Contributions
Abstract: P510
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 19 Neurodegeneration
Background: Leptomeningeal contrast enhancement (LMCE) on fluid attenuation inversion recovery (FLAIR) magnetic resonance imaging (MRI) is supposed to be a possible biomarker of disability and cortical atrophy in multiple sclerosis (MS). Recent studies consider LMCE to be associated with leptomeningeal B-cell infiltrates. In this study, we aimed to assess the prevalence of LMCE foci and their impact on neurodegeneration and disability.
Materials: LMCE were detected with a 3 Tesla scanner on post-contrast fluid attenuated inversion-recovery (FLAIR) sequence, using a specific MRI protocol based on original study by M.Absinta et al., 2015. Lesions were detected and characterized by two independent neuroscientists in a blinded fashion. Expanded Disability Status Scale (EDSS) score, number of relapses during 5 years from MS onset and number of contrast-enhancing lesions on T1 weighted MRI were counted. Statistical analysis of covariates (ANCOVA) including age, sex, disease duration and age at clinical onset was performed to determine the impact of LMCE on brain atrophy.
Results: 54 patients with MS were included into the study. LMCE was detected in 41% (22/54) patients. LMCE-positive patients had longer disease duration (p=0,0098) and higher EDSS score (p=0,039), but neither a higher relapse rate (p=0,091), nor older age (p=0.071). LMCE-positive patients had no difference in frequency of contrast-enhancing lesions on T1-wheighted images compared to LMCE-negative patients (p=0,3842). The statistical analysis revealed a significant effect of LMCE on the grey matter volume
(% intracortical volume (mean ± SD)): 44.8 ± 2.8 for LMCE-negative vs. 43.8 ± 2.9 for LMCE positive, p=0.0391. LMCE showed no significant effect on normalized cortical volume: 33.4 ± 2.1 for LMCE-negative vs. 32.7 ± 2.3 for LMCE positive, p=0.0912.
Conclusions: LMCE was shown to be an independent and significant biomarker of grey matter atrophy. LMCE is associated with longer disease duration and higher level of disability in MS. More studies are needed to define the pathogenesis of LMCE formation and its relevance to the clinical practice.
Disclosure: The study was supported with the research grant from the Russian Science Foundation (project #16-15-10203).
Gleb Makshakov has received honoraria for lectures and speaking in the past 2 years from Genzyme and Roche.
Evgeniy Magonov has received honoraria for lectures in the last 2 years from GE Healthcare.
Natalia Totolyan has received honoraria for lectures and speaking from Genzyme, Janssen and Roche. Other authors declare no potential conflict of interests regarding the publication of this paper.
Abstract: P510
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 19 Neurodegeneration
Background: Leptomeningeal contrast enhancement (LMCE) on fluid attenuation inversion recovery (FLAIR) magnetic resonance imaging (MRI) is supposed to be a possible biomarker of disability and cortical atrophy in multiple sclerosis (MS). Recent studies consider LMCE to be associated with leptomeningeal B-cell infiltrates. In this study, we aimed to assess the prevalence of LMCE foci and their impact on neurodegeneration and disability.
Materials: LMCE were detected with a 3 Tesla scanner on post-contrast fluid attenuated inversion-recovery (FLAIR) sequence, using a specific MRI protocol based on original study by M.Absinta et al., 2015. Lesions were detected and characterized by two independent neuroscientists in a blinded fashion. Expanded Disability Status Scale (EDSS) score, number of relapses during 5 years from MS onset and number of contrast-enhancing lesions on T1 weighted MRI were counted. Statistical analysis of covariates (ANCOVA) including age, sex, disease duration and age at clinical onset was performed to determine the impact of LMCE on brain atrophy.
Results: 54 patients with MS were included into the study. LMCE was detected in 41% (22/54) patients. LMCE-positive patients had longer disease duration (p=0,0098) and higher EDSS score (p=0,039), but neither a higher relapse rate (p=0,091), nor older age (p=0.071). LMCE-positive patients had no difference in frequency of contrast-enhancing lesions on T1-wheighted images compared to LMCE-negative patients (p=0,3842). The statistical analysis revealed a significant effect of LMCE on the grey matter volume
(% intracortical volume (mean ± SD)): 44.8 ± 2.8 for LMCE-negative vs. 43.8 ± 2.9 for LMCE positive, p=0.0391. LMCE showed no significant effect on normalized cortical volume: 33.4 ± 2.1 for LMCE-negative vs. 32.7 ± 2.3 for LMCE positive, p=0.0912.
Conclusions: LMCE was shown to be an independent and significant biomarker of grey matter atrophy. LMCE is associated with longer disease duration and higher level of disability in MS. More studies are needed to define the pathogenesis of LMCE formation and its relevance to the clinical practice.
Disclosure: The study was supported with the research grant from the Russian Science Foundation (project #16-15-10203).
Gleb Makshakov has received honoraria for lectures and speaking in the past 2 years from Genzyme and Roche.
Evgeniy Magonov has received honoraria for lectures in the last 2 years from GE Healthcare.
Natalia Totolyan has received honoraria for lectures and speaking from Genzyme, Janssen and Roche. Other authors declare no potential conflict of interests regarding the publication of this paper.