Comparison of cortical lesion frequency by type as detected by 3T and 7T multi-contrast MRI in patients with multiple sclerosis

2018 ◽  
Author(s):  
Josefina Maranzano
Keyword(s):  
Multiple Sclerosis ◽  
Cortical Lesion ◽  
Lesion Frequency

scholarly journals Changes in Cerebrospinal Fluid Balance of TNF and TNF Receptors in Naïve Multiple Sclerosis Patients: Early Involvement in Compartmentalised Intrathecal Inflammation

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1712
Author(s):  
Roberta Magliozzi ◽  
Francesco Pezzini ◽  
Mairi Pucci ◽  
Stefania Rossi ◽  
Francesco Facchiano ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Immune Cell ◽  
Protein Pattern ◽  
Fold Change ◽  
Cortical Lesion ◽  
Control Group ◽  
Lesion Volume ◽  
Mri Features ◽  
Csf Levels ◽  
Multiple Sclerosis Patients

An imbalance of TNF signalling in the inflammatory milieu generated by meningeal immune cell infiltrates in the subarachnoid space in multiple sclerosis (MS), and its animal model may lead to increased cortical pathology. In order to explore whether this feature may be present from the early stages of MS and may be associated with the clinical outcome, the protein levels of TNF, sTNF-R1 and sTNF-R2 were assayed in CSF collected from 122 treatment-naïve MS patients and 36 subjects with other neurological conditions at diagnosis. Potential correlations with other CSF cytokines/chemokines and with clinical and imaging parameters at diagnosis (T0) and after 2 years of follow-up (T24) were evaluated. Significantly increased levels of TNF (fold change: 7.739; p < 0.001), sTNF-R1 (fold change: 1.693; p < 0.001) and sTNF-R2 (fold change: 2.189; p < 0.001) were detected in CSF of MS patients compared to the control group at T0. Increased TNF levels in CSF were significantly (p < 0.01) associated with increased EDSS change (r = 0.43), relapses (r = 0.48) and the appearance of white matter lesions (r = 0.49). CSF levels of TNFR1 were associated with cortical lesion volume (r = 0.41) at T0, as well as with new cortical lesions (r = 0.56), whilst no correlation could be found between TNFR2 levels in CSF and clinical or MRI features. Combined correlation and pathway analysis (ingenuity) of the CSF protein pattern associated with TNF expression (encompassing elevated levels of BAFF, IFN-γ, IL-1β, IL-10, IL-8, IL-16, CCL21, haptoglobin and fibrinogen) showed a particular relationship to the interaction between innate and adaptive immune response. The CSF sTNF-R1-associated pattern (encompassing high levels of CXCL13, TWEAK, LIGHT, IL-35, osteopontin, pentraxin-3, sCD163 and chitinase-3-L1) was mainly related to altered T cell and B cell signalling. Finally, the CSF TNFR2-associated pattern (encompassing high CSF levels of IFN-β, IFN-λ2, sIL-6Rα) was linked to Th cell differentiation and regulatory cytokine signalling. In conclusion, dysregulation of TNF and TNF-R1/2 pathways associates with specific clinical/MRI profiles and can be identified at a very early stage in MS patients, at the time of diagnosis, contributing to the prediction of the disease outcome.

scholarly journals Comparison of Multiple Sclerosis Cortical Lesion Types Detected by Multicontrast 3T and 7T MRI

2019 ◽  
Vol 40 (7) ◽  
pp. 1162-1169 ◽  
Author(s):  
J. Maranzano ◽  
M. Dadar ◽  
D.A. Rudko ◽  
D. De Nigris ◽  
C. Elliott ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cortical Lesion

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.

scholarly journals Ultrahigh-resolution MRI Reveals Extensive Cortical Demyelination in a Nonhuman Primate Model of Multiple Sclerosis

2020 ◽  
Vol 31 (1) ◽  
pp. 439-447 ◽  
Author(s):  
Maxime Donadieu ◽  
Hannah Kelly ◽  
Diego Szczupak ◽  
Jing-Ping Lin ◽  
Yeajin Song ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Proteolipid Protein ◽  
Common Marmoset ◽  
Cortical Lesion ◽  
Tissue Preparation ◽  
Cortical Lesions ◽  
Primate Model ◽  
Relevant Animal Model ◽  
Primary Driver

