Retrograde trans-synaptic visual pathway degeneration in multiple sclerosis: A case series
Open accessAbstract
Background: Trans-synaptic degeneration (TSD) describes the propagation of neuronal injury through synaptic pathways in the human nervous system and may be linked to the accelerated retinal atrophy seen in multiple sclerosis (MS). Results: We report six cases where homonymous, hemi-macular ganglion cell + inner plexiform (GCIP) thickness reduction was seen in conjunction with posterior visual pathway lesions. Macular microcystoid changes of the inner nuclear layer (INL) were seen in a subset of three subjects. Conclusion: Our findings highlight the utility of assessing regional GCIP changes to identify potential retrograde TSD in MS and demonstrate that INL changes may be an accompaniment in such instances.
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Assessing GCIPL thickness maps for patterns of regional macular injury might provide insight into vascular etiologies of optic neuropathy, such as when altitudinal thinning is present, or optic chiasm, optic tract, thalamic and/or retrogeniculate pathology.
“Assessing the GCIPL thickness maps for patterns of regional macular injury might provide insight into vascular etiologies of optic neuropathy, such as when altitudinal thinning is present, or optic chiasm, optic tract, thalamic and/or retrogeniculate pathology. 80 -83”
From The use of optical coherence tomography and visual evoked potentials in the 2024 McDonald diagnostic criteria for multiple sclerosis (2025) · cites this paper as [83]
The Discussion (page unavailable) says regional hemi-macular GCIP thinning may help localize injury in the lateral geniculate nucleus or posterior visual pathway; it reports optic-radiation and visual-cortex lesions and notes that terminal optic-tract involvement could not be excluded. This supports the thalamic and retrogeniculate parts of the claim, but the paper does not address optic-chiasm pathology, vascular optic neuropathy, or altitudinal thinning. (LLM, conf=0.87)
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Research works printed but not linked: 10
- [1]Jindahra P Petrie A Plant GT The time course of retrograde trans-synaptic degeneration following occipital lobe damage in humans. Brain 2012; 135(Pt 2): 534– 541. 22300877
- [2]Klistorner A Sriram P Vootakuru N Axonal loss of retinal neurons in multiple sclerosis associated with optic radiation lesions. Neurology 2014; 82: 2165– 2172. 24838786 PMC4113462
- [3]Gabilondo I Martínez-Lapiscina EH Martínez-Heras E Trans-synaptic axonal degeneration in the visual pathway in multiple sclerosis. Ann Neurol 2014; 75(1): 98– 107. 24114885
- [4]Oh J Sotirchos ES Saidha S In vivo demonstration of homonymous hemimacular loss of retinal ganglion cells due to a thalamic lesion using optical coherence tomography. JAMA Neurol 2013; 70(3): 410– 411. 23303271 PMC5894493
- [5]Tur C Goodkin O Altmann DR Longitudinal evidence for anterograde trans-synaptic degeneration after optic neuritis. Brain 2016; 139(3): 816– 828. 26912640 PMC5839599
- [6]Saidha S Sotirchos ES Ibrahim MA Microcystic macular oedema, thickness of the inner nuclear layer of the retina, and disease characteristics in multiple sclerosis: A retrospective study. Lancet Neurol 2012; 11(11): 963– 972. 23041237 PMC3533139
- [7]Sotirchos ES Saidha S Byraiah G In vivo identification of morphologic retinal abnormalities in neuromyelitis optica. Neurology 2013; 80(15): 1406– 1414. 23516321 PMC3662269
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Saidha, S., Green, A. J., Leocani, L., Vidal-Jordana, A., Kenney, R. C., Bsteh, G., Outteryck, O., Thompson, A., Montalban, X., Coetzee, T., et al. (2025) · The Lancet Neurology · doi:10.1016/s1474-4422(25)00275-3 · Cited by 66 · see citing works
Self-citation
- Authors
- Al-Louzi, O., Button, J., Newsome, S. D., Calabresi, P. A., & Saidha, S.
- Affiliations
- The Division of Neuroimmunology and Neurological Infections, Department of Neurology, The Johns Hopkins hospital, Baltimore, MD, USA
- Johns Hopkins University (US)
- Corresponding author
- Saidha, Shiv
- Venue
- Multiple Sclerosis Journal
- Publisher
- SAGE Publications
- Published
- 2017-04-07
- Volume
- 23
- Issue
- 7
- Pages
- 1035-1039
- ISSN
- 1352-4585 (ISSN-L)
- 1477-0970
- PMC
- PMC5451303
- OpenAlex
- W2604991722
- Cited by
- 40
- References
- 0
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 6 · 2023: 8 · 2022: 1 · 2021: 3 · 2020: 6 · 2019: 3 · 2018: 2 · 2017: 1 · 2016: 1
- FWCI
- 2.58
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Multiple Sclerosis Journal (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Race to Erase MS grant to SS
- Genentech corporation grant to SS
- National Institute of Neurological Disorders and Stroke (5R01NS082347)
- Topics
- Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
- Health Sciences › Medicine › Ophthalmology › Glaucoma and retinal disorders
- Health Sciences › Medicine › Ophthalmology › Drug-Induced Ocular Toxicity
- Keywords
- transsynaptic degeneration, multiple sclerosis, retinal atrophy, ganglion cell-inner plexiform layer thickness, inner nuclear layer, homonymous visual field defects, retinal degeneration
- MeSH terms
- Adult, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Predictive Value of Tests, Retinal Ganglion Cells, Retrograde Degeneration, Synapses, Vision, Ocular, Visual Pathways, Multiple Sclerosis, Relapsing-Remitting, Tomography, Optical Coherence
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