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Progressive retinal changes in pediatric multiple sclerosis
Giulia Longoni1, Robert A Brown2, Ade Oyefiade3
1Department of Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, ON, Canada; Department of Pediatrics, Division of Neurology, University of Toronto, Toronto, ON, Canada.
Insights
Acute demyelinating episodes, especially the first optic neuritis, significantly damage retinal neuroaxonal structure in pediatric acquired demyelinating syndromes. Chronic changes also contribute to retinal thinning in pediatric multiple sclerosis.
Area of Science:
- Ophthalmology
- Neuroscience
- Pediatrics
Background:
- Pediatric acquired demyelinating syndromes (ADS) involve acute inflammatory attacks on myelin.
- Retinal neuroaxonal damage is a key indicator of neurological disease progression.
- Understanding drivers of retinal damage in pediatric ADS is crucial for prognosis.
Purpose of the Study:
- To differentiate the impact of acute demyelination versus chronic degeneration on retinal neuroaxonal damage in pediatric ADS.
- To quantify the effects of optic neuritis and non-optic neuritis relapses on retinal thickness.
- To assess long-term retinal changes in pediatric multiple sclerosis (MS).
Main Methods:
- Optical coherence tomography (OCT) was used to measure retinal nerve fiber layer (RNFL) and ganglion cell layer-inner plexiform layer (GCIPL) thickness.
- Data from pediatric participants with MS, monophasic ADS, and healthy controls were analyzed.
- Multivariable mixed effects models assessed associations between demyelinating episodes and retinal layer thickness changes over time.
Main Results:
- The initial optic neuritis (ON) episode caused significant RNFL and GCIPL thinning in both monophasic ADS and MS.
- Non-ON relapses were associated with smaller but significant reductions in RNFL and GCIPL thickness in MS.
- Pediatric MS patients exhibited progressive GCIPL thinning, independent of acute demyelinating events.
Conclusions:
- Acute demyelinating episodes, particularly the first ON, prominently impact retinal neuroaxonal structure in pediatric ADS.
- Non-ON relapses and chronic neurodegenerative processes also contribute to retinal thinning in pediatric MS.
- OCT is a valuable tool for monitoring neuroaxonal damage in pediatric demyelinating diseases.
Abstract:
Objectives To determine to what extent acute demyelinating episodes versus chronic degenerative phenomena drive retinal neuroaxonal damage in pediatric acquired demyelinating syndromes (ADS). Methods We acquired optical coherence tomography (OCT) data (follow-up range: 2 weeks - 5 years, at variable intervals from presentation) in pediatric participants who had multiple sclerosis (MS), monophasic ADS, or were healthy. Multivariable mixed effects models were used to assess the association of the number of demyelinating episodes (either optic neuritis [ON], or non-ON relapses) with changes in retinal nerve fiber layer (RNFL) or ganglion cell layer-inner plexiform layer (GCIPL) thickness. Results 64 OCT sans from 23 MS, and 33 scans from 12 monophasic ADS participants were compared with 68 scans from 62 healthy participants. The first ON episode had the biggest impact on RNFL or GCIPL thickness in monophasic ADS (RNFL: -7.9 µm, CI=5.5, p = 0.0056; GCIPL: -8.4 µm, CI=4.4, p = 0.0002) and MS (RNFL: -16 µm, CI = 3.7, p < 10-6; GCIPL: -15 µm, CI = 2.6, p < 10-6). Non-ON relapses were also associated with small but significant retinal thickness reductions in MS (RNFL: -2.6 µm/relapse, CI = 1.4, p = 0.0003; GCIPL: -2.8 µm/relapse, CI = 0.89, p < 10-6). MS participants showed progressive GCIPL thinning independent of acute demyelinating episodes (-2.7 µm/year, CI = 1.9, p = 0.0058). Conclusions We showed a prominent impact of early ON episodes on OCT measures of neuroaxonal structure in patients with ADS. We also demonstrated negative effects of non-ON relapses, and the presence of chronic retinal neurodegenerative changes, in youth with MS.
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