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Author Spotlight: Ex Vivo OCT-Based Multimodal Imaging of Human Donor Eyes for Research into Age-Related Macular Degeneration
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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.

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Summary
This summary is machine-generated.

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.

Keywords:
Optical coherence tomography (OCT)Pediatric acquired demyelinating disordersPediatric multiple sclerosis

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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.