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NMOSD and MOGAD
NMOSD (AQP4 antibodies) and MOGAD (MOG antibodies) are inflammatory diseases that mimic multiple sclerosis but differ from it: severe attacks of the optic nerve and spinal cord, an antibody mechanism, and different treatments — and some MS drugs even worsen them.
Why it matters in the exam
Questions present severe or bilateral optic neuritis, a myelitis spanning 3 or more vertebral segments, or unexplained hiccups and vomiting (area postrema syndrome), and ask for the right test (serum AQP4 and MOG antibodies) and treatment. The discriminating point: drugs such as interferon beta, natalizumab and fingolimod suit MS but may worsen NMOSD. They also ask about the link to autoimmune diseases such as lupus and Sjögren's, and about MOGAD in children, which usually presents as ADEM. In NMOSD the CSF usually lacks oligoclonal bands, unlike MS, and the cell count may be relatively high. Early brain MRI may be normal or show lesions that are not typical of MS. Each NMOSD attack may leave permanent disability, so prevention starts right after diagnosis rather than after another attack.
Key points
- NMOSD is mediated by AQP4 antibodies and mainly hits the optic nerve and spinal cord.
- Myelitis of 3 or more segments and area postrema syndrome are key signs.
- MOGAD is more common in children (ADEM), with marked disc swelling and better recovery.
- Attacks are treated with high-dose steroids and early plasma exchange.
- Interferon, natalizumab and fingolimod may worsen NMOSD.
Summary table
| Feature | NMOSD with AQP4 | MOGAD |
|---|---|---|
| Population | Mainly women, sometimes with lupus or Sjögren's | Children and adults, no clear sex preference; in children often ADEM |
| Optic nerve | Severe neuritis, sometimes bilateral, chiasm involvement, partial recovery | Bilateral neuritis with marked disc swelling and perineural enhancement; better recovery |
| Spinal cord and brain | Long myelitis (3 or more segments); area postrema syndrome (hiccups and vomiting); brainstem | Conus or long myelitis; diffuse lesions |
| Attack treatment | High-dose steroids and early plasma exchange | High-dose steroids with a slow taper; plasma exchange for a severe attack |
| Prevention | Eculizumab, ravulizumab, inebilizumab, satralizumab, rituximab; not MS drugs such as interferon | After a relapse: immunoglobulin, rituximab or immunosuppressants |
A free exam question
באילו אתרים ממוקם הנזק הראשוני הנגרם ע"י הנוגדנים נגד החלבון aquaporin-4 ? (the question as examined, in Hebrew)
- א. astrocytes
- ב. myelin sheath
- ג. oligodendrocytes
- ד. spinal and retinal ganglion neurons
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Sources
- International Consensus Diagnostic Criteria for Neuromyelitis Optica Spectrum Disorders (Wingerchuk et al., Neurology), 2015 — AQP4-IgG positive and negative criteria
- International MOGAD Panel Proposed Criteria (Banwell et al., Lancet Neurology), 2023 — Diagnosis of MOG antibody-associated disease
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.