In-vivo mapping of thalamic pathological mechanisms in pediatric patients with MS
ECTRIMS Online Library. De Meo E. 09/13/19; 279569; 311
Ermelinda De Meo
Ermelinda De Meo
Contributions
Abstract

Abstract: 311

Type: Scientific Session

Abstract Category: Clinical aspects of MS - Paediatric MS

E. De Meo1,2, L. Storelli1, L. Moiola2, M.P. Amato3, A. Ghezzi4, P. Veggiotti5,6, R. Capra7, M.A. Rocca1,2, M. Filippi1,2

1Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, 2Department of Neurology, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, 3Department of Neurology, University of Florence, Florence, 4Multiple Sclerosis Center, ASST Valle Olona, Gallarate Hospital, Gallarate, 5Pediatric Neurology Unit, V. Buzzi Children's Hospital, 6Biomedical and Clinical Science Department, University of Milan, Milan, 7Multiple Sclerosis Center, Spedali Civili of Brescia, Brescia, Italy

Introduction: Both local inflammatory demyelination and changes secondary to axonal transection of fibers passing through focal white matter (WM) lesions can account for thalamic abnormalities in multiple sclerosis (MS) patients. Assessing location of microstructural abnormalities within the thalamus as a function of distance from cerebrospinal fluid (CSF) in pediatric MS patients could help to define whether at beginning of disease, thalamic damage is due to CSF-mediated factors or thalamic neurodegeneration associated with macroscopic damage.
Aims: To investigate in-vivo, the pathological mechanisms underlying microstructural thalamic damage in pediatric MS patients by applying quantitative MRI techniques and to assess their contribution to clinical disability.
Methods: Sixty-eight pediatric MS patients and 24 age- and sex-matched healthy controls (HC) underwent 3T MRI and clinical evaluation. As quantitative-MRI metrics, we assessed diffusion tensor imaging measures - fractional anisotropy (FA) and mean diffusivity (MD)- and T1/T2-weighted ratio in whole thalamus and thalamic white matter (WM). We tested for: differences in thalamic volume and quantitative-MRI measures globally and within concentric bands originating from CSF/thalamus interface; relation between thalamic, cortical, and WM metrics; and contribution of MRI metrics to clinical disability.
Results: Compared to HC, pediatric-MS patients had increased FA in the whole thalamus, reduced FA with increased MD in thalamic WM, but no atrophy. In pediatric-MS, considering whole thalamus and thalamic WM, significant abnormalities of FA were observed in bands nearest to CSF and in those nearest to WM, while significant abnormalities of MD and T1/T2-weighted ratio were observed only in thalamic regions next to CSF. Significant correlations were found between the abnormalities detected at CSF/thalamus interface and cortical thickness, while the alterations described at thalamus/WM interface correlated with lesion volumes. No correlations were found between thalamic damage and clinical disability.
Conclusions: The abnormalities observed suggest that thalamic damage is determined by heterogeneous pathological processes according to the interface examined, confirming the thalamus as a critical barometer of neuronal pathology in MS.
Disclosure: Partially supported by grants from Italian Ministry of Health (GR2009-1529671) and Fondazione Italiana Sclerosi Multipla (FISM2016/R/23).
E De Meo, L. Storelli, and P. Veggiotti have nothing to disclose.
L. Moiola has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Sanofi-Genzyme, Novartis, Teva, Merck-Serono, Biogen, Roche, Excemed.
M.P. Amato has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen, Byer, Merck, Roche, Sanofi, and Teva, she has received research support from Biogen, Byer, Italian MS Society, Novartis, Sanofi, and Teva.
A. Ghezzi has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen Idec, Merk-Serono, Novartis, Genzyme, Teva Neuroscience, Serono Symposia Int Found., and Almirall.
R. Capra has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Novartis, Biogen, Teva, Genzyme and Sanofi-Aventis
M.A. Rocca received speakers honoraria from Biogen Idec, Novartis, Genzyme, Sanofi-Aventis, Teva, Merck Serono, and Roche and receives research support from the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla.
M. Filippi is Editor-in-Chief of the Journal of Neurology; received compensation for consulting services and/or speaking activities from Biogen Idec, Merck-Serono, Novartis, Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Merck-Serono, Novartis, Teva Pharmaceutical Industries, Roche, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA).

