White Matter Disease on MRI
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Direct answer
White matter hyperintensities on T2/FLAIR MRI are read as patterns, not as spots, and the pattern that organises the differential is anatomy plus symmetry plus clinical tempo. Small-vessel ischaemic disease gives periventricular and deep confluencing lesions in an older hypertensive or diabetic patient, graded by the Fazekas scale; multiple sclerosis gives perivenular ovoid lesions perpendicularly tracking the ventricles — Dawson fingers — with juxtacortical, infratentorial and spinal lesions satisfying dissemination in space; PRES produces parieto-occipital vasogenic oedema in eclampsia or severe hypertension; osmotic demyelination centres on the central pons sparing the periphery; PML is asymmetric, progressive and immunosuppression-linked; and the leukodystrophies are symmetric, confluent and progressive in children. Symmetry, age and tempo convert a picture of "white spots" into one of six diagnoses.
What you must remember
- Dawson fingers: periventricular ovoid lesions oriented perpendicular to the ventricular wall, representing perivenular inflammation — the named MS sign, alongside juxtacortical U-fibre lesions, infratentorial pontocerebellar involvement and asymmetric spinal cord plaques.
- McDonald dissemination in space: at least one T2 lesion in two or more of periventricular, juxtacortical, infratentorial or spinal cord regions; optic nerve involvement counts clinically.
- Fazekas scale: periventricular and deep white matter hyperintensities graded 0-3 each (none, caps or thin rim, smooth halo or confluence, large confluent); grade 3 with microbleeds and lacunes in a hypertensive patient is advanced small-vessel disease.
- PRES: posterior predominant parieto-occipital vasogenic oedema, often symmetric, in eclampsia, hypertension or immunosuppression — Indian maternal postpartum clinics see it after eclampsia, and it largely reverses with blood-pressure control.
- Osmotic demyelination (central pontine myelinolysis): symmetric central pontine T2 hyperintensity sparing the ventral pons and periphery, after rapid sodium correction in hyponatraemia; extrapontine basal ganglia variants occur.
- NMO spectrum: longitudinally extensive transverse myelitis over three or more segments with AQP4 antibodies, plus optic neuritis — Dawson fingers are conspicuously absent.
- PML: asymmetric, frontoparietal, T2-bright lesions with little enhancement, in HIV or natalizumab-treated patients; Susac (corpus callosum snowballs) and ADEM (monophasic, post-infectious, paediatric) complete the exam shortlist.
Sorting one white-matter consult
A 28-year-old woman has two episodes of transient sensory loss weeks apart. FLAIR shows periventricular ovoid lesions perpendicular to the lateral ventricles, a juxtacortical frontal lesion and a cerebellar peduncle plaque. Periventricular plus juxtacortical plus infratentorial satisfies McDonald dissemination in space, and two clinical episodes at different times satisfy dissemination in time — clinically isolated syndrome has become MS, and disease-modifying therapy begins.
Contrast a 22-year-old with postpartum headache and seizures after eclampsia: symmetric parieto-occipital FLAIR hyperintensity with no restricted diffusion. That is PRES — vasogenic, not cytotoxic oedema — and the ADC map showing increased diffusivity is the confirmatory detail distinguishing it from posterior-circulation infarction. Control the pressure and repeat in a fortnight to show resolution.
A third: a 50-year-old hyponatraemic alcoholic corrected rapidly develops quadriparesis; MRI shows a symmetric bright triangle in the central pons with an unaffected rim. Osmotic demyelination — and the lesson is that the sodium was corrected too fast, a management question wearing a radiology mask.
Where students slip
The commonest slip is reading every white spot in a 60-year-old as MS: age-appropriate small-vessel disease is periventricular rim-like and deep punctate without juxtacortical or infratentorial lesions, and the exam expects the Fazekas vocabulary for it. The second is ignoring the cord: a long segmental cord lesion redirects the diagnosis toward NMO spectrum disorder, where AQP4 antibody testing — increasingly available in Indian reference labs — outranks MRI follow-up. Third, tempo: acutely developing symmetric posterior lesions in a hypertensive or postpartum patient are PRES, not leukodystrophy, and slowly progressive symmetric confluent change in a child is a leukodystrophy until proven otherwise. A viva favourite is why osmotic demyelination spares the periphery — the outer pons has different osmolyte adaptation and blood supply — and the quotable rule remains sodium correction limits of about 8-10 mmol/L per day.
Frequently asked questions
What are Dawson fingers and which disease do they indicate?
Periventricular ovoid lesions oriented perpendicular to the lateral ventricle walls along medullary veins, characteristic of multiple sclerosis.
How does Fazekas grading describe small-vessel ischaemic white matter change?
Periventricular and deep white matter hyperintensities are each graded 0 to 3 from absent through confluent, with higher grades indicating advanced small-vessel disease and dementia risk.
Which MRI pattern defines PRES?
Predominantly parieto-occipital, often symmetric vasogenic oedema with increased diffusivity, occurring with eclampsia, hypertension or immunosuppression, which typically resolves after blood-pressure control.
What distinguishes osmotic demyelination on MRI?
Symmetric central pontine T2 hyperintensity sparing the peripheral pons, following rapid correction of hyponatraemia, with possible extrapontine basal ganglia involvement.
How is NMO spectrum disorder distinguished from multiple sclerosis on imaging?
Longitudinally extensive spinal cord lesions of three or more segments and optic nerve involvement, without periventricular Dawson fingers, suggest NMO spectrum disorder, confirmed by AQP4 antibodies.