scholarly journals No association between cortical lesions and leptomeningeal enhancement on 7-Tesla MRI in multiple sclerosis

2019 ◽  
Vol 26 (2) ◽  
pp. 165-176 ◽  
Author(s):  
Mehrnaz Ighani ◽  
Samuel Jonas ◽  
Izlem Izbudak ◽  
Seongjin Choi ◽  
Alfonso Lema-Dopico ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cortical Thickness ◽  
7 Tesla ◽  
Focal Lesion ◽  
Cortical Lesions ◽  
Leptomeningeal Enhancement ◽  
Meningeal Inflammation ◽  
Cortical Gray Matter ◽  
Inflammatory Processes ◽  
Magnetic Resonance Imaging Mri

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.

Association of retinal atrophy with cortical lesions and leptomeningeal enhancement in multiple sclerosis on 7T MRI

2021 ◽  
pp. 135245852110233
Author(s):  
Ryan Mizell ◽  
Hegang Chen ◽  
Jeffrey Lambe ◽  
Shiv Saidha ◽  
Daniel M Harrison
Keyword(s):  
Multiple Sclerosis ◽  
7 Tesla ◽  
Retinal Layer ◽  
Inner Plexiform Layer ◽  
Cortical Lesions ◽  
Post Contrast ◽  
Leptomeningeal Enhancement ◽  
Retinal Layers ◽  
Meningeal Inflammation ◽  
Retinal Atrophy

Background: Retinal atrophy in multiple sclerosis (MS) as measured by optical coherence tomography (OCT) correlates with demyelinating lesions and brain atrophy, but its relationship with cortical lesions (CLs) and meningeal inflammation is not well known. Objectives: To evaluate the relationship of retinal layer atrophy with leptomeningeal enhancement (LME) and CLs in MS as visualized on 7 Tesla (7T) magnetic resonance imaging (MRI). Methods: Forty participants with MS underwent 7T MRI of the brain and OCT. Partial correlation and mixed-effects regression evaluated relationships between MRI and OCT findings. Results: All participants had CLs and 32 (80%) participants had LME on post-contrast MRI. Ganglion cell/inner plexiform layer (GCIPL) thickness correlated with total CL volume ( r =−0.45, p < 0.01). Participants with LME at baseline had thinner macular retinal nerve fiber layer (mRNFL; p = 0.01) and GCIPL ( p < 0.01). Atrophy in various retinal layers was faster in those with certain patterns of LME. For example, mRNFL declined –1.113 (–1.974, –0.252) μm/year faster in those with spread/fill-pattern LME foci at baseline compared with those without ( p = 0.01). Conclusion: This study associates MRI findings of LME and cortical pathology with thinning of retinal layers as measured by OCT, suggesting a common link between meningeal inflammation, CLs, and retinal atrophy in MS.

scholarly journals 7T MRI cerebral leptomeningeal enhancement is common in relapsing-remitting multiple sclerosis and is associated with cortical and thalamic lesions

2019 ◽  
Vol 26 (2) ◽  
pp. 177-187 ◽  
Author(s):  
Jonathan Zurawski ◽  
Shahamat Tauhid ◽  
Renxin Chu ◽  
Fariha Khalid ◽  
Brian C Healy ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Three Dimensional ◽  
Leptomeningeal Enhancement ◽  
Meningeal Inflammation ◽  
Relapsing Remitting ◽  
Fluid Attenuated Inversion Recovery ◽  
Thalamic Lesions ◽  
Remitting Multiple Sclerosis ◽  
Magnetic Resonance Imaging Mri ◽  
Relapsing Remitting Multiple Sclerosis

Background: Meningeal inflammation may contribute to gray matter (GM) involvement in multiple sclerosis (MS) and is proposed to manifest as magnetic resonance imaging (MRI) leptomeningeal enhancement (LME). Objective: To investigate how LME relates to GM lesions in relapsing-remitting multiple sclerosis (RRMS) at 7T. Methods: A total of 30 RRMS subjects (age (mean ± standard deviation (SD)): 44.0 ± 11.3 years, 93% on disease-modifying treatment) and 15 controls underwent gadolinium-enhanced three-dimensional (3D) MP2RAGE (magnetization-prepared 2 rapid gradient-echo) and fluid-attenuated inversion recovery (FLAIR) MRI. LME, cortical lesions (CLs), thalamic lesions (TLs), and white matter (WM) lesions were expert-quantified. Wilcoxon rank-sum, two-sample t-tests, Spearman correlations, and regression models were employed. Results: Two-thirds (20/30) of MS subjects and 1/15 controls (6.7%) had LME. LME+ MS subjects had 2.7 ± 1.5 foci, longer disease duration (14.9 ± 10.4 vs. 8.1 ± 5.7 years, p = 0.028), increased CL number (21.5 ± 12.6 vs. 5.5 ± 5.0, p < 0.001) and volume (0.80 ± 1.13 vs. 0.13 ± 0.13 mL, p = 0.002), and increased TL number (3.95 ± 2.11 vs. 0.70 ± 1.34, p < 0.001) and volume (0.106 ± 0.09 vs. 0.007 ± 0.01 mL, p < 0.001) versus LME– subjects. LME focus number correlated more highly with CL ( rs = 0.50, p = 0.01) and TL ( rs = 0.81, p < 0.001) than WM lesion ( rs = 0.34, p > 0.05) volume. Similar LME–CL number associations were observed in unadjusted and WM lesion–adjusted comparisons (both p < 0.001). Conclusion: Cerebral LME is common in RRMS at 7T and is independently associated with GM injury. We hypothesize that cerebrospinal fluid (CSF)-related inflammation links cortical and thalamic injury.

