Contributions
Abstract: P554
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - OCT
Background: Leptomeningeal contrast enhancement (LM CE) has been recently described in multiple sclerosis (MS) patients, as potential in-vivo marker of cortical pathology. Optical coherence tomography (OCT) is utilized for early outcome detection of post-inflammatory optic nerve events as well as for assessing the progression of different central nervous system (CNS) pathologies by quantifying the Retinal Nerve Fiber Layer Thickness (RNFLT) and Total macular volume (TMV). We hypothesized that if the LM CE is a marker of neurodegeneration in MS, it would be associated with decrease in RNFLT and TMV as measured by OCT.
Objective: To investigate the association of presence and frequency of LM CE and loss of RNFL thickness and TMV on OCT.
Methods: 81 MS patients (relapsing-remitting (RR): 48, progressive (PMS): 33) were enrolled in the present study. Presence and number of LM CE foci were assessed using 3D fluid-attenuated inversion recovery MRI sequence obtained 10 min after single dose of gadolinium injection on 3T scanner. RNFLT in superior, inferior, nasal and temporal quadrants were obtained for both eyes using OCT (Spectralis, Heidelberg, Germany). The OCT differences between subjects with and without LM CE were evaluated. We also explored the association between number of LM CE foci and OCT measures.
Results: Of the 81 MS patients participating in the study, 35 (43.2%) showed presence of LM CE. PMS patients (n=19, 57.6%) showed significantly higher prevalence of LM CE compared to RRMS (n=16, 33.3%, p=0.026). No age (p=0.362), sex (p=0.347) or disease duration (p=0.227) differences were found between subjects with and without LM CE. MS patients with LM CE showed significantly decreased RNFLT (81.7 vs. 88.4 µm, p=0.046) and decreased TMV (7.4 vs. 8.1 mm3, p=0.036) compared to subjects without LM CE. The most robust regional RNFLT differences between MS patients with and without LM CE were observed in superior and inferior temporal quadrants (p< 0.05). There were significant associations between increased number of LM CE foci, and decreased RNFLT (r=-0.3, p=0.025) and decreased TMV (r=-0.36, p=0.012), which were more robust in RRMS than PMS patients.
Conclusions: These findings suggest that LM CE is associated with atrophy of the retina nerve layer and macula, suggesting that LM CE is a potential biomarker of neurodegeneration occurring in the CNS independent and/or coexisting with an ongoing inflammatory process.
Disclosure:
Robert Zivadinov received personal compensation from Teva Pharmaceuticals, Biogen Idec, EMD Serono, Genzyme-Sanofi, Claret Medical, IMS Health and Novartis for speaking and consultant fees. He received financial support for research activities from Teva Pharmaceuticals, Genzyme-Sanofi, Novartis, Claret Medical, Intekrin and IMS Health.
Deepa Ramasamy, Sirin Gandhi, Jesper Hagemeier, Dejan Jakimovski, Ivo Paunkoski, Ellen Carl, Ahmed Sanai have nothing to disclose.
Channa Kolb has received speaker honoraria from Novartis, Genzyme and Biogen-Idec.
David Hojnacki has received speaker honoraria and consultant fees from Biogen Idec, Teva Pharmaceutical Industries Ltd., EMD Serono, Pfizer Inc, and Novartis.
Bianca Weinstock- Guttman has participated in speaker´s bureaus and served as a consultant for Biogen Idec, Teva Neuroscience, EMD Serono, Novartis, Genzyme & Sanofi, Mylan Inc., and Acorda Therapeutics, Inc. Dr. Weinstock-Guttman also has received grant/research support from the agencies listed in the previous sentence as well as Questcor Pharmaceuticals, Inc., and Shire. She serves in the editorial board for BMC Neurology, Journal of International MS, Journal of Multiple Sclerosis.
Abstract: P554
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - OCT
Background: Leptomeningeal contrast enhancement (LM CE) has been recently described in multiple sclerosis (MS) patients, as potential in-vivo marker of cortical pathology. Optical coherence tomography (OCT) is utilized for early outcome detection of post-inflammatory optic nerve events as well as for assessing the progression of different central nervous system (CNS) pathologies by quantifying the Retinal Nerve Fiber Layer Thickness (RNFLT) and Total macular volume (TMV). We hypothesized that if the LM CE is a marker of neurodegeneration in MS, it would be associated with decrease in RNFLT and TMV as measured by OCT.
Objective: To investigate the association of presence and frequency of LM CE and loss of RNFL thickness and TMV on OCT.
Methods: 81 MS patients (relapsing-remitting (RR): 48, progressive (PMS): 33) were enrolled in the present study. Presence and number of LM CE foci were assessed using 3D fluid-attenuated inversion recovery MRI sequence obtained 10 min after single dose of gadolinium injection on 3T scanner. RNFLT in superior, inferior, nasal and temporal quadrants were obtained for both eyes using OCT (Spectralis, Heidelberg, Germany). The OCT differences between subjects with and without LM CE were evaluated. We also explored the association between number of LM CE foci and OCT measures.
Results: Of the 81 MS patients participating in the study, 35 (43.2%) showed presence of LM CE. PMS patients (n=19, 57.6%) showed significantly higher prevalence of LM CE compared to RRMS (n=16, 33.3%, p=0.026). No age (p=0.362), sex (p=0.347) or disease duration (p=0.227) differences were found between subjects with and without LM CE. MS patients with LM CE showed significantly decreased RNFLT (81.7 vs. 88.4 µm, p=0.046) and decreased TMV (7.4 vs. 8.1 mm3, p=0.036) compared to subjects without LM CE. The most robust regional RNFLT differences between MS patients with and without LM CE were observed in superior and inferior temporal quadrants (p< 0.05). There were significant associations between increased number of LM CE foci, and decreased RNFLT (r=-0.3, p=0.025) and decreased TMV (r=-0.36, p=0.012), which were more robust in RRMS than PMS patients.
Conclusions: These findings suggest that LM CE is associated with atrophy of the retina nerve layer and macula, suggesting that LM CE is a potential biomarker of neurodegeneration occurring in the CNS independent and/or coexisting with an ongoing inflammatory process.
Disclosure:
Robert Zivadinov received personal compensation from Teva Pharmaceuticals, Biogen Idec, EMD Serono, Genzyme-Sanofi, Claret Medical, IMS Health and Novartis for speaking and consultant fees. He received financial support for research activities from Teva Pharmaceuticals, Genzyme-Sanofi, Novartis, Claret Medical, Intekrin and IMS Health.
Deepa Ramasamy, Sirin Gandhi, Jesper Hagemeier, Dejan Jakimovski, Ivo Paunkoski, Ellen Carl, Ahmed Sanai have nothing to disclose.
Channa Kolb has received speaker honoraria from Novartis, Genzyme and Biogen-Idec.
David Hojnacki has received speaker honoraria and consultant fees from Biogen Idec, Teva Pharmaceutical Industries Ltd., EMD Serono, Pfizer Inc, and Novartis.
Bianca Weinstock- Guttman has participated in speaker´s bureaus and served as a consultant for Biogen Idec, Teva Neuroscience, EMD Serono, Novartis, Genzyme & Sanofi, Mylan Inc., and Acorda Therapeutics, Inc. Dr. Weinstock-Guttman also has received grant/research support from the agencies listed in the previous sentence as well as Questcor Pharmaceuticals, Inc., and Shire. She serves in the editorial board for BMC Neurology, Journal of International MS, Journal of Multiple Sclerosis.