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The anterior visual pathway is frequently affected in multiple sclerosis (MS), but how axonal damage extends from the site of the lesion to neuronal bodies in the retina or lateral geniculate nucleus is poorly understood. Thanks to optical coherence tomography (OCT), it is possible to map and quantify the retrograde diffusion of axonal damage to the retina.1 Lesions in the anterior optic pathway promote significant atrophy of retinal nerve fibre layer (RNFL), which develops in the first 3 months after damage and remains stable after 3 months. Moreover, it has been recently demonstrated that retinal damage in MS is complex and may distinctly affect retinal layers, combining either layer thinning (suggesting the presence of synapse loss and neuronal loss) or layer thickening (suggesting the presence of oedema and inflammation). In fact, the analysis of the ganglion cell/inner plexiform layer (ganglion cell layer (GCL)+inner plexiform layer complex (IPL)) and inner nuclear layer (INL) better correlates with functional disability and prognosis than with RNFL atrophy.2 Acute focal lesions of the optic tracts are infrequently recognised in MS, and they constitute an excellent opportunity to study retrograde axonal degeneration. Previous studies with OCT have shown the homonymous hemimacular atrophy ipsilateral to the optic tract lesion as a specific pattern of retinal atrophy in optic tract lesions,3 with a preferential impact on the GCL.4
A patient with relapsing–remitting MS presented with non-painful, new onset, acute bilateral visual deficit. Automated visual field tests demonstrated non-congruent bilateral homonymous right hemianopsia (figure 1A). Visual acuity (Snellen chart) and colour …
Contributors IG, EFP and SOP performed OCT studies and analysis; MS, SL, NS and AS performed patient evaluation; PV and BSD reviewed data and wrote the manuscript.
Funding This work was supported by grants to PV from the Instituto de Salud Carlos III, Spain (FIS PS09/00259 and RETICS program RD07/0060/01) and by an unrestricted grant from Roche Postdoctoral Fund (RPF-ID046). IG was supported by a fellowship from the Instituto de Salud Carlos III, Spain (Rio Ortega program CM11/00240).
Competing interests Iñigo Gabilondo has received travel and accommodation expenses from Novartis for national and international congresses. Maria Sepulveda has no conflicts of interest to disclose. Santiago Ortiz-Pérez has received consultancy fees from Novartis. Elena Martínez-Lapiscina has received travel and accommodation expenses from Novartis, Biogen, Teva, Sanofi Aventis, Lundbeck and Bayer for national and international congresses. Elena Fraga-Pumar, Sara llufriu and Nuria Sola have no conflicts of interest to disclose. Albert Saiz has received remuneration for consulting services and for giving lectures from Bayer-Schering, Merck-Serono, Biogen-Idec, Sanofi-Aventis, Teva Pharmaceutical Industries and Novartis. Bernardo Sanchez-Dalmau has received travel and accommodation expenses from Novartis for national and international congresses. PV has received consultancy fees from Roche, Novartis, MedImmune, TFS, Heidelberg Engineering, Digna Biotech and Neurotec Farma and research grants from Novartis and Roche and is founder and hold stocks in Bionure Farma.
Patient consent Obtained.
Ethics approval IRB of the Hospital Clinic of Barcelona.
Provenance and peer review Not commissioned; externally peer reviewed.
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