TO PATIENT SITE

Not a Monophasic Disease*

OVER TIME, RELAPSES ARE NOT ONLY POSSIBLE—THEY MAY BE INEVITABLE1,2

Up to 92.7% of patients with neuromyelitis optica spectrum disorder (NMOSD) who are aquaporin-4 immunoglobulin G positive (AQP4-IgG+) have had a relapse,† with those relapses potentially resulting in permanent disability.2-4

*80-90% of cases have a relapsing disease course.5

†The terms “attack” and “relapse” are used interchangeably.

This is a hypothetical patient.

THE FIRST NMOSD ATTACK CAN BE A PROGNOSTIC INDICATOR OF FUTURE DISABILITY2

Myelitis attack3

Having more than 1 myelitis attack in the first year can predict more severe long-term disability.‡

Optic neuritis attack2

The severity of the first optic neuritis attack is a predictor of vision loss over time.‡

‡

Retrospective study of 106 patients with AQP4-IgG+ NMOSD based on a 4-year review of medical records from 3 tertiary centers in the United Kingdom and Japan; median disease duration at last follow-up was 75 months.2

EVERY NMOSD ATTACK PUTS PATIENTS AT RISK OF IRREVERSIBLE DAMAGE3

76%

of patients did not fully recover from the first myelitis or optic neuritis attack.§

  • By the time of diagnosis, some patients may have already experienced multiple attacks and have irreversible nervous system damage§

After disease onset, the median time to first attack was 8.5 to 14 months.2,3§∥

§

Retrospective study based on the German NEMOS registry that evaluated 175 Caucasian patients with NMOSD (defined by Wingerchuk, et al 2006) and known AQP4 antibody status.3

∥

Retrospective study of 106 patients with AQP4-IgG+ NMOSD based on a 4-year review of medical records from 3 tertiary centers in the United Kingdom and Japan; median disease duration at last follow-up was 75 months.2

COMPLEMENT ACTIVATION IS AN IMPORTANT CAUSE OF ASTROCYTE DESTRUCTION IN NMOSD3,6-9

COMPLEMENT IN NMOSD

EXPLORE THE CURRENT NMOSD TREATMENT LANDSCAPE

SEE CURRENT TREATMENTS
References: 1. Wingerchuk DM, Hogancamp WF, O’Brien PC, Weinshenker BG. The
clinical course of neuromyelitis optica (Devic’s syndrome). Neurology. 1999;53(5):1107-1114. 2. Kitley J, Leite MI, Nakashima I, et al. Prognostic factors
and disease course in aquaporin-4 antibody-positive patients with neuromyelitis optica spectrum disorder from the United Kingdom and Japan. Brain. 2012;135(pt
6):1834-1849. 3. Jarius S, Ruprecht K, Wildemann B, et al. Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: a multicentre study of 175 patients. J Neuroinflammation. 2012;9:14. 4. Jiao Y, Fryer JP, Lennon VA,
et al. Updated estimate of AQP4-IgG serostatus and disability outcome in neuromyelitis optica. Neurology. 2013;81(14):1197-1204. 5. Borisow M, Mori M, Kuwabara S, Scheel M, Paul F. Diagnosis and Treatment of NMO Spectrum Disorder and MOG-Encephalomyelitis. Front Neurol. 2018;9:888. 6. Piatek P, Domowicz M, Lewkowicz N, et al. C5a-preactivated neutrophils are critical for autoimmune-induced astrocyte dysregulation in neuromyelitis optica spectrum disorder.
Front Immunol. 2018;9:1694. 7. Winkler
A, Wrzos C, Haberl M, et al. Blood-brain barrier resealing in neuromyelitis optica occurs independently of astrocyte regeneration. J Clin Invest. 2021;131(5):e141694. 8. Chamberlain JL, Huda S, Whittam DH, Matiello M, Morgan
BP, Jacob A. 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. 9. Mealy MA, Kessler RA, Rimler Z, et al. Mortality in neuromyelitis optica is strongly associated with African ancestry. Neurol Neuroimmunol Neuroinflamm. 2018;5(4):e468.