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Longitudinal Characterization of Cortical Lesion Development and Evolution in Multiple Sclerosis with 7.0-T MRI.
Radiology 2019; 291(3):740-749R

Abstract

Background Cortical lesions develop early in multiple sclerosis (MS) and play a major role in disease progression. MRI at 7.0 T shows high sensitivity for detection of cortical lesions as well as better spatial resolution and signal-to-noise ratio compared with lower field strengths. Purpose To longitudinally characterize (a) the development and evolution of cortical lesions in multiple sclerosis across the cortical width, sulci, and gyri; (b) their relation with white matter lesion accrual; and (c) the contribution of 7.0-T cortical and white matter lesion load and cortical thickness to neurologic disability. Materials and Methods Twenty participants with relapsing-remitting MS and 13 with secondary progressive MS, along with 10 age-matched healthy controls, were prospectively recruited from 2010 to 2016 to acquire, in two imaging sessions (mean interval, 1.5 years), 7.0-T MRI T2*-weighted gradient-echo images (0.33 × 0.33 × 1.0 mm3) for cortical and white matter lesion segmentation and 3.0-T T1-weighted images for cortical surface reconstruction and cortical thickness estimation. Cortical lesions were sampled through the cortex to quantify cortical lesion distribution. The Expanded Disability Status Scale (EDSS) was used to assess neurologic disability. Nonparametric statistics assessed differences between and within groups in MRI metrics of cortical and white matter lesion burden; regression analysis explored associations of disability with MRI metrics. Results Twenty-five of 31 (81%) participants developed new cortical lesions per year (intracortical, 1.3 ± 1.7 vs leukocortical, 0.7 ± 1.9; P = .04), surpassing white matter lesion accrual (cortical, 2.0 ± 2.8 vs white matter, 0.7 ± 0.6; P = .01). In contrast to white matter lesions, cortical lesion accrual was greater in participants with secondary progressive MS than with relapsing-remitting MS (3.6 lesions/year ± 4.2 vs 1.1 lesions/year ± 0.9, respectively; P = .03) and preferentially localized in sulci. Total cortical lesion volume independently predicted baseline EDSS (β = 1.5, P < .001) and EDSS changes at follow-up (β = 0.5, P = .003). Conclusion Cortical lesions predominantly develop intracortically and within sulci, suggesting an inflammatory cerebrospinal fluid-mediated lesion pathogenesis. Cortical lesion accumulation was prominent at 7.0 T and independently predicted neurologic disability progression. © RSNA, 2019 Online supplemental material is available for this article. See also the editorial by Filippi and Rocca in this issue.

Authors+Show Affiliations

From the A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Bldg 149, 13th St, Charleston, MA 02129 (C.A.T., T.E.G., E.H., R.A.O., C.L., C.M.); Harvard Medical School, Boston, MA (C.A.T., T.E.G., E.H., C.L., C.M.); Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden (T.E.G.); Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy (M.P.S.); Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA (J.A.S.); and Department of Neurosciences, University of California San Diego, San Diego, CA (R.P.K.).From the A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Bldg 149, 13th St, Charleston, MA 02129 (C.A.T., T.E.G., E.H., R.A.O., C.L., C.M.); Harvard Medical School, Boston, MA (C.A.T., T.E.G., E.H., C.L., C.M.); Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden (T.E.G.); Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy (M.P.S.); Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA (J.A.S.); and Department of Neurosciences, University of California San Diego, San Diego, CA (R.P.K.).From the A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Bldg 149, 13th St, Charleston, MA 02129 (C.A.T., T.E.G., E.H., R.A.O., C.L., C.M.); Harvard Medical School, Boston, MA (C.A.T., T.E.G., E.H., C.L., C.M.); Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden (T.E.G.); Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy (M.P.S.); Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA (J.A.S.); and Department of Neurosciences, University of California San Diego, San Diego, CA (R.P.K.).From the A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Bldg 149, 13th St, Charleston, MA 02129 (C.A.T., T.E.G., E.H., R.A.O., C.L., C.M.); Harvard Medical School, Boston, MA (C.A.T., T.E.G., E.H., C.L., C.M.); Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden (T.E.G.); Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy (M.P.S.); Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA (J.A.S.); and Department of Neurosciences, University of California San Diego, San Diego, CA (R.P.K.).From the A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Bldg 149, 13th St, Charleston, MA 02129 (C.A.T., T.E.G., E.H., R.A.O., C.L., C.M.); Harvard Medical School, Boston, MA (C.A.T., T.E.G., E.H., C.L., C.M.); Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden (T.E.G.); Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy (M.P.S.); Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA (J.A.S.); and Department of Neurosciences, University of California San Diego, San Diego, CA (R.P.K.).From the A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Bldg 149, 13th St, Charleston, MA 02129 (C.A.T., T.E.G., E.H., R.A.O., C.L., C.M.); Harvard Medical School, Boston, MA (C.A.T., T.E.G., E.H., C.L., C.M.); Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden (T.E.G.); Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy (M.P.S.); Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA (J.A.S.); and Department of Neurosciences, University of California San Diego, San Diego, CA (R.P.K.).From the A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Bldg 149, 13th St, Charleston, MA 02129 (C.A.T., T.E.G., E.H., R.A.O., C.L., C.M.); Harvard Medical School, Boston, MA (C.A.T., T.E.G., E.H., C.L., C.M.); Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden (T.E.G.); Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy (M.P.S.); Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA (J.A.S.); and Department of Neurosciences, University of California San Diego, San Diego, CA (R.P.K.).From the A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Bldg 149, 13th St, Charleston, MA 02129 (C.A.T., T.E.G., E.H., R.A.O., C.L., C.M.); Harvard Medical School, Boston, MA (C.A.T., T.E.G., E.H., C.L., C.M.); Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden (T.E.G.); Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy (M.P.S.); Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA (J.A.S.); and Department of Neurosciences, University of California San Diego, San Diego, CA (R.P.K.).From the A. A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Bldg 149, 13th St, Charleston, MA 02129 (C.A.T., T.E.G., E.H., R.A.O., C.L., C.M.); Harvard Medical School, Boston, MA (C.A.T., T.E.G., E.H., C.L., C.M.); Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden (T.E.G.); Department of Health Sciences (DISSAL), University of Genoa, Genoa, Italy (M.P.S.); Department of Neurology, Beth Israel Deaconess Medical Center, Boston, MA (J.A.S.); and Department of Neurosciences, University of California San Diego, San Diego, CA (R.P.K.).

