Hello,
Any drusen seen?
I also wonder whether the 2 recent transient events could represent something other than migraine, such as transient hemodynamic compromise or even a cardiac arrhythmia producing hypoperfusion in already predisposed optic nerves.
The original presentation at age 20 would still be unusual for this mechanism, although the apparently near-simultaneous bilateral onset is interesting.
Any history of GI blood loss, ulcers, melena, or significant anemia preceding either event?
Did his MRA/CTA demonstrate any anomalous carotid or ophthalmic circulation? Rare developmental variants can occasionally create situations where one carotid circulation substantially supplies both ophthalmic circulations or otherwise produces unusual anterior circulation hemodynamics. May be worthwhile to evaluate if this has not already been assessed.
Overall this does seem more consistent with AION as you suggest rather than MOG-related disease, particularly given the lack of steroid responsiveness, absence of MRI enhancement, and persistently negative antibodies. Were the initial antibody studies obtained before steroid treatment?
What still seems important to explain mechanistically is the bilateral involvement at age 20 and then the new event now, especially since the more recently affected eye may already have been somewhat "decompressed" from prior NFL loss over time. I assume the more recent OCT still demonstrated swelling OS? I am having a little trouble seeing it clearly on my iPhone.
Jade