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Osmotic demyelination syndrome (ODS) is a non-inflammatory demyelinating disorder of the central nervous system that occurs following rapid correction of chronic hyponatremia. It includes:

Central pontine myelinolysis (CPM) – affects the central pons
Extrapontine myelinolysis (EPM) – affects basal ganglia, thalami, cerebral cortex, or cerebellum </aside>

https://youtu.be/jeF3qw1Z_3E?si=gyvd2Urc_fZdAyms

https://www.youtube.com/watch?v=SWaM54mCWNg

https://youtu.be/fUAX9AtUDwU

Etiology

Risk Factors:

Cause	Notes
Rapid correction of hyponatremia	Most common and well-established cause
• Correction by >8–10 mmol/L/24 h in chronic hyponatremia is considered unsafe.
Hyponatremia risk factors	Burns, SIADH, adrenal insufficiency
Chronic alcoholism	↑ risk due to malnutrition and electrolyte derangement
Malnutrition / liver disease	Seen in liver transplant patients
Hyperosmolar states	Hyperglycemia, dialysis disequilibrium

Pathophysiology

Rapid shift in osmolality leads to oligodendrocyte apoptosis, BBB disruption, and inflammatory demyelination
The centrally located myelinated fibers in the pons are highly susceptible
Sparing of axons and neurons is typical

Clinical Features

Presentation	Description
Biphasic illness	Initial improvement post-Na+ correction → delayed worsening (2–6 days later)
Pseudobulbar palsy	Dysarthria, dysphagia, emotional lability
Quadriparesis/quadriplegia	From corticospinal tract involvement
"Locked-in" syndrome	Severe cases with pontine damage and preserved consciousness
Movement disorders	Parkinsonism, dystonia, chorea (in extrapontine forms)
Seizures, confusion	If cortex or thalami involved

Radiology

https://youtu.be/N0ghdirpfaI?si=eednIPB4TPBmuhSx

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MRI shows characteristic symmetric T2 hyperintensities in the central pons and/or deep gray structures, often without enhancement.

Timing: Imaging may be normal in the first 24–48 hours. Abnormalities often appear 2–10 days after clinical symptoms. </aside>