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Ganglion Cell Layer Compared With Inner Plexiform Layer Atrophy After Optic Neuritis Associated With NMOSD, MOGAD,

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Ganglion cell layer (GCL) thinning, not inner plexiform layer (IPL) thinning, is the primary driver of vision loss in optic neuritis (ON) associated with multiple sclerosis (MS), MOGAD, and AQP4+NMOSD. This GCL atrophy pattern is consistent across these neuroinflammatory conditions.

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Area of Science:

  • Neuro-ophthalmology
  • Neuroimmunology
  • Retinal imaging

Background:

  • Optic neuritis (ON) is a key manifestation of multiple sclerosis (MS), aquaporin-4-IgG seropositive neuromyelitis optica spectrum disorder (AQP4+NMOSD), and myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD).
  • Previous optical coherence tomography (OCT) studies show greater macular inner retinal thinning in AQP4+NMOSD-ON and MOGAD-ON compared to MS-ON.
  • The distinct contributions of the ganglion cell layer (GCL) and inner plexiform layer (IPL) to this thinning have not been fully elucidated.

Purpose of the Study:

  • To investigate the differential thinning of the GCL and IPL in eyes with ON secondary to MS, AQP4+NMOSD, and MOGAD.
  • To compare the GCL and IPL thinning patterns across these distinct neuroinflammatory conditions.
  • To analyze the longitudinal changes in GCL and IPL thickness following acute ON.

Main Methods:

  • Cross-sectional analysis of retinal imaging data from patients with MS-ON, AQP4+NMOSD-ON, MOGAD-ON, and healthy controls (HC).
  • Longitudinal analysis of OCT scans from patients within 30 days of a first ON episode to track GCL and IPL thinning over time.
  • Calculation of the GCL/GCIPL ratio to assess the relative contribution of GCL thinning.

Main Results:

  • Cross-sectionally, GCL and IPL volumes were reduced in AQP4-ON and MOGAD-ON compared to MS-ON.
  • The GCL/GCIPL ratio was lower in all ON groups versus HC and was significantly lower in AQP4-ON and MOGAD-ON compared to MS-ON.
  • Longitudinally, the GCL/GCIPL ratio was already reduced within one month of acute ON and further decreased with greater GCIPL volume loss.

Conclusions:

  • More severe inner retinal atrophy after ON is primarily driven by GCL thinning rather than IPL thinning.
  • This pattern of GCL-predominant atrophy is consistent across MS-ON, AQP4+NMOSD-ON, and MOGAD-ON.
  • These findings enhance understanding of the microstructural changes in the inner retina following ON in various neuroinflammatory diseases.