Contributions
Abstract: P1136
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Background: Rich expression of aquaporin 4 water channels (AQP4) has been described in peri-ependymal regions of the brain, with which white matter lesions in AQP4 antibody positive neuromyelitis optica spectrum disorders (NMOSD) co-localize.
Objective: To investigate and compare occult tissue alterations in peri-ependymal regions in patients with NMOSD versus healthy controls (HC) and multiple sclerosis (MS) patients by applying quantitative T1 mapping at 7 Tesla (T).
Methods: Eleven NMOSD patients (all female; mean±SD age 39.6±12.6 years, range 21-69 years; mean±SD disease duration 9.5±8.0 years, range 1-29 years; median EDSS 4, range 1.5-5) seropositive for AQP4 antibodies, 7 patients with relapsing-remitting MS and 10 HCs underwent 7T MRI. The imaging protocol included T2*w imaging and a 3D MP2RAGE sequence yielding quantitative T1 maps as well as conventional T1 weighted (T1w) images. We semi-automatically segmented the normal-appearing peri-ependymal areas of the cerebral aqueduct, as well as the lateral, third, and fourth ventricles to quantify the T1 relaxation times within these areas.
Results: We could not observe any T1 changes in peri-ependymal areas differentiating NMOSD patients from HC (all p>0.05). In contrast, T1 was longer in patients with MS compared to NMOSD (lateral ventricle p=0.056, third ventricle p=0.153, fourth ventricle p=0.016), as well as in comparison to HC (third ventricle (p=0.027), fourth ventricle (p=0.013), lateral ventricle (p=0.043).
Conclusion: In contrast to our initial hypothesis and different from MS, in NMOSD patients we could not detect even subtle T1 time changes within lesion-free and normal-appearing peri-ependymal brain regions. Our findings suggest a more focal and less diffuse brain pathology in NMOSD in contrast to MS.
Disclosure: Baptiste Pasquier, and Nadja Borisow have nothing to disclose. Judith Bellmann-Strobl has received travel grants and speaking fees from Bayer Healthcare, Biogen Idec, Merck Serono, sanofi-aventis/Genzyme, Teva Pharmaceuticals, and Novartis. Klemens Ruprecht was supported by the German Ministry of Education and Research (BMBF/KKNMS, Competence Network Multiple Sclerosis) and has received research support from Novartis and Merck Serono as well as speaking fees and travel grants from Guthy Jackson Charitable Foundation, Bayer Healthcare, Biogen Idec, Merck Serono, sanofi-aventis/Genzyme, Teva Pharmaceuticals, Roche and Novartis. Thoralf Niendorf has nothing to disclose related to this work. Tobias Derfuss received speaker fees, research support, travel support, and/or served on Advisory Boards or Steering Committees of Novartis Pharma, Merck, Biogen, Teva, Bayer-Schering, GeNeuro, Mitsubishi Pharma, MedDay, Roche, and Genzyme; he received research support from Biogen, Novartis, Swiss National Research Foundation, University of Basel, and Swiss MS Society. Jens Wuerfel is CEO of MIAC AG Basel, Switzerland. He served on scientific advisory boards of Actelion, Biogen, Genzyme-Sanofi, Novartis, and Roche. He is or was supported by grants of the EU (Horizon2020), German Federal Ministeries of Education and Research (BMBF) and of Economic Affairs and Energy (BMWI).Friedemann Paul serves on the scientific advisory board for Novartis; received speaker honoraria and travel funding from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an academic editor for PLoS ONE; is an associate Editor for Neurology® Neuroimmunology & Neuroinflammation; consulted for SanofiGenzyme, Biogen Idec, MedImmune, Shire, and Alexion; and received research support from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Alexion, Merck Serono, German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy Jackson Charitable Foundation, and National Multiple Sclerosis of the USA. Tim Sinnecker has received travel support from Actelion and Roche, and speaker fees from Biogen. He is employee of the Medical Image Analysis Center AG in Basel.
