Retinal Optical Coherence Tomography in Neuromyelitis Optica

Oertel, Frederike Cosima; Specovius, Svenja; Zimmermann, Hanna; Chien, Claudia; Motamedi, Seyedamirhosein; Bereuter, Charlotte; Cook, Lawrence J.; Peixoto, Marco Aurélio Lana; Fontanelle, Mariana Andrade; Kim, Ho Jin; Hyun, Jae‐Won; Palace, Jacqueline; Roca-Fernández, Adriana; Leite, Maria Isabel; Sharma, Srilakshmi M; Ashtari, Fereshteh; Kafieh, Rahele; Dehghani, Alireza; Pourazizi, Mohsen; Pandit, Lekha; D’Cunha, Anitha; Aktaş, Orhan; Ringelstein, Marius; Albrecht, Philipp; May, Eugene; Tongco, Caryl; Leocani, Letizia; Pisa, Marco; Radaelli, Marta; Martínez-Lapiscina, Elena H.; Stiebel‐Kalish, Hadas; Siritho, Sasitorn; Sèze, Jérôme De; Senger, Thomas; Havla, Joachim; Marignier, Romain; Calvo, Álvaro Cobo; Bichuetti, Denis Bernardi; Tavares, Ivan Maynart; Asgari, Nasrin; Soelberg, Kerstin; Altıntaş, Ayşe; Yıldırım, Rengin; Tanriverdi, Uygur; Jacob, Anu; Huda, Saif; Rimler, Zoe; Reid, Allyson; Mao-Draayer, Yang; Castillo, Ibis Soto de; Petzold, Axel; Green, Ari J.; Yeaman, Michael R.; Smith, Terry J.; Brandt, Alexander U.; Paul, Friedemann

doi:10.1212/nxi.0000000000001068

Cited by 49 publications

(32 citation statements)

References 41 publications

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“…GCIP and pRNFL thinning was shown to occur in MS and NMOSD patients with and without prior ON. 5 , 6 , 32 Therefore, we suggest that motion perception relies on the structural integrity of the retina and represents a clinical correlate of neuro-axonal damage. The fact that we reproduced the association of motion perception impairment with pRNFL and GCIP thinning in NMOSD supports this idea, as the effect of axonal loss was shown to be stronger in NMOSD than in MS. 6 , 22 This concept would also explain motion perception impairment in non-demyelinating diseases such as glaucoma, which features RNFL and GCIP damage as a consequence of increased intraocular pressure.…”

Section: Discussionmentioning

confidence: 92%

Impaired motion perception is associated with functional and structural visual pathway damage in multiple sclerosis and neuromyelitis optica spectrum disorders

et al. 2021

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Background: Decreased motion perception has been suggested as a marker for visual pathway demyelination in optic neuritis (ON) and/or multiple sclerosis (MS). Objectives: To examine the influence of neuro-axonal damage on motion perception in MS and neuromyelitis optica spectrum disorders (NMOSD). Methods: We analysed motion perception with numbers-from-motion (NFM), visual acuity, (multifocal (mf)) VEP, optical coherence tomography in patients with MS ( n = 38, confirmatory cohort n = 43), NMOSD ( n = 13) and healthy controls ( n = 33). Results: NFM was lower compared with controls in MS ( B = −12.37, p < 0.001) and NMOSD ( B = −34.5, p < 0.001). NFM was lower in ON than in non-ON eyes ( B = −30.95, p = 0.041) in NMOSD, but not MS. In MS and NMOSD, lower NFM was associated with worse visual acuity ( B = −139.4, p < 0.001/ B = −77.2, p < 0.001) and low contrast letter acuity ( B = 0.99, p = 0.002/ B = 1.6, p < 0.001), thinner peripapillary retinal nerve fibre layer ( B = 1.0, p < 0.001/ B = 0.92, p = 0.016) and ganglion cell/inner plexiform layer ( B = 64.8, p < 0.001/ B = 79.5, p = 0.006), but not with VEP P100 latencies. In the confirmatory MS cohort, lower NFM was associated with thinner retinal nerve fibre layer ( B = 1.351, p < 0.001) and increased mfVEP P100 latencies ( B = −1.159, p < 0.001). Conclusions: Structural neuro-axonal visual pathway damage is an important driver of motion perception impairment in MS and NMOSD.

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Section: Discussionmentioning

confidence: 92%

Impaired motion perception is associated with functional and structural visual pathway damage in multiple sclerosis and neuromyelitis optica spectrum disorders

et al. 2021

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“…The international CROCTINO program uses OCT as a standardized method to assess the clinical course and pathophysiology of NMOSD as well as to monitor therapeutic efficacy [ 131 , 132 ]. OCT was shown to provide unique insights into the identification of foveal pitting in NMOSD likely due to the loss of Müller cells [ 133 ].…”

