Contributions
Abstract: P1058
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: Increased supratentorial gray matter (GM) atrophy in patients after the first demyelinating event suggestive of MS is associated with a greater risk of conversion to clinically definite multiple sclerosis (CDMS). However, few studies have investigated as to whether or not early disease activity is associated with cerebellar GM atrophy as well. Increasing evidence suggests that the cerebellum is involved beyond just motor control and that individual cerebellar lobules have distinct functions. Thus, treating the cerebellum as a whole may be insufficient to unravel its role with respect to disease progression.
Objective: To investigate the association between regional cerebellar GM atrophy and conversion to CDMS in CIS patients.
Methods: 216 CIS patients were scanned at baseline and after two years of follow-up on the same 1.5T MRI scanner. Patients were divided into 2 groups based on CDMS status within the 2-year time period of the study. CDMS was characterized by the development of a second clinical attack. The scanning protocol included a high resolution T1-weighted image with 1mm isotropic resolution. The Spatially Unbiased Infratentorial and cerebellar Template (SUIT) was used to calculate total cerebellar GM and individual lobular volumes at both time points and percent changes were derived. Total lobular volumes (including left, right and vermis, as applicable) were used to reduce the number of statistical analyses. Binary logistic regression, controlling for age, sex, and time from the first event to baseline assessment, assessed the association between cerebellar GM volumes and conversion to CDMS.
Results: GM atrophy within the cerebellum as a whole was associated with conversion to CDMS (p = 0.048, odds ratio (OR)=.943) [-1.4 vs. -2.8 percent change for those who remained CIS vs. progressed to CDMS]. Atrophy within lobules Crus I (p=.023, OR=.953) [-1.5 vs. 3.7], VIIIb (p=.044, OR=.944) [-1.3 vs. -2.8], IX (p=.022, OR=.926) [-1.4 vs. -2.8], and X (p=.024, OR=.965) [-1.8 vs. -4.9] was significantly associated with conversion to CDMS.
Conclusions: Conversion to CDMS is associated with cerebellar GM atrophy and appears to be regionally specific. These findings further highlight the role of cerebellar pathology from the earliest stages of MS.
Disclosure:
Study disclosure:
The study is an investigator-initiated study that was supported Czech Ministry of Education project Progres Q27/LF1. The MRI acquisition part of the study was supported by Gedeon Richter and Biogen Idec. The MRI analysis part was supported in part by Biogen Idec.
Author disclosure:
N Bergsland has nothing to disclose.
T. Uher received financial support for conference travel and honoraria from Biogen Idec, Novartis, Roche, Genzyme and Merck Serono, as well as support for research activities from Biogen Idec.
D Horakova received compensation for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, Bayer, Sanofi Genzyme, Roche, and Teva, as well as support for research activities from Biogen Idec. D Ramasamy has nothing to disclose.
M Vaneckova received financial support for research activities from Biogen Idec.
Z Seidl received financial support for research activities from Biogen Idec.
J Krasensky received financial support for research activities from Biogen Idec.
E Havrdova received speaker honoraria and consultant fees from Biogen Idec, Merck Serono, Novartis, Genzyme and Teva, as well as support for research activities from Biogen Idec and Merck Serono.
R Zivadinov received personal compensation from EMD Serono, Genzyme-Sanofi, Novartis, Claret-Medical, Celgene for speaking and consultant fees. He received financial support for research activities from Claret Medical, Genzyme-Sanofi, QuintilesIMS Health, Novartis and Intekrin-Coherus.
Abstract: P1058
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: Increased supratentorial gray matter (GM) atrophy in patients after the first demyelinating event suggestive of MS is associated with a greater risk of conversion to clinically definite multiple sclerosis (CDMS). However, few studies have investigated as to whether or not early disease activity is associated with cerebellar GM atrophy as well. Increasing evidence suggests that the cerebellum is involved beyond just motor control and that individual cerebellar lobules have distinct functions. Thus, treating the cerebellum as a whole may be insufficient to unravel its role with respect to disease progression.
Objective: To investigate the association between regional cerebellar GM atrophy and conversion to CDMS in CIS patients.
Methods: 216 CIS patients were scanned at baseline and after two years of follow-up on the same 1.5T MRI scanner. Patients were divided into 2 groups based on CDMS status within the 2-year time period of the study. CDMS was characterized by the development of a second clinical attack. The scanning protocol included a high resolution T1-weighted image with 1mm isotropic resolution. The Spatially Unbiased Infratentorial and cerebellar Template (SUIT) was used to calculate total cerebellar GM and individual lobular volumes at both time points and percent changes were derived. Total lobular volumes (including left, right and vermis, as applicable) were used to reduce the number of statistical analyses. Binary logistic regression, controlling for age, sex, and time from the first event to baseline assessment, assessed the association between cerebellar GM volumes and conversion to CDMS.
Results: GM atrophy within the cerebellum as a whole was associated with conversion to CDMS (p = 0.048, odds ratio (OR)=.943) [-1.4 vs. -2.8 percent change for those who remained CIS vs. progressed to CDMS]. Atrophy within lobules Crus I (p=.023, OR=.953) [-1.5 vs. 3.7], VIIIb (p=.044, OR=.944) [-1.3 vs. -2.8], IX (p=.022, OR=.926) [-1.4 vs. -2.8], and X (p=.024, OR=.965) [-1.8 vs. -4.9] was significantly associated with conversion to CDMS.
Conclusions: Conversion to CDMS is associated with cerebellar GM atrophy and appears to be regionally specific. These findings further highlight the role of cerebellar pathology from the earliest stages of MS.
Disclosure:
Study disclosure:
The study is an investigator-initiated study that was supported Czech Ministry of Education project Progres Q27/LF1. The MRI acquisition part of the study was supported by Gedeon Richter and Biogen Idec. The MRI analysis part was supported in part by Biogen Idec.
Author disclosure:
N Bergsland has nothing to disclose.
T. Uher received financial support for conference travel and honoraria from Biogen Idec, Novartis, Roche, Genzyme and Merck Serono, as well as support for research activities from Biogen Idec.
D Horakova received compensation for travel, speaker honoraria and consultant fees from Biogen Idec, Novartis, Merck, Bayer, Sanofi Genzyme, Roche, and Teva, as well as support for research activities from Biogen Idec. D Ramasamy has nothing to disclose.
M Vaneckova received financial support for research activities from Biogen Idec.
Z Seidl received financial support for research activities from Biogen Idec.
J Krasensky received financial support for research activities from Biogen Idec.
E Havrdova received speaker honoraria and consultant fees from Biogen Idec, Merck Serono, Novartis, Genzyme and Teva, as well as support for research activities from Biogen Idec and Merck Serono.
R Zivadinov received personal compensation from EMD Serono, Genzyme-Sanofi, Novartis, Claret-Medical, Celgene for speaking and consultant fees. He received financial support for research activities from Claret Medical, Genzyme-Sanofi, QuintilesIMS Health, Novartis and Intekrin-Coherus.