| Core idea |
Diffuse HIV-related white matter injury (encephalopathy), often with global brain atrophy |
Opportunistic demyelination from JC virus reactivation in severe immunosuppression |
| Distribution |
Symmetric deep/periventricular WM (centrum semiovale, periventricular), ± basal ganglia involvement; tends to be diffuse |
Multifocal, asymmetric subcortical WM; classically parieto-occipital; U-fibre involvement is common; can hit cerebellar peduncles/brainstem |
| Mass effect |
None / minimal |
None / minimal (big lesions can look “busy” but usually little mass effect) |
| Enhancement |
Usually none |
Classically none; can enhance in IRIS (new/worsening enhancement after ART) |
| DWI |
Often no marked restriction (may be subtle/variable) |
Peripheral “leading edge” restriction can be a big clue (active demyelination rim) |
| Cortex / U-fibres |
Tends to spare U-fibres (not a perfect rule) |
Involves U-fibres early/commonly (subcortical scalloped margin) |
| Atrophy |
Prominent diffuse atrophy (out of proportion for age) is a classic exam hint |
Atrophy not the primary feature (can develop later) |
| Clinical tempo |
Subacute cognitive decline, gait issues, behavioural change; improves/stabilises with ART |
Subacute focal neuro deficits, visual symptoms, language/motor; often progressive without immune reconstitution |
| “Gotcha” |
Can look like nonspecific leukoencephalopathy → don’t overcall PML if it’s very symmetric + atrophic |
Don’t dismiss because there’s no enhancement/mass effect; think PML when asymmetric U-fibre lesions in immunosuppressed |
