A case of central pontine myelinolysis in a patient on regular hemodialysis Shingo Kubo Division of Nephrology, Department of Internal Medicine, Ehime

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A case of central pontine myelinolysis in a patient on regular hemodialysis Shingo Kubo Division of Nephrology, Department of Internal Medicine, Ehime Rousai Hospital A case of central pontine myelinolysis (CPM) caused by hyponatremia in a patient on regular hemodialysis (HD) is reported. A 51-year-old woman with a history of diabetes mellitus for 15 years started HD in July 1995. There were no serious clinical problems, except for intermittent diarrhea due to a previous operation for a thrombus of the supraintestinal artery and a poorly controlled blood glucose level. General fatigue occurred around August 10, 1996. A few days later, gait disturbance and dysarthria appeared, while a brain computerized tomography revealed no abnormalities. Additional intake of salt was recommended, because hyponatremia of 125mEq/l was also found. Magnetic resonance imaging on August 21 revealed a low intensity area in the central pons. Several lines of evidence led to the diagnosis of CPM. The deliberate slow correction of serum sodium concentration by administration of sodium (170mEq/day), reinforcement of medication for diarrhea, control of water volume and strict correction of the blood glucose level improved the neurological disorders. It was considered that loss of sodium due to intermittent severe diarrhea and anorexia as well as water excess due to inadequate dry weight and hyperosmolarity with high blood glucose level were the main causes of her hyponatremia. There was also a possibility that unexpected rapid correction of her serum sodium concentration by the normal dialysate composition (Na; 140mEq/l) during HD caused or exacerbated the CPM. In conclu sion, it is necessary to diagnose immediately and to treat deliberately a case of CPM, because HD therapy has a tendency to bring on an imbalance and unexpected rapid correction of electrolyte concentration.

A: Computerized tomography on August 13 showed no abnormal ities. B: Magnetic resornance imaging (MRI) on August 21 revealed a low intensity area located symmetrically in the central pons.(t2 - weighted image) C: The previous low intensity area almost disappeared. (MRI on November 27; T2-weighted image)

1) Adams RD, Victor M, Mancall EL: Central pontine myelinolysis. A hitherto undescribed disease occur ring in alcoholic and malnourished patients, Arch Neurol Psychiatry 81: 154-172, 1958 2) Tomlinson B, Pierides A, Bradley W: Central pontine myelinolysis. Two cases with associated electrolyte disturbance. Q J Med 45: 373-386, 1976 3) Sterns RH, Riggs JE, Schochet SS: Osmotic demyelination syndrome following correction of hyponatremia. N Engl J Med 314: 1535-1542, 1986 4) Klieinschmidt-DeMasters BK, Norenberg MD: Rapid correction of hyponatremia causes demyelination: Relation to central pontine myelinolysis. Science 211: 1068-1079, 1981 5) Laureno R: Central pontine myelinolysis following rapid correction of hyponatremia. Ann Neurol 13: 232-242, 1983 7) McCormic WF, Danniel CM: Central pontine myelinolysis. Arch Intern Med 119: 444-478, 1967 8) Kandt RS, Heldrich FJ, Moser HW: Recovery from probable central pontine myelinolysis associated with addison's disease. Arch Neurol 40: 118-119, 1983 9) Norenberg MD: A hypothesis of osmotic endoth elial injury: A pathogenetic mechanism in central pontine myelinolysis. Ann Neurol 40: 66-69, 1983 10) Messert B, Orrison WW, Hawkin MJ, Quaglieri CE: Central pontine myelinolysis: Considerations on etiology, diagnosis and treatment. Neurology 29: 147-160, 1979

14) DeWitt LD, Buonanno FS, Kistler JP, Zeffiro T, DeLaPaz RL, Brady TJ, Rosen BR, Pykett IL : Central pontine myelinolysis: Demonstration by nuclear magnetic resonance. Neurology (Cleve land) 34: 570-576, 1984