MOGAD Relapse During Pregnancy
29-year-old woman at 14 weeks' gestation presents with 5 days of bilateral blurred vision, nausea, vomiting, hiccups, and unsteady gait. MRI shows bilateral optic neuritis extending to the chiasm and a lesion in the area postrema. AQP4-IgG is negative; MOG-IgG is positive. She had a single episode of unilateral optic neuritis 2 years ago with good recovery and has not been on maintenance therapy. She is eager to avoid another attack during pregnancy but is concerned about fetal risk. The neurologist must choose acute therapy and plan long-term immunosuppression.
1. What acute treatment would you give for this attack, and how would you monitor response?
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I would give IV methylprednisolone 1 g daily for 5 days as first-line acute therapy. Corticosteroids are acceptable in pregnancy and are the standard initial treatment for MOGAD attacks. If vision or gait does not improve, or if symptoms are severe, I would escalate to plasma exchange. I would monitor visual acuity, fields, color vision, swallowing, and gait, and obtain follow-up MRI if there is clinical worsening.
Supportive care includes antiemetics, thromboprophylaxis if immobilized, glucose monitoring, and mental health support. I would avoid live vaccines during steroids and coordinate with obstetrics. The presence of area postrema involvement and bilateral optic neuritis makes this a disabling attack, so I would not delay treatment while awaiting repeat antibody results.
2. Which maintenance therapy would you start, and when? Address pregnancy and MOGAD relapse risk.
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She has had a second attack, so maintenance therapy is reasonable, but MOGAD can be monophasic and the decision should be shared. Azathioprine is the most pregnancy-compatible conventional option and can be started during pregnancy with close monitoring of blood counts and liver tests. Mycophenolate is contraindicated because of teratogenicity. Rituximab can be considered for severe relapsing disease, but pregnancy timing and neonatal B-cell effects require counseling; it is often deferred until after delivery unless attacks are frequent and severe.
I would start azathioprine after the acute attack, counsel her that relapse risk may persist through pregnancy and postpartum, and involve maternal-fetal medicine. I would not use a teratogenic agent simply because of one prior episode.
3. How would you counsel her about delivery and postpartum risk?
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I would reassure her that MOGAD is not by itself an indication for cesarean delivery; obstetric indications should guide delivery. I would plan continued immunosuppression through pregnancy and postpartum, because autoimmune relapse risk can increase after delivery. She should have a low threshold for reporting new visual, bulbar, or gait symptoms, and follow-up MRI should be reserved for new deficits rather than routine screening.
I would coordinate with obstetrics, anesthesia, and neonatology if she is on immunosuppression. Breastfeeding is generally compatible with azathioprine, but if rituximab is used, timing and infant monitoring need individualized discussion. The key is continuity of care rather than stopping therapy abruptly after delivery.