Maria Petracca1, Christian Cordano2, Maria Cellerino3, Julia Button4, Stephen Krieger5, Roxana Vancea5, Rezwan Ghassemi5, Colleen Farrell5, Aaron Miller5, Peter A Calabresi4, Fred Lublin5, Matilde Inglese6. 1. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA/Department of Neuroscience, Reproductive Sciences and Odontostomatology, University of Naples Federico II, Naples, Italy. 2. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics and Maternal and Perinatal Sciences, University of Genoa, Genoa, Italy/Department of Neurology, University of California -San Francisco, San Francisco, CA, USA. 3. Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics and Maternal and Perinatal Sciences, University of Genoa, Genoa, Italy. 4. Division of Neuroimmunology and Neurological Infections, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. 5. Department of Neurology, Icahn School of Medicine at Mount Sinai, New York, NY, USA. 6. Departments of Neurology, Radiology and Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY, USA/Department of Neuroscience, Rehabilitation, Ophthalmology, Genetics and Maternal and Perinatal Sciences, University of Genoa, Genoa, Italy.
Abstract
BACKGROUND: Retinal atrophy in multiple sclerosis (MS) is secondary to optic nerve focal inflammation and to injury of the posterior visual pathway. OBJECTIVES: To investigate the contribution of cortical lesions (CLs) to retinal pathology in primary-progressive multiple sclerosis (PPMS). METHODS: We performed a cross-sectional evaluation of 25 patients and 20 controls, relating magnetic resonance imaging (MRI) metrics of visual pathway integrity with parameters derived from spectral-domain optical coherence tomography (peripapillary retinal nerve fiber layer (RNFL) thickness, ganglion cell + inner plexiform layer (GCIPL) thickness, and macular volume (MV)). RESULTS: Mean RNFL, GCIPL thickness, and MV were significantly reduced in patients compared to controls. MV and GCIPL thickness were significantly correlated with visual acuity. RNFL thinning was associated with thalamus and visual cortex volume (respectively, p = 0.01 and p < 0.05). In addition to thalamic volume, GCIPL thinning was associated with CLs and intracortical lesion number and volume, leucocortical lesion volume (all p ⩽ 0.05) while MV decrease was associated with CLs volume ( p = 0.05) and intracortical lesion number and volume ( p < 0.05). CONCLUSION: Our results suggest that RNFL thinning and GCIPL thinning/MV decrease may be explained by alternative mechanisms including retrograde trans-synaptic degeneration and/or a common pathophysiologic process affecting both the brain with CLs and the retina with neuronal loss.
BACKGROUND:Retinal atrophy in multiple sclerosis (MS) is secondary to optic nerve focal inflammation and to injury of the posterior visual pathway. OBJECTIVES: To investigate the contribution of cortical lesions (CLs) to retinal pathology in primary-progressive multiple sclerosis (PPMS). METHODS: We performed a cross-sectional evaluation of 25 patients and 20 controls, relating magnetic resonance imaging (MRI) metrics of visual pathway integrity with parameters derived from spectral-domain optical coherence tomography (peripapillary retinal nerve fiber layer (RNFL) thickness, ganglion cell + inner plexiform layer (GCIPL) thickness, and macular volume (MV)). RESULTS: Mean RNFL, GCIPL thickness, and MV were significantly reduced in patients compared to controls. MV and GCIPL thickness were significantly correlated with visual acuity. RNFL thinning was associated with thalamus and visual cortex volume (respectively, p = 0.01 and p < 0.05). In addition to thalamic volume, GCIPL thinning was associated with CLs and intracortical lesion number and volume, leucocortical lesion volume (all p ⩽ 0.05) while MV decrease was associated with CLs volume ( p = 0.05) and intracortical lesion number and volume ( p < 0.05). CONCLUSION: Our results suggest that RNFL thinning and GCIPL thinning/MV decrease may be explained by alternative mechanisms including retrograde trans-synaptic degeneration and/or a common pathophysiologic process affecting both the brain with CLs and the retina with neuronal loss.
Entities:
Keywords:
Multiple sclerosis; cortical lesions; magnetic resonance imaging; neurodegeneration; retina
Authors: Christian Cordano; Bardia Nourbakhsh; Hao H Yiu; Nico Papinutto; Eduardo Caverzasi; Ahmed Abdelhak; Frederike C Oertel; Alexandra Beaudry-Richard; Adam Santaniello; Simone Sacco; Daniel J Bennett; Apraham Gomez; Christina J Sigurdson; Stephen L Hauser; Roberta Magliozzi; Bruce A C Cree; Roland G Henry; Ari J Green Journal: Neurology Date: 2022-08-29 Impact factor: 11.800
Authors: Valentina Poretto; Maria Petracca; Catarina Saiote; Enricomaria Mormina; Jonathan Howard; Aaron Miller; Fred D Lublin; Matilde Inglese Journal: Mult Scler J Exp Transl Clin Date: 2017-05-18