ECTRIMS eLearning

Demographic analysis and lesion characterization of leptomeningeal enhancement in multiple sclerosis
ECTRIMS Learn. Engisch R. 10/25/17; 199542; EP1522
Renate Engisch
Renate Engisch
Contributions
Abstract

Abstract: EP1522

Type: ePoster

Abstract Category: Pathology and pathogenesis of MS - 21 Imaging

Background: B-cell lymphoid aggregates have been implicated in meningeal inflammation, cortical grey matter demyelination, and disability progression in multiple sclerosis (MS) (1). Gadolinium-enhanced 3D-FLAIR (Gd-3D-FLAIR) MRI has recently been shown to identify foci of leptomeningeal enhancement (LME) in MS (2), thought to be an imaging biomarker for leptomeningeal inflammation. Awareness of demographics and lesion characteristics will facilitate determining if LME is a potential biomarker for anti-B cell therapies.
Goals: To analyze LME in MS patients in community-based practice by determining demographic and lesion characteristics, including relative frequency of LME by MS-subtype and disease modifying therapy (DMT), and correlation with disease activity.
Methods: MRI exams in MS patients showing LME were reviewed for demographics, disease subtype, and DMT, and lesions were analyzed for concurrent disease activity, location and morphology, and stability over time.
Results: 18 MS patients revealed 34 LMEs (mean 1.9, range 1-4), including 15 (83%) with relapsing remitting (RR), and 3 (17%) with secondary progressive (SP) MS. LME was seen with various DMTs and in patients receiving no treatment. 1 patient had imaging signs of active disease. Lesions were equally distributed between right and left, with 9 frontal, 13 parietal, 8 occipital, 3 temporal, and 1 cingulate lesions. Lesion morphology showed 11 rounded dots, 21 curvilinear lesions, and 1 globular lesion. 7 patients had prior exams ranging from 6-21 months, with 1 patient revealing 1 new lesion over a 10 month follow up.
Conclusions:
1) In the community outpatient setting, LME is more likely to be seen in RRMS.
2) LME can be seen with a variety of DMTs.
3) LME is generally stable and unrelated to white matter disease activity.
References:
1. Howell OW, Reeves CA, Nicholas R, et al. Meningeal inflammation is widespread and linked to cortical pathology in multiple sclerosis. Brain 2011; 134:2755-2771.
2. Absinta M, Vuolo L, Rao A, et al. Gadolinium-based MRI characterization of leptomeningeal inflammation in multiple sclerosis. Neurology 2015; 85:18-28.
Disclosure:
David S. Titelbaum, M.D.: nothing relevant to disclose
Renate Engisch, M.D.: nothing relevant to disclose
Eric D. Schwartz, M.D.: nothing relevant to disclose
Salvatore Q. Napoli, M.D.: nothing relevant to disclose
Joshua D. Katz, M.D.: nothing relevant to disclose
Ellen S. Lathi, M.D.: nothing relevant to disclose

Abstract: EP1522

Type: ePoster

Abstract Category: Pathology and pathogenesis of MS - 21 Imaging

Background: B-cell lymphoid aggregates have been implicated in meningeal inflammation, cortical grey matter demyelination, and disability progression in multiple sclerosis (MS) (1). Gadolinium-enhanced 3D-FLAIR (Gd-3D-FLAIR) MRI has recently been shown to identify foci of leptomeningeal enhancement (LME) in MS (2), thought to be an imaging biomarker for leptomeningeal inflammation. Awareness of demographics and lesion characteristics will facilitate determining if LME is a potential biomarker for anti-B cell therapies.
Goals: To analyze LME in MS patients in community-based practice by determining demographic and lesion characteristics, including relative frequency of LME by MS-subtype and disease modifying therapy (DMT), and correlation with disease activity.
Methods: MRI exams in MS patients showing LME were reviewed for demographics, disease subtype, and DMT, and lesions were analyzed for concurrent disease activity, location and morphology, and stability over time.
Results: 18 MS patients revealed 34 LMEs (mean 1.9, range 1-4), including 15 (83%) with relapsing remitting (RR), and 3 (17%) with secondary progressive (SP) MS. LME was seen with various DMTs and in patients receiving no treatment. 1 patient had imaging signs of active disease. Lesions were equally distributed between right and left, with 9 frontal, 13 parietal, 8 occipital, 3 temporal, and 1 cingulate lesions. Lesion morphology showed 11 rounded dots, 21 curvilinear lesions, and 1 globular lesion. 7 patients had prior exams ranging from 6-21 months, with 1 patient revealing 1 new lesion over a 10 month follow up.
Conclusions:
1) In the community outpatient setting, LME is more likely to be seen in RRMS.
2) LME can be seen with a variety of DMTs.
3) LME is generally stable and unrelated to white matter disease activity.
References:
1. Howell OW, Reeves CA, Nicholas R, et al. Meningeal inflammation is widespread and linked to cortical pathology in multiple sclerosis. Brain 2011; 134:2755-2771.
2. Absinta M, Vuolo L, Rao A, et al. Gadolinium-based MRI characterization of leptomeningeal inflammation in multiple sclerosis. Neurology 2015; 85:18-28.
Disclosure:
David S. Titelbaum, M.D.: nothing relevant to disclose
Renate Engisch, M.D.: nothing relevant to disclose
Eric D. Schwartz, M.D.: nothing relevant to disclose
Salvatore Q. Napoli, M.D.: nothing relevant to disclose
Joshua D. Katz, M.D.: nothing relevant to disclose
Ellen S. Lathi, M.D.: nothing relevant to disclose

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