Differentiating between MS, NMOSD, and MOGAD - MS Nurse PRO
Differentiating between MS, NMOSD, and MOGAD

Differentiating between MS, NMOSD, and MOGAD


Over recent years, the identification of specific autoantibody-associated conditions distinct from MS, including neuromyelitis optica spectrum disorder (NMOSD) and myelin oligodendrocyte glycoprotein-antibody disease (MOGAD), has changed the concept of inflammatory demyelinating disorders of the central nervous system (CNS) (Lennon et al., 2014; Sechi et al., 2022).

Awareness of the specific features that define each demyelinating disorder is crucial for a nurse in shaping a correct diagnosis and timely initiation of an appropriate treatment together with a neurologist. Hence, the blog will expand on NMOSD and MOGAD, with a focus on how to differentiate them from MS.


NMOSD (also known as Devic’s disease) is an autoimmune condition of the CNS, causing inflammation to the optic nerve and spinal cord. It is a rare disease with a worldwide prevalence between 0.5 and 10 per 100,000 persons (Hor et al., 2020). It can occur at any age but appears most often in females between the ages of 30–50 years, with a median age of disease onset at 40 years (Etemadifar et al., 2015).

NMOSD is a relapsing disease where relapses are followed by periods of some recovery. The most common relapses in NMOSD are optic neuritis, transverse myelitis, and area postrema syndrome, resulting in symptoms including eye pain, loss of vision, muscle weakness, paralysis, loss of bowel and bladder control, and severe nausea, vomiting, and hiccups (taken from The Sumaira Foundation).

Relapses in NMOSD are often very severe and can result in incomplete recovery, leading to an accumulation of damage and permanent disability (Kessler et al., 2016). Preventing attacks through early and ongoing treatment is therefore important to prevent long-term permanent disability.


MOGAD is an immune-mediated disorder that mainly targets the CNS. It is associated with the presence of antibodies directed against myelin oligodendrocyte glycoprotein (MOG) (Sharma et al., 2022).

MOGAD appears to be equally common among males and females. It presents in both adults and in children in different ways:

  • In children, MOGAD more commonly causes attacks on the brain, resulting in symptoms including confusion, incoordination, double vision, nausea and vomiting.
  • In adults, MOGAD often causes damage to the eyes (optic neuritis) and/or spinal cord (transverse myelitis) resulting in symptoms similar to NMOSD (e.g., loss of vision, weakness, paralysis).

Differentiating NMOSD and MOGAD from MS

The neurological manifestations of NMOSD and MOGAD may mimic those of MS, often leading to misdiagnosis. DMTs used to treat MS can be ineffective against NMOSD, with evidence showing that some can even aggravate it further (Min et al., 2012; Gelfand et al., 2014). It is therefore important to distinguish between these disorders owing to the differences in both therapeutic and diagnostic implications (Fadda et al., 2022).

The following table highlights some of the differences to look out for between the disorders (Sechi et al., 2022; Fadda et al., 2022):


NMOSD (AQP4 +ve_
Commonly affected age




Sex (female:male)





Any, mostly Caucasian

Any, African-American and Asian at higher risk

Any, unclear ethnic differences

Disease course

Relapsing (85%) or progressive from onset (15%); secondary progression can develop in relapsing form

Relapsing (>95%); progressive course extremely rare

Relapsing (50%) or monophasic (50%); progressive course is rare

Recovery from attacks

Generally good

Often incomplete, leading to permanent CNS damage

Generally good despite severe attacks

Key symptoms

Often fatigue or cognitive impairment

Severe vision impairment

Vision impairment, often with better recovery than in NMOSD

Area postrema syndrome


Sometimes seen





Sometimes seen


AQP4 antibody seronegative

AQP4 antibody seropositive

The presence of aquaporin 4 (AQP4) antibodies is very specific to a diagnosis of NMOSD, with the antibody being detected in up to 80% of patients with NMOSD. More stringent clinical criteria, with additional neuroimaging findings, are required for diagnosis of NMOSD without AQP4-IgG or when serologic testing is unavailable (Wingerchuk et al., 2015).

Find out more...

For more information about NMOSD and MOGAD, visit The Sumaira Foundation. The Sumaira Foundation is dedicated to raising global awareness of NMOSD and MOGAD, building communities of support for patients and their caregivers, funding research and patient advocacy.


  1. Lennon VA, et al. Lancet 2004;364:2106–2112
  2. Sechi E, et al. Front Neurol. 2022;13:885218
  3. Glisson C. Neuromyelitis optica spectrum disorders. UpToDate. Available at https://www.uptodate.com/contents/neuromyelitis-optica-spectrum-disorders. Accessed 02/12/22
  4. Hor JY, et al. Front Neurol. 2020;11:501
  5. Etemadifar M, et al. Mult Scler Int. 2015;2015:174720
  6. The Sumaira Foundation. What to know about NMO. Available at https://www.sumairafoundation.org/what-to-know-about-nmo/ Accessed 02/12/22
  7. Kessler RA, et al. Neurol Neuroimmunol Neuroinflamm. 2016;3:e269
  8. Sharma G, et al. Curr Protein Pept Sci. 2022;23:384–394
  9. Min JH, et al. Mult Scler. 2012;18:113
  10. Gelfand JM, et al. Neurol Neuroimmunol Neuroinflamm. 2014;1:e34
  11. Fadda G, et al. Front Neurol. 2022;13:1011579
  12. Wingerchuk DM, et al. Neurology 2015; 85:177–189
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