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

J Korean Neurol Assoc > Volume 11(2); 1993 > Article

Journal of the Korean Neurological Association 1993;11(2): 248-253.

고나트륨성, 고혈당성, 비케톤성 고삼투압성 혼수 후에 발생한 중심성 뇌교 수초용해 (Central Pontine Myelinolysis)

김상윤, 유경호,송홍기,김승현,이병철

한림대학교 신경과.

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

Sang-Yun Kim, M.D., Kyung-Ho Yu, M.D., Hong-Ki Song, M.D., Seung-Hyun Kim, M.D., Byung-Chul Lee, M.D.

Department of Neurology, College of Medicine Hallym University

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.