Introduction
Demyelinating diseases are disorders characterized by destruction of the myelin sheath in the CNS. MRI is the modality of choice for diagnosis, staging, and follow-up.
The most common example is multiple sclerosis (MS), but other demyelinating conditions (ADEM, NMOSD, MOG disease) must also be considered.
MRI Protocol for Demyelinating Diseases
- T1-weighted (± contrast): hypointense “black holes.”
- T2-weighted / FLAIR: hyperintense white matter plaques.
- DWI/ADC: differentiates acute demyelination from stroke.
- Post-contrast T1: shows active lesions (enhancement).
- Spinal cord sequences: sagittal T2, axial T2, STIR.
Typical MRI Findings in Demyelinating Diseases
1. Multiple Sclerosis (MS)
- Brain lesions:
- T2/FLAIR hyperintense plaques in periventricular, juxtacortical, infratentorial, and spinal cord regions.
- “Dawson’s fingers” → ovoid lesions perpendicular to ventricles (classic).
- Black holes on T1 (chronic axonal loss).
- Contrast enhancement → active lesions.
- Spinal cord:
- Short segment (<2 vertebral bodies).
- Peripheral / asymmetric lesions.
2. Acute Disseminated Encephalomyelitis (ADEM)
- Post-infectious or post-vaccination.
- MRI features:
- Large, poorly marginated, asymmetric T2 hyperintensities.
- Involves both white and grey matter (basal ganglia, thalami).
- Usually monophasic.
3. Neuromyelitis Optica Spectrum Disorder (NMOSD)
- Autoimmune against aquaporin-4.
- MRI features:
- Optic nerve: long, bilateral involvement.
- Spinal cord: longitudinally extensive transverse myelitis (≥3 vertebral segments).
- Brain: periependymal lesions around 3rd and 4th ventricles, area postrema.
4. MOG-Associated Disease (MOGAD)
- Anti-MOG antibody-related.
- MRI features:
- Bilateral optic neuritis .
- ADEM-like large lesions in children.
- Spinal cord: longitudinal lesions, often with conus involvement.
| Feature | Multiple Sclerosis (MS) | ADEM | NMOSD | MOGAD |
|---|---|---|---|---|
| Typical Age | Young adults (20–40 yrs) | Children, young adults | Any age (often young females) | Children & young adults |
| Clinical Course | Relapsing–remitting / progressive | Monophasic, post-infection/vaccine | Relapsing, severe attacks | Relapsing, steroid responsive |
| Brain MRI | • Periventricular ovoid plaques (Dawson’s fingers) • Juxtacortical + infratentorial lesions • Black holes on T1 | • Large, asymmetric, poorly marginated lesions • Grey + white matter involvement • Often basal ganglia, thalamus | • Less brain involvement • Lesions around 3rd/4th ventricles, aqueduct, area postrema | • ADEM-like large lesions in children • Cortical/subcortical involvement • Fluffy/ill-defined |
| Optic Nerve | Short segment, unilateral | Can be involved, usually mild | Bilateral, long segment involvement | Bilateral, long & severe optic neuritis |
| Spinal Cord MRI | • Short lesions (<2 vertebral bodies)• Peripheral/asymmetric | • Large but short lesions possible | Longitudinally extensive transverse myelitis (≥3 vertebral segments) | • Long lesions common• Often involves conus medullaris |
| Enhancement | • Variable: active lesions enhance• Incomplete rings possible | • Patchy enhancement | • Variable, cord & optic nerve enhancement | • Patchy or ring-like enhancement |
| Key Differentiator | Dawson’s fingers + short cord lesions | Large, ill-defined, grey + white matter lesions | Long cord lesions + bilateral optic neuritis | Long optic neuritis + conus involvement |
Differential Diagnosis (MRI Clues)
- Ischemia: wedge-shaped, vascular territory, restricted diffusion.
- Tumefactive demyelination: >2 cm, incomplete ring enhancement, less mass effect than neoplasm.
- Infection: rim-enhancing abscess (restricted diffusion).
Key Teaching Points
- MS: Dawson’s fingers, short segment cord lesions.
- ADEM: large, ill-defined, grey + white matter lesions.
- NMOSD: long spinal cord lesions, bilateral optic neuritis.
- MOGAD: optic neuritis + conus medullaris involvement.
- MRI contrast → separates active vs chronic lesions.
✅ Conclusion
MRI is the cornerstone in evaluating demyelinating diseases. By analyzing location, morphology, lesion length, and enhancement patterns, radiologists can differentiate MS from ADEM, NMOSD, and MOG disease — guiding early diagnosis and management.
