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Longitudinal Retinal Changes in MOGAD.

Frederike Cosima Oertel1,2,3, Elias S Sotirchos4, Hanna G Zimmermann1,2

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Summary
This summary is machine-generated.

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) does not show retinal damage independent of optic neuritis (ON) attacks. However, retinal changes persist for up to 12 months post-ON, indicating distinct MOGAD disease mechanisms.

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Area of Science:

  • Neuro-immunology
  • Ophthalmology
  • Neuroscience

Background:

  • Myelin oligodendrocyte glycoprotein antibody (MOG-IgG)-associated disease (MOGAD) causes severe optic neuritis (ON), leading to retinal neuro-axonal loss.
  • Optical coherence tomography (OCT) is crucial for quantifying retinal changes in MOGAD.

Purpose of the Study:

  • To investigate whether retinal atrophy, independent of ON attacks, is detectable in MOGAD patients.
  • To assess the longitudinal changes in retinal layers after ON in MOGAD.

Main Methods:

  • Eighty MOGAD patients and 139 healthy controls (HCs) underwent OCT imaging using Spectralis and Cirrus devices.
  • Quantified macular ganglion cell and inner plexiform layer (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL).

Main Results:

  • MOGAD eyes with ON history showed lower GCIPL and pRNFL compared to MOGAD eyes without ON history and HCs.
  • MOGAD eyes without ON history had reduced GCIPL volume compared to HCs (Spectralis cohort).
  • pRNFL thinning was greater in MOGAD-ON patients with recent ON (within 6-12 months) versus those with remote ON (>12 months).

Conclusions:

  • MOGAD does not exhibit attack-independent retinal damage.
  • Neuroaxonal damage or edema resolution may continue for up to 12 months post-ON in MOGAD.
  • These findings highlight distinct pathomechanisms and OCT changes post-ON in MOGAD compared to other ON forms.