Retinal Optical Coherence Tomography in Neuromyelitis Optica
Date
2021Author
Yildirim, Rengin
Havla, Joachim
Marignier, Romain
Calvo, Alvaro Cobo
Bichuetti, Denis
Tavares, Ivan Maynart
Asgari, Nasrin
Soelberg, Kerstin
Altintas, Ayse
Tanriverdi, Uygur
Jacob, Anu
Huda, Saif
Rimler, Zoe
Bereuter, Charlotte
Lana Peixoto, Marco Aurelio
Fontanelle, Mariana Andrade
Kim, Ho Jin
Hyun, Jae-Won
Palace, Jacqueline
Roca-Fernandez, Adriana
Leite, Maria Isabel
Sharma, Srilakshmi
Ashtari, Fereshteh
Kafieh, Rahele
Dehghani, Alireza
Pourazizi, Mohsen
Pandit, Lekha
D'Cunha, Anitha
Aktas, Orhan
Ringelstein, Marius
Albrecht, Philipp
May, Eugene
Tongco, Caryl
Leocani, Letizia
Pisa, Marco
Radaelli, Marta
Reid, Allyson
Mao-Draayer, Yang
Soto de Castillo, Ibis
Petzold, Axel
Green, Ari J.
Yeaman, Michael R.
Smith, Terry
Brandt, Alexander U.
Paul, Friedemann
Oertel, Frederike Cosima
Specovius, Svenja
Zimmermann, Hanna G.
Chien, Claudia
Motamedi, Seyedamirhosein
Cook, Lawrence
Martinez-Lapiscina, Elena H.
Stiebel-Kalish, Hadas
Siritho, Sasitorn
de Seze, Jerome
Senger, Thomas
Metadata
Show full item recordAbstract
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 mu m) was reduced compared with HC (GCIP layer: 81.4 +/- 5.7 mu m, p < 0.001). GCIP layer loss (-22.7 mu m) after the first ON was higher than after the next (-3.5 mu m) 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.
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