TY - JOUR
T1 - No association between cortical lesions and leptomeningeal enhancement on 7-Tesla MRI in multiple sclerosis
AU - Ighani, Mehrnaz
AU - Jonas, Samuel
AU - Izbudak, Izlem
AU - Choi, Seongjin
AU - Lema-Dopico, Alfonso
AU - Hua, Jun
AU - O’Connor, Erin E.
AU - Harrison, Daniel M.
N1 - Publisher Copyright:
© The Author(s), 2019.
PY - 2020/2/1
Y1 - 2020/2/1
N2 - Background: Autopsy data suggest a causative link between meningeal inflammation and cortical lesions (CLs) in multiple sclerosis (MS). Objective: To use leptomeningeal enhancement (LME) and CLs on 7-Tesla (7T) magnetic resonance imaging (MRI) to investigate associations between meningeal inflammation and cortical pathology. Methods: Forty-one participants with MS underwent 7T MRI of the brain. CLs and foci of LME were quantified. Results: All MS participants had CLs; 27 (65.8%) had >1 focus of LME. Except for hippocampal CL count (ρ = 0.32 with spread/fill-sulcal pattern LME, p = 0.042), no significant correlations were seen between LME and CLs. Mean cortical thickness correlated with the number of LME foci (ρ = –0.43, p = 0.005). Participants with relapsing–remitting multiple sclerosis (RRMS) showed no correlation with neocortical CLs, but significant correlations were seen between LME and hippocampal lesion count (ρ = 0.39, p = 0.030), normalized cortical gray matter (GM) volume (ρ = –0.49, p = 0.005), and mean cortical thickness (ρ = –0.59, p < 0.001). Conclusion: This study supports a relationship between LME and cortical GM atrophy but does not support an association of LME and neocortical CLs. This may indicate that meningeal inflammation is involved with neurodegenerative inflammatory processes, rather than focal lesion development.
AB - Background: Autopsy data suggest a causative link between meningeal inflammation and cortical lesions (CLs) in multiple sclerosis (MS). Objective: To use leptomeningeal enhancement (LME) and CLs on 7-Tesla (7T) magnetic resonance imaging (MRI) to investigate associations between meningeal inflammation and cortical pathology. Methods: Forty-one participants with MS underwent 7T MRI of the brain. CLs and foci of LME were quantified. Results: All MS participants had CLs; 27 (65.8%) had >1 focus of LME. Except for hippocampal CL count (ρ = 0.32 with spread/fill-sulcal pattern LME, p = 0.042), no significant correlations were seen between LME and CLs. Mean cortical thickness correlated with the number of LME foci (ρ = –0.43, p = 0.005). Participants with relapsing–remitting multiple sclerosis (RRMS) showed no correlation with neocortical CLs, but significant correlations were seen between LME and hippocampal lesion count (ρ = 0.39, p = 0.030), normalized cortical gray matter (GM) volume (ρ = –0.49, p = 0.005), and mean cortical thickness (ρ = –0.59, p < 0.001). Conclusion: This study supports a relationship between LME and cortical GM atrophy but does not support an association of LME and neocortical CLs. This may indicate that meningeal inflammation is involved with neurodegenerative inflammatory processes, rather than focal lesion development.
KW - 7 Tesla
KW - 7T MRI
KW - Leptomeningeal enhancement
KW - cortical lesions
KW - hippocampal lesions
KW - meningeal inflammation
KW - multiple sclerosis
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U2 - 10.1177/1352458519876037
DO - 10.1177/1352458519876037
M3 - Article
C2 - 31573837
AN - SCOPUS:85074010474
SN - 1352-4585
VL - 26
SP - 165
EP - 176
JO - Multiple Sclerosis Journal
JF - Multiple Sclerosis Journal
IS - 2
ER -