Neuromyelitis optica spectrum disorder historical perspective
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Julinka Auta Fernandes
Overview
Neuromyelitis optica spectrum disorder (NMOSD) has its historical roots in the optic nerve and spinal cord syndrome characterized by Eugène Devic and Fernand Gault in 1894, although similar cases had been reported earlier.[1] Discovery of a specific serum autoantibody in 2004[2] and identification of aquaporin-4 as its target in 2005 transformed understanding of the disease.[3] International diagnostic criteria published in 2015 recognized a broader clinical spectrum.[4] Larger trials published from 2019 onward established the relapse-prevention benefits of new targeted therapies.[5]
Discovery
Neuromyelitis optica spectrum disorder may be represented in nineteenth-century reports associating visual loss with spinal cord disease. Giovanni Battista Pescetto described a possible early case in 1844, and Thomas Clifford Allbutt's 1870 report helped attract sustained clinical interest.[1]
In 1894, Devic presented the association of acute myelitis and optic neuritis in Lyon, France. That year, his student Gault published a doctoral thesis reviewing previous reports and analyzing Devic's case. Their work introduced the term neuromyelitis optica (NMO). The eponym Devic's disease was proposed by Peppo Acchioté in 1907.[1]
Development of the Disease Concept and Diagnostic Criteria
Neuromyelitis optica spectrum disorder evolved from a clinically described opticospinal syndrome into a disease classified using antibody findings and characteristic clinical and imaging presentations.[4]
Antibody Discoveries (2004–2005)
Neuromyelitis optica spectrum disorder research changed in 2004, when Vanda Lennon and colleagues described a serum autoantibody called neuromyelitis optica immunoglobulin G (NMO-IgG) that helped distinguish the condition from multiple sclerosis (MS).[2]
In 2005, Lennon and colleagues identified aquaporin-4 (AQP4), a water-channel protein expressed on astrocytes, as the antibody's target. These antibodies subsequently became known as aquaporin-4 immunoglobulin G antibodies (AQP4-IgG). This discovery provided a biological basis for distinguishing antibody-positive disease from MS.[3]
Diagnostic Criteria (2006–2015)
Neuromyelitis optica spectrum disorder was more clearly distinguished from MS through the 2006 revision of criteria for classical NMO, which incorporated serum antibody status alongside clinical findings and magnetic resonance imaging (MRI) features.[6]
In 2015, the International Panel for Neuromyelitis Optica Diagnosis (IPND) published consensus criteria that unified classical NMO and its broader spectrum under NMOSD. The criteria recognized optic nerve, spinal cord, area postrema, other brainstem, diencephalic, and cerebral presentations, with separate requirements according to AQP4-IgG status.[4]
Distinction from Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease
Neuromyelitis optica spectrum disorder was further differentiated from related inflammatory disorders by the publication of international diagnostic criteria for myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) in 2023. These criteria formalized recognition of MOGAD as a separate disease, despite overlapping optic neuritis and myelitis presentations.[7]
Landmark Events in the Development of Treatment Strategies
Neuromyelitis optica spectrum disorder relapse prevention initially relied on immunosuppressants and evidence from small studies, before larger trials supported targeted therapies.[5]
- 2005: Bruce Cree and colleagues published an early open-label study of rituximab, providing preliminary evidence for B-cell depletion as a relapse-prevention strategy.[8]
- 2019: Randomized trials demonstrated reduced attack risk with eculizumab, a complement inhibitor, and inebilizumab, a B-cell-depleting antibody, in predominantly or exclusively AQP4-IgG-positive study populations.[5]
- 2019–2020: Trials of satralizumab, an interleukin-6 receptor-blocking antibody, evaluated both addition to existing immunosuppression and monotherapy, establishing relapse-prevention benefits in AQP4-IgG-positive disease.[5]
- 2023: An open-label trial of ravulizumab, a longer-acting complement inhibitor, used an external placebo comparator and provided additional evidence for relapse prevention in AQP4-IgG-positive NMOSD.[5]
- 2026: The Middle East and North Africa Committee for Treatment and Research in Multiple Sclerosis (MENACTRIMS) published consensus guidelines integrating antibody-based diagnosis and modern immunotherapies into regional clinical practice.[9]
References
- ↑ 1.0 1.1 1.2 Jarius, S; Wildemann, B (2013). "The history of neuromyelitis optica". Journal of Neuroinflammation. 10: 8. doi:10.1186/1742-2094-10-8. PMID 23320783.
- ↑ 2.0 2.1 Lennon, VA; Wingerchuk, DM; Kryzer, TJ; et al. (2004). "A serum autoantibody marker of neuromyelitis optica: distinction from multiple sclerosis". The Lancet. 364 (9451): 2106–2112. doi:10.1016/S0140-6736(04)17551-X. PMID 15589308.
- ↑ 3.0 3.1 Lennon, VA; Kryzer, TJ; Pittock, SJ; et al. (2005). "IgG marker of optic-spinal multiple sclerosis binds to the aquaporin-4 water channel". Journal of Experimental Medicine. 202 (4): 473–477. doi:10.1084/jem.20050304. PMID 16087714.
- ↑ 4.0 4.1 4.2 Wingerchuk, DM; Banwell, B; Bennett, JL; et al. (2015). "International consensus diagnostic criteria for neuromyelitis optica spectrum disorders". Neurology. 85 (2): 177–189. doi:10.1212/WNL.0000000000001729. PMID 26092914.
- ↑ 5.0 5.1 5.2 5.3 5.4 Kümpfel, T; Giglhuber, K; Aktas, O; et al. (2024). "Update on the diagnosis and treatment of neuromyelitis optica spectrum disorders (NMOSD) - revised recommendations of the Neuromyelitis Optica Study Group (NEMOS). Part II: Attack therapy and long-term management". Journal of Neurology. 271 (1): 141–176. doi:10.1007/s00415-023-11910-z. PMID 37676297 Check
|pmid=value (help). - ↑ Wingerchuk, DM; Lennon, VA; Pittock, SJ; et al. (2006). "Revised diagnostic criteria for neuromyelitis optica". Neurology. 66 (10): 1485–1489. doi:10.1212/01.wnl.0000216139.44259.74. PMID 16717206.
- ↑ Banwell, B; Bennett, JL; Marignier, R; et al. (2023). "Diagnosis of myelin oligodendrocyte glycoprotein antibody-associated disease: International MOGAD Panel proposed criteria". The Lancet Neurology. 22 (3): 268–282. doi:10.1016/S1474-4422(22)00431-8. PMID 36706773 Check
|pmid=value (help). - ↑ Cree, BA; Lamb, S; Morgan, K; et al. (2005). "An open label study of the effects of rituximab in neuromyelitis optica". Neurology. 64 (7): 1270–1272. doi:10.1212/01.WNL.0000159399.81861.D5. PMID 15824362.
- ↑ Yamout, B; Gouider, R; Al-Roughani, R; et al. (2026). "Consensus Recommendations for the Diagnosis and Treatment of Neuromyelitis Optica Spectrum Disorders (NMOSD): The MENACTRIMS Guidelines". CNS Drugs. 40 (3): 283–303. doi:10.1007/s40263-025-01260-x. PMID 41591715 Check
|pmid=value (help).