Contributions
Abstract: EP1543
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: Cortical lesions (CL) are believed to play a role in the accumulation of physical and cognitive disability in multiple sclerosis (MS). Up to date, no study has investigated the metabolic behavior of CL.
Aim: To analyze the absolute 18F-FDG metabolism of CL in MS patients by means of a fully integrated 3T-Positron Emission Tomography/Magnetic Resonance Imaging (3T 18F-PET/MRI) system.
Methods: Fifteen early relapsing remitting MS (eRRMS) with no sign of cognitive impairment (CI) and fifteen RRMS with significantly longer disease duration and clinical evidence of CI (CI-RRMS) were enrolled in the study. Physical and cognitive evaluations were done by EDSS and Rao´s BRB. Dynamic 18F-FDG-PET/MRI (Siemens Biograph 3TMRI/PET System) data were analyzed with Patlak plot method to obtain absolute metabolic rate of glucose (aMRglu). CL and white matter (WM) lesions were identified on 3DFLAIR and 3DDIR images, respectively.
Results: eRRMS had lower CL volume and number than CI-RRMS and, despite the limited number of patients, the differences were significant (p=0.02 and p=0.01, respectively). The great majority of CL (68.0%) showed aMRGlu values in the range of the surrounding apparently normal cortex, but 17.8% had significantly increased aMRGlu values and 14.2% were hypometabolic. aMRGlu inversely correlated with CL number and volume in both left (p=0.01, r=-0.49 and p=0.02, r=-0.42) and right parietal (p=0.02, r=-0.43 and p=0.03, r=-0.39) lobes.
Interpretation: CL were found to differ in aMRGlu values. Whether the metabolic state of CL reflects their evolution from an initial hypermatabolic inflammatory phase (potentially excitotoxic) to a final hypo-metabolic neurodegenerative phase merits to be investigated. Indeed, the metabolism of CL might be the link between inflammation and neurodegeneration in MS.
Disclosure: Poggiali D, Cecchin D, Favaretto A, Lazzarotto A, Margoni M, Frigo AC, Zucchetta P, Causin F and Bui F have nothing to disclose. Alice Riccardi has received onoraria from Biogen, Novartis, Teva and Merck Serono. Puthenparampil Marco received travel grant from Novartis, Sanofi-Genzyme, Biogen Idec, Almirall, Teva and Sanofi Aventis and honoraria from Almirall; he has been consultant for Genzyme Federle Lisa has received funding for travel from Novartis, Merck Serono, Biogen Idec, Sanofi-Genzyme, Bayer Schering Pharma, Almirall, Teva and honoraria from MerkSerono, Teva and Almirall. Miante Silvia received travel grant form Biogen Idec, Novartis, Sanofi Aventis and Teva Zito Antonio has nothing to disclose. Erica Stropparo has nothing to disclose. Cazzola Chiara has nothing to disclose. Toffanin Elisabetta has nothing to disclose. Ruggiero Susanna has nothing to disclose. Mario Ermani has nothing to disclose. Francesca Grassivaro has nothing to disclose. Davide Poggiali received travel grant from Biogen Idec, Novartis, Sanofi Aventis and Teva. Rinaldi Francesca serves as an advisory board member of Biogen-Idec and has received funding for travel and speaker honoraria from Merck Serono, Biogen Idec, Sanofi-Aventis, Teva and Bayer Schering Pharma. Perini Paola has received funding for travel and speaker honoraria from Merck Serono, Biogen Idec, Sanofi-Aventis, and Bayer Schering Pharma and has been consultant for Merck Serono, Biogen Idec and Teva; Gallo Paolo has been a consultant for Bayer Schering, Biogen Idec, Genzyme, Merck Serono and Novartis; has received funding for travel and speaker honoraria from Merck-Serono, Biogen Idec, Sanofi-Aventis, Novartis Pharma and Bayer-Schering Pharma, Teva; has received research support from Bayer, Biogen Idec/Elan, MerkSerono, Genzyme and Teva; and has received research grant from the University of Padova, Veneto Region of Italy, the Italian Association for Multiple Sclerosis, the Italian Ministry of Public Health.
