J Korean Neurol Assoc.  1993 Jun;11(2):248-253.

Central Pontine Myelinolysis after Hypernatremic, Hyperglycemic, non-ketotic Hyperosmolar Coma

• Kim SY
• Yu KH
• Song HK
• Kim SH
• Lee BC

Abstract

Until recently the mechanism involved in the genesis of central pontine myelinolysis (CPM) has been obscure. During the past decade, attention has been drawn to the rapid correction or over-correction of hyponatremia as an important causative factor. Whether the myelinolytic lesions are related to a shift in osmolality or more specifically linked to changes in the sodium ion remains to be elucidated. But more recently, organic osmolytes known previously as idiogenic osmoles appear as an important factor that play an important role in the cellular adaptation to osmolality changes and in the occurance of the central pontine myelirrolysis. Another noteworthy feature of CPM is that patients already afflicted with certain serious, debilitating illnesses-malnourished alcoholcs, advanced systemic cancer. Acute and chronic infection, chronic liver disease, renal transplantation, and chronic hemodialysis, severe burn, etc. are at greater risk for the CPM than healthy people. In this case, a patient with history of chronic alcohol abuse and central pontine myelinolysis is described. He suffered relatively suddenly developed quadriparesis after an episode of hypematremic. Hyperglycemic. Non-ketotic hyperosmolar coma But hyponatremia or rapid correction of hvponatremia never occurred. We conclude that CPM of this case was induced by the disturbance of serum osmolality resulted from hyperglycemia and/or hypernatremia.

MeSH Terms

Alcoholism
Burns
Coma*
Humans
Hyperglycemia
Hypernatremia
Hyponatremia
Kidney Transplantation
Liver Diseases
Myelinolysis, Central Pontine*
Osmolar Concentration
Quadriplegia
Renal Dialysis
Sodium
Sodium