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Psychiatry · Substance use: osmotic demyelination after sodium correction
Sample itemA malnourished chronic drinker is admitted with a serum sodium of 106 mmol/L, and the level is corrected to 128 mmol/L within 24 hours. Four days later he develops dysarthria, dysphagia and flaccid quadriparesis, and becomes unable to move anything except his eyes. What is the most likely diagnosis?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Central pontine myelinolysis
Rapid correction of chronic hyponatraemia in alcoholics and the malnourished causes osmotic demyelination, classically of the basis pontis. It produces a delayed quadriparesis, pseudobulbar signs and a locked-in state, and prevention depends on limiting correction to a slow rate.
Option by option
A. Wernicke encephalopathy
Wernicke encephalopathy presents with confusion, ophthalmoplegia and ataxia, and is not linked to sodium correction.
B. Central pontine myelinolysis (correct)
Correct. Delayed quadriparesis with preserved eye movements after rapid sodium correction is typical of pontine demyelination.
C. Hepatic encephalopathy
Hepatic encephalopathy causes fluctuating consciousness and asterixis, not a locked-in state following sodium correction.
D. Marchiafava-Bignami disease
Marchiafava-Bignami disease involves corpus callosum demyelination in malnourished drinkers and is not tied to sodium correction.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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