TY - JOUR
T1 - Longitudinal Retinal Changes in MOGAD
AU - with the GJCF International Clinical Consortium for NMOSD and the CROCTINO study group
AU - Oertel, Frederike Cosima
AU - Sotirchos, Elias S.
AU - Zimmermann, Hanna G.
AU - Motamedi, Seyedamirhosein
AU - Specovius, Svenja
AU - Asseyer, Eva Susanna
AU - Chien, Claudia
AU - Cook, Lawrence
AU - Vasileiou, Eleni
AU - Filippatou, Angeliki
AU - Calabresi, Peter A.
AU - Saidha, Shiv
AU - Pandit, Lekha
AU - D'Cunha, Anitha
AU - Outteryck, Olivier
AU - Zéphir, Hélène
AU - Pittock, Sean
AU - Flanagan, Eoin P.
AU - Bhatti, M. Tariq
AU - Rommer, Paulus S.
AU - Bsteh, Gabriel
AU - Zrzavy, Tobias
AU - Kuempfel, Tania
AU - Aktas, Orhan
AU - Ringelstein, Marius
AU - Albrecht, Philipp
AU - Ayzenberg, Ilya
AU - Pakeerathan, Thivya
AU - Knier, Benjamin
AU - Aly, Lilian
AU - Asgari, Nasrin
AU - Soelberg, Kerstin
AU - Marignier, Romain
AU - Tilikete, Caroline Froment
AU - Cobo Calvo, Alvaro
AU - Villoslada, Pablo
AU - Sanchez-Dalmau, Bernardo
AU - Martinez-Lapiscina, Elena H.
AU - Llufriu, Sara
AU - Green, Ari J.
AU - Yeaman, Michael R.
AU - Smith, Terry J.
AU - Brandt, Alexander U.
AU - Chen, John
AU - Paul, Friedemann
AU - Havla, Joachim
AU - Altintas, Ayse
AU - Ashtari, Fereshte
AU - Bichuetti, Denis
AU - Stiebel-Kalish, Hadas
N1 - Publisher Copyright:
© 2022 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.
PY - 2022/9
Y1 - 2022/9
N2 - Objective: Patients with myelin oligodendrocyte glycoprotein antibody (MOG-IgG)-associated disease (MOGAD) suffer from severe optic neuritis (ON) leading to retinal neuro-axonal loss, which can be quantified by optical coherence tomography (OCT). We assessed whether ON-independent retinal atrophy can be detected in MOGAD. Methods: Eighty patients with MOGAD and 139 healthy controls (HCs) were included. OCT data was acquired with (1) Spectralis spectral domain OCT (MOGAD: N = 66 and HCs: N = 103) and (2) Cirrus high-definition OCT (MOGAD: N = 14 and HCs: N = 36). Macular combined ganglion cell and inner plexiform layer (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) were quantified. Results: At baseline, GCIPL and pRNFL were lower in MOGAD eyes with a history of ON (MOGAD-ON) compared with MOGAD eyes without a history of ON (MOGAD-NON) and HCs (p < 0.001). MOGAD-NON eyes had lower GCIPL volume compared to HCs (p < 0.001) in the Spectralis, but not in the Cirrus cohort. Longitudinally (follow-up up to 3 years), MOGAD-ON with ON within the last 6–12 months before baseline exhibited greater pRNFL thinning than MOGAD-ON with an ON greater than 12 months ago (p < 0.001). The overall MOGAD cohort did not exhibit faster GCIPL thinning compared with the HC cohort. Interpretation: Our study suggests the absence of attack-independent retinal damage in patients with MOGAD. Yet, ongoing neuroaxonal damage or edema resolution seems to occur for up to 12 months after ON, which is longer than what has been reported with other ON forms. These findings support that the pathomechanisms underlying optic nerve involvement and the evolution of OCT retinal changes after ON is distinct in patients with MOGAD. ANN NEUROL 2022;92:476–485.
AB - Objective: Patients with myelin oligodendrocyte glycoprotein antibody (MOG-IgG)-associated disease (MOGAD) suffer from severe optic neuritis (ON) leading to retinal neuro-axonal loss, which can be quantified by optical coherence tomography (OCT). We assessed whether ON-independent retinal atrophy can be detected in MOGAD. Methods: Eighty patients with MOGAD and 139 healthy controls (HCs) were included. OCT data was acquired with (1) Spectralis spectral domain OCT (MOGAD: N = 66 and HCs: N = 103) and (2) Cirrus high-definition OCT (MOGAD: N = 14 and HCs: N = 36). Macular combined ganglion cell and inner plexiform layer (GCIPL) and peripapillary retinal nerve fiber layer (pRNFL) were quantified. Results: At baseline, GCIPL and pRNFL were lower in MOGAD eyes with a history of ON (MOGAD-ON) compared with MOGAD eyes without a history of ON (MOGAD-NON) and HCs (p < 0.001). MOGAD-NON eyes had lower GCIPL volume compared to HCs (p < 0.001) in the Spectralis, but not in the Cirrus cohort. Longitudinally (follow-up up to 3 years), MOGAD-ON with ON within the last 6–12 months before baseline exhibited greater pRNFL thinning than MOGAD-ON with an ON greater than 12 months ago (p < 0.001). The overall MOGAD cohort did not exhibit faster GCIPL thinning compared with the HC cohort. Interpretation: Our study suggests the absence of attack-independent retinal damage in patients with MOGAD. Yet, ongoing neuroaxonal damage or edema resolution seems to occur for up to 12 months after ON, which is longer than what has been reported with other ON forms. These findings support that the pathomechanisms underlying optic nerve involvement and the evolution of OCT retinal changes after ON is distinct in patients with MOGAD. ANN NEUROL 2022;92:476–485.
UR - http://www.scopus.com/inward/record.url?scp=85134148770&partnerID=8YFLogxK
U2 - 10.1002/ana.26440
DO - 10.1002/ana.26440
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C2 - 35703428
AN - SCOPUS:85134148770
SN - 0364-5134
VL - 92
SP - 476
EP - 485
JO - Annals of Neurology
JF - Annals of Neurology
IS - 3
ER -