Abstract: EP1543
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Background: Cortical lesions (CL) are believed to play a role in the accumulation of physical and cognitive disability in multiple sclerosis (MS). Up to date, no study has investigated the metabolic behavior of CL.
Aim: To analyze the absolute 18F-FDG metabolism of CL in MS patients by means of a fully integrated 3T-Positron Emission Tomography/Magnetic Resonance Imaging (3T 18F-PET/MRI) system.
Methods: Fifteen early relapsing remitting MS (eRRMS) with no sign of cognitive impairment (CI) and fifteen RRMS with significantly longer disease duration and clinical evidence of CI (CI-RRMS) were enrolled in the study. Physical and cognitive evaluations were done by EDSS and Rao´s BRB. Dynamic 18F-FDG-PET/MRI (Siemens Biograph 3TMRI/PET System) data were analyzed with Patlak plot method to obtain absolute metabolic rate of glucose (aMRglu). CL and white matter (WM) lesions were identified on 3DFLAIR and 3DDIR images, respectively.
Results: eRRMS had lower CL volume and number than CI-RRMS and, despite the limited number of patients, the differences were significant (p=0.02 and p=0.01, respectively). The great majority of CL (68.0%) showed aMRGlu values in the range of the surrounding apparently normal cortex, but 17.8% had significantly increased aMRGlu values and 14.2% were hypometabolic. aMRGlu inversely correlated with CL number and volume in both left (p=0.01, r=-0.49 and p=0.02, r=-0.42) and right parietal (p=0.02, r=-0.43 and p=0.03, r=-0.39) lobes.
Interpretation: CL were found to differ in aMRGlu values. Whether the metabolic state of CL reflects their evolution from an initial hypermatabolic inflammatory phase (potentially excitotoxic) to a final hypo-metabolic neurodegenerative phase merits to be investigated. Indeed, the metabolism of CL might be the link between inflammation and neurodegeneration in MS.
Disclosure: Poggiali D, Cecchin D, Favaretto A, Lazzarotto A, Margoni M, Frigo AC, Zucchetta P, Causin F and Bui F have nothing to disclose. Alice Riccardi has received onoraria from Biogen, Novartis, Teva and Merck Serono. Puthenparampil Marco received travel grant from Novartis, Sanofi-Genzyme, Biogen Idec, Almirall, Teva and Sanofi Aventis and honoraria from Almirall; he has been consultant for Genzyme Federle Lisa has received funding for travel from Novartis, Merck Serono, Biogen Idec, Sanofi-Genzyme, Bayer Schering Pharma, Almirall, Teva and honoraria from MerkSerono, Teva and Almirall. Miante Silvia received travel grant form Biogen Idec, Novartis, Sanofi Aventis and Teva Zito Antonio has nothing to disclose. Erica Stropparo has nothing to disclose. Cazzola Chiara has nothing to disclose. Toffanin Elisabetta has nothing to disclose. Ruggiero Susanna has nothing to disclose. Mario Ermani has nothing to disclose. Francesca Grassivaro has nothing to disclose. Davide Poggiali received travel grant from Biogen Idec, Novartis, Sanofi Aventis and Teva. Rinaldi Francesca serves as an advisory board member of Biogen-Idec and has received funding for travel and speaker honoraria from Merck Serono, Biogen Idec, Sanofi-Aventis, Teva and Bayer Schering Pharma. Perini Paola has received funding for travel and speaker honoraria from Merck Serono, Biogen Idec, Sanofi-Aventis, and Bayer Schering Pharma and has been consultant for Merck Serono, Biogen Idec and Teva; Gallo Paolo has been a consultant for Bayer Schering, Biogen Idec, Genzyme, Merck Serono and Novartis; has received funding for travel and speaker honoraria from Merck-Serono, Biogen Idec, Sanofi-Aventis, Novartis Pharma and Bayer-Schering Pharma, Teva; has received research support from Bayer, Biogen Idec/Elan, MerkSerono, Genzyme and Teva; and has received research grant from the University of Padova, Veneto Region of Italy, the Italian Association for Multiple Sclerosis, the Italian Ministry of Public Health.