of the histopathology of myelinolysis and multiple sclerosis.Left.

Microscopic pathology of the pontine lesion, showing abundant macrophages and glial response without inflammation. (Original magnification, x20.) Right. Microscopic pathology from a lesion of acute multiple sclerosis with intense perivascular inflammation. (Original magnification, x20.).

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