Contributions
Abstract: P735
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Pathology
Introduction: Thalamic pathology is common in multiple sclerosis (MS) where it contributes to neurological disability. Initial data at 7 Tesla (7T) magnetic resonance imaging (MRI) have found a positive correlation between thalamic and cortical lesion load, suggesting that thalamic lesion assessment may be a simple estimate of overall gray matter (GM) lesion burden in MS. Other studies, however, have reported that thalamic degeneration in MS is more closely related to white matter (WM) pathology.
Aim: To characterize, in a large cohort of subjects with either relapsing-remitting or secondary progressive MS (RRMS, SPMS), thalamic lesion types and their association with cortical and WM lesion burden using 7T MRI.
Methods: Eighty-eight MS patients (61 RRMS, 27 SPMS; age 42±9.11 years; disease duration 9±9.2 years; median EDSS 2.5, range 0-8) underwent 7T T2* imaging (0.33x0.33x1.0 mm3) for semi-automated segmentation of thalamic, cortical (intracortical and leukocortical), and WM lesions using Slicer. Lesion volume was assessed using FSL. Thalamic lesions were classified in ovoid (discrete ovoid areas) and periventricular (diffuse lesions lining the periventricular surface), and if they were venular (a venule had to be present in the lesion within two view planes: sagittal, axial, or coronal) or non-venular.
Results: Thalamic lesions were identified in 39/88 patients. The mean±SD overall thalamic lesion volume was 96±175 mm3. In both RRMS and SPMS, ovoid lesions were the most common thalamic lesion type (mean±SD volume = 68±94 mm3) followed by the periventricular type (mean±SD volume = 28±101 mm3). Slightly more than half of overall thalamic lesions disclosed a perivenular pattern (mean±SD lesion volume: 52±72 mm3 for perivenular, 44±162 mm3 for non-perivenular). There was no correlation between overall thalamic lesion load or individual thalamic lesion subtypes and either cortical (either total, intra- or leuko-cortical) (p ranging from 0.547 to 0.913 by Spearman test) or WM lesion loads (p ranging from 0.251to 0.667 by Spearman test).
Discussion: Our data suggest that thalamic and cortical lesion pathology in MS may not share common pathogenetic mechanisms, indicating that both measures might be needed for an accurate estimation of GM pathology in the disease. 7T T2* imaging shows the ability to characterize distinct thalamic lesion patterns that could be used in future studies for better understanding thalamic pathology in MS.
Disclosure: This study was supported by the Clafin Award; the National Institute of Health (NIH R01NS07832201 A1); the National Multiple Sclerosis Society (NMSS; RG 4729A2/1); the US Army, Department of Defense (DoD; W81XWH13-10112). A. Mehndiratta: nothing to disclose. C.A. Treaba: nothing to disclose. V. Barletta: nothing to disclose. E. Herranz has received research support by the NMSS fellowship FG150705459. R. Ouellette: nothing to disclose. J. Sloane: nothing to disclose. C. Mainero has received research support from EMD Merck Serono.
Abstract: P735
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Pathology
Introduction: Thalamic pathology is common in multiple sclerosis (MS) where it contributes to neurological disability. Initial data at 7 Tesla (7T) magnetic resonance imaging (MRI) have found a positive correlation between thalamic and cortical lesion load, suggesting that thalamic lesion assessment may be a simple estimate of overall gray matter (GM) lesion burden in MS. Other studies, however, have reported that thalamic degeneration in MS is more closely related to white matter (WM) pathology.
Aim: To characterize, in a large cohort of subjects with either relapsing-remitting or secondary progressive MS (RRMS, SPMS), thalamic lesion types and their association with cortical and WM lesion burden using 7T MRI.
Methods: Eighty-eight MS patients (61 RRMS, 27 SPMS; age 42±9.11 years; disease duration 9±9.2 years; median EDSS 2.5, range 0-8) underwent 7T T2* imaging (0.33x0.33x1.0 mm3) for semi-automated segmentation of thalamic, cortical (intracortical and leukocortical), and WM lesions using Slicer. Lesion volume was assessed using FSL. Thalamic lesions were classified in ovoid (discrete ovoid areas) and periventricular (diffuse lesions lining the periventricular surface), and if they were venular (a venule had to be present in the lesion within two view planes: sagittal, axial, or coronal) or non-venular.
Results: Thalamic lesions were identified in 39/88 patients. The mean±SD overall thalamic lesion volume was 96±175 mm3. In both RRMS and SPMS, ovoid lesions were the most common thalamic lesion type (mean±SD volume = 68±94 mm3) followed by the periventricular type (mean±SD volume = 28±101 mm3). Slightly more than half of overall thalamic lesions disclosed a perivenular pattern (mean±SD lesion volume: 52±72 mm3 for perivenular, 44±162 mm3 for non-perivenular). There was no correlation between overall thalamic lesion load or individual thalamic lesion subtypes and either cortical (either total, intra- or leuko-cortical) (p ranging from 0.547 to 0.913 by Spearman test) or WM lesion loads (p ranging from 0.251to 0.667 by Spearman test).
Discussion: Our data suggest that thalamic and cortical lesion pathology in MS may not share common pathogenetic mechanisms, indicating that both measures might be needed for an accurate estimation of GM pathology in the disease. 7T T2* imaging shows the ability to characterize distinct thalamic lesion patterns that could be used in future studies for better understanding thalamic pathology in MS.
Disclosure: This study was supported by the Clafin Award; the National Institute of Health (NIH R01NS07832201 A1); the National Multiple Sclerosis Society (NMSS; RG 4729A2/1); the US Army, Department of Defense (DoD; W81XWH13-10112). A. Mehndiratta: nothing to disclose. C.A. Treaba: nothing to disclose. V. Barletta: nothing to disclose. E. Herranz has received research support by the NMSS fellowship FG150705459. R. Ouellette: nothing to disclose. J. Sloane: nothing to disclose. C. Mainero has received research support from EMD Merck Serono.