Section: Potential Biomarkers In Nmosdmentioning

confidence: 99%

“…GC-IPL thickness associated with visual ability in NMOSD-ON eyes leads to more severe retinal thinning and visual impairment than that found in MS [ 134 ]. A cross-sectional collaborative retrospective study reported that the average GC-IPL loss was 22.7 μm after the first ON attack, and the average loss after a recurrent episode was 3.5 μm, with noticeable subclinical GC-IPL loss in non-optic neuritis (NON) eyes [ 132 ]. NMOSD-NON eyes exhibited reduced thickness in the GC-IPL but not in the pRNFL compared with normal eyes, and relative changes in the parvocellular layer of NMOSD-NON eyes were not fully confirmed in recent studies [ 132 , 134 , 135 ].…”

Section: Optic Nerve Structure In Nmosdmentioning

confidence: 99%

Neuromyelitis Optica Spectrum Disorder: From Basic Research to Clinical Perspectives

Huang

Wang

Chang

et al. 2022

IJMS

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Neuromyelitis optica spectrum disorder (NMOSD) is an inflammatory disease of the central nervous system characterized by relapses and autoimmunity caused by antibodies against the astrocyte water channel protein aquaporin-4. Over the past decade, there have been significant advances in the biologic knowledge of NMOSD, which resulted in the IDENTIFICATION of variable disease phenotypes, biomarkers, and complex inflammatory cascades involved in disease pathogenesis. Ongoing clinical trials are looking at new treatments targeting NMOSD relapses. This review aims to provide an update on recent studies regarding issues related to NMOSD, including the pathophysiology of the disease, the potential use of serum and cerebrospinal fluid cytokines as disease biomarkers, the clinical utilization of ocular coherence tomography, and the comparison of different animal models of NMOSD.

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“…The retina is part of the central nervous system, and OCT-derived intraretinal layer thickness or volume measurements, which are typically measured within the macular region, are promising noninvasive biomarkers querying neuronal structures. For instance, the combined macular ganglion cell and inner plexiform layer (GCIPL) shows thinning in eyes affected by optic neuritis (ON) [ 2 , 3 ], multiple sclerosis (MS) [ 4 ], neuromyelitis optica spectrum disorders (NMOSD) [ 5 ] and Alzheimer’s disease [ 6 ]. GCIPL is a potential biomarker predicting disease activity in patients with early MS [ 7 , 8 ] and of cognitive decline in Parkinson’s disease [ 9 ].…”

Section: Introductionmentioning

confidence: 99%

“…GCIPL is a potential biomarker predicting disease activity in patients with early MS [ 7 , 8 ] and of cognitive decline in Parkinson’s disease [ 9 ]. The macular inner nuclear layer (INL) may be affected by inflammatory activity in MS and related disorders [ 10 ] or Müller cell damage in NMOSD [ 5 , 11 , 12 ]. In glaucoma, thinning of inner retinal layers such as GCIPL and the retinal nerve fiber layer (RNFL) may appear before visual function loss and is a potential biomarker for early diagnosis [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

Intraretinal Layer Segmentation Using Cascaded Compressed U-Nets

et al. 2022

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Reliable biomarkers quantifying neurodegeneration and neuroinflammation in central nervous system disorders such as Multiple Sclerosis, Alzheimer’s dementia or Parkinson’s disease are an unmet clinical need. Intraretinal layer thicknesses on macular optical coherence tomography (OCT) images are promising noninvasive biomarkers querying neuroretinal structures with near cellular resolution. However, changes are typically subtle, while tissue gradients can be weak, making intraretinal segmentation a challenging task. A robust and efficient method that requires no or minimal manual correction is an unmet need to foster reliable and reproducible research as well as clinical application. Here, we propose and validate a cascaded two-stage network for intraretinal layer segmentation, with both networks being compressed versions of U-Net (CCU-INSEG). The first network is responsible for retinal tissue segmentation from OCT B-scans. The second network segments eight intraretinal layers with high fidelity. At the post-processing stage, we introduce Laplacian-based outlier detection with layer surface hole filling by adaptive non-linear interpolation. Additionally, we propose a weighted version of focal loss to minimize the foreground–background pixel imbalance in the training data. We train our method using 17,458 B-scans from patients with autoimmune optic neuropathies, i.e., multiple sclerosis, and healthy controls. Voxel-wise comparison against manual segmentation produces a mean absolute error of 2.3 μm, outperforming current state-of-the-art methods on the same data set. Voxel-wise comparison against external glaucoma data leads to a mean absolute error of 2.6 μm when using the same gold standard segmentation approach, and 3.7 μm mean absolute error in an externally segmented data set. In scans from patients with severe optic atrophy, 3.5% of B-scan segmentation results were rejected by an experienced grader, whereas this was the case in 41.4% of B-scans segmented with a graph-based reference method. The validation results suggest that the proposed method can robustly segment macular scans from eyes with even severe neuroretinal changes.

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Retinal Optical Coherence Tomography in Neuromyelitis Optica

Cited by 49 publications

References 41 publications

Impaired motion perception is associated with functional and structural visual pathway damage in multiple sclerosis and neuromyelitis optica spectrum disorders

Impaired motion perception is associated with functional and structural visual pathway damage in multiple sclerosis and neuromyelitis optica spectrum disorders

Neuromyelitis Optica Spectrum Disorder: From Basic Research to Clinical Perspectives

Intraretinal Layer Segmentation Using Cascaded Compressed U-Nets

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