Abstract: P1136
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Background: Rich expression of aquaporin 4 water channels (AQP4) has been described in peri-ependymal regions of the brain, with which white matter lesions in AQP4 antibody positive neuromyelitis optica spectrum disorders (NMOSD) co-localize.
Objective: To investigate and compare occult tissue alterations in peri-ependymal regions in patients with NMOSD versus healthy controls (HC) and multiple sclerosis (MS) patients by applying quantitative T1 mapping at 7 Tesla (T).
Methods: Eleven NMOSD patients (all female; mean±SD age 39.6±12.6 years, range 21-69 years; mean±SD disease duration 9.5±8.0 years, range 1-29 years; median EDSS 4, range 1.5-5) seropositive for AQP4 antibodies, 7 patients with relapsing-remitting MS and 10 HCs underwent 7T MRI. The imaging protocol included T2*w imaging and a 3D MP2RAGE sequence yielding quantitative T1 maps as well as conventional T1 weighted (T1w) images. We semi-automatically segmented the normal-appearing peri-ependymal areas of the cerebral aqueduct, as well as the lateral, third, and fourth ventricles to quantify the T1 relaxation times within these areas.
Results: We could not observe any T1 changes in peri-ependymal areas differentiating NMOSD patients from HC (all p>0.05). In contrast, T1 was longer in patients with MS compared to NMOSD (lateral ventricle p=0.056, third ventricle p=0.153, fourth ventricle p=0.016), as well as in comparison to HC (third ventricle (p=0.027), fourth ventricle (p=0.013), lateral ventricle (p=0.043).
Conclusion: In contrast to our initial hypothesis and different from MS, in NMOSD patients we could not detect even subtle T1 time changes within lesion-free and normal-appearing peri-ependymal brain regions. Our findings suggest a more focal and less diffuse brain pathology in NMOSD in contrast to MS.
Disclosure: Baptiste Pasquier, and Nadja Borisow have nothing to disclose. Judith Bellmann-Strobl has received travel grants and speaking fees from Bayer Healthcare, Biogen Idec, Merck Serono, sanofi-aventis/Genzyme, Teva Pharmaceuticals, and Novartis. Klemens Ruprecht was supported by the German Ministry of Education and Research (BMBF/KKNMS, Competence Network Multiple Sclerosis) and has received research support from Novartis and Merck Serono as well as speaking fees and travel grants from Guthy Jackson Charitable Foundation, Bayer Healthcare, Biogen Idec, Merck Serono, sanofi-aventis/Genzyme, Teva Pharmaceuticals, Roche and Novartis. Thoralf Niendorf has nothing to disclose related to this work. Tobias Derfuss received speaker fees, research support, travel support, and/or served on Advisory Boards or Steering Committees of Novartis Pharma, Merck, Biogen, Teva, Bayer-Schering, GeNeuro, Mitsubishi Pharma, MedDay, Roche, and Genzyme; he received research support from Biogen, Novartis, Swiss National Research Foundation, University of Basel, and Swiss MS Society. Jens Wuerfel is CEO of MIAC AG Basel, Switzerland. He served on scientific advisory boards of Actelion, Biogen, Genzyme-Sanofi, Novartis, and Roche. He is or was supported by grants of the EU (Horizon2020), German Federal Ministeries of Education and Research (BMBF) and of Economic Affairs and Energy (BMWI).Friedemann Paul serves on the scientific advisory board for Novartis; received speaker honoraria and travel funding from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an academic editor for PLoS ONE; is an associate Editor for Neurology® Neuroimmunology & Neuroinflammation; consulted for SanofiGenzyme, Biogen Idec, MedImmune, Shire, and Alexion; and received research support from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Alexion, Merck Serono, German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy Jackson Charitable Foundation, and National Multiple Sclerosis of the USA. Tim Sinnecker has received travel support from Actelion and Roche, and speaker fees from Biogen. He is employee of the Medical Image Analysis Center AG in Basel.