Contributions
Abstract: P464
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Progressive MS
Introduction: Among relapsing remitting (RR) MS patients, a larger number of early attacks predicts faster disease evolution. We set out to elucidate the relationship between early relapses and grey matter pathological changes, and to explore baseline factors, affecting the long-term prognosis.
Methods: By using 3D Double Inversion Recovery, 3D T1 weighted imaging and Freesurfer analysis, we assessed the number and volume of cortical lesions (CLs), and the rate of cortical thinning, among RR MS patients with 1 (n = 116), 2 (n = 53) and ≥3 (n = 50) relapses during the first 2 years, followed for a mean of 7 years. The multivariate cox regression model estimated the risk of conversion to secondary progressive (SP) MS, according to early clinical and MRI features.
Results: During the observation period, patients with high early relapses frequency entered the SP phase in larger percentage (≥ 3 attacks = 54.0%, 2 attacks = 30.2%, 1 attack = 13.8%; p< 0.001) and in shorter time (≥ 3 attacks = 68.0, 2 attacks = 80.5, 1 attack = 79.0 median months; p< 0.001). At clinical onset, the 3 groups had similar global cortical thickness, but patients with higher number of early attacks were distinguished by a larger volume of CLs (mean mm3 volume: ≥3 attacks = 544.0; 2 attacks = 379.5; 1 attack = 181.6; p< 0.001). In addition, they accrued in the long term significantly higher volume of cortical lesions (mean mm3 increase: ≥3 attacks = 790.5; 2 attacks = 138.8; 1 attack = 118.8; p< 0.001) and more severe global cortical atrophy (global cortical thickness: ≥ 3 attacks = 2.26; 2 attacks = 2.36;
1 attack = 2.38 mean mm; p< 0.001). Among all RR MS patients, larger volume of baseline CLs predicted shorter time to reach the SP phase (84.5, 103.5, 136.1 mean months in the group with large, intermediate and small volume, respectively; p< 0.001). The multivariate model estimated that the risk of experiencing a progressive course was significantly higher, among patients older at onset
(HR=2.02; p< 0.001), with a larger volume of baseline cortical lesions (HR = 2.06; p=0.008) and with ≥3 early relapses (HR= 6.38; p< 0.001).
Conclusions: Patients with frequent early relapses develop more prominent focal and diffuse cortical damage over time, accounting for their faster disease evolution. The number of early attacks and the extent of baseline focal cortical damage can be used for selecting groups at high risk of progression, who may potentially benefit from early aggressive treatment.
Disclosure:
Dr Scalfari received honoraria for speaking from Teva and Genzyme and travel support from Teva, Biogen and Genzyme.
Dr Romualdi: nothing to disclose
Dr Mattoscio received financial support for travel, accommodation and scientific meeting expenses from Biogen Idec, Genzyme, Novartis and Teva.
Dr Muraro received honoraria for speaking and travel support from Merck Serono, Biogen, Bayer and Novartis.
Dr Nicholas received honoraria for speaking from Bayer, Biogen, Genzyme, Merck Serono, Roche, and funds from Biogen, Genzyme, Novartis.
Dr Calabrese received payment for development of educational presentations from Biogen, Genzyme, Teva, Bayer-Schering, and support for travel from Novartis, Genzyme, Biogen, Merck Serono, Bayer-Schering, Teva
Abstract: P464
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Progressive MS
Introduction: Among relapsing remitting (RR) MS patients, a larger number of early attacks predicts faster disease evolution. We set out to elucidate the relationship between early relapses and grey matter pathological changes, and to explore baseline factors, affecting the long-term prognosis.
Methods: By using 3D Double Inversion Recovery, 3D T1 weighted imaging and Freesurfer analysis, we assessed the number and volume of cortical lesions (CLs), and the rate of cortical thinning, among RR MS patients with 1 (n = 116), 2 (n = 53) and ≥3 (n = 50) relapses during the first 2 years, followed for a mean of 7 years. The multivariate cox regression model estimated the risk of conversion to secondary progressive (SP) MS, according to early clinical and MRI features.
Results: During the observation period, patients with high early relapses frequency entered the SP phase in larger percentage (≥ 3 attacks = 54.0%, 2 attacks = 30.2%, 1 attack = 13.8%; p< 0.001) and in shorter time (≥ 3 attacks = 68.0, 2 attacks = 80.5, 1 attack = 79.0 median months; p< 0.001). At clinical onset, the 3 groups had similar global cortical thickness, but patients with higher number of early attacks were distinguished by a larger volume of CLs (mean mm3 volume: ≥3 attacks = 544.0; 2 attacks = 379.5; 1 attack = 181.6; p< 0.001). In addition, they accrued in the long term significantly higher volume of cortical lesions (mean mm3 increase: ≥3 attacks = 790.5; 2 attacks = 138.8; 1 attack = 118.8; p< 0.001) and more severe global cortical atrophy (global cortical thickness: ≥ 3 attacks = 2.26; 2 attacks = 2.36;
1 attack = 2.38 mean mm; p< 0.001). Among all RR MS patients, larger volume of baseline CLs predicted shorter time to reach the SP phase (84.5, 103.5, 136.1 mean months in the group with large, intermediate and small volume, respectively; p< 0.001). The multivariate model estimated that the risk of experiencing a progressive course was significantly higher, among patients older at onset
(HR=2.02; p< 0.001), with a larger volume of baseline cortical lesions (HR = 2.06; p=0.008) and with ≥3 early relapses (HR= 6.38; p< 0.001).
Conclusions: Patients with frequent early relapses develop more prominent focal and diffuse cortical damage over time, accounting for their faster disease evolution. The number of early attacks and the extent of baseline focal cortical damage can be used for selecting groups at high risk of progression, who may potentially benefit from early aggressive treatment.
Disclosure:
Dr Scalfari received honoraria for speaking from Teva and Genzyme and travel support from Teva, Biogen and Genzyme.
Dr Romualdi: nothing to disclose
Dr Mattoscio received financial support for travel, accommodation and scientific meeting expenses from Biogen Idec, Genzyme, Novartis and Teva.
Dr Muraro received honoraria for speaking and travel support from Merck Serono, Biogen, Bayer and Novartis.
Dr Nicholas received honoraria for speaking from Bayer, Biogen, Genzyme, Merck Serono, Roche, and funds from Biogen, Genzyme, Novartis.
Dr Calabrese received payment for development of educational presentations from Biogen, Genzyme, Teva, Bayer-Schering, and support for travel from Novartis, Genzyme, Biogen, Merck Serono, Bayer-Schering, Teva