Abstract Cortical lesions are a primary driver of disability in multiple sclerosis (MS). However, noninvasive detection of cortical lesions with in vivo magnetic resonance imaging (MRI) remains challenging. Experimental autoimmune encephalomyelitis (EAE) in the common marmoset is a relevant animal model of MS for investigating the pathophysiological mechanisms leading to brain damage. This study aimed to characterize cortical lesions in marmosets with EAE using ultrahigh-field (7 T) MRI and histological analysis. Tissue preparation was optimized to enable the acquisition of high-spatial resolution (50-μm isotropic) T2*-weighted images. A total of 14 animals were scanned in this study, and 70% of the diseased animals presented at least one cortical lesion on postmortem imaging. Cortical lesions identified on MRI were verified with myelin proteolipid protein immunostaining. An optimized T2*-weighted sequence was developed for in vivo imaging and shown to capture 65% of cortical lesions detected postmortem. Immunostaining confirmed extensive demyelination with preserved neuronal somata in several cortical areas of EAE animals. Overall, this study demonstrates the relevance and feasibility of the marmoset EAE model to study cortical lesions, among the most important yet least understood features of MS.

Neuropsychological impairment in multiple sclerosis patients: the role of (juxta)cortical lesion on FLAIR

2000 ◽  
Vol 6 (4) ◽  
pp. 280-285 ◽  
Author(s):  
R.H.C. Lazeron ◽  
D.W. Langdon ◽  
M. Filippi ◽  
J.H.T.M. van Waesberghe ◽  
V.L. Stevenson ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Neuropsychological Impairment ◽  
Cortical Lesion ◽  
Multiple Sclerosis Patients

scholarly journals Disease-Modifying Drugs Reduce Cortical Lesion Accumulation and Atrophy Progression in Relapsing-Remitting Multiple Sclerosis: Results from a 48-Month Extension Study

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Francesca Rinaldi ◽  
Paola Perini ◽  
Matteo Atzori ◽  
Alice Favaretto ◽  
Dario Seppi ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Glatiramer Acetate ◽  
Reference Population ◽  
Cortical Atrophy ◽  
Cortical Lesion ◽  
Disease Modifying Drugs ◽  
Relapsing Remitting ◽  
The Mean ◽  
Disease Modifying ◽  
Relapsing Remitting Multiple Sclerosis

Cortical lesions (CLs) and atrophy are pivotal in multiple sclerosis (MS) pathology. This study determined the effect of disease modifying drugs (DMDs) on CL development and cortical atrophy progression in patients with relapsing-remitting MS (RRMS) over 48 months. Patients (n=165) were randomized to sc IFNβ-1a 44 μg, im IFNβ-1a 30 μg, or glatiramer acetate 20 mg. The reference population comprised 50 DMD-untreated patients with RRMS. After 24 months, 43 of the untreated patients switched to DMDs. The four groups of patients were followed up for an additional 24 months. At 48 months the mean standard deviation number of new CLs was significantly lower in patients treated with sc IFNβ-1a (1.4 ± 1.0, range 0–5) compared with im IFNβ-1a (2.3 ± 1.3, range 0–6,P=0.004) and glatiramer acetate (2.2 ± 1.5, range 0–7,P=0.03). Significant reductions in CL accumulation and new white matter and gadolinium-enhancing lesions were also observed in the 43 patients who switched to DMDs after 24 months, compared with the 24 months of no treatment. Concluding, this study confirms that DMDs significantly reduce CL development and cortical atrophy progression compared with no treatment.

scholarly journals Temporal Lobe Epilepsy as a Unique Manifestation of Multiple Sclerosis

2003 ◽  
Vol 30 (3) ◽  
pp. 228-232 ◽  
Author(s):  
Antonio Gambardella ◽  
Paola Valentino ◽  
Angelo Labate ◽  
Grazia Sibilia ◽  
Francesca Ruscica ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Brain Mri ◽  
Epileptic Seizures ◽  
Cortical Lesion ◽  
Temporal Region ◽  
Antiepileptic Medication ◽  
Long Term Follow Up

Objective:To report on five patients with temporal lobe epilepsy (TLE) as the unique manifestation of multiple sclerosis (MS).Methods:Among 350 consecutive MS patients, we identified 16/350 (4.6%) who also had epileptic seizures. Here, we review their electrophysiological and clinical features.Results:Five of these 16 patients (four female, one male; mean age 34.2 years; range 31 to 38) with MS and epileptic seizures had an extremely homogeneous clinical picture characterized by TLE as the unique manifestation of MS, even at long follow-up (mean: five years; range 4 to 10). In all patients, seizures started in the second or third decade. Brain MRI revealed at least one juxta-cortical lesion within the temporal region. Antiepileptic medication was always effective.Conclusions:The present study provides the first evidence of a peculiar form of MS characterized by TLE as the unique manifestation of the disease with no disability or MS relapses at long-term follow-up.

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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