Marco Pisa1, Francesco Ratti1, Marco Vabanesi1, Marta Radaelli1, Simone Guerrieri1, Lucia Moiola2, Vittorio Martinelli2, Giancarlo Comi3, Letizia Leocani4. 1. University Vita-Salute San Raffaele, Milan, Italy. 2. Department of Neurology, Hospital San Raffaele, Milan, Italy/Institute of Experimental Neurology (INSPE), San Raffaele Scientific Institute, Milan, Italy. 3. Department of Clinical Neurophysiology, Hospital San Raffaele, Milan, Italy/ Department of Neurorehabilitation, Hospital San Raffaele, Milan, Italy/ Department of Neurology, Hospital San Raffaele, Milan, Italy/ Institute of Experimental Neurology (INSPE), San Raffaele Scientific Institute, Milan, Italy/ University Vita-Salute San Raffaele, Milan, Italy. 4. Department of Neurorehabilitation and Department of Clinical Neurophysiology, Hospital San Raffaele, Milan, Italy/ INSPE, Institute of Experimental Neurology (INSPE), San Raffaele Scientific Institute, Milan, Italy/ University Vita-Salute San Raffaele, Milan, Italy.
Abstract
BACKGROUND: Neuroretinal atrophy is associated with whole-brain atrophy and disease activity in multiple sclerosis (MS). Recent findings support that subclinical visual pathway involvement might also occur in neuromyelitis optica spectrum disorders (NMOSDs). OBJECTIVE: The objective of this study is to assess retinal thinning in MS and NMOSD and its association with disease activity. METHODS: In total, 27 NMOSD and 54 propensity-score-matched MS patients underwent optical coherence tomography, visual acuity, and visual-evoked potentials at 2.4 years apart, in addition to routine clinical and magnetic resonance imaging (MRI) assessment. We excluded eyes with acute optic neuritis. RESULTS: In NMOSD, we detected peripapillary retinal nerve fiber layer (pRNFL) thinning in patients with disease activity during follow-up (-0.494 µm/year), but not in stable patients (-0.012 µm/year). Macular ganglion cell-inner plexiform layer (GCIPL) thinning occurred instead in all patients (-0.279 µm/year). Relapsing-remitting multiple sclerosis (RRMS) meeting NEDA-3 criteria had no pRNFL or GCIPL thinning during follow-up. Active-disease RRMS and progressive MS, both active and stable, displayed pRNFL (-0.724, -0.586, -0.556 µm/year, respectively) and GCIPL loss. CONCLUSION: In MS, neuroretinal atrophy was associated with disease activity but occurred in progressive MS even when achieving NEDA-3 criteria. In NMOSD, pRNFL thinning was associated with non-ocular relapses due to a spreading of inflammatory activity. GCIPL thinning was found in all patients, supporting a primary retinal pathology targeting AQP4-rich structures.
BACKGROUND:Neuroretinal atrophy is associated with whole-brain atrophy and disease activity in multiple sclerosis (MS). Recent findings support that subclinical visual pathway involvement might also occur in neuromyelitis optica spectrum disorders (NMOSDs). OBJECTIVE: The objective of this study is to assess retinal thinning in MS and NMOSD and its association with disease activity. METHODS: In total, 27 NMOSD and 54 propensity-score-matched MS patients underwent optical coherence tomography, visual acuity, and visual-evoked potentials at 2.4 years apart, in addition to routine clinical and magnetic resonance imaging (MRI) assessment. We excluded eyes with acute optic neuritis. RESULTS: In NMOSD, we detected peripapillary retinal nerve fiber layer (pRNFL) thinning in patients with disease activity during follow-up (-0.494 µm/year), but not in stable patients (-0.012 µm/year). Macular ganglion cell-inner plexiform layer (GCIPL) thinning occurred instead in all patients (-0.279 µm/year). Relapsing-remitting multiple sclerosis (RRMS) meeting NEDA-3 criteria had no pRNFL or GCIPL thinning during follow-up. Active-disease RRMS and progressive MS, both active and stable, displayed pRNFL (-0.724, -0.586, -0.556 µm/year, respectively) and GCIPL loss. CONCLUSION: In MS, neuroretinal atrophy was associated with disease activity but occurred in progressive MS even when achieving NEDA-3 criteria. In NMOSD, pRNFL thinning was associated with non-ocular relapses due to a spreading of inflammatory activity. GCIPL thinning was found in all patients, supporting a primary retinal pathology targeting AQP4-rich structures.
Authors: Angeliki G Filippatou; Eleni S Vasileiou; Yufan He; Kathryn C Fitzgerald; Grigorios Kalaitzidis; Jeffrey Lambe; Maureen A Mealy; Michael Levy; Yihao Liu; Jerry L Prince; Ellen M Mowry; Shiv Saidha; Peter A Calabresi; Elias S Sotirchos Journal: J Neuroophthalmol Date: 2021-05-17 Impact factor: 4.415
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