Vision in Multiple Sclerosis: The Story, Structure-Function Correlations, and Models for Neuroprotection

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Title Journal of Neuro-Ophthalmology, December 2011, Volume 31, Issue 4
Date 2011-12
Language eng
Format application/pdf
Type Text
Publication Type Journal Article
Collection Neuro-Ophthalmology Virtual Education Library: Journal of Neuro-Ophthalmology Archives: https://novel.utah.edu/jno/
Publisher Lippincott, Williams & Wilkins
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah
Rights Management © North American Neuro-Ophthalmology Society
ARK ark:/87278/s6jx1m0m
Setname ehsl_novel_jno
ID 227244
Reference URL https://collections.lib.utah.edu/ark:/87278/s6jx1m0m

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Title Vision in Multiple Sclerosis: The Story, Structure-Function Correlations, and Models for Neuroprotection
Creator Sakai, Reiko E; Feller Daniel J; Galetta, Kristin M; Galetta, Steven L; Balcer, Laura J
Affiliation Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA
Abstract Visual dysfunction is one of the most common clinical manifestations of multiple sclerosis (MS). Just over a decade ago, MS clinical trials did not include visual outcomes, but experts recognized the need for more sensitive measures of visual function. Low-contrast letter acuity emerged as the leading candidate to measure visual disability in MS, and subsequent studies found low-contrast acuity testing to correlate well with brain MRI lesion burden, visual-evoked potentials, quality of life (QOL), and retinal nerve fiber layer (RNFL) loss, as measured by optical coherence tomography (OCT). OCT in MS has allowed for assessment of structure-function correlations that make the anterior visual pathway and acute optic neuritis (ON) ideal models for testing novel agents for neuroprotection and repair. New therapies that reduce axonal loss by neuroprotective or myelin repair mechanisms can now be assessed noninvasively by OCT and coupled with visual function data. Based on OCT studies in MS, RNFL thickness is reduced significantly among patients (92 ?m) vs controls (105 ?m) and is particularly reduced in MS eyes with a history of ON (85 ?m). Worsening of visual function by a clinically significant ? 7 letters or approximately 1.5 lines for low-contrast acuity is associated with approximately 4.5 ?m reductions in RNFL thickness in MS eyes. Longitudinal studies of OCT have also shown RNFL axonal loss over time that occurs even in the absence of acute ON and that correlates with clinically meaningful worsening of vision and QOL, even in patients with benign MS. The latest OCT investigations involve high-resolution spectral-domain (SD) OCT with segmentation and measurement of specific retinal layers using computerized algorithms. These methods allow quantitation of ganglion cell (neuronal) layer loss and axonal degeneration in MS in vivo. In this review, we examine the data from these studies and ongoing trials that highlight the entity of ON as a model to investigate neuroprotection and neurorepair. In doing so, we also present representative group data from studies that have examined visual function, OCT measures, and QOL scales in patients with MS and ON and disease-free controls. These data, and those from recent meta-analyses, may be used to provide reference values for the development of clinical trial protocols.
Subject Contrast Sensitivity; Evoked Potentials, Visual; Humans; Magnetic Resonance Imaging; Multiple Sclerosis; Optic Neuritis; Quality of Life; Tomography, Optical Coherence; Vision Disorders; Vision, Ocular; Visual Acuity; Visual Pathways
OCR Text Show
Format application/pdf
Publication Type Journal Article
Collection Neuro-Ophthalmology Virtual Education Library: Journal of Neuro-Ophthalmology Archives: https://novel.utah.edu/jno/
Publisher Lippincott, Williams & Wilkins
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah
Rights Management © North American Neuro-Ophthalmology Society
Setname ehsl_novel_jno
ID 227235
Reference URL https://collections.lib.utah.edu/ark:/87278/s6jx1m0m/227235
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