2018
DOI: 10.1136/jnnp-2018-318382
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Retinal ganglion cell loss in neuromyelitis optica: a longitudinal study

Abstract: This study clearly shows GCIP loss independent of ON attacks in aquaporin4-antibody-seropositive NMOSD. Potential explanations for progressive GCIP thinning include primary retinopathy, drug-induced neurodegeneration and retrograde neuroaxonal degeneration from lesions or optic neuropathy. pRNFL thickening in the patients presenting with attacks during F/U might be indicative of pRNFL susceptibility to inflammation.

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Cited by 87 publications
(97 citation statements)
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“…Note that in this study optic nerve diameters were measured in the cisternal segment 7 mm anterior to the OC, since contrast heterogeneity and motion artifacts in the orbital part rendered orbital assessment difficult in 25% of the patients. The observation that smaller OC dimensions were also found in NMOSD-NON (compared to HC and NMOSD-ON) supports microstructural changes in the optic pathway independent of ON [26], which have been described in NMOSD [5,27,43,44]. In concordance with a study by Harrigan et al [16], the optic nerve diameter was smaller in patients with a history of ON compared to HC but not in patients without ON.…”
Section: Discussionsupporting
confidence: 89%
“…Note that in this study optic nerve diameters were measured in the cisternal segment 7 mm anterior to the OC, since contrast heterogeneity and motion artifacts in the orbital part rendered orbital assessment difficult in 25% of the patients. The observation that smaller OC dimensions were also found in NMOSD-NON (compared to HC and NMOSD-ON) supports microstructural changes in the optic pathway independent of ON [26], which have been described in NMOSD [5,27,43,44]. In concordance with a study by Harrigan et al [16], the optic nerve diameter was smaller in patients with a history of ON compared to HC but not in patients without ON.…”
Section: Discussionsupporting
confidence: 89%
“…In line with the clinical experience that disability is almost exclusively attack-related in NMOSD, some studies did not find progressive retinal thinning independent of ON (258). However, recent work has suggested that there is attack-independent ganglion cell loss in NMOSD-a finding whose clinical relevance needs to be further investigated (259). In addition, foveal changes have been detected in NMOSD patients without clinical evidence of optic neuritis of affection of the visual system, which suggests that AQP4 ab may directly target astrocytic Mueller cells in the retina, thus causing a primary retinal astrocytopathy (188,260,261).…”
Section: Neuromyelitis Optica Spectrum Disorders (Nmosd)mentioning
confidence: 86%
“…33 We recently reported progressive GCIPL loss without ON in a longitudinal study investigating an overlapping cohort. 34 Further evidence for a primary retinopathy comes from Tian et al 35 reporting inner retinal layer thinning independent from ON. Significant changes in vascularization of the fovea were also shown in patients with AQP4-IgG-seropositive NMOSD in comparison to HCs using OCT angiography.…”
Section: Discussionmentioning
confidence: 99%