Ting Shen1, Yuyi You2, Sukanya Arunachalam3, Ariadna Fontes4, Sidong Liu5, Vivek Gupta1, John Parratt4, Chenyu Wang6, Michael Barnett6, Joshua Barton7, Nitin Chitranshi1, Ling Zhu3, Clare L Fraser3, Stuart L Graham8, Alexander Klistorner9, Con Yiannikas4. 1. Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia. 2. Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia; Save Sight Institute, The University of Sydney, Sydney, Australia. Electronic address: yuyi.you@gmail.com. 3. Save Sight Institute, The University of Sydney, Sydney, Australia. 4. Australia Department of Neurology, Royal North Shore Hospital, Sydney, Australia. 5. Save Sight Institute, The University of Sydney, Sydney, Australia; Brain and Mind Centre, The University of Sydney, Sydney, Australia. 6. Brain and Mind Centre, The University of Sydney, Sydney, Australia; Sydney Neuroimaging Analysis Centre, Sydney, Australia. 7. Brain and Mind Centre, The University of Sydney, Sydney, Australia. 8. Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia; Save Sight Institute, The University of Sydney, Sydney, Australia. 9. Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia; Save Sight Institute, The University of Sydney, Sydney, Australia; Brain and Mind Centre, The University of Sydney, Sydney, Australia.
Abstract
PURPOSE: To assess differential patterns of axonal loss and demyelination in the optic nerve in multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD). DESIGN: Cross-sectional study. PARTICIPANTS: One hundred ninety-two participants, including 136 MS patients (272 eyes), 19 NMOSD patients (38 eyes), and 37 healthy control participants (74 eyes). METHODS: All participants underwent spectral-domain OCT scans and multifocal visual evoked potential (mfVEP) recordings. High-resolution magnetic resonance imaging (MRI) with the diffusion protocol also was performed in all patients. MAIN OUTCOME MEASURES: Ganglion cell-inner plexiform layer (GCIPL) thickness and mfVEP amplitude and latency at 5 eccentricities; global and temporal retinal nerve fiber layer thickness. RESULTS: In optic neuritis (ON) eyes, the NMOSD patients had more severe GCIPL loss (P < 0.001) and mfVEP amplitude reduction (P < 0.001) compared with MS patients, whereas in contrast, mfVEP latency delay was more evident in MS patients (P < 0.001). The NMOSD patients showed more morphologic and functional loss at the foveal to parafoveal region, whereas the MS patients showed evenly distributed damage at the macula. Correlation analysis demonstrated a strong structure-function (OCT-mfVEP) association in the NMOSD patients, which was only moderate in the MS patients. In non-ON (NON) eyes, the MS patients showed significantly thinner GCIPL than controls (P < 0.001), whereas no GCIPL loss was observed in NON eyes in NMOSD. In addition, a significant correlation was found between all OCT and mfVEP measures in MS patients, but not in NMOSD patients. MRI demonstrated significant lesional load in the optic radiation in MS compared to NMOSD eyes (P = 0.002), which was related to the above OCT and mfVEP changes in NON eyes. CONCLUSIONS: Our study demonstrated different patterns of ON damage in NMOSD and MS. In MS, the ON damage was less severe, with demyelination as the main pathologic component, whereas in NMOSD, axonal loss was more severe compared with myelin loss. The disproportional mfVEP amplitude and latency changes suggested predominant axonal damage within the anterior visual pathway as the main clinical feature of NMOSD, in contrast to MS, where demyelination spreads along the entire visual pathway.
PURPOSE: To assess differential patterns of axonal loss and demyelination in the optic nerve in multiple sclerosis (MS) and neuromyelitis optica spectrum disorders (NMOSD). DESIGN: Cross-sectional study. PARTICIPANTS: One hundred ninety-two participants, including 136 MSpatients (272 eyes), 19 NMOSD patients (38 eyes), and 37 healthy control participants (74 eyes). METHODS: All participants underwent spectral-domain OCT scans and multifocal visual evoked potential (mfVEP) recordings. High-resolution magnetic resonance imaging (MRI) with the diffusion protocol also was performed in all patients. MAIN OUTCOME MEASURES: Ganglion cell-inner plexiform layer (GCIPL) thickness and mfVEP amplitude and latency at 5 eccentricities; global and temporal retinal nerve fiber layer thickness. RESULTS: In optic neuritis (ON) eyes, the NMOSD patients had more severe GCIPL loss (P < 0.001) and mfVEP amplitude reduction (P < 0.001) compared with MSpatients, whereas in contrast, mfVEP latency delay was more evident in MSpatients (P < 0.001). The NMOSD patients showed more morphologic and functional loss at the foveal to parafoveal region, whereas the MSpatients showed evenly distributed damage at the macula. Correlation analysis demonstrated a strong structure-function (OCT-mfVEP) association in the NMOSD patients, which was only moderate in the MSpatients. In non-ON (NON) eyes, the MSpatients showed significantly thinner GCIPL than controls (P < 0.001), whereas no GCIPL loss was observed in NON eyes in NMOSD. In addition, a significant correlation was found between all OCT and mfVEP measures in MSpatients, but not in NMOSD patients. MRI demonstrated significant lesional load in the optic radiation in MS compared to NMOSD eyes (P = 0.002), which was related to the above OCT and mfVEP changes in NON eyes. CONCLUSIONS: Our study demonstrated different patterns of ON damage in NMOSD and MS. In MS, the ON damage was less severe, with demyelination as the main pathologic component, whereas in NMOSD, axonal loss was more severe compared with myelin loss. The disproportional mfVEP amplitude and latency changes suggested predominant axonal damage within the anterior visual pathway as the main clinical feature of NMOSD, in contrast to MS, where demyelination spreads along the entire visual pathway.
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