Grey matter abnormalities in multiple sclerosis: proton magnetic resonance spectroscopic imaging

2001 ◽  
Vol 7 (4) ◽  
pp. 221-226 ◽  
Author(s):  
Rakesh Sharma ◽  
Ponnada A Narayana ◽  
Jerry S Wolinsky
Keyword(s):  
Multiple Sclerosis ◽  
Magnetic Resonance ◽  
Proton Magnetic Resonance ◽  
Magnetization Transfer ◽  
Spectroscopic Imaging ◽  
Magnetic Resonance Spectroscopic Imaging ◽  
Relapsing Remitting ◽  
Cortical Gray Matter ◽  
Magnetic Resonance Imaging Mri ◽  
Mri Characteristics

Pathologically defined abnormalities in the cortical gray matter (GM) are well described in multiple sclerosis (MS) but are infrequently seen by conventional magnetic resonance imaging (MRI). We systematically evaluated 52 relapsing - remitting MS patients and 20 normal volunteers with high resolution MRI and short echo proton magnetic resonance spectroscopic imaging (MRSI). Individual tissue contributions to the spectroscopic voxels were estimated based on MRI that incorporated both CSF suppression and magnetization transfer, or double inversion images in which both CSF and GM were suppressed. Strong resonances in the 0.8 to 1.5 p.p.m. spectral region were observed in 13 MS patients. Image segmentation based on the MRI characteristics of tissues contributing to the spectroscopic voxels showed that these additional peaks originated mainly from GM. The presence of these additional peaks suggests that the normal appearance GM on MRI, is biochemically abnormal in a substantial proportion of relapsing-remitting MS patients.

Heterogeneous pathological processes account for thalamic degeneration in multiple sclerosis: Insights from 7 T imaging

2017 ◽  
Vol 24 (11) ◽  
pp. 1433-1444 ◽  
Author(s):  
Céline Louapre ◽  
Sindhuja T Govindarajan ◽  
Costanza Giannì ◽  
Nancy Madigan ◽  
Jacob A Sloane ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Progressive Multiple Sclerosis ◽  
Lesion Volume ◽  
Thalamic Lesion ◽  
Cortical Lesions ◽  
Focal Lesions ◽  
Thalamic Degeneration ◽  
Relapsing Remitting ◽  
Thalamic Lesions ◽  
Magnetic Resonance Imaging Mri

Background: Thalamic degeneration impacts multiple sclerosis (MS) prognosis. Objective: To investigate heterogeneous thalamic pathology, its correlation with white matter (WM), cortical lesions and thickness, and as function of distance from cerebrospinal fluid (CSF). Methods: In 41 MS subjects and 17 controls, using 3 and 7 T imaging, we tested for (1) differences in thalamic volume and quantitative T2* (q-T2*) (2) globally and (3) within concentric bands originating from the CSF/thalamus interface; (4) the relation between thalamic, cortical, and WM metrics; and (5) the contribution of magnetic resonance imaging (MRI) metrics to clinical scores. We also assessed MS thalamic lesion distribution as a function of distance from CSF. Results: Thalamic lesions were mainly located next to the ventricles. Thalamic volume was decreased in MS versus controls ( p < 10−2); global q-T2* was longer in secondary progressive multiple sclerosis (SPMS) only ( p < 10−2), indicating myelin and/or iron loss. Thalamic atrophy and longer q-T2* correlated with WM lesion volume ( p < 0.01). In relapsing-remitting MS, q-T2* thalamic abnormalities were located next to the WM ( p < 0.01 (uncorrected), p = 0.09 (corrected)), while they were homogeneously distributed in SPMS. Cortical MRI metrics were the strongest predictors of clinical outcome. Conclusion: Heterogeneous pathological processes affect the thalamus in MS. While focal lesions are likely mainly driven by CSF-mediated factors, overall thalamic degeneration develops in association with WM lesions.

