What are the MRI features of Osmotic Demyelination Syndrome (ODS)?

MRI Features of Osmotic Demyelination Syndrome

Osmotic demyelination syndrome (ODS) demonstrates characteristic symmetric T2/FLAIR hyperintensity and T1 hypointensity in the central pons ("central pontine myelinolysis"), often with additional extrapontine involvement in the basal ganglia, thalami, and cerebral white matter, showing restricted diffusion in acute phases that may predict clinical outcomes. 1, 2

Classic Pontine Features

Central pontine involvement is the hallmark finding:

• Symmetric T2 hyperintensity centrally located in the pons, characteristically sparing the peripheral pontine fibers and corticospinal tracts (creating a "trident" appearance) 1, 2
• T1 hypointensity in the same distribution 1
• FLAIR hyperintensity matching the T2 abnormality 1
• The lesions typically spare the ventrolateral pons, distinguishing ODS from vascular infarction 2

Critical distinction from other pontine pathology: Unlike amyloid angiopathy or cerebrovascular disease which show asymmetric or peripheral pontine involvement, ODS demonstrates symmetric central pontine lesions 3. This symmetric central distribution is a "red flag" feature that helps differentiate ODS from multiple sclerosis or other demyelinating conditions 3.

Extrapontine Manifestations

Extrapontine myelinolysis (EPM) occurs in 10-50% of ODS cases:

• Basal ganglia (putamen, caudate) showing bilateral symmetric T2/FLAIR hyperintensity 4, 5
• Thalami with similar signal characteristics 5
• Cerebral white matter involvement, particularly in deep white matter regions 5
• Cerebellum in some cases 2

Temporal progression insight: Extrapontine lesions may actually precede central pontine changes, with restricted diffusion appearing first in the basal ganglia before pontine involvement becomes evident 4. This suggests that early MRI showing isolated extrapontine restricted diffusion in high-risk patients may predict subsequent pontine involvement 4.

Advanced MRI Sequences

Diffusion-weighted imaging (DWI) provides critical prognostic information:

• Acute phase (first week): Restricted diffusion with hyperintensity on DWI and reduced ADC values in affected regions 6, 5
• Prognostic value: The degree and duration of ADC reduction correlates with clinical severity and recovery potential 6
• Normalization of ADC values (typically within 1-4 weeks) parallels clinical improvement and suggests better prognosis 6
• Persistent ADC reduction beyond 1 month indicates poor prognosis 6

Important caveat: Unlike acute ischemic stroke, ODS shows mildly elevated ADC values in subacute/chronic phases, distinguishing it from pure cytotoxic edema and suggesting a mixed demyelinating process rather than simple demyelination 5.

Temporal Evolution on MRI

Biphasic imaging pattern:

• Days 1-3: MRI may be normal despite clinical symptoms; DWI is most sensitive for early detection 4
• Days 4-7: Classic T2/FLAIR hyperintensity becomes apparent with restricted diffusion 1, 6
• Weeks 2-4: ADC values normalize in patients with good recovery 6
• Months 1-4: T2/FLAIR hyperintensity may persist despite clinical improvement, or completely resolve in favorable cases 6

Clinical pitfall: The lag between symptom onset and MRI abnormalities means that a negative initial MRI does not exclude ODS 4. Repeat imaging at 3-7 days is warranted when clinical suspicion remains high 4.

Diagnostic Algorithm

When to suspect ODS on imaging:

1. Symmetric central pontine T2/FLAIR hyperintensity with peripheral sparing in any patient with recent sodium fluctuations 1, 2
2. Bilateral basal ganglia restricted diffusion in high-risk patients (alcoholism, liver disease, dialysis, malnutrition) even before pontine changes appear 4
3. Normonatremic patients with unexplained neurological deterioration following trauma, surgery, or critical illness—ODS can occur without documented hyponatremia 1

Optimal imaging protocol:

• Sagittal and axial T1-weighted sequences 1
• Axial T2-weighted and FLAIR sequences 1, 2
• DWI with ADC mapping (essential for early detection and prognosis) 6, 4, 5
• Contrast enhancement is typically not necessary for diagnosis but may show mild enhancement in some cases 7

Key differentiating features from mimics:

• Unlike NMOSD: No longitudinally extensive spinal cord lesions, no area postrema involvement 3
• Unlike MS: Symmetric rather than asymmetric distribution, central rather than perivenular location 3
• Unlike ischemic stroke: Symmetric distribution, characteristic central pontine location with peripheral sparing 3