Longitudinal Retinal Changes in MOGAD

Frederike Cosima Oertel; Elias S. Sotirchos; Hanna G. Zimmermann; Seyedamirhosein Motamedi; Svenja Specovius; Eva Susanna Asseyer; Claudia Chien; Lawrence Cook; Eleni Vasileiou; Angeliki Filippatou; Peter A. Calabresi; Shiv Saidha; Lekha Pandit; Anitha D'Cunha; Olivier Outteryck; Hélène Zéphir; Sean Pittock; Eoin P. Flanagan; M. Tariq Bhatti; Paulus S. Rommer; Gabriel Bsteh; Tobias Zrzavy; Tania Kuempfel; Orhan Aktas; Marius Ringelstein; Philipp Albrecht; Ilya Ayzenberg; Thivya Pakeerathan; Benjamin Knier; Lilian Aly; Nasrin Asgari; Kerstin Soelberg; Romain Marignier; Caroline Froment Tilikete; Alvaro Cobo Calvo; Pablo Villoslada; Bernardo Sanchez-Dalmau; Elena H. Martinez-Lapiscina; Sara Llufriu; Ari J. Green; Michael R. Yeaman; Terry J. Smith; Alexander U. Brandt; John Chen; Friedemann Paul; Joachim Havla; with the GJCF International Clinical Consortium for NMOSD and the CROCTINO study group

doi:10.1002/ana.26440

Longitudinal Retinal Changes in MOGAD

Frederike Cosima Oertel, Elias S. Sotirchos, Hanna G. Zimmermann, Seyedamirhosein Motamedi, Svenja Specovius, Eva Susanna Asseyer, Claudia Chien, Lawrence Cook, Eleni Vasileiou, Angeliki Filippatou, Peter A. Calabresi, Shiv Saidha, Lekha Pandit, Anitha D'Cunha, Olivier Outteryck, Hélène Zéphir, Sean Pittock, Eoin P. Flanagan, M. Tariq Bhatti, Paulus S. RommerGabriel Bsteh, Tobias Zrzavy, Tania Kuempfel, Orhan Aktas, Marius Ringelstein, Philipp Albrecht, Ilya Ayzenberg, Thivya Pakeerathan, Benjamin Knier, Lilian Aly, Nasrin Asgari, Kerstin Soelberg, Romain Marignier, Caroline Froment Tilikete, Alvaro Cobo Calvo, Pablo Villoslada, Bernardo Sanchez-Dalmau, Elena H. Martinez-Lapiscina, Sara Llufriu, Ari J. Green, Michael R. Yeaman, Terry J. Smith, Alexander U. Brandt, John Chen, Friedemann Paul^*, Joachim Havla, with the GJCF International Clinical Consortium for NMOSD and the CROCTINO study group

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Abstract

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.

Originalsprog	Engelsk
Tidsskrift	Annals of Neurology
Vol/bind	92
Udgave nummer	3
Sider (fra-til)	476-485
ISSN	0364-5134
DOI	https://doi.org/10.1002/ana.26440
Status	Udgivet - sep. 2022

Bibliografisk note

Funding Information:
J.H. and F.C.O. would like to thank Charlotte Bereuter, Angelika Bamberger, and Luise Böhm for their excellent technical support. This study was funded in part by the Guthy‐Jackson Charitable Foundation. J.H. is (partially) funded by the German Federal Ministry of Education and Research (Grant Numbers 01ZZ1603[A‐D] and 01ZZ1804[A‐H] DIFUTURE). F.C.O. received research support by the German Association of Neurology (Deutsche Gesellschaft für Neurologie) in context of this work and would like to thank the American Academy of Neurology (AAN) and the National Multiple Sclerosis Society (NMSS) for their research support. Open Access funding enabled and organized by Projekt DEAL.

Publisher Copyright:
© 2022 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.

Dokumenter og links

10.1002/ana.26440Licens: CC BY-NC

Open Access VersionForlagets udgivne version, 997 KBLicens: CC BY-NC

Citationsformater

Oertel, F. C., Sotirchos, E. S., Zimmermann, H. G., Motamedi, S., Specovius, S., Asseyer, E. S., Chien, C., Cook, L., Vasileiou, E., Filippatou, A., Calabresi, P. A., Saidha, S., Pandit, L., D'Cunha, A., Outteryck, O., Zéphir, H., Pittock, S., Flanagan, E. P., Bhatti, M. T., ... with the GJCF International Clinical Consortium for NMOSD and the CROCTINO study group (2022). Longitudinal Retinal Changes in MOGAD. Annals of Neurology, 92(3), 476-485. https://doi.org/10.1002/ana.26440

