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.
View Volume: https://doi.org/10.9734/bpi/ctmmr/v4
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