Abstract: 311

Type: Scientific Session

Abstract Category: Clinical aspects of MS - Paediatric MS

E. De Meo1,2, L. Storelli1, L. Moiola2, M.P. Amato3, A. Ghezzi4, P. Veggiotti5,6, R. Capra7, M.A. Rocca1,2, M. Filippi1,2

1Neuroimaging Research Unit, Institute of Experimental Neurology, Division of Neuroscience, 2Department of Neurology, Institute of Experimental Neurology, Division of Neuroscience, San Raffaele Scientific Institute, Vita-Salute San Raffaele University, Milan, 3Department of Neurology, University of Florence, Florence, 4Multiple Sclerosis Center, ASST Valle Olona, Gallarate Hospital, Gallarate, 5Pediatric Neurology Unit, V. Buzzi Children's Hospital, 6Biomedical and Clinical Science Department, University of Milan, Milan, 7Multiple Sclerosis Center, Spedali Civili of Brescia, Brescia, Italy

Introduction: Both local inflammatory demyelination and changes secondary to axonal transection of fibers passing through focal white matter (WM) lesions can account for thalamic abnormalities in multiple sclerosis (MS) patients. Assessing location of microstructural abnormalities within the thalamus as a function of distance from cerebrospinal fluid (CSF) in pediatric MS patients could help to define whether at beginning of disease, thalamic damage is due to CSF-mediated factors or thalamic neurodegeneration associated with macroscopic damage.
Aims: To investigate in-vivo, the pathological mechanisms underlying microstructural thalamic damage in pediatric MS patients by applying quantitative MRI techniques and to assess their contribution to clinical disability.
Methods: Sixty-eight pediatric MS patients and 24 age- and sex-matched healthy controls (HC) underwent 3T MRI and clinical evaluation. As quantitative-MRI metrics, we assessed diffusion tensor imaging measures - fractional anisotropy (FA) and mean diffusivity (MD)- and T1/T2-weighted ratio in whole thalamus and thalamic white matter (WM). We tested for: differences in thalamic volume and quantitative-MRI measures globally and within concentric bands originating from CSF/thalamus interface; relation between thalamic, cortical, and WM metrics; and contribution of MRI metrics to clinical disability.
Results: Compared to HC, pediatric-MS patients had increased FA in the whole thalamus, reduced FA with increased MD in thalamic WM, but no atrophy. In pediatric-MS, considering whole thalamus and thalamic WM, significant abnormalities of FA were observed in bands nearest to CSF and in those nearest to WM, while significant abnormalities of MD and T1/T2-weighted ratio were observed only in thalamic regions next to CSF. Significant correlations were found between the abnormalities detected at CSF/thalamus interface and cortical thickness, while the alterations described at thalamus/WM interface correlated with lesion volumes. No correlations were found between thalamic damage and clinical disability.
Conclusions: The abnormalities observed suggest that thalamic damage is determined by heterogeneous pathological processes according to the interface examined, confirming the thalamus as a critical barometer of neuronal pathology in MS.
Disclosure: Partially supported by grants from Italian Ministry of Health (GR2009-1529671) and Fondazione Italiana Sclerosi Multipla (FISM2016/R/23).
E De Meo, L. Storelli, and P. Veggiotti have nothing to disclose.
L. Moiola has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Sanofi-Genzyme, Novartis, Teva, Merck-Serono, Biogen, Roche, Excemed.
M.P. Amato has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen, Byer, Merck, Roche, Sanofi, and Teva, she has received research support from Biogen, Byer, Italian MS Society, Novartis, Sanofi, and Teva.
A. Ghezzi has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen Idec, Merk-Serono, Novartis, Genzyme, Teva Neuroscience, Serono Symposia Int Found., and Almirall.
R. Capra has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Novartis, Biogen, Teva, Genzyme and Sanofi-Aventis
M.A. Rocca received speakers honoraria from Biogen Idec, Novartis, Genzyme, Sanofi-Aventis, Teva, Merck Serono, and Roche and receives research support from the Italian Ministry of Health and Fondazione Italiana Sclerosi Multipla.
M. Filippi is Editor-in-Chief of the Journal of Neurology; received compensation for consulting services and/or speaking activities from Biogen Idec, Merck-Serono, Novartis, Teva Pharmaceutical Industries; and receives research support from Biogen Idec, Merck-Serono, Novartis, Teva Pharmaceutical Industries, Roche, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla, and ARiSLA (Fondazione Italiana di Ricerca per la SLA).

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