Contributions
Abstract: P1749
Type: Poster Sessions
Abstract Category: N/A
Introduction: Cortical atrophy is well established as a feature of multiple sclerosis (MS) and is correlated to clinical and neuropsychological measures. Recent studies, demonstrated specific clinically relevant patterns of cortical atrophy in MS. However, the temporal evolution of cortical thinning as well as its association with white matter (WM) lesions and disease progression is still poorly understood. In this study, we aimed to investigate longitudinal changes of cortical thickness (CTh) and their correlation to lesion volume and clinical outcomes in relapse-onset MS.
Methods: 231 MS patients (180 relapsing remitting (RR) and 51 secondary progressive (SP) MS) underwent annual standardized clinical (including expanded disability status scale (EDSS)) and MRI examinations over 6 years. CTh was estimated using a fully automated pipeline (CIVET) after WM lesion filling on 3D T1w MPRAGE images acquired at a single 1.5T scanner. In addition, T2 WM lesion volume (T2LV) was measured. Vertex-wise longitudinal analysis was performed using a linear mixed effect model. The results were corrected for multiplicity using the false discovery rate approach (q< 0.05).
Results: EDSS worsening over time was associated with cortical thinning in bilateral visual association areas, inferior gyri and insula, the left premotor cortex as well as the right orbitofrontal cortex, parahippocampal and cingulate gyri. Longer disease duration and higher T2LV were associated with extended bilateral CTh reduction on average, but not with CTh progression over time. Higher age was associated with bilateral frontotemporal CTh reduction including the primary somatosensory and motor cortex, the prefrontal cortex and the parahippocampal gyri as well as the right visual association area and orbitofrontal cortex, while displaying faster extended bilateral CTh reduction over time. CTh did not differ between RRMS and SPMS.
Conclusions: In MS, cortical thinning occurs and a specific cortical atrophy pattern is related to disease worsening over 6 years, after correcting for age- and disease duration-dependent cortical changes. T2LV was associated with a diffuse cortical thinning, but did not predict the temporal evolution of CTh over 6 years, suggesting that focal inflammatory events occurring in the WM do not drive the immediate loss of cortical grey matter.
Disclosure: Charidimos Tsagkas has no disclosures.
M. Mallar Chakravarty has no disclosures.
Laura Gaetano was a temporary employee of Novartis AG.
Yvonne Naegelin has no disclosures.
Amann Michael has no disclosures.
K.Parmar: K.P. holds a grant of the Baasch-Medicus foundation. Her institution (University Hospital Basel) received speakers honoraria from Novartis and ExceMED and travel support by Novartis Switzerland.
Athina Papadopoulou has consulted for Teva, received speaker-fee from Sanofi-Genzyme and travel support from Bayer AG, Teva, UCB-Pharma AG and Roche. Her research was/is being supported by the University of Basel, the Swiss Multiple Sclerosis Society, the Swiss National Science Foundation and the “Stiftung zur Förderung der gastroenterologischen und allgemeinen klinischen Forschung sowie
der medizinischen Bildauswertung”.
J. Wuerfel: CEO of MIAC AG, Basel, Switzerland; speaker honoraria (Bayer, Biogen, Novartis, Teva); advisory boards and research grants (Biogen, Novartis); supported by the German Ministry of Science (BMBF/KKNMS) and German Ministry of Economy (BMWi).
Ludwig Kappos´ Institution (University Hospital Basel) received in the last 3 years and used exclusively for research support at the Department: steering committee, advisory board and consultancy fees from Actelion, Alkermes, Almirall, Bayer, Biogen, Celgene/Receptos, df-mp, Excemed, GeNeuro SA, Genzyme, Japan Tobacco, Merck, Minoryx, Mitsubishi Pharma, Novartis, Roche, sanofi-aventis, Santhera, Teva, Vianex and royalties for Neurostatus-UHB products. The Research of the MS Center in Basel has been supported by grants from Bayer, Biogen, Novartis, the Swiss MS Society, the Swiss National Research Foundation, the European Union and Roche Research Foundations
Till Sprenger:The current (DKD Helios Klinik Wiesbaden) or previous (University Hospital Basel) institutions of Till Sprenger have received payments for speaking or consultation from: Biogen Idec, Eli Lilly, Allergan, Actelion, ATI, Mitsubishi Pharma, Novartis, Genzyme, and Teva. Dr. Sprenger received research grants from the Swiss MS Society, Novartis Pharmaceuticals Switzerland, EFIC-Grünenthal grant, and Swiss National Science foundation.
Stefano Magon has received research support from Swiss MS Society, Swiss National Science Foundation, University of Basel and Stiftung zur Förderung der gastroenterologischen und allgemeinen klinischen Forschung sowie
der medizinischen Bildauswertung University Hospital Basel. He also received travel support from Biogen and Genzyme.
Abstract: P1749
Type: Poster Sessions
Abstract Category: N/A
Introduction: Cortical atrophy is well established as a feature of multiple sclerosis (MS) and is correlated to clinical and neuropsychological measures. Recent studies, demonstrated specific clinically relevant patterns of cortical atrophy in MS. However, the temporal evolution of cortical thinning as well as its association with white matter (WM) lesions and disease progression is still poorly understood. In this study, we aimed to investigate longitudinal changes of cortical thickness (CTh) and their correlation to lesion volume and clinical outcomes in relapse-onset MS.
Methods: 231 MS patients (180 relapsing remitting (RR) and 51 secondary progressive (SP) MS) underwent annual standardized clinical (including expanded disability status scale (EDSS)) and MRI examinations over 6 years. CTh was estimated using a fully automated pipeline (CIVET) after WM lesion filling on 3D T1w MPRAGE images acquired at a single 1.5T scanner. In addition, T2 WM lesion volume (T2LV) was measured. Vertex-wise longitudinal analysis was performed using a linear mixed effect model. The results were corrected for multiplicity using the false discovery rate approach (q< 0.05).
Results: EDSS worsening over time was associated with cortical thinning in bilateral visual association areas, inferior gyri and insula, the left premotor cortex as well as the right orbitofrontal cortex, parahippocampal and cingulate gyri. Longer disease duration and higher T2LV were associated with extended bilateral CTh reduction on average, but not with CTh progression over time. Higher age was associated with bilateral frontotemporal CTh reduction including the primary somatosensory and motor cortex, the prefrontal cortex and the parahippocampal gyri as well as the right visual association area and orbitofrontal cortex, while displaying faster extended bilateral CTh reduction over time. CTh did not differ between RRMS and SPMS.
Conclusions: In MS, cortical thinning occurs and a specific cortical atrophy pattern is related to disease worsening over 6 years, after correcting for age- and disease duration-dependent cortical changes. T2LV was associated with a diffuse cortical thinning, but did not predict the temporal evolution of CTh over 6 years, suggesting that focal inflammatory events occurring in the WM do not drive the immediate loss of cortical grey matter.
Disclosure: Charidimos Tsagkas has no disclosures.
M. Mallar Chakravarty has no disclosures.
Laura Gaetano was a temporary employee of Novartis AG.
Yvonne Naegelin has no disclosures.
Amann Michael has no disclosures.
K.Parmar: K.P. holds a grant of the Baasch-Medicus foundation. Her institution (University Hospital Basel) received speakers honoraria from Novartis and ExceMED and travel support by Novartis Switzerland.
Athina Papadopoulou has consulted for Teva, received speaker-fee from Sanofi-Genzyme and travel support from Bayer AG, Teva, UCB-Pharma AG and Roche. Her research was/is being supported by the University of Basel, the Swiss Multiple Sclerosis Society, the Swiss National Science Foundation and the “Stiftung zur Förderung der gastroenterologischen und allgemeinen klinischen Forschung sowie
der medizinischen Bildauswertung”.
J. Wuerfel: CEO of MIAC AG, Basel, Switzerland; speaker honoraria (Bayer, Biogen, Novartis, Teva); advisory boards and research grants (Biogen, Novartis); supported by the German Ministry of Science (BMBF/KKNMS) and German Ministry of Economy (BMWi).
Ludwig Kappos´ Institution (University Hospital Basel) received in the last 3 years and used exclusively for research support at the Department: steering committee, advisory board and consultancy fees from Actelion, Alkermes, Almirall, Bayer, Biogen, Celgene/Receptos, df-mp, Excemed, GeNeuro SA, Genzyme, Japan Tobacco, Merck, Minoryx, Mitsubishi Pharma, Novartis, Roche, sanofi-aventis, Santhera, Teva, Vianex and royalties for Neurostatus-UHB products. The Research of the MS Center in Basel has been supported by grants from Bayer, Biogen, Novartis, the Swiss MS Society, the Swiss National Research Foundation, the European Union and Roche Research Foundations
Till Sprenger:The current (DKD Helios Klinik Wiesbaden) or previous (University Hospital Basel) institutions of Till Sprenger have received payments for speaking or consultation from: Biogen Idec, Eli Lilly, Allergan, Actelion, ATI, Mitsubishi Pharma, Novartis, Genzyme, and Teva. Dr. Sprenger received research grants from the Swiss MS Society, Novartis Pharmaceuticals Switzerland, EFIC-Grünenthal grant, and Swiss National Science foundation.
Stefano Magon has received research support from Swiss MS Society, Swiss National Science Foundation, University of Basel and Stiftung zur Förderung der gastroenterologischen und allgemeinen klinischen Forschung sowie
der medizinischen Bildauswertung University Hospital Basel. He also received travel support from Biogen and Genzyme.