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30964421

Citation

Treaba, Constantina A., et al. "Longitudinal Characterization of Cortical Lesion Development and Evolution in Multiple Sclerosis With 7.0-T MRI." Radiology, vol. 291, no. 3, 2019, pp. 740-749.
Treaba CA, Granberg TE, Sormani MP, et al. Longitudinal Characterization of Cortical Lesion Development and Evolution in Multiple Sclerosis with 7.0-T MRI. Radiology. 2019;291(3):740-749.
Treaba, C. A., Granberg, T. E., Sormani, M. P., Herranz, E., Ouellette, R. A., Louapre, C., ... Mainero, C. (2019). Longitudinal Characterization of Cortical Lesion Development and Evolution in Multiple Sclerosis with 7.0-T MRI. Radiology, 291(3), pp. 740-749. doi:10.1148/radiol.2019181719.
Treaba CA, et al. Longitudinal Characterization of Cortical Lesion Development and Evolution in Multiple Sclerosis With 7.0-T MRI. Radiology. 2019;291(3):740-749. PubMed PMID: 30964421.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Longitudinal Characterization of Cortical Lesion Development and Evolution in Multiple Sclerosis with 7.0-T MRI. AU - Treaba,Constantina A, AU - Granberg,Tobias E, AU - Sormani,Maria Pia, AU - Herranz,Elena, AU - Ouellette,Russell A, AU - Louapre,Céline, AU - Sloane,Jacob A, AU - Kinkel,Revere P, AU - Mainero,Caterina, Y1 - 2019/04/09/ PY - 2019/4/10/pubmed PY - 2019/4/10/medline PY - 2019/4/10/entrez SP - 740 EP - 749 JF - Radiology JO - Radiology VL - 291 IS - 3 N2 - Background Cortical lesions develop early in multiple sclerosis (MS) and play a major role in disease progression. MRI at 7.0 T shows high sensitivity for detection of cortical lesions as well as better spatial resolution and signal-to-noise ratio compared with lower field strengths. Purpose To longitudinally characterize (a) the development and evolution of cortical lesions in multiple sclerosis across the cortical width, sulci, and gyri; (b) their relation with white matter lesion accrual; and (c) the contribution of 7.0-T cortical and white matter lesion load and cortical thickness to neurologic disability. Materials and Methods Twenty participants with relapsing-remitting MS and 13 with secondary progressive MS, along with 10 age-matched healthy controls, were prospectively recruited from 2010 to 2016 to acquire, in two imaging sessions (mean interval, 1.5 years), 7.0-T MRI T2*-weighted gradient-echo images (0.33 × 0.33 × 1.0 mm3) for cortical and white matter lesion segmentation and 3.0-T T1-weighted images for cortical surface reconstruction and cortical thickness estimation. Cortical lesions were sampled through the cortex to quantify cortical lesion distribution. The Expanded Disability Status Scale (EDSS) was used to assess neurologic disability. Nonparametric statistics assessed differences between and within groups in MRI metrics of cortical and white matter lesion burden; regression analysis explored associations of disability with MRI metrics. Results Twenty-five of 31 (81%) participants developed new cortical lesions per year (intracortical, 1.3 ± 1.7 vs leukocortical, 0.7 ± 1.9; P = .04), surpassing white matter lesion accrual (cortical, 2.0 ± 2.8 vs white matter, 0.7 ± 0.6; P = .01). In contrast to white matter lesions, cortical lesion accrual was greater in participants with secondary progressive MS than with relapsing-remitting MS (3.6 lesions/year ± 4.2 vs 1.1 lesions/year ± 0.9, respectively; P = .03) and preferentially localized in sulci. Total cortical lesion volume independently predicted baseline EDSS (β = 1.5, P < .001) and EDSS changes at follow-up (β = 0.5, P = .003). Conclusion Cortical lesions predominantly develop intracortically and within sulci, suggesting an inflammatory cerebrospinal fluid-mediated lesion pathogenesis. Cortical lesion accumulation was prominent at 7.0 T and independently predicted neurologic disability progression. © RSNA, 2019 Online supplemental material is available for this article. See also the editorial by Filippi and Rocca in this issue. SN - 1527-1315 UR - https://www.unboundmedicine.com/medline/citation/30964421/Longitudinal_Characterization_of_Cortical_Lesion_Development_and_Evolution_in_Multiple_Sclerosis_with_7_0_T_MRI_ L2 - http://pubs.rsna.org/doi/10.1148/radiol.2019181719?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -