Contributions
Abstract: P577
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: New or enlarging T2-hyperintense white matter lesions (WML) are associated with clinical disease progression in multiple sclerosis (MS). The impact of WML shrinking, which might be a sign of repair, has not been investigated to the best of our knowledge.
Aim: We aimed at assessing causes and clinical relevance of WML shrinking in early MS patients.
Methods: We performed 3 consecutive brain MRI scans (3D, 3T, FLAIR and T1w +/- gadolinium) at baseline (MRI1) and after 1 (MRI2) and 3 years (MRI3) in a cohort of 152 early (mean disease duration
1 year) MS patients. All patients were therapy naïve at baseline and most of them treated with different disease modifying drugs (DMD) at MRI 2 and 3. We determined total WML volumes at all time points by an automatic lesion segmentation tool (LST version 2.0.15, lesion growth algorithm) and extracted the number of gadolinium-enhancing and new WML from the radiology report. The volume of WML decrease and increase (MRI1-2; 2-3) was determined by LST's longitudinal pipeline based on changes of each individual WML. Clinical disability was measured simultaneously to each MRI scan by Expanded Disability Status Scale (EDSS). We determined the association of WML decrease (MRI1-2; MRI 2-3) with EDSS at MRI3, EDSS change between MRI1 and 3, number of relapses within the study period and with the number of new (MRI2) and gadolinium-enhancing WML (MRI1; 2) by partial correlation analyses correcting for age, gender, DMD and total WML volume (MRI1; 2).
Results: WML decrease between MRI1 and 2 was associated with none of the clinical parameters but with the number of gadolinium-enhancing WML at MRI1 (r 0.215, p 0.009). WML decrease between MRI2 and 3 was also associated with the number of gadolinium-enhancing WML at MRI1 (r 0.268, p 0.002);
it was further associated with the number of new (r 0.299, p = 0.001) and gadolinium-enhancing
(r 0.225, p 0.01) WML at MRI2 but with none of the clinical parameters. EDSS was low at all 3 time points (mean EDSS MRI1, 2, 3; 1.2, 1.1, 1.2) and correlated with total WML volume only at time point 2
(r 0.243, p 0.003) but not 1 or 3.
Conclusion: In treated MS patients, WML decrease as observable during the first years after diagnosis with conventional MRI, seems to reflect disease activity at baseline rather than repair processes.
Disclosure:
Viola Biberacher has received intramural research support from the Komission für Klinische Forschung (KKF), Klinikum rechts der Isar, Technische Universität München.
Paul Schmidt has nothing to disclose.
Sophia Grahl has nothing to disclose.
Annkathrin Beer has nothing to disclose.
Dorothea Buck has received compensation for activities with Bayer HealthCare, BiogenIdec, MerckSerono, and Novartis. She is supported by the Abirisk Consortium.
Achim Berthele reports grants from Bayer Healthcare, personal fees from Biogen, Merck Serono, Teva, Novartis, and Genzyme, and compensations for clinical trials from Biogen, Novartis, Genzyme, Roche, Teva, and Alexion Pharmaceuticals - outside the submitted work”.
Muna-Miriam Hoshi reports a travel grant from Bayer Health Care for participation in the annual Meeting of German Neurologic Society 2016.
Jan Kirschke has received research funding from the European Research Council and the German Research Foundation, travel support from Kaneka Europe as well as speaker honoraria from Philips Healthcare; all not related to this work.
Claus Zimmer has nothing to disclose.
Bernhard Hemmer has served on scientific advisory boards for F. Hoffmann-La Roche Ltd, Novartis, Bayer AG, and Genentech; he has served as DMSC member for AllergyCare; he or his institution have received speaker honoraria from Biogen Idec, Teva Neuroscience, Merck Serono, Medimmune, Novartis, Desitin, and F. Hoffmann-La Roche Ltd; his institution has received research support from Chugai Pharmaceuticals and Hoffmann-La-Roche; holds part of two patents; one for the detection of antibodies and T cells against KIR4.1 in a subpopulation of MS patients and one for genetic determinants of neutralizing antibodies to interferon β.
Mark Mühlau received research support from Merck Serono and Novartis.
