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Astrocytic Outer Retinal Layer Thinning Is Not a Feature in Aqp4-Igg Seropositive Neuromyelitis Optica Spectrum Disorders Publisher Pubmed



Lu A1, 2 ; Zimmermann HG1, 2 ; Specovius S1, 2 ; Motamedi S1, 2 ; Chien C1, 2 ; Bereuter C1, 2 ; Lanapeixoto MA3 ; Fontenelle MA3 ; Ashtari F4 ; Kafieh R5 ; Dehghani A6 ; Pourazizi M6 ; Pandit L7 ; Dcunha A7 Show All Authors
Authors
  1. Lu A1, 2
  2. Zimmermann HG1, 2
  3. Specovius S1, 2
  4. Motamedi S1, 2
  5. Chien C1, 2
  6. Bereuter C1, 2
  7. Lanapeixoto MA3
  8. Fontenelle MA3
  9. Ashtari F4
  10. Kafieh R5
  11. Dehghani A6
  12. Pourazizi M6
  13. Pandit L7
  14. Dcunha A7
  15. Kim HJ8
  16. Hyun JW8
  17. Jung SK9
  18. Leocani L10
  19. Pisa M10
  20. Radaelli M10
  21. Siritho S11
  22. May EF12
  23. Tongco C12
  24. De Seze J13
  25. Senger T13
  26. Palace J14
  27. Rocafernandez A14
  28. Leite MI14
  29. Sharma SM15
  30. Stiebelkalish H16, 17
  31. Asgari N18
  32. Soelberg KK19
  33. Martinezlapiscina EH20
  34. Havla J21
  35. Maodraayer Y22
  36. Rimler Z23
  37. Reid A23
  38. Marignier R24
  39. Cobocalvo A24, 25
  40. Altintas A26
  41. Tanriverdi U27
  42. Yildirim R28
  43. Aktas O29
  44. Ringelstein M29, 30
  45. Albrecht P29
  46. Tavares IM31
  47. Bichuetti DB32
  48. Jacob A33
  49. Huda S33
  50. De Castillo IS34
  51. Petzold A35
  52. Green AJ36
  53. Yeaman MR37, 38
  54. Smith TJ39, 40
  55. Cook L41
  56. Paul F1, 2, 42
  57. Brandt AU1, 2, 43
  58. Oertel FC1, 2, 36

Source: Journal of Neurology, Neurosurgery and Psychiatry Published:2022


Abstract

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. © Author(s) (or their employer(s)) 2022.
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