Fighting NMOSD Every Day

What is neuromyelitis optica spectrum disorder (NMOSD)?

NMOSD is a rare and devastating disorder that affects the central nervous system (CNS), in which complement activation due to anti-AQP4 antibodies plays a significant role in the disease process.1-5 Patients with NMOSD can experience unpredictable attacks, also referred to as relapses, which can lead to long-term disability.6-8


NMOSD primarily affects the optic nerve and the spinal cord. The most common symptoms of NMOSD are optic neuritis and transverse myelitis.

Approximately three-quarters (73%) of all patients with NMOSD have anti-AQP4 autoantibodies.9 In patients with anti-AQP4 antibody-positive NMOSD, the body’s own immune system can turn against itself to produce autoantibodies against anti-AQP4, a protein in certain cells in the eyes, brain, and spinal cord that is critical for the survival of nerve cells. The binding of anti-AQP4 autoantibodies to specific cells in the CNS activates the complement cascade, another part of the immune system. Complement activation by anti-AQP4 autoantibodies can cause destruction of vital cells in the CNS, leading to demyelination and to the death of neurons, predominantly in the spinal cord and optic nerve.1,10,11

Symptom locations of NMOSD on the human body

Some symptoms of NMOSD3-7

  • Problems with vision including eye pain and blindness
  • Severe weakness and impaired mobility
  • Paralysis
  • Sensory and motor disability
  • Respiratory dysfunction/failure
  • Loss of bowel, bladder function


  1. Wingerchuk DM, Lennon VA, Lucchinetti CF, Pittock SJ, Weinshenker BG. The spectrum of neuromyelitis optica. Lancet Neurol. 2007;6(9):805-815.
  2. Wingerchuk DM. Diagnosis and treatment of neuromyelitis optica. Neurologist. 2007;13(1):2-11.
  3. Wingerchuk DM, Weinshenker BG. Neuromyelitis optica. Curr Treat Options Neurol. 2008;10(1):55-66.
  4. Tüzün E, Kürtüncü M, Türkoğlu R, et al. Enhanced complement consumption in neuromyelitis optica and Behcet’s disease patients. J Neuroimmunol. 2011;233(1-2):211-215.
  5. Kuroda H, Fujihara K, Takano R, et al. Increase of complement fragment C5a in cerebrospinal fluid during exacerbation of neuromyelitis optica. J Neuroimmunol. 2013;254(1-2):178-182.
  6. 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(6):1834-1849.
  7. Jarius S, Ruprecht K, Wildemann B, et al. Contrasting disease patterns in seropositive and seronegative neuromyelitis optica: a multicentre study of 175 patients. J Neuroinflamm. 2012;9:14.
  8. Wingerchuk DM, Hogancamp WF, O’Brien PC, Weinshenker BG. The clinical course of neuromyelitis optica (Devic’s syndrome). Neurology. 1999;53(5):1107-1114.
  9. Hamid SHM, Whittam D, Mutch K, Linaker S, Solomon T, Das K, et al. What proportion of AQP4-IgG-negative NMO spectrum disorder patients are MOG-IgG positive? A cross sectional study of 132 patients. J Neurol. 2017;264(10):2088-2094.
  10. Papadopoulos MC, Bennett JL, Verkman AS. Treatment of neuromyelitis optica: state-of-the-art and emerging therapies. Nat Rev Neurol. 2014;10(9):493.
  11. Takata K, Matsuzaki T, Tajika Y. Aquaporins: water channel proteins of the cell membrane. Prog Histochem Cytochem. 2004;39(1):1-83.

I’m hoping my story will inspire others to continue to fight for themselves.”