Contributions
Abstract: P1106
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Introduction: A couple of recent MS studies have used source-based morphometry (SBM), a novel multivariate MRI approach, to show distinct patterns of grey matter (GM) atrophy or white matter (WM) disruption, respectively. It is not known, however, whether patterns of GM atrophy and WM disruption coexist and are interrelated.
Objectives: To use SBM to explore the link between patterns of GM atrophy and WM disruption and their clinical relevance in relapsing-remitting (RR) MS patients.
Methods: We assessed RRMS patients (n=41, age=35.6±10.4 years) with disease duration= 9.1±7 years, median Expanded Disability Status Scale (EDSS)=1.5 (range: 0-6), cognitive impairment (on the Rao Battery) in 22%. Patient data were compared with those of age-matched normal controls (NC, n=28, age=33.2±10 years). Brain MRI was acquired at 3T. Distinct patterns of GM atrophy and WM disruption were assessed, respectively, on the maps of GM and diffusion tensor imaging such as fractional anisotropy (FA) with SBM using independent component analysis. Statistical threshold was set at p< 0.05 corrected for multiple comparisons across space.
Results: GM atrophy was significantly present in MS patients in 3 of 6 patterns: deep GM (pattern 1), sensorimotor cortex (pattern 2) and posterior GM (pattern 3). Moreover, MS patients showed significantly lower FA in 2 of 4 patterns: callosal splenium and corticospinal tract (pattern 1), posterior corona radiata (PCR)/thalamic radiation (PTR) (pattern 2). All GM patterns correlated closely with WM pattern 2 (r=0.62 to 0.67, p< 0.001). GM patterns 1 and 3 correlated with EDSS (r=-0.33 to -0.4, p=0.03 to 0.01) and cognitive tests (Symbol Digit Modality Test: r=0.52, p< 0.001; Selective Reminding Test: r=0.40, p=0.01). WM patterns correlated with EDSS (r=-0.45 to -0.54, p< 0.003), but not with cognitive tests.
Conclusions: In a group of RRMS with low disability accrual, GM atrophy and WM disruption occur in distinct anatomical patterns that are closely interrelated. Both GM patterns of atrophy and WM patterns of tissue disruption showed significant relevance for physical disability, while GM patterns of atrophy were related to cognitive impairment. SBM is a novel and promising approach capturing clinically relevant tissue damage with high specificity.
Disclosure: Jian Zhang, Antonio Giorgio, Claudia Vinciguerra, Maria Laura Stromillo, Marzia Mortilla, Riccardo Tappa Brocci have nothing to disclose.
Emilio Portaccio serves on a scientific advisory board for Biogen-Idec, Merck Serono and Bayer. He received honoraria and research grants from Merck Serono, Biogen Idec, Bayer Schering, Novartis, Teva, Genzyme.
Maria Pia Amato is member of Advisory Boards for Biogen, Merck, Teva, Novartis, Sanofi Aventis, Genzyme, Almirall and Roche. She received honoraria for speaking from Biogen, Merck, Novartis, Teva, Genzyme, Almirall and Sanofi Aventis. She is member of Editorial Board and Associate Editor of BMC Neurology Member of the Editorial Board of Multiple Sclerosis Journal research grants from Biogen, Merk, Bayer, Sanofi Aventis, Teva.
Nicola De Stefano has received honoraria from Biogen-Idec, Genzyme, Merck Serono, Novartis, Roche and Teva for consulting services, speaking and travel support. He serves on advisory boards for Merck Serono, Novartis, Biogen-Idec, Roche, and Genzyme, he has received research grant support from the Italian MS Society.
Abstract: P1106
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - MRI and PET
Introduction: A couple of recent MS studies have used source-based morphometry (SBM), a novel multivariate MRI approach, to show distinct patterns of grey matter (GM) atrophy or white matter (WM) disruption, respectively. It is not known, however, whether patterns of GM atrophy and WM disruption coexist and are interrelated.
Objectives: To use SBM to explore the link between patterns of GM atrophy and WM disruption and their clinical relevance in relapsing-remitting (RR) MS patients.
Methods: We assessed RRMS patients (n=41, age=35.6±10.4 years) with disease duration= 9.1±7 years, median Expanded Disability Status Scale (EDSS)=1.5 (range: 0-6), cognitive impairment (on the Rao Battery) in 22%. Patient data were compared with those of age-matched normal controls (NC, n=28, age=33.2±10 years). Brain MRI was acquired at 3T. Distinct patterns of GM atrophy and WM disruption were assessed, respectively, on the maps of GM and diffusion tensor imaging such as fractional anisotropy (FA) with SBM using independent component analysis. Statistical threshold was set at p< 0.05 corrected for multiple comparisons across space.
Results: GM atrophy was significantly present in MS patients in 3 of 6 patterns: deep GM (pattern 1), sensorimotor cortex (pattern 2) and posterior GM (pattern 3). Moreover, MS patients showed significantly lower FA in 2 of 4 patterns: callosal splenium and corticospinal tract (pattern 1), posterior corona radiata (PCR)/thalamic radiation (PTR) (pattern 2). All GM patterns correlated closely with WM pattern 2 (r=0.62 to 0.67, p< 0.001). GM patterns 1 and 3 correlated with EDSS (r=-0.33 to -0.4, p=0.03 to 0.01) and cognitive tests (Symbol Digit Modality Test: r=0.52, p< 0.001; Selective Reminding Test: r=0.40, p=0.01). WM patterns correlated with EDSS (r=-0.45 to -0.54, p< 0.003), but not with cognitive tests.
Conclusions: In a group of RRMS with low disability accrual, GM atrophy and WM disruption occur in distinct anatomical patterns that are closely interrelated. Both GM patterns of atrophy and WM patterns of tissue disruption showed significant relevance for physical disability, while GM patterns of atrophy were related to cognitive impairment. SBM is a novel and promising approach capturing clinically relevant tissue damage with high specificity.
Disclosure: Jian Zhang, Antonio Giorgio, Claudia Vinciguerra, Maria Laura Stromillo, Marzia Mortilla, Riccardo Tappa Brocci have nothing to disclose.
Emilio Portaccio serves on a scientific advisory board for Biogen-Idec, Merck Serono and Bayer. He received honoraria and research grants from Merck Serono, Biogen Idec, Bayer Schering, Novartis, Teva, Genzyme.
Maria Pia Amato is member of Advisory Boards for Biogen, Merck, Teva, Novartis, Sanofi Aventis, Genzyme, Almirall and Roche. She received honoraria for speaking from Biogen, Merck, Novartis, Teva, Genzyme, Almirall and Sanofi Aventis. She is member of Editorial Board and Associate Editor of BMC Neurology Member of the Editorial Board of Multiple Sclerosis Journal research grants from Biogen, Merk, Bayer, Sanofi Aventis, Teva.
Nicola De Stefano has received honoraria from Biogen-Idec, Genzyme, Merck Serono, Novartis, Roche and Teva for consulting services, speaking and travel support. He serves on advisory boards for Merck Serono, Novartis, Biogen-Idec, Roche, and Genzyme, he has received research grant support from the Italian MS Society.