@article{272ccf1b313840b4a78d99f0b2e38cc9,

title = "Longitudinal Retinal Changes in MOGAD",

abstract = "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.",

keywords = "Case-Control Studies, Cohort Studies, Humans, Immunologic Deficiency Syndromes/complications, Longitudinal Studies, Myelin-Oligodendrocyte Glycoprotein/immunology, Optic Neuritis/complications, Retina/diagnostic imaging, Retinal Degeneration/etiology, Retinal Neurons, Tomography, Optical Coherence/methods",

author = "Oertel, {Frederike Cosima} and Sotirchos, {Elias S.} and Zimmermann, {Hanna G.} and Seyedamirhosein Motamedi and Svenja Specovius and Asseyer, {Eva Susanna} and Claudia Chien and Lawrence Cook and Eleni Vasileiou and Angeliki Filippatou and Calabresi, {Peter A.} and Shiv Saidha and Lekha Pandit and Anitha D'Cunha and Olivier Outteryck and H{\'e}l{\`e}ne Z{\'e}phir and Sean Pittock and Flanagan, {Eoin P.} and Bhatti, {M. Tariq} and Rommer, {Paulus S.} and Gabriel Bsteh and Tobias Zrzavy and Tania Kuempfel and Orhan Aktas and Marius Ringelstein and Philipp Albrecht and Ilya Ayzenberg and Thivya Pakeerathan and Benjamin Knier and Lilian Aly and Nasrin Asgari and Kerstin Soelberg and Romain Marignier and Tilikete, {Caroline Froment} and {Cobo Calvo}, Alvaro and Pablo Villoslada and Bernardo Sanchez-Dalmau and Martinez-Lapiscina, {Elena H.} and Sara Llufriu and Green, {Ari J.} and Yeaman, {Michael R.} and Smith, {Terry J.} and Brandt, {Alexander U.} and John Chen and Friedemann Paul and Joachim Havla and {with the GJCF International Clinical Consortium for NMOSD and the CROCTINO study group}",

note = "Funding Information: J.H. and F.C.O. would like to thank Charlotte Bereuter, Angelika Bamberger, and Luise B{\"o}hm for their excellent technical support. This study was funded in part by the Guthy‐Jackson Charitable Foundation. J.H. is (partially) funded by the German Federal Ministry of Education and Research (Grant Numbers 01ZZ1603[A‐D] and 01ZZ1804[A‐H] DIFUTURE). F.C.O. received research support by the German Association of Neurology (Deutsche Gesellschaft f{\"u}r Neurologie) in context of this work and would like to thank the American Academy of Neurology (AAN) and the National Multiple Sclerosis Society (NMSS) for their research support. Open Access funding enabled and organized by Projekt DEAL. Publisher Copyright: {\textcopyright} 2022 The Authors. Annals of Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.",

year = "2022",

month = sep,

doi = "10.1002/ana.26440",

language = "English",

volume = "92",

pages = "476--485",

journal = "Annals of Neurology",

issn = "0364-5134",

publisher = "Wiley",

number = "3",

}

Oertel, FC, Sotirchos, ES, Zimmermann, HG, Motamedi, S, Specovius, S, Asseyer, ES, Chien, C, Cook, L, Vasileiou, E, Filippatou, A, Calabresi, PA, Saidha, S, Pandit, L, D'Cunha, A, Outteryck, O, Zéphir, H, Pittock, S, Flanagan, EP, Bhatti, MT, Rommer, PS, Bsteh, G, Zrzavy, T, Kuempfel, T, Aktas, O, Ringelstein, M, Albrecht, P, Ayzenberg, I, Pakeerathan, T, Knier, B, Aly, L, Asgari, N, Soelberg, K, Marignier, R, Tilikete, CF, Cobo Calvo, A, Villoslada, P, Sanchez-Dalmau, B, Martinez-Lapiscina, EH, Llufriu, S, Green, AJ, Yeaman, MR, Smith, TJ, Brandt, AU, Chen, J, Paul, F, Havla, J & with the GJCF International Clinical Consortium for NMOSD and the CROCTINO study group 2022, 'Longitudinal Retinal Changes in MOGAD', Annals of Neurology, bind 92, nr. 3, s. 476-485. https://doi.org/10.1002/ana.26440

TY - JOUR

T1 - Longitudinal Retinal Changes in MOGAD

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 - with the GJCF International Clinical Consortium for NMOSD and the CROCTINO study group

N1 - Funding Information: J.H. and F.C.O. would like to thank Charlotte Bereuter, Angelika Bamberger, and Luise Böhm for their excellent technical support. This study was funded in part by the Guthy‐Jackson Charitable Foundation. J.H. is (partially) funded by the German Federal Ministry of Education and Research (Grant Numbers 01ZZ1603[A‐D] and 01ZZ1804[A‐H] DIFUTURE). F.C.O. received research support by the German Association of Neurology (Deutsche Gesellschaft für Neurologie) in context of this work and would like to thank the American Academy of Neurology (AAN) and the National Multiple Sclerosis Society (NMSS) for their research support. Open Access funding enabled and organized by Projekt DEAL. 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.

KW - Case-Control Studies

KW - Cohort Studies

KW - Humans

KW - Immunologic Deficiency Syndromes/complications

KW - Longitudinal Studies

KW - Myelin-Oligodendrocyte Glycoprotein/immunology

KW - Optic Neuritis/complications

KW - Retina/diagnostic imaging

KW - Retinal Degeneration/etiology

KW - Retinal Neurons

KW - Tomography, Optical Coherence/methods

U2 - 10.1002/ana.26440

DO - 10.1002/ana.26440

M3 - Journal article

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 -

Longitudinal Retinal Changes in MOGAD

Abstract

Bibliografisk note

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