Retinal Optical Coherence Tomography in Neuromyelitis Optica

Other authors

Institut Català de la Salut

[Oertel FC] Experimental and Clinical Research Center, Max Delbruck Center for Molecular Medicine and Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany. NeuroCure Clinical Research Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Germany. Department of Neurology, University of California San Francisco, CA. [Specovius S, Zimmermann HG, Chien C, Motamedi S, Bereuter C] Experimental and Clinical Research Center, Max Delbruck Center for Molecular Medicine and Charité- Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Germany. NeuroCure Clinical Research Center, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Germany. [Cobo-Calvo A] Biomedical Center and University Hospital, Ludwig-Maximilians Universitaet Muenchen, Munich, Germany. Neurology, Multiple Sclerosis, Myelin Disorders and Neuroinflammation, Pierre Wertheimer Neurological Hospital, Hospices Civils de Lyon, France. Centre d’Esclerosi Múltiple de Catalunya (CEMCAT), Barcelona, Spain. Servei de Neurologia-Neuroimmunologia, Vall d’Hebron Hospital Universitari, Barcelona, Spain. Universitat Autònoma de Barcelona, Bellaterra, Spain

Vall d'Hebron Barcelona Hospital Campus

Publication date

2022-05-12T08:25:48Z

2022-05-12T08:25:48Z

2021-11



Abstract

Retina; Pérdida visual


Retina; Visual loss


Retina; Pèrdua visual


Background and Objectives To determine optic nerve and retinal damage in aquaporin-4 antibody (AQP4-IgG)-seropositive neuromyelitis optica spectrum disorders (NMOSD) in a large international cohort after previous studies have been limited by small and heterogeneous cohorts. Methods The cross-sectional Collaborative Retrospective Study on retinal optical coherence tomography (OCT) in neuromyelitis optica collected retrospective data from 22 centers. Of 653 screened participants, we included 283 AQP4-IgG–seropositive patients with NMOSD and 72 healthy controls (HCs). Participants underwent OCT with central reading including quality control and intraretinal segmentation. The primary outcome was thickness of combined ganglion cell and inner plexiform (GCIP) layer; secondary outcomes were thickness of peripapillary retinal nerve fiber layer (pRNFL) and visual acuity (VA). Results Eyes with ON (NMOSD-ON, N = 260) or without ON (NMOSD-NON, N = 241) were assessed compared with HCs (N = 136). In NMOSD-ON, GCIP layer (57.4 ± 12.2 μm) was reduced compared with HC (GCIP layer: 81.4 ± 5.7 μm, p < 0.001). GCIP layer loss (−22.7 μm) after the first ON was higher than after the next (−3.5 μm) and subsequent episodes. pRNFL observations were similar. NMOSD-NON exhibited reduced GCIP layer but not pRNFL compared with HC. VA was greatly reduced in NMOSD-ON compared with HC eyes, but did not differ between NMOSD-NON and HC. Discussion Our results emphasize that attack prevention is key to avoid severe neuroaxonal damage and vision loss caused by ON in NMOSD. Therapies ameliorating attack-related damage, especially during a first attack, are an unmet clinical need. Mild signs of neuroaxonal changes without apparent vision loss in ON-unaffected eyes might be solely due to contralateral ON attacks and do not suggest clinically relevant progression but need further investigation.


Guthy-Jackson Charitable Foundation (GJCF) and German Research Foundation (DFG).

Document Type

Article


Published version

Language

English

Publisher

Wolters Kluwer Health

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Attribution-NonCommercial-NoDerivatives 4.0 International

http://creativecommons.org/licenses/by-nc-nd/4.0/

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