Abstract: P577
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: New or enlarging T2-hyperintense white matter lesions (WML) are associated with clinical disease progression in multiple sclerosis (MS). The impact of WML shrinking, which might be a sign of repair, has not been investigated to the best of our knowledge.
Aim: We aimed at assessing causes and clinical relevance of WML shrinking in early MS patients.
Methods: We performed 3 consecutive brain MRI scans (3D, 3T, FLAIR and T1w +/- gadolinium) at baseline (MRI1) and after 1 (MRI2) and 3 years (MRI3) in a cohort of 152 early (mean disease duration
1 year) MS patients. All patients were therapy naïve at baseline and most of them treated with different disease modifying drugs (DMD) at MRI 2 and 3. We determined total WML volumes at all time points by an automatic lesion segmentation tool (LST version 2.0.15, lesion growth algorithm) and extracted the number of gadolinium-enhancing and new WML from the radiology report. The volume of WML decrease and increase (MRI1-2; 2-3) was determined by LST's longitudinal pipeline based on changes of each individual WML. Clinical disability was measured simultaneously to each MRI scan by Expanded Disability Status Scale (EDSS). We determined the association of WML decrease (MRI1-2; MRI 2-3) with EDSS at MRI3, EDSS change between MRI1 and 3, number of relapses within the study period and with the number of new (MRI2) and gadolinium-enhancing WML (MRI1; 2) by partial correlation analyses correcting for age, gender, DMD and total WML volume (MRI1; 2).
Results: WML decrease between MRI1 and 2 was associated with none of the clinical parameters but with the number of gadolinium-enhancing WML at MRI1 (r 0.215, p 0.009). WML decrease between MRI2 and 3 was also associated with the number of gadolinium-enhancing WML at MRI1 (r 0.268, p 0.002);
it was further associated with the number of new (r 0.299, p = 0.001) and gadolinium-enhancing
(r 0.225, p 0.01) WML at MRI2 but with none of the clinical parameters. EDSS was low at all 3 time points (mean EDSS MRI1, 2, 3; 1.2, 1.1, 1.2) and correlated with total WML volume only at time point 2
(r 0.243, p 0.003) but not 1 or 3.
Conclusion: In treated MS patients, WML decrease as observable during the first years after diagnosis with conventional MRI, seems to reflect disease activity at baseline rather than repair processes.
Disclosure:
Viola Biberacher has received intramural research support from the Komission für Klinische Forschung (KKF), Klinikum rechts der Isar, Technische Universität München.
Paul Schmidt has nothing to disclose.
Sophia Grahl has nothing to disclose.
Annkathrin Beer has nothing to disclose.
Dorothea Buck has received compensation for activities with Bayer HealthCare, BiogenIdec, MerckSerono, and Novartis. She is supported by the Abirisk Consortium.
Achim Berthele reports grants from Bayer Healthcare, personal fees from Biogen, Merck Serono, Teva, Novartis, and Genzyme, and compensations for clinical trials from Biogen, Novartis, Genzyme, Roche, Teva, and Alexion Pharmaceuticals - outside the submitted work”.
Muna-Miriam Hoshi reports a travel grant from Bayer Health Care for participation in the annual Meeting of German Neurologic Society 2016.
Jan Kirschke has received research funding from the European Research Council and the German Research Foundation, travel support from Kaneka Europe as well as speaker honoraria from Philips Healthcare; all not related to this work.
Claus Zimmer has nothing to disclose.
Bernhard Hemmer has served on scientific advisory boards for F. Hoffmann-La Roche Ltd, Novartis, Bayer AG, and Genentech; he has served as DMSC member for AllergyCare; he or his institution have received speaker honoraria from Biogen Idec, Teva Neuroscience, Merck Serono, Medimmune, Novartis, Desitin, and F. Hoffmann-La Roche Ltd; his institution has received research support from Chugai Pharmaceuticals and Hoffmann-La-Roche; holds part of two patents; one for the detection of antibodies and T cells against KIR4.1 in a subpopulation of MS patients and one for genetic determinants of neutralizing antibodies to interferon β.
Mark Mühlau received research support from Merck Serono and Novartis.