Contributions
Abstract: EP1552
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Introduction: Thalamic atrophy, a prominent feature in multiple sclerosis (MS), may occur as a consequence of intrinsic thalamic pathology and/or due to distant injury in white matter tracts. Magnetic resonance fingerprinting (MRF) is a new MRI approach that provides direct estimates of quantitative relaxation times from fast acquisition.
Objectives: To investigate quantitative MR properties using MRF in the thalamus of MS patients compared with controls, and to correlate extrathalamic involvement with quantitative changes in thalamic tissue.
Methods: Nine patients with relapsing remitting (RR) MS (disease duration [DD] ≤ 5 years, EDSS ≤ 2),
9 patients with secondary progressive (SP) MS (DD ≥10 years, EDSS ≥ 4.0), and 8 age/gender matched controls were recruited. Clinical measures included EDSS, MSFC, and neurocognitive testing. MRI of the brain was conducted with FISP-MRF protocol (1000 images, 1.2 x 1.2mm, 20 slices, 5mm slice thickness) and conventional MRI (T1-weighted MPRAGE, 3D FLAIR, and 3D T2). Thalami were segmented using an atlas-based approach. Lesions (T1/T2) and white matter structures were segmented. Mean T1 and T2 relaxation times were measured within each region of interest (thalamus, frontal normal appearing white matter, corpus callosum, caudate, T1 lesions, and T2 lesions). Differences between controls, RRMS, and SPMS were analyzed by ANCOVA with age as covariate. Correlations were assessed between MRI and clinical measures using Pearson test.
Results: Thalamic volumes were significantly different between controls (20.5 ml, SD: 0.7), RRMS (20.2 ml, SD: 1.4), and SPMS patients (16.6 ml (1.7ml) (p< 0.001). Thalamic T1 and T2 relaxation did not show consistent differences in controls, RRMS and SPMS. There was no correlation between thalamic volume and T1 and T2 relaxation times from the thalamus. In contrast, significant correlations were found between thalamic volume and T1 relaxation times from white matter T2 lesions (r=-0.74, p< 0.001) and T1 lesions (r=-0.61, p=0.01). Significant correlations were found between thalamic volume and SDMT (r=0.78, p< 0.001) and EDSS (r=-0.67, p< 0.002).
Conclusions: Thalamic volume distinguishes MS from controls, RR from SPMS, and correlates with both physical and cognitive measures of impairment. Thalamic atrophy reflects extrathalamic injury measured in T1 and T2 lesions with no clear relationship between thalamic volume and intra-thalamic T2 and T1 relaxation times.
Disclosure: Study was funded by Sanofi/Genzyme
DO has received research support from NIH, NMSS, Genzyme, Novartis, and Genetech, and consulting fees from Genentech and Novartis.
KN has received speaking fees from Genzyme and and License fee from Biogen.
KS has recieved Salary support from Novartis and Genzyme for research work.
BT has no relevant disclosures.
KM has no relevant disclosures.
DM has no relevant disclosures.
AS has no relevant disclosures.
OK has no relevant disclosures.
SR has no relevant disclosures.
JC reports compensation for consulting for Adamas, Celgene, Mallinckrodt, Merck, and Novartis, and as a Co-Editor of Multiple Sclerosis Journal - Experimental, Translational and Clinical.
ML has no relevant disclosures.
VG has no relevant disclosures.
MG has no relevant disclosures.
Abstract: EP1552
Type: ePoster
Abstract Category: Pathology and pathogenesis of MS - 21 Imaging
Introduction: Thalamic atrophy, a prominent feature in multiple sclerosis (MS), may occur as a consequence of intrinsic thalamic pathology and/or due to distant injury in white matter tracts. Magnetic resonance fingerprinting (MRF) is a new MRI approach that provides direct estimates of quantitative relaxation times from fast acquisition.
Objectives: To investigate quantitative MR properties using MRF in the thalamus of MS patients compared with controls, and to correlate extrathalamic involvement with quantitative changes in thalamic tissue.
Methods: Nine patients with relapsing remitting (RR) MS (disease duration [DD] ≤ 5 years, EDSS ≤ 2),
9 patients with secondary progressive (SP) MS (DD ≥10 years, EDSS ≥ 4.0), and 8 age/gender matched controls were recruited. Clinical measures included EDSS, MSFC, and neurocognitive testing. MRI of the brain was conducted with FISP-MRF protocol (1000 images, 1.2 x 1.2mm, 20 slices, 5mm slice thickness) and conventional MRI (T1-weighted MPRAGE, 3D FLAIR, and 3D T2). Thalami were segmented using an atlas-based approach. Lesions (T1/T2) and white matter structures were segmented. Mean T1 and T2 relaxation times were measured within each region of interest (thalamus, frontal normal appearing white matter, corpus callosum, caudate, T1 lesions, and T2 lesions). Differences between controls, RRMS, and SPMS were analyzed by ANCOVA with age as covariate. Correlations were assessed between MRI and clinical measures using Pearson test.
Results: Thalamic volumes were significantly different between controls (20.5 ml, SD: 0.7), RRMS (20.2 ml, SD: 1.4), and SPMS patients (16.6 ml (1.7ml) (p< 0.001). Thalamic T1 and T2 relaxation did not show consistent differences in controls, RRMS and SPMS. There was no correlation between thalamic volume and T1 and T2 relaxation times from the thalamus. In contrast, significant correlations were found between thalamic volume and T1 relaxation times from white matter T2 lesions (r=-0.74, p< 0.001) and T1 lesions (r=-0.61, p=0.01). Significant correlations were found between thalamic volume and SDMT (r=0.78, p< 0.001) and EDSS (r=-0.67, p< 0.002).
Conclusions: Thalamic volume distinguishes MS from controls, RR from SPMS, and correlates with both physical and cognitive measures of impairment. Thalamic atrophy reflects extrathalamic injury measured in T1 and T2 lesions with no clear relationship between thalamic volume and intra-thalamic T2 and T1 relaxation times.
Disclosure: Study was funded by Sanofi/Genzyme
DO has received research support from NIH, NMSS, Genzyme, Novartis, and Genetech, and consulting fees from Genentech and Novartis.
KN has received speaking fees from Genzyme and and License fee from Biogen.
KS has recieved Salary support from Novartis and Genzyme for research work.
BT has no relevant disclosures.
KM has no relevant disclosures.
DM has no relevant disclosures.
AS has no relevant disclosures.
OK has no relevant disclosures.
SR has no relevant disclosures.
JC reports compensation for consulting for Adamas, Celgene, Mallinckrodt, Merck, and Novartis, and as a Co-Editor of Multiple Sclerosis Journal - Experimental, Translational and Clinical.
ML has no relevant disclosures.
VG has no relevant disclosures.
MG has no relevant disclosures.