Neuromyelitis Optica Spectrum Disorder Medical Slides

Emphasize that MS treatments can worsen NMOSD: interferon-beta increases relapse rate, fingolimod and natalizumab are ineffective and potentially harmful. Present the key differentiating features: AQP4-IgG positivity (75-80% of NMOSD), longitudinally extensive transverse myelitis (≥3 vertebral segments vs short segments in MS), severe optic neuritis with poor recovery, area postrema syndrome (intractable hiccups/vomiting), and brain MRI not meeting Barkhof criteria for MS.

Present the three landmark phase 3 trials: PREVENT (eculizumab, complement C5 inhibitor, 94% reduction in relapse risk), N-MOmentum (inebilizumab, anti-CD19 B-cell depletion, 73% reduction), and SAkura (satralizumab, IL-6 receptor inhibitor, 55-74% reduction depending on AQP4 status). Rituximab, while lacking phase 3 RCT data, remains widely used based on extensive retrospective evidence and lower cost.

Present MOG antibody disease (MOGAD) as a distinct entity from AQP4+ NMOSD with different demographics (equal sex distribution, younger onset), typically monophasic or less frequently relapsing course, better recovery, different MRI patterns (bilateral optic neuritis, conus-predominant myelitis, fluffy cortical lesions), and different treatment responses. Emphasize that MOG-IgG testing should be performed in AQP4-seronegative patients with NMOSD phenotype, as it changes prognosis and management.