Photo Credit: Mohammed Haneefa Nizamudeen
The following is a summary of “Trans-Synaptic Degeneration in the Visual Pathway in Patients With Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease,” published in the March 2024 issue of Neurology by Bollo et al.
Researchers conducted a retrospective study to investigate if retinal neurodegeneration occurs in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) patients independent of optic neuritis (ON) and if ON triggers further nerve cell degeneration in these patients.
They involved 34 adult patients diagnosed with MOGAD) and 23 HC. Clinical, optical coherence tomography (OCT), and MRI data were collected. Peripapillary retinal nerve fiber layer (pRNFL) and ganglion cell inner plexiform layer (GCIPL) measurements were obtained using Heidelberg Spectralis. FreeSurfer7 software was utilized to obtain measurements of the lateral geniculate nucleus (LGN), occipital volume fractions (relative to total estimated intracranial volume), and occipital cortical thickness. For the anterior visual pathway, eyes categorized based on the presence or absence of ON (Eye-ON and Eye-NON) were analyzed and compared with eyes from healthy controls (Eye-HC). OCT and brain volumetric measurements analysis were conducted comparing MOGAD patients with ON (MOGAD-ON), MOGAD patients without ON (MOGAD-NON), and HC groups. Analysis of covariance with Bonferroni-adjusted post hoc tests was used to assess differences between groups, and linear regression analysis was employed to evaluate associations between OCT/MRI measurements; age and sex were accounted for as covariates.
The results showed that 24 (70.5%) patients had a prior ON. The median pRNFL and GCIPL thickness (in micrometers) were significantly reduced in Eye-ON compared to Eye-NON and HC (pRNFL: 69.4 (17.3), 89.6 (13.7), 98.2 (11.7), P<0.001; GCIPL: 55.8 (8.7), 67.39 (8.7), 72.6 (4.5), P<0.001). Both pRNFL and GCIPL thickness negatively correlated with the number of ON episodes (P=0.025 and P=0.031, respectively). The LGN volume fraction was significantly lower in patients with MOGAD-ON compared to HC (0.33 (0.05) vs. 0.39 (0.04), P=0.002). Occipital cortical thickness was lower in MOGAD-ON compared to MOGAD-NON and HC (P=0.010). In patients with MOGAD-ON, pRNFL correlated with LGN volume (P=0.006), occipital thickness (P=0.002), and the medial occipital cortex (P=0.002) but not the lateral occipital lobe.
Investigators concluded that MOGAD with ON showed retinal thinning (worse with more ON episodes) and wider brain damage compared to no-ON MOGAD or HCs.