In a 42‑year‑old man with myelin‑oligodendrocyte glycoprotein antibody‑associated disease who developed bilateral optic neuritis treated with intravenous methylprednisolone 1 g daily followed by an oral prednisolone taper, and now presents with left‑eye central serous retinopathy causing visual decline, what are the appropriate subsequent treatment options?

Management of Steroid-Induced Central Serous Retinopathy in MOGAD

The immediate priority is to discontinue or rapidly taper oral prednisolone to the lowest possible dose, as corticosteroids are the direct cause of the central serous retinopathy and continued exposure will prevent resolution and cause permanent photoreceptor damage. 1, 2

Immediate Corticosteroid Management

Discontinue or aggressively taper prednisolone immediately because:

• Central serous retinopathy (CSR) is directly precipitated and worsened by glucocorticoids, making it the only "inflammatory" chorioretinal disease that deteriorates with steroid exposure 2
• Photoreceptor atrophy in the fovea occurs after approximately 4 months of persistent subretinal fluid, resulting in irreversible vision loss despite eventual retinal reattachment 1, 2
• The FDA explicitly lists CSR-related complications (blurred vision, exophthalmos) as adverse effects of systemic prednisone 3

Critical pitfall: Premature or rapid steroid withdrawal in MOGAD causes relapses in 50-60% of patients during corticosteroid dose reduction 4. This creates a therapeutic dilemma requiring immediate steroid-sparing immunotherapy.

Steroid-Sparing Immunotherapy for MOGAD Maintenance

Initiate intravenous immunoglobulin (IVIG) as first-line steroid-sparing therapy because:

• IVIG has demonstrated effectiveness as a steroid-sparing agent in recurrent-relapsing inflammatory optic neuropathy in multiple case series 4
• A 2025 case report documented successful IVIG maintenance in steroid-dependent MOG-associated optic neuritis, reducing annual relapse rate from 1.15 to 0.27 times/year while tapering prednisolone from 35 mg to 5 mg daily 5
• Standard dosing is 2 g/kg divided over 2-5 days, administered every 4 weeks 4

Alternative steroid-sparing agents if IVIG is unavailable or fails:

• Rituximab is the most commonly utilized chronic immunotherapy for relapsing MOGAD 6, 7
• Azathioprine, mycophenolate mofetil are additional options for relapsing disease 6
• These agents allow corticosteroid tapering while preventing MOGAD relapses 8, 6

Central Serous Retinopathy-Specific Management

For the acute CSR (2 weeks duration):

• Observation is appropriate for the first 3-4 months in most cases, as acute CSR has a high rate of spontaneous subretinal fluid resolution once the inciting corticosteroid is removed 1, 2
• However, treatment should be considered before 4 months if there is angiographic evidence of ongoing foveal leakage or signs of chronic CSR alterations, because photoreceptor atrophy typically occurs after 4 months of symptoms 2

If CSR persists beyond 3-4 months despite steroid cessation:

• Half-dose or half-fluence photodynamic therapy (PDT) with verteporfin is the treatment of choice, guided by indocyanine green angiography (ICGA) and fluorescein angiography (FA) 1, 2
• PDT is more effective and safer than argon laser treatment for chronic CSR 2
• Micropulse diode laser photocoagulation is an effective alternative 2

Mineralocorticoid receptor antagonists (spironolactone 25-50 mg daily) may be considered:

• 57% of spironolactone-treated patients achieved complete subretinal fluid resolution at 6 months versus 32% with conservative treatment 1
• However, recurrence rates remain high (33%) and efficacy is inferior to PDT 1
• This option is less relevant in steroid-induced CSR where removing the inciting agent is paramount 1

Monitoring Protocol

Weekly ophthalmology follow-up initially with:

• Optical coherence tomography (OCT) to monitor subretinal fluid resolution 1
• Visual acuity and Amsler grid testing
• Fundoscopy to assess for persistent leakage or complications

Neurology follow-up every 2-4 weeks during steroid taper to:

• Monitor for MOGAD relapse (vision changes, eye pain, new neurological symptoms) 4, 7
• Adjust IVIG dosing and steroid taper rate based on clinical stability 5
• Retest MOG-IgG antibodies at 6-12 months, as transient seronegativity can occur 4

Critical Pitfalls to Avoid

• Do not continue oral prednisolone at current dose: This guarantees CSR progression and permanent vision loss 1, 2
• Do not taper steroids without initiating steroid-sparing therapy: This will trigger MOGAD relapse in 50-60% of cases 4
• Do not wait 4 months to treat CSR if there is evidence of photoreceptor damage on OCT: Outer segment atrophy and granular debris indicate urgent need for intervention 1, 2
• Do not use MS-directed therapies (interferon-β): These increase relapse rates in MOGAD 9

Algorithmic Summary

1. Day 1-3: Ophthalmology confirms CSR on OCT; begin aggressive prednisolone taper (e.g., reduce by 5-10 mg every 3-5 days toward 5-10 mg daily target)
2. Day 1-7: Initiate IVIG 2 g/kg over 2-5 days as steroid-sparing agent 4, 5
3. Week 2-4: Continue IVIG monthly; taper prednisolone to 5-10 mg daily if clinically stable
4. Week 4-12: Monitor CSR with weekly OCT; if subretinal fluid persists or worsens, obtain FA/ICGA to plan PDT 1
5. Month 3-4: If CSR has not resolved, proceed with half-dose PDT 1, 2
6. Month 6-12: Maintain IVIG monthly; attempt to discontinue prednisolone entirely if no MOGAD relapses 5