A recent study showed significant retinal damage in patients with double-antibody seronegative neuromyelitis optica spectrum disorders following optic neuritis.
Frederike C. Oertel, MD, PhD
(Credit: LinkedIn)
Newly published in Neurology Neuroimmunology & Neuroinflammation, a cross-sectional study revealed that patients with double-antibody seronegative neuromyelitis optica spectrum disorders (DN-NMOSD) were marked by severe retinal damage after optic neuritis (ON) and retinal neurodegeneration that was independent of ON attack. A majority of the damage occurred in the first ON episode, which suggests the need for better diagnostic markers in DN-NMOSD to facilitate an earlier diagnosis as well as for effective and early treatments.1
In this DN-NMOSD cohort (48 eyes), patients had a median history of 6 attacks (interquartile range: 5-9) within the 5 (±4) years since onset. Myelitis and ON were the most common attack types. In DN-NMOSD eyes after ON, peripapillary retinal nerve fiber layer thickness (pRNFL; P <.001) and GCIPL (P = .023) were thinner compared with eyes of healthy controls (HCs, 49 eyes). Even after only 1 ON episode, DN-NMOSD eyes already had considerable neuroaxonal loss compared with HCs.
Conducted by lead author Frederike C. Oertel, MD, PhD, an assistant professor of translational neuroimmunology at Charité-Universitätsmedizin Berlin, in Germany, and colleagues, the study assessed data of 25 patients with DN-NMOSD with and without a history of ON along with data from 25 patients with aquaporin-4-antibody seropositive NMOSD (AQP4-NMOSD) and from 25 HCs for comparison analysis. All the groups, matched for age and sex,were included from the collaborative retrospective study of retinal optical coherence tomography (OCT) in neuromyelitis optica, known as the CROCTINO study.2 The patients underwent OCT with central postprocessing and local neurologic examination and antibody testing. Authors noted that retinal neurodegeneration quantified as pRNFL and combined ganglion cell and inner plexiform layer thickness (GCIPL).
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In DN-NMOSD eyes without a history of ON, findings showed that pRNFL (P = .027) and GCIPL (p = 0.022) were also reduced in comparison with eyes of the HCs. Despite this, there was no reports of difference in pRNFL and GCIPL between DN-NMOSD and AQP4-NMOSD (46 eyes) for the whole group and for subsets with a history of ON and without a history of ON-as well as between variances of retinal layer thicknesses. Overall, authors noted that the patients with DN-NMOSD presented with homogeneous clinical and imaging findings in this study, potentially suggesting a common retinal pathology in these patients.
All told, the study did not include functional assessments, details of optic nerve involvement on orbital MRI, or descriptions of acute management. The absence of imaging of the retina and optic nerve during acute attacks in the study limited the understanding of acute ON-related damage patterns in DN-NMOSD. Also, authors noted that the ON diagnosis was made clinically, and lacked uniform paraclinical measures to confirm ON status across the study. Moreover, antibody testing, especially for MOG-IgG, was performed at most centers as part of clinical routines instead of in CSF and not at predefined or consistent time points. Researchers noted that this combined with the use of different cell-based assays at various centers, may have influenced test sensitivity. Therefore, authors noted that they cannot rule out the potential influence of center-specific distribution and effects on these results.
