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White matter diseases on MRI
Multiple sclerosis disseminates in space (periventricular, juxtacortical, infratentorial, spinal cord) and in time, NMOSD causes long spinal cord and optic nerve lesions, ADEM is a single event in a child after infection, and PML is a non-enhancing subcortical lesion in an immunosuppressed patient.
Why it matters in the exam
Under McDonald 2017, dissemination in space (DIS) is at least one T2 lesion in two of four areas: periventricular, cortical or juxtacortical, infratentorial and spinal cord. Dissemination in time (DIT) is enhancing and non-enhancing lesions on the same scan, or a new lesion on a later scan. Typical lesions: ovoid and perpendicular to the ventricles (Dawson fingers), in the corpus callosum body, with the "central vein sign". In the spinal cord: a short lesion (less than two vertebral segments), peripheral and dorsolateral.
NMOSD (AQP4 antibodies): a spinal cord lesion of 3 or more vertebral segments (LETM) in the centre of the cord, long optic neuritis reaching the chiasm, and lesions in the area postrema (nausea and hiccups) and around the third and fourth ventricles. ADEM: mainly children, after infection or vaccination, encephalopathy, large bilateral asymmetric lesions in the white matter and deep nuclei — all "of the same age" and usually a single episode. PML (JC virus): in HIV patients with low CD4 or on natalizumab; a subcortical lesion involving the U-fibres, asymmetric, without mass effect and without or with little enhancement, dark on T1.
Small vessel disease: periventricular and deep white matter foci (Fazekas grading), lacunes and microbleeds — a few such foci are common in normal ageing. Mimics: alcohol — Wernicke (medial thalami, mammillary bodies, periaqueductal), Marchiafava-Bignami in the corpus callosum, and osmotic demyelination in the central pons after rapid correction of hyponatraemia. Herpes encephalitis — mesial temporal lobe and insula, bilateral and asymmetric. CJD — restricted diffusion in the cortex (cortical ribboning) and basal ganglia. Mesial temporal sclerosis in epilepsy — a small hippocampus bright on T2 with loss of internal architecture.
Key points
- DIS: two of four areas; DIT: enhancing and non-enhancing together.
- Multiple sclerosis in the cord — short and peripheral.
- NMOSD — 3 segments or more, central.
- ADEM — child, after infection, lesions of the same age.
- PML — subcortical, no enhancement or mass effect.
Summary table
| Disease | Key feature | Spinal cord | Clinical clue |
|---|---|---|---|
| Multiple sclerosis | Dawson fingers, corpus callosum, central vein | Short, peripheral | Young woman, relapsing episodes |
| NMOSD | Area postrema, long optic nerve to the chiasm | 3 segments or more, central | AQP4 antibodies |
| ADEM | Large lesions of the same age, deep nuclei | May be involved | Child after infection, encephalopathy |
| PML | Subcortical, U-fibres, no mass effect | Not typical | HIV or natalizumab |
| Small vessel disease | Fazekas, lacunes | Not involved | Age, hypertension |
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Sources
- McDonald Criteria for Multiple Sclerosis (Thompson et al.), 2017 revision — MRI dissemination in space and time
- MAGNIMS–CMSC–NAIMS Consensus Recommendations on the Use of MRI in Multiple Sclerosis, 2021 — Diagnosis and monitoring
- International Consensus Diagnostic Criteria for Neuromyelitis Optica Spectrum Disorders, 2015 — Imaging features
Sources are given for further reading; the text is written afresh and not copied from them.
Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.