TY - JOUR
T1 - Astrocytic outer retinal layer thinning is not a feature in AQP4-IgG seropositive neuromyelitis optica spectrum disorders
AU - GJCF International Clinical Consortium for NMOSD
AU - Lu, Angelo
AU - Zimmermann, Hanna G.
AU - Specovius, Svenja
AU - Motamedi, Seyedamirhosein
AU - Chien, Claudia
AU - Bereuter, Charlotte
AU - Lana-Peixoto, Marco A.
AU - Fontenelle, Mariana Andrade
AU - Ashtari, Fereshteh
AU - Kafieh, Rahele
AU - Dehghani, Alireza
AU - Pourazizi, Mohsen
AU - Pandit, Lekha
AU - D’Cunha, Anitha
AU - Kim, Ho Jin
AU - Hyun, Jae Won
AU - Jung, Su Kyung
AU - Leocani, Letizia
AU - Pisa, Marco
AU - Radaelli, Marta
AU - Siritho, Sasitorn
AU - May, Eugene F.
AU - Tongco, Caryl
AU - De Sèze, Jérôme
AU - Senger, Thomas
AU - Palace, Jacqueline
AU - Roca-Fernández, Adriana
AU - Leite, Maria Isabel
AU - Sharma, Srilakshmi M.
AU - Stiebel-Kalish, Hadas
AU - Asgari, Nasrin
AU - Soelberg, Kerstin Kathrine
AU - Martinez-Lapiscina, Elena H.
AU - Havla, Joachim
AU - Mao-Draayer, Yang
AU - Rimler, Zoe
AU - Reid, Allyson
AU - Marignier, Romain
AU - Cobo-Calvo, Alvaro
AU - Altintas, Ayse
AU - Tanriverdi, Uygur
AU - Yildirim, Rengin
AU - Aktas, Orhan
AU - Ringelstein, Marius
AU - Albrecht, Philipp
AU - Tavares, Ivan Maynart
AU - Bichuetti, Denis Bernardi
AU - Jacob, Anu
AU - Huda, Saif
AU - de Castillo, Ibis Soto
N1 - Publisher Copyright:
© Author(s) (or their employer(s)) 2022.
PY - 2022/2
Y1 - 2022/2
N2 - Background Patients with anti-aquaporin-4 antibody seropositive (AQP4-IgG+) neuromyelitis optica spectrum disorders (NMOSDs) frequently suffer from optic neuritis (ON) leading to severe retinal neuroaxonal damage. Further, the relationship of this retinal damage to a primary astrocytopathy in NMOSD is uncertain. Primary astrocytopathy has been suggested to cause ON-independent retinal damage and contribute to changes particularly in the outer plexiform layer (OPL) and outer nuclear layer (ONL), as reported in some earlier studies. However, these were limited in their sample size and contradictory as to the localisation. This study assesses outer retinal layer changes using optical coherence tomography (OCT) in a multicentre cross-sectional cohort. Method 197 patients who were AQP4-IgG+ and 32 myelin-oligodendrocyte-glycoprotein antibody seropositive (MOG-IgG+) patients were enrolled in this study along with 75 healthy controls. Participants underwent neurological examination and OCT with central postprocessing conducted at a single site. Results No significant thinning of OPL (25.02±2.03 µm) or ONL (61.63±7.04 µm) were observed in patients who were AQP4-IgG+ compared with patients who were MOG-IgG + with comparable neuroaxonal damage (OPL: 25.10±2.00 µm; ONL: 64.71±7.87 µm) or healthy controls (OPL: 24.58±1.64 µm; ONL: 63.59±5.78 µm). Eyes of patients who were AQP4-IgG+ (19.84±5.09 µm, p=0.027) and MOG-IgG + (19.82±4.78 µm, p=0.004) with a history of ON showed parafoveal OPL thinning compared with healthy controls (20.99±5.14 µm); this was not observed elsewhere. Conclusion The results suggest that outer retinal layer loss is not a consistent component of retinal astrocytic damage in AQP4-IgG+ NMOSD. Longitudinal studies are necessary to determine if OPL and ONL are damaged in late disease due to retrograde trans-synaptic axonal degeneration and whether outer retinal dysfunction occurs despite any measurable structural correlates.
AB - Background Patients with anti-aquaporin-4 antibody seropositive (AQP4-IgG+) neuromyelitis optica spectrum disorders (NMOSDs) frequently suffer from optic neuritis (ON) leading to severe retinal neuroaxonal damage. Further, the relationship of this retinal damage to a primary astrocytopathy in NMOSD is uncertain. Primary astrocytopathy has been suggested to cause ON-independent retinal damage and contribute to changes particularly in the outer plexiform layer (OPL) and outer nuclear layer (ONL), as reported in some earlier studies. However, these were limited in their sample size and contradictory as to the localisation. This study assesses outer retinal layer changes using optical coherence tomography (OCT) in a multicentre cross-sectional cohort. Method 197 patients who were AQP4-IgG+ and 32 myelin-oligodendrocyte-glycoprotein antibody seropositive (MOG-IgG+) patients were enrolled in this study along with 75 healthy controls. Participants underwent neurological examination and OCT with central postprocessing conducted at a single site. Results No significant thinning of OPL (25.02±2.03 µm) or ONL (61.63±7.04 µm) were observed in patients who were AQP4-IgG+ compared with patients who were MOG-IgG + with comparable neuroaxonal damage (OPL: 25.10±2.00 µm; ONL: 64.71±7.87 µm) or healthy controls (OPL: 24.58±1.64 µm; ONL: 63.59±5.78 µm). Eyes of patients who were AQP4-IgG+ (19.84±5.09 µm, p=0.027) and MOG-IgG + (19.82±4.78 µm, p=0.004) with a history of ON showed parafoveal OPL thinning compared with healthy controls (20.99±5.14 µm); this was not observed elsewhere. Conclusion The results suggest that outer retinal layer loss is not a consistent component of retinal astrocytic damage in AQP4-IgG+ NMOSD. Longitudinal studies are necessary to determine if OPL and ONL are damaged in late disease due to retrograde trans-synaptic axonal degeneration and whether outer retinal dysfunction occurs despite any measurable structural correlates.
UR - http://www.scopus.com/inward/record.url?scp=85123648130&partnerID=8YFLogxK
U2 - 10.1136/jnnp-2021-327412
DO - 10.1136/jnnp-2021-327412
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C2 - 34711650
AN - SCOPUS:85123648130
SN - 0022-3050
VL - 93
SP - 188
EP - 195
JO - Journal of Neurology, Neurosurgery and Psychiatry
JF - Journal of Neurology, Neurosurgery and Psychiatry
IS - 2
ER -