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| Year : 2000 | Volume
: 48
| Issue : 1 | Page : 97 |
Pontine and extrapontine myelinolysis following rapid correction of hyponatremia.
Srivastava T, Singh P, Sharma B
Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
Correspondence Address:
Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarh, 160012, India.
How to cite this article:
Srivastava T, Singh P, Sharma B. Pontine and extrapontine myelinolysis following rapid correction of hyponatremia. Neurol India 2000;48:97 |
A 45 year female presented with pain epigastrium and vomiting for 5 days. Serum sodium was 116 mmol/L which was rapidly corrected to 142 mmol/L within 24 hours. Over the days following correction of hyponatraemia, there was progressive obtundation in sensorium. There was hyperreflexia, quadriparesis and bilateral sixth nerve palsies. MRI brain showed abnormal hyperintensity on T2W image in the central pons [Figure. 1] and the121 caudate head and putamen bilateral symmetrically [Figure. 2]. T1W image shows hypointensity in the basal ganglion [Figure. 3].
Comments
Pontine signal abnormalities have a broard differential diagnosis that include infarct, demyelination, gliomas, metastasis and encephalitis. Bilateral symmetrical signal changes in the basal ganglionhave a differential diagnosis of hypoxia, CO poisoning, Wilson's disease, Wernicke's encephalopathy, Leigh's disease etc. However, pontine and concomitant basal ganglion involvement is fairly specific for osmotic pontine and extrapontine myelionlysis. Rapid correction of hyponatremia is well known cause for osmotic myelionlysis.
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