
Contributions
Abstract: P987
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - Paediatric MS
Background: It has been widely demonstrated that multiple sclerosis (MS) onset during the childhood may lead to a failure of age-expected maturation processes in the gray matter (GM) and white matter (WM). Considering the role of cortical GM for cognitive functioning, we explored cortical abnormalities in pediatric MS patients and their contribution to cognitive impairment.
Methods: Seventy pediatric MS patients and 26 age and sex-matched healthy controls (HC) underwent 3T MRI acquisition and clinical evaluation. Patients also underwent an extensive neuropsychological evaluation and patients with > 3 abnormal tests were classified as cognitively impaired (CI). Cortical surface reconstruction and mean cortical thickness and surface area measurement were performed using FreeSurfer. Correlations between cortical abnormalities and WM lesion volumes were explored.
Results: Thirteen patients were CI. Compered to HC, pediatric MS patients showed a widespread reduction of cortical surface area in bilateral brain regions belonging to frontal and parietal cortex and the insula. They also showed reduced cortical thickness in bilateral frontal regions and the right insula. Compared to CP, CI pediatric MS patients showed reduced surface area in the left frontal pole, lingual and fusiform gyri and in the right middle fontal cortex. They also showed reduced cortical thickness in left frontal pole, lingual and fusiform gyri and in right orbitofrontal cortex and temporal pole. Significant correlations were found between reduction of cortical surface area in left frontal regions and WM lesion volume (r ranging from -0.25 to -0.30, p< 0.05).
Conclusions: Cortical abnormalities both in terms of cortical thinning and surface area reduction occur in pediatric MS patients and are only partially related to WM lesions. Cortical abnormalities in frontal and temporal cortex contribute to cognitive impairment in these patients. The lack of correlation between reduction of cortical thickness and WM lesions suggests the presence of early primary GM degeneration as well as an effect of the disease on cortical developmental trajectories.
Funding: Partially supported by Italian Ministry of Health (GR-2009-1529671) and Fondazione Italiana Sclerosi Multipla (FISM-2016-R-23).
Disclosure: E. De Meo, L. Moiola, P. Veggiotti, and A. Falini have nothing to disclose.
M.P. Amato has received research grants and honoraria as a speaker and member of advisory boards from Bayer, Biogen Idec, Merck Serono, Novartis, Sanofi Genzyme, Teva, and Almirall.
A. Ghezzi received honoraria for speaking from Biogen-Idec, Merck-Serono, Novartis, Genzyme, Teva, and Allergan, and for consultancy from Merck-Serono, Teva, Novartis, and Biogen-Idec; and received support for participation in national and international congresses from Schering, Biogen-Idec, Merck-Serono, Novartis, Genzyme, and Teva.
R. Capra received consulting fees from Novartis and Biogen and lecture fees and/or travel grants from Novartis, Biogen, Genzyme, and Sanofi-Aventis.
G. Comi has received consulting fees for participating on advisory boards from Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Actelion and honorarium for speaking activities for Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Biogen, ExceMED.
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).
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.
Abstract: P987
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - Paediatric MS
Background: It has been widely demonstrated that multiple sclerosis (MS) onset during the childhood may lead to a failure of age-expected maturation processes in the gray matter (GM) and white matter (WM). Considering the role of cortical GM for cognitive functioning, we explored cortical abnormalities in pediatric MS patients and their contribution to cognitive impairment.
Methods: Seventy pediatric MS patients and 26 age and sex-matched healthy controls (HC) underwent 3T MRI acquisition and clinical evaluation. Patients also underwent an extensive neuropsychological evaluation and patients with > 3 abnormal tests were classified as cognitively impaired (CI). Cortical surface reconstruction and mean cortical thickness and surface area measurement were performed using FreeSurfer. Correlations between cortical abnormalities and WM lesion volumes were explored.
Results: Thirteen patients were CI. Compered to HC, pediatric MS patients showed a widespread reduction of cortical surface area in bilateral brain regions belonging to frontal and parietal cortex and the insula. They also showed reduced cortical thickness in bilateral frontal regions and the right insula. Compared to CP, CI pediatric MS patients showed reduced surface area in the left frontal pole, lingual and fusiform gyri and in the right middle fontal cortex. They also showed reduced cortical thickness in left frontal pole, lingual and fusiform gyri and in right orbitofrontal cortex and temporal pole. Significant correlations were found between reduction of cortical surface area in left frontal regions and WM lesion volume (r ranging from -0.25 to -0.30, p< 0.05).
Conclusions: Cortical abnormalities both in terms of cortical thinning and surface area reduction occur in pediatric MS patients and are only partially related to WM lesions. Cortical abnormalities in frontal and temporal cortex contribute to cognitive impairment in these patients. The lack of correlation between reduction of cortical thickness and WM lesions suggests the presence of early primary GM degeneration as well as an effect of the disease on cortical developmental trajectories.
Funding: Partially supported by Italian Ministry of Health (GR-2009-1529671) and Fondazione Italiana Sclerosi Multipla (FISM-2016-R-23).
Disclosure: E. De Meo, L. Moiola, P. Veggiotti, and A. Falini have nothing to disclose.
M.P. Amato has received research grants and honoraria as a speaker and member of advisory boards from Bayer, Biogen Idec, Merck Serono, Novartis, Sanofi Genzyme, Teva, and Almirall.
A. Ghezzi received honoraria for speaking from Biogen-Idec, Merck-Serono, Novartis, Genzyme, Teva, and Allergan, and for consultancy from Merck-Serono, Teva, Novartis, and Biogen-Idec; and received support for participation in national and international congresses from Schering, Biogen-Idec, Merck-Serono, Novartis, Genzyme, and Teva.
R. Capra received consulting fees from Novartis and Biogen and lecture fees and/or travel grants from Novartis, Biogen, Genzyme, and Sanofi-Aventis.
G. Comi has received consulting fees for participating on advisory boards from Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Actelion and honorarium for speaking activities for Novartis, Teva Pharmaceutical Ind. Ltd, Sanofi, Genzyme, Merck Serono, Bayer, Biogen, ExceMED.
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).
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.