scholarly journals Profiles of cortical inflammation in multiple sclerosis by 11C-PBR28 MR-PET and 7 Tesla imaging

2019 ◽  
Vol 26 (12) ◽  
pp. 1497-1509 ◽  
Author(s):  
Elena Herranz ◽  
Céline Louapre ◽  
Constantina Andrada Treaba ◽  
Sindhuja T Govindarajan ◽  
Russell Ouellette ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Disease Burden ◽  
Relative Difference ◽  
Tracer Uptake ◽  
Microglia Activation ◽  
Inactive Disease ◽  
7 Tesla ◽  
Cortical Lesion ◽  
Cortical Lesions ◽  
Cortical Areas

Background: Neuroinflammation with microglia activation is thought to be closely related to cortical multiple sclerosis (MS) lesion pathogenesis. Objective: Using 11C-PBR28 and 7 Tesla (7T) imaging, we assessed in 9 relapsing–remitting multiple sclerosis (RRMS) and 10 secondary progressive multiple sclerosis (SPMS) patients the following: (1) microglia activation in lesioned and normal-appearing cortex, (2) cortical lesion inflammatory profiles, and (3) the relationship between neuroinflammation and cortical integrity. Methods: Mean 11C-PBR28 uptake was measured in focal cortical lesions, cortical areas with 7T quantitative T2* (q-T2*) abnormalities, and normal-appearing cortex. The relative difference in cortical 11C-PBR28 uptake between patients and 14 controls was used to classify cortical lesions as either active or inactive. Disease burden was investigated according to cortical lesion inflammatory profiles. The relation between q-T2* and 11C-PBR28 uptake along the cortex was assessed. Results: 11C-PBR28 uptake was abnormally high in cortical lesions in RRMS and SPMS; in SPMS, tracer uptake was significantly increased also in normal-appearing cortex. 11C-PBR28 uptake and q-T2* correlated positively in many cortical areas, negatively in some regions. Patients with high cortical lesion inflammation had worse clinical outcome and higher intracortical lesion burden than patients with low inflammation. Conclusion: 11C-PBR28 and 7T imaging reveal distinct profiles of cortical inflammation in MS, which are related to disease burden.

A clinically feasible 7-Tesla protocol for the identification of cortical lesions in Multiple Sclerosis

2020 ◽  
Vol 30 (8) ◽  
pp. 4586-4594 ◽  
Author(s):  
Sirio Cocozza ◽  
Mirco Cosottini ◽  
Alessio Signori ◽  
Lazar Fleysher ◽  
Mohamed Mounir El Mendili ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
7 Tesla ◽  
Cortical Lesions

scholarly journals Quantitative 7-Tesla Imaging of Cortical Myelin Changes in Early Multiple Sclerosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Valeria Barletta ◽  
Elena Herranz ◽  
Constantina A. Treaba ◽  
Ambica Mehndiratta ◽  
Russell Ouellette ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Quantitative Mri ◽  
7 Tesla ◽  
Cortical Lesion ◽  
Healthy Controls ◽  
Cortical Lesions ◽  
Lesion Analysis ◽  
Cortical Map ◽  
The Brain

Cortical demyelination occurs early in multiple sclerosis (MS) and relates to disease outcome. The brain cortex has endogenous propensity for remyelination as proven from histopathology study. In this study, we aimed at characterizing cortical microstructural abnormalities related to myelin content by applying a novel quantitative MRI technique in early MS. A combined myelin estimation (CME) cortical map was obtained from quantitative 7-Tesla (7T) T2* and T1 acquisitions in 25 patients with early MS and 19 healthy volunteers. Cortical lesions in MS patients were classified based on their myelin content by comparison with CME values in healthy controls as demyelinated, partially demyelinated, or non-demyelinated. At follow-up, we registered changes in cortical lesions as increased, decreased, or stable CME. Vertex-wise analysis compared cortical CME in the normal-appearing cortex in 25 MS patients vs. 19 healthy controls at baseline and investigated longitudinal changes at 1 year in 10 MS patients. Measurements from the neurite orientation dispersion and density imaging (NODDI) diffusion model were obtained to account for cortical neurite/dendrite loss at baseline and follow-up. Finally, CME maps were correlated with clinical metrics. CME was overall low in cortical lesions (p = 0.03) and several normal-appearing cortical areas (p &lt; 0.05) in the absence of NODDI abnormalities. Individual cortical lesion analysis revealed, however, heterogeneous CME patterns from extensive to partial or absent demyelination. At follow-up, CME overall decreased in cortical lesions and non-lesioned cortex, with few areas showing an increase (p &lt; 0.05). Cortical CME maps correlated with processing speed in several areas across the cortex. In conclusion, CME allows detection of cortical microstructural changes related to coexisting demyelination and remyelination since the early phases of MS, and shows to be more sensitive than NODDI and relates to cognitive performance.

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