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Demyelinating Disorders of the Nervous System Due to Osmotic Disequilibrium | Chapter 04 | Current Trends in Medicine and Medical Research Vol. 4

Introduction: In central nervous system (CNS), oligodendrocytes form myelin. In peripheral nervous system large proportions of axons are unmyelinated, instead they are ensheathed by non myelinating schwann cells  and  arranged  in  Remak  bundles.  Osmotic  demyelination  (ODS)  syndrome  is  a neurologic disorder that can occur after rapid correction of hyponatremia. Acute hypernatremia results in  sudden  shrinkage  of  brain  cells  leading  to  parenchymal  or  subarachnoid hemorrhages  and/or subdural hematomas mainly in pediatric patients.

Aim: Our aim is to present a case of hypernatremia which has led on to a flaccid quadriparesis due to brain  stem  demyelination.  Rapid  correction  of  hypernatremia  as  a  cause  for  pyramidal  tract demyelination is not documented in the literature.

Presentation  of  Case: A 53 year old male was brought to the emergency services with suspected stroke. He was treated with intravenous mannitol and oral glycerine from the primary health centre. We detected hypoglycemia (blood sugarwas 50mg/dl-Ref range: ≤70 mg%) and dextrose was given intravenously. Subsequently the patient went into a hypernatremic state with serum sodium 170 milli equivalents  /liter  which  was  corrected  rapidly.  This  was  corrected  over  48  hours  to  140 milli equalents/litre. The rate of correction exceeded 0.62 millimols/liter/hour (Ideal: 0.5 mmol/L/h). On the 6th  day  the  patient  developed  acute  quadriparesis.  Magnetic  resonance  imaging  (MRI)  of  brain revealed  bilateral  symmetric  demyelination  of  the  corticospinal  tracts.  Over  six  months  the neurological deficit improved with complete resolution of the changes in previous MRI.

Discussion: Osmotic Demyelination Syndrome (ODS) has been a recognized complication of rapid correction of hyponatremia. Experiments in animals and clinical experience suggest that correction of chronic hyponatremia should be kept at a slow rate to combat this complication. The characteristic sites  include  pons  and  basal  ganglia.  Such  a  complication  has  not  been  described  due  to  rapid correction of hypernatremia. This is probably the first case report in the literature where acute onset of quadriparesis resulted from demyelination of the pyramidal tract consequent to a rapid correction of hypernatremia. We had to wait about 6 months for the patient to obtain a complete functional recovery and the neuro imaging was repeated after 6 months to confirm the disappearance of the initial findings thus implicating rapid correction of hypernatremia as the cause of his morbidity.

Conclusion: This  is  the  first  time  extrapontine  reversible  myelinolysis  due  to  rapid  correction  of hypernatremia has been documented. To prevent this potentially fatal complication it will be prudent if hypernatremia  is  corrected  slowly.  Osmotic  Demyelination  Syndrome  (ODS)  can  occur  with  rapid correction of hyponatremia or hypernatremia. The first of its kind our report highlights the importance of rate of correction of Sodium in the brain which may functionally interfere with the rapidly conducting fibers rich in oligodendrocytes resulting in transient or permanent neuronal dysfunction.

Author(s) Details

Dr. C. Rajasekharan
Department of Medicine, Medical College Hospital, Thiruvananthapuram, Kerala, 695011, India.

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