For NMOSD patients, the next relapse could strike at any time
Relapses in neuromyelitis optica spectrum disorder (NMOSD) are sudden, frequent, and unpredictable.1–3
Complement-mediated destruction of viral central nervous system (CNS) cells can lead to severe recurrent attacks of optic neuritis and myelitis resulting in rapid development of permanent neurological deficits.4–9
  • Increased burden of disease: Over 70% of patients report relapses negatively impact their quality of life*10
  • Accumulation of disability: Up to 18% of patients can develop permanent bilateral visual disability within 6 years of disease onset, and 34% of patients can develop permanent motor disability within 6 years†11
  • Poor recovery of essential functions: 76% of patients experience only partial or no recovery from myelitis after the first attack‡12
NMOSD is a complex disease. To learn more about its mechanism of disease, see the video below.
NMOSD can deeply affect a person's life. Discover the burden of NMOSD below.
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Relapse triggered by complement activation is a reality in NMOSD. Address its potentially devastating impact.4–8

* Based on a cross-sectional survey which was used to assess physical, emotional, and socioeconomic burden of NMOSD on quality of life among 193 patients.10

† Based on a case record study of clinical outcomes and prognostic characteristics of NMO in 106 AQP4 antibody-positive patients fro the UK and Japan.11

‡ Based on a multicentre, retrospective study of 175 Caucasian patients with NMOSD (78.3% of them AQP4 antibody-positive) to analyse clinical and paraclinical features associated with NMO spectrum disorders.12

AQP4, aquaporin-4; NMO, neuromyelitis optica; NMOSD, neuromyelitis optica spectrum disorder.
Wingerchuk M D, et al. Network meta-analysis of food and drug administration-approved treatment options for adults 
with aquaporin-4 immunoglobulin G-positive neuromyelitis optica spectrum disorder. Neurol Ther. 2022;11(1):123–135. Jasiak-Zatonska M, et al. The immunology of neuromyelitis optica-current knowledge, clinical implications, controversies and future perspectives. Int J Mol Sci. 2016;17(3):273. Mandler RN. Neuromyelitis optica – Devic’s syndrome, update. Autoimmun Rev. 2006;5(8):537–543. Piatek P, et al. C5a-preactivated neutrophils are critical for autoimmune-induced astrocyte dysregulation in neuromyelitis 
optica spectrum disorder. Front Immunol. 2018;9:1694. Winkler A, et al. Blood-brain barrier resealing in neuromyelitis optica occurs independently of astrocyte regeneration. 
J Clin Invest. 2021;131(5):e141694. Papadopoulos MC, et al. Aquaporin water channels in the nervous system. Nat Rev Neurosci. 2013;14(4):265–277. Kuroda H, et al. Increase of complement fragment C5a in cerebrospinal fluid during exacerbation of neuromyelitis optica. J Neuroimmunol. 2013;254(1-2):178–82. Chamberlain LJ, et al. Role of complement and potential of complement inhibitors in myasthenia gravis and neuromyelitis optica spectrum disorders: a brief review. J Neurol. 2021;268(5):1643–1664. Jiao Y, et al. Updated estimate of AQP4-IgG serostatus and disability outcome in neuromyelitis optica. Neurology. 2013;81(14):1197–1204. Beekman J, et al. Neuromyelitis optica spectrum disorder: Patient experience and quality of life. Neurol Neuroimmunol Neuroinflamm. 2019;6(4):e580. Kitley J, et al. Prognostic factors and disease course in aquaporin-4 antibody-positive patients with neuromyelitis optica spectrum disorder form the United Kingdom and Japan. Brain. 2012;135(6):1834–1849. Jarius S, et al. Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: a multicentre study of 175 patients. J. Neuroinflammation. 2012;9(1):14.