ArticleJournal of neurology2025
Progressive retinal and microvascular neurodegeneration in neuromyelitis optica spectrum disorders: a longitudinal SS-OCT/OCTA study.
Article in Journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Cerebrovascular risk factors impact on brain atrophy and DTI-ALPS decrease in neuromyelitis optica spectrum disorder.Journal of neurology · 2026Article
- Longitudinal retinal microvascular changes and their association with white matter hyperintensities in neuromyelitis optica spectrum disorder.Frontiers in neurologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
Abstract
backgroundEmerging evidence suggests that subclinical visual pathway impairment might occur in neuromyelitis optica spectrum disorder (NMOSD) independently of optic neuritis (ON). This prospective longitudinal cohort study aims to characterize dynamic retinal neurodegeneration and microvascular alterations in NMOSD.
methodsThe quantitative parameters from swept-source optical coherence tomography (SS-OCT) and SS-OCT angiography (SS-OCTA) included the macular retinal nerve fiber layer (RNFL) thickness, ganglion cell-inner plexiform layer (GCIPL) thickness, superficial vascular complex (SVC) density, and deep vascular complex (DVC) density. Multivariable linear mixed-effects models adjusted for age, sex, treatment, follow-up time, and ON history were used to analyze correlations between SS-OCT/OCTA parameters and clinical features.
resultsCross-sectional analysis demonstrated significant reductions in the RNFL thickness (33.91 ± 8.90 vs. 38.88 ± 4.00 μm, p < 0.001), GCIPL thickness (54.89 ± 11.06 vs. 64.42 ± 5.28 μm, p < 0.001), and SVC density (38.17 ± 10.21% vs. 45.96 ± 3.83%, p < 0.001) in NMOSD patients versus healthy controls, along with reduced RNFL thickness (33.91 ± 8.90 μm vs. 36.22 ± 8.62 μm; p = 0.011) and SVC density (38.17 ± 10.21% vs. 40.66 ± 6.62%; p = 0.016) relative to patients with multiple sclerosis. Longitudinal analysis demonstrated a progressive decline in GCIPL thickness (- 0.18 µm/year, IQR: - 1.69 to 1.72 µm/year, p = 0.047), SVC density (- 1.11%/year, IQR:-2.90% to 0.87%/year, p = 0.003), and DVC density (- 1.88%/year, IQR: - 3.52% to 0.50%/year, p = 0.004) from baseline among clinically stable NMOSD patients. The annual degradation rate of GCIPL thickness showed significant inverse correlations with baseline logMAR visual acuity (p < 0.001), ON frequency (p < 0.001) and baseline EDSS scores (p = 0.039). DISCUSSION: Our findings indicate that progressive retinal neurodegeneration and microvascular loss persist independently of clinical relapse, positioning SS-OCT/OCTA metrics as sensitive biomarkers for subclinical progression and supporting their integration into the framework of disease monitoring and treatment response assessment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.