A 58-year-old man with chronic liver disease and severe hyponatremia (Na 118 mEq/L) is admitted. His serum sodium is corrected at 12 mEq/L over 24 hours. On day 3, he develops progressive quadriparesis, dysphagia, and dysarthria. Axial MRI brain at the pons level shows a characteristic non-enhancing T2-hyperintense lesion in the central region of the structure marked **A**, sparing the periphery, with a "bat wing" appearance on imaging. Which of the following best explains this clinical and radiological presentation?

Explanation

## Why Central pontine myelinolysis (osmotic demyelination syndrome) due to rapid correction of chronic hyponatremia is right Central pontine myelinolysis (CPM) is a demyelinating disorder of the central pons caused by RAPID CORRECTION of chronic hyponatremia. The clinical presentation—progressive quadriparesis, dysphagia, and dysarthria developing 1–7 days after Na+ correction—is pathognomonic. The MRI finding of a non-enhancing, T2-hyperintense lesion in the central pons with a characteristic "bat wing" or "trident sign" appearance (sparing the periphery) is the diagnostic hallmark. This case demonstrates overcorrection (12 mEq/L/24 h exceeds the safe limit of 6–8 mEq/L/24 h for chronic hyponatremia), placing the patient at high risk. The structure marked **A** (pons) is the primary site of demyelination in CPM, and the clinical syndrome reflects damage to the compact motor and brainstem pathways within it (Gray's Anatomy 42e Ch 22; Harrison 21e Ch 439). ## Why each distractor is wrong - **Acute basilar artery thrombosis causing locked-in syndrome**: While basilar artery occlusion does cause locked-in syndrome with bilateral pyramidal tract infarction and CN VI/VII destruction, the MRI would show ACUTE INFARCTION (restricted diffusion, enhancement, acute ischemic changes) rather than the non-enhancing, demyelinating T2 lesion described. Locked-in syndrome also presents acutely, not over 3 days post-Na correction. The clinical timeline and imaging pattern do not fit acute stroke. - **Millard-Gubler syndrome from medial pontine infarction**: Millard-Gubler syndrome presents with ipsilateral CN VI and CN VII palsies plus contralateral hemiparesis. It is caused by MEDIAL pontine infarction (basilar artery territory), not demyelination, and would show acute ischemic changes on MRI, not the characteristic central demyelinating lesion. The clinical presentation lacks the cranial nerve findings (CN VI/VII palsies) expected in this syndrome. - **Foville syndrome with inability to look toward the affected side**: Foville syndrome results from MEDIAL pontine infarction affecting the CN VI nucleus and PPRF (paramedian pontine reticular formation), causing ipsilateral gaze palsy in addition to CN VI and CN VII palsies and contralateral hemiparesis. Like Millard-Gubler, it is an acute ischemic stroke, not a demyelinating process, and would not produce the characteristic non-enhancing central pontine T2 lesion. The patient has no gaze palsy or cranial nerve findings. **High-Yield:** Central pontine myelinolysis = demyelination of central pons from RAPID Na+ correction of chronic hyponatremia; safe correction rate ≤6–8 mEq/L/24 h; MRI shows non-enhancing T2-hyperintense "bat wing" lesion sparing periphery; clinical syndrome includes quadriparesis, dysphagia, dysarthria, and locked-in appearance. [cite: Gray's Anatomy 42e Ch 22; Harrison 21e Ch 439]