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Basic Neuroscience · Neuropharmacology

MS vs NMOSD vs MOGAD

Distinguishing the three main inflammatory demyelinating diseases. Confirm AQP4-IgG and MOG-IgG serostatus (cell-based assay) before long-term treatment — misdiagnosis leads to harmful or ineffective therapy.

Feature Multiple Sclerosis NMOSD (AQP4-IgG) MOGAD (MOG-IgG)
Target antigenNone identified (T-cell–mediated CNS demyelination)AQP4 water channel on astrocytesMOG on the oligodendrocyte / myelin surface
DemographicsYoung adults; F:M ~3:1Median ~40 y; F:M up to ~9:1; more common in non-white populationsAll ages incl. children; F ≈ M
Optic neuritisUsually unilateral, mild–moderateSevere, may be bilateral; posterior/chiasmal; poor recoveryOften bilateral, painful, with disc edema; usually good recovery
MyelitisShort-segment, partialLETM ≥3 vertebral segments, central cordLETM, often conus/cauda; H-sign on axial
Other hallmark attacksBrainstem/cerebellar, cognitiveArea postrema (intractable nausea/vomiting/hiccups), diencephalic, narcolepsyADEM (esp. children); cortical encephalitis with seizures (FLAMES)
Brain MRIPeriventricular ovoid (Dawson fingers), juxtacortical, infratentorialPeriependymal (around 3rd/4th ventricle & area postrema), diencephalicFluffy / ill-defined, ADEM-like, often resolves; cortical FLAIR-hyperintensity
CSF oligoclonal bandsPositive ~85–95%Usually negative (<20%)Usually negative
SerologyNo specific antibodyAQP4-IgG (cell-based assay)MOG-IgG (cell-based assay); low/transient titers can be false-positive
CourseRelapsing → secondary progressive; progression independent of relapsesRelapsing; no progressive phase — disability is attack-drivenMonophasic or relapsing; disability attack-related
Attack recoveryUsually moderateOften severe / incompleteOften good
Acute treatmentIV methylprednisolone ± PLEXIV steroids + early PLEXIV steroids (steroid-responsive/dependent) ± IVIG/PLEX
MaintenanceDMTs (interferons → anti-CD20; see MS DMT sheet)Eculizumab, ravulizumab, inebilizumab, satralizumab (FDA); rituximabOff-label: rituximab (less reliable), IVIG, MMF, azathioprine — no FDA-approved therapy
⚠ Key pitfallMS DMTs (IFN-β, natalizumab, fingolimod) WORSEN NMOSDDon’t over-call on a low/transient MOG titer; re-test if uncertain
Bottom line: MS — OCB-positive, short lesions, progressive course, treat with DMTs. NMOSD — AQP4-IgG, LETM & area postrema, severe attacks, treat with complement/IL-6/anti-CD20 (never MS DMTs). MOGAD — MOG-IgG, ADEM/bilateral ON, steroid-responsive, often monophasic; no approved therapy.

Neuro-Pharmacology — NeurologyResident.Net by Ahmed Koriesh