Long optic neuritis, longitudinally extensive myelitis and area postrema lesions point away from MS towards aquaporin-4 NMOSD or MOG antibody disease — the treatment differs and some MS drugs worsen NMOSD.
Orient first
- NMOSD (AQP4): long posterior optic nerve and chiasm involvement; myelitis ≥ 3 vertebral segments centrally; area postrema and periependymal lesions.
- MOGAD: anterior, bilateral optic neuritis with perineural enhancement; conus involvement; fluffy ADEM-like brain lesions; H-sign in the cord grey matter.
- MS: short peripheral cord lesions, Dawson fingers, juxtacortical and central vein sign.
Acquire the study
- MRI brain (FLAIR, T2, DWI, post-gadolinium T1), orbits (fat-saturated coronal T2 and post-contrast T1) and whole spine (sagittal and axial T2, STIR, post-contrast T1).
The manoeuvre
- Orbits: length of optic nerve involvement on coronal fat-saturated T2; posterior/chiasmal (NMOSD) vs anterior with perineural enhancement (MOGAD).
- Spine sagittal T2: lesion length in vertebral segments; central grey matter (H-sign on axial) vs peripheral.
- Brain FLAIR: area postrema, periependymal third and fourth ventricles, hypothalamus.
- Post-gadolinium T1: cloud-like (NMOSD) or leptomeningeal enhancement (MOGAD).
- Compare against MS features: Dawson fingers, juxtacortical U-fibre lesions, central vein sign on SWI.
What confirms it
- A compatible lesion pattern with AQP4-IgG or MOG-IgG positivity.
What licenses you to exclude it
- Typical MS features (periventricular ovoid lesions perpendicular to the ventricles, short peripheral cord lesions, central vein sign) make NMOSD unlikely.
The classic misread
- Calling a longitudinally extensive lesion MS without testing for antibodies.