Management Differences Between NMOSD/MOGAD and MS
The critical management difference is that NMOSD and MOGAD require B-cell depleting therapies (rituximab, inebilizumab) or immunosuppression as first-line prevention, while MS-specific disease-modifying therapies (interferons, natalizumab, fingolimod) are not only ineffective but potentially harmful in NMOSD and MOGAD. 1, 2
Acute Attack Management
NMOSD and MOGAD
- High-dose intravenous methylprednisolone is first-line for acute attacks 1
- Plasma exchange or immunoadsorption should be initiated early if steroids fail, as MOG-IgG and AQP4-IgG positive patients show particular responsiveness to antibody-depleting treatments 1, 3
- Slow steroid taper is mandatory - both NMOSD and MOGAD carry high risk of flare-ups after rapid steroid cessation, requiring close monitoring during tapering 1, 3, 4
MS
- High-dose corticosteroids for acute relapses
- Plasma exchange reserved for severe, steroid-refractory attacks
- Standard steroid taper without the same flare-up risk seen in NMOSD/MOGAD
Long-Term Preventive Therapy
NMOSD (AQP4-IgG Positive)
- Start preventive therapy immediately after first attack - NMOSD has relapsing course in most cases 2
- FDA-approved options with Class 1 evidence: 2
- Eculizumab (complement inhibitor)
- Inebilizumab (anti-CD19 B-cell depleting)
- Satralizumab (IL-6 receptor antagonist)
- Rituximab (anti-CD20, off-label but Class 1 evidence)
- Avoid MS therapies: Beta-interferons, natalizumab, and fingolimod are ineffective or may exacerbate disease 2
MOGAD
- Preventive therapy reserved for relapsing disease only - MOGAD is much more likely to be monophasic than NMOSD 2
- No FDA-approved therapies or Class 1 evidence exists 2
- Observational benefit reported from: 1, 2
- Monitor for steroid-dependent course - frequent flare-ups after IV methylprednisolone withdrawal indicate need for maintenance therapy 4
MS
- Multiple FDA-approved disease-modifying therapies including:
- Injectable therapies (interferons, glatiramer acetate)
- Oral agents (fingolimod, dimethyl fumarate, teriflunomide, others)
- Infusion therapies (natalizumab, ocrelizumab, alemtuzumab)
- Treatment selection based on disease activity and risk stratification
Critical Therapeutic Pitfalls
Drugs That Worsen NMOSD/MOGAD
- Beta-interferons, natalizumab, and fingolimod - approved for MS but can exacerbate NMOSD due to differences in immunopathogenesis 1, 2
- This represents the most dangerous consequence of misdiagnosis
B-Cell Targeted Therapy Differences
- Rituximab increases eosinophil counts in NMOSD patients 5
- Inebilizumab increases CD3+ T cell and CD3+CD8+ T cell ratios in NMOSD patients 5
- Eosinophil quantities and ratios are higher in rituximab-treated versus inebilizumab-treated patients 5
Monitoring Requirements
NMOSD/MOGAD Specific
- MOG-IgG titers are disease-activity dependent - higher during acute attacks, lower in remission and on immunosuppression 6
- Retest if initially negative but clinical suspicion high: during acute attacks, treatment-free intervals, or 1-3 months after plasma exchange/IVIG 6
- Four MOGAD patients relapsed after MOG-IgG turned negative - seronegative relapses can occur 7
- Close monitoring during steroid taper to detect early flare-ups 1, 3
MS
- Standard MRI surveillance protocols
- Clinical relapse monitoring
- No antibody titer monitoring required
Prognosis Implications
Disease Course Patterns
- NMOSD: Relapsing course in most cases, requires immediate preventive therapy 2
- MOGAD: More likely monophasic, especially in children; adults experience relapsing course in approximately 80% 3, 2
- MOGAD with brainstem involvement: When brainstem involved in first attack, 12-fold increased likelihood of second attack at same location (OR=12.22) 7
- MS: Variable course patterns (relapsing-remitting, secondary progressive, primary progressive)