Systemic pathology: central pontine myelinolysis: practice question

A Pathology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Pathology · Systemic pathology: central pontine myelinolysis

Sample item

A malnourished alcoholic man with sodium 108 mEq/L is given hypertonic saline, and sodium rises to 128 mEq/L within a day. Three days later he develops flaccid quadriparesis, dysarthria and difficulty with eye movement. MRI shows a symmetrical lesion in the basis pontis. What is the mechanism?

AT-cell mediated autoimmune attack on myelinBOsmotic injury to oligodendrocytes from rapid sodium correctionCThiamine-dependent mamillary body necrosisDReactivation of JC virus in oligodendrocytes

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

B. Osmotic injury to oligodendrocytes from rapid sodium correction

Rapid correction of chronic hyponatraemia shrinks brain cells that have adapted to a low osmolality. Oligodendrocytes are especially vulnerable, so myelin is lost in the pons while axons are preserved. Alcoholism, malnutrition and liver disease increase the risk.

Option by option

A. T-cell mediated autoimmune attack on myelin
Autoimmune T-cell attack describes multiple sclerosis, with relapsing lesions in different sites.
B. Osmotic injury to oligodendrocytes from rapid sodium correction (correct)
Correct. Rapid osmotic shifts injure oligodendrocytes, causing demyelination in the pons.
C. Thiamine-dependent mamillary body necrosis
Thiamine deficiency causes Wernicke encephalopathy with mamillary body and periaqueductal lesions.
D. Reactivation of JC virus in oligodendrocytes
JC virus causes progressive multifocal leukoencephalopathy in immunosuppressed patients, not after 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.

Questions about this Pathology question

What is the answer to this Pathology question?

The best answer is B, Osmotic injury to oligodendrocytes from rapid sodium correction. Rapid correction of chronic hyponatraemia shrinks brain cells that have adapted to a low osmolality.

Why is "T-cell mediated autoimmune attack on myelin" not the answer?

Autoimmune T-cell attack describes multiple sclerosis, with relapsing lesions in different sites.

Why is "Thiamine-dependent mamillary body necrosis" not the answer?

Thiamine deficiency causes Wernicke encephalopathy with mamillary body and periaqueductal lesions.

Why is "Reactivation of JC virus in oligodendrocytes" not the answer?

JC virus causes progressive multifocal leukoencephalopathy in immunosuppressed patients, not after sodium correction.

What concept does this question test?

It tests Systemic pathology: central pontine myelinolysis in Pathology. Oligodendrocytes are especially vulnerable, so myelin is lost in the pons while axons are preserved. Alcoholism, malnutrition and liver disease increase the risk.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Systemic pathology: central pontine myelinolysis?

Learn each disease as a bundle: cause, key histology, markers, and the clinical hallmark. Then use the flashcards and the other Pathology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.