Central pontine and extrapontine myelinolysis after correction of hyponatremia

BACKGROUND- Central pontine myelinolysis can cause pseudobulbar palsy, quadriplegia, and death attributable to symmetric myelin damage in the center of the basis pontis. Extrapontine myelinolysis symmetrically affects thalamocapsular regions, neostriatum, and other territories. Myelinolysis usually results from the rapid correction of hyponatremia. REVIEW SUMMARY- The clinical spectrum of myelinolysis includes seemingly asymptomatic cases, transient encephalopathies, mutism, behavioral changes, stupor, and coma in addition to the classic syndrome of spastic quadriparesis and pseudobulbar palsy. As paralysis resolves, movement disorders or ataxia may become evident. Magnetic resonance imaging is the best diagnostic test, but the lesions may not be visible until 1 to 2 weeks after the onset of the illness. Myelinolysis can follow a rapid (greater than or equal to 10 mEq/L/d) rise in sodium regardless of the cause of hyponatremia and method of therapy. It is more to occur after correction of chronic hyponatremia (greater than or equal to 48-hour duration) than acute hyponatremia. CONCLUSIONS- To minimize the incidence of myelinolysis, the therapeutic rise in sodium associated with the management of hyponatremia should be less than 10 mEq/L on the first day of treatment whenever possible. An even slower rate of correction is adequate after hyponatremic symptoms are controlled. Because the rise in sodium is unpredictable in a given individual, frequent monitoring of the sodium level is necessary. Should the sodium rise more quickly than anticipated, relowering of the sodium level may help minimize morbidity. The administration of dilute fluid and deamino-8-D-arginine vasopressin has been used for this purpose in the initial days of myelinolytic symptoms. When severe symptoms of myelinolysis are established despite all efforts, supportive care may allow good recovery over the following months.