Contributions
Abstract: P719
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - Neuro-ophthalmology
Background: dynamic visual functions have been previously suggested to better reflect the demyelinative damage to the optic nerve by a first-time optic neuritis (ON) episode.
Objective: to examine whether past conclusions regarding vision and vision-related measures in clinically acute ON patients hold true in progressive multiple sclerosis (MS) patients in whom disease load may alter the picture.
Methods: 48 progressive MS patients, with and without prior ON (21 ON, 27 non-ON), underwent a battery of behavioural tests, as well as visual evoked potential (VEP) and optical coherence tomography (OCT) tests, at two time-points, 66.1±10.4 days apart. Behavioural tests included object-from-motion based tests, colour, visual acuity, and low contrast letter acuity. P100 measurements were extracted from VEP data and retinal nerve fibre layer (RNFL) thickness and macular volume from OCT data. Data were analysed for stability between visits and for correlation between behavioural and electrophysiological data.
Results: all measures were found to be stable between visits, suggesting no change in disease status. Significant differences were found in all measures between the affected and fellow eyes of ON patients and in the VEP latencies between the affected ON eye and the non-ON eyes. Motion perception was found to correlate with VEP latencies of both ON eyes (affected and fellow) but not of the non-ON eyes. RNFL thickness was correlated with the VEP latencies of non-ON eyes but not of either ON eye.
Conclusions: Despite the passage of time, previous ON episodes still leave their mark, persistently prolonged VEP latencies, in the patient´s visual system. Additionally, even years after the acute episode, all visual measures of the affected eyes are notably reduced compared to the fellow eyes. Motion perception, as a tool reflecting myelination levels along the visual pathway, still showed its usefulness in advanced-stage MS. In the non-ON eyes, axonal loss, as reflected by RNFL thinning, appears to explain the prolongation of conduction velocities, unlike in ON eyes, where demyelination appears to be the main mechanism involved. Lastly, we have shown that the visual measures assessed in this study are replicable over short durations, attesting their applicability as valid follow-up tools in therapeutic studies.
Disclosure: YB, NR and NL were funded by the National Multiple Sclerosis Society (research grant 5128-A) and the Applebaum Foundation. HZ received speaker honoraria from Teva and Bayer. FP serves on the scientific advisory board for Novartis; received speaker honoraria and travel funding from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an academic editor for PLoS ONE; is an associate editor for Neurology® Neuroimmunology & Neuroinflammation; consulted for SanofiGenzyme, Biogen Idec, MedImmune, Shire, and Alexion; and received research support from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Alexion, Merck Serono, German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy Jackson Charitable Foundation, and National Multiple Sclerosis of the USA. HGS, PP and DK have nothing to disclose.
Abstract: P719
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - Neuro-ophthalmology
Background: dynamic visual functions have been previously suggested to better reflect the demyelinative damage to the optic nerve by a first-time optic neuritis (ON) episode.
Objective: to examine whether past conclusions regarding vision and vision-related measures in clinically acute ON patients hold true in progressive multiple sclerosis (MS) patients in whom disease load may alter the picture.
Methods: 48 progressive MS patients, with and without prior ON (21 ON, 27 non-ON), underwent a battery of behavioural tests, as well as visual evoked potential (VEP) and optical coherence tomography (OCT) tests, at two time-points, 66.1±10.4 days apart. Behavioural tests included object-from-motion based tests, colour, visual acuity, and low contrast letter acuity. P100 measurements were extracted from VEP data and retinal nerve fibre layer (RNFL) thickness and macular volume from OCT data. Data were analysed for stability between visits and for correlation between behavioural and electrophysiological data.
Results: all measures were found to be stable between visits, suggesting no change in disease status. Significant differences were found in all measures between the affected and fellow eyes of ON patients and in the VEP latencies between the affected ON eye and the non-ON eyes. Motion perception was found to correlate with VEP latencies of both ON eyes (affected and fellow) but not of the non-ON eyes. RNFL thickness was correlated with the VEP latencies of non-ON eyes but not of either ON eye.
Conclusions: Despite the passage of time, previous ON episodes still leave their mark, persistently prolonged VEP latencies, in the patient´s visual system. Additionally, even years after the acute episode, all visual measures of the affected eyes are notably reduced compared to the fellow eyes. Motion perception, as a tool reflecting myelination levels along the visual pathway, still showed its usefulness in advanced-stage MS. In the non-ON eyes, axonal loss, as reflected by RNFL thinning, appears to explain the prolongation of conduction velocities, unlike in ON eyes, where demyelination appears to be the main mechanism involved. Lastly, we have shown that the visual measures assessed in this study are replicable over short durations, attesting their applicability as valid follow-up tools in therapeutic studies.
Disclosure: YB, NR and NL were funded by the National Multiple Sclerosis Society (research grant 5128-A) and the Applebaum Foundation. HZ received speaker honoraria from Teva and Bayer. FP serves on the scientific advisory board for Novartis; received speaker honoraria and travel funding from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an academic editor for PLoS ONE; is an associate editor for Neurology® Neuroimmunology & Neuroinflammation; consulted for SanofiGenzyme, Biogen Idec, MedImmune, Shire, and Alexion; and received research support from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Alexion, Merck Serono, German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy Jackson Charitable Foundation, and National Multiple Sclerosis of the USA. HGS, PP and DK have nothing to disclose.