ArticleJournal of neurology, neurosurgery, and psychiatry2025
Investigating colour vision and its structural correlates 15 years following a first demyelinating event.
Article in Journal of neurology, neurosurgery, and psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Fifteen-Year Longitudinal Changes in Peripapillary Retinal Nerve Fiber Layer Thickness in Multiple Sclerosis.Journal of clinical medicine · 2026Article
- Digital Color Vision Testing Reveals Widespread Cone Dysfunction in Multiple Sclerosis Independent of Optic Neuritis.European neurology · 2026Article
- Optical coherence tomography angiography reveals insights into complementary vascular and neurodegenerative mechanisms in multiple sclerosis.Brain communications · 2026Article
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Authors and funding
5 authors.
Funding
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Abstract
backgroundWe investigated the long-term colour and contrast vision outcomes, 15 years after a first demyelinating event, with their structural correlates using optical coherence tomography (OCT) and brain MRI.
methodsPatients recruited with their first demyelinating event, were invited~15 years later to undergo clinical assessments, OCT and brain MRI and were clinically classified according to multiple sclerosis (MS) phenotypes. Linear mixed models evaluated associations between visual outcomes, MS phenotypes and OCT measures.
results94 patients were evaluated after a median of 14.3 years. 111 eyes affected by optic neuritis and 77 unaffected eyes were studied. Optic neuritis eyes displayed worse colour vision than unaffected eyes. Unaffected eyes showed worse colour vision in relapsing-remitting MS and secondary progressive MS (SPMS) than clinically isolated syndrome, while no similar discriminatory ability was seen for OCT measures. However, ganglion cell inner plexiform layer (GCIPL) was superior to peripapillary retinal nerve fibre layer (pRNFL) in predicting all visual outcomes. Worse colour vision was associated with lower retinal thicknesses and higher brain T2 lesion load; adding MRI volumetrics to macular GCIPL predictors did not improve model prediction of visual outcomes.
conclusionsColour vision was impaired in unaffected eyes, especially in SPMS. GCIPL thinning underpinned this impairment more than pRNFL, suggesting neuroaxonal loss as the pathobiological substrate. The correlation between worse colour vision and increasing T2 lesion load suggests that colour dysfunction reflects overall greater disease burden. Quantitative evaluation of colour vision in addition to OCT may be useful to assess disease severity in patients after a first demyelinating event.
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