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The association between intra- and juxta-cortical pathology and cognitive impairment in multiple sclerosis by quantitative T2* mapping at 7 T MRI.

ABSTRACT: Using quantitative T2* at 7 Tesla (T) magnetic resonance imaging, we investigated whether impairment in selective cognitive functions in multiple sclerosis (MS) can be explained by pathology in specific areas and/or layers of the cortex. Thirty-one MS patients underwent neuropsychological evaluation, acquisition of 7 T multi-echo T2* gradient-echo sequences, and 3 T anatomical images for cortical surfaces reconstruction. Seventeen age-matched healthy subjects served as controls. Cortical T2* maps were sampled at various depths throughout the cortex and juxtacortex. Relation between T2*, neuropsychological scores and a cognitive index (CI), calculated from a principal component analysis on the whole battery, was tested by a general linear model. Cognitive impairment correlated with T2* increase, independently from white matter lesions and cortical thickness, in cortical areas highly relevant for cognition belonging to the default-mode network (p < 0.05 corrected). Dysfunction in different cognitive functions correlated with longer T2* in selective cortical regions, most of which showed longer T2* relative to controls. For most tests, this association was strongest in deeper cortical layers. Executive dysfunction, however, was mainly related with pathology in juxtameningeal cortex. T2* explained up to 20% of the variance of the CI, independently of conventional imaging metrics (adjusted-R2: 52-67%, p < 5.10- 4). Location of pathology across the cortical width and mantle showed selective correlation with impairment in differing cognitive domains. These findings may guide studies at lower field strength designed to develop surrogate markers of cognitive impairment in MS.

SUBMITTER: Louapre C

PROVIDER: S-EPMC5107649 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

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The association between intra- and juxta-cortical pathology and cognitive impairment in multiple sclerosis by quantitative T2* mapping at 7 T MRI.

Louapre Céline C Govindarajan Sindhuja T ST Giannì Costanza C Madigan Nancy N Nielsen A Scott AS Sloane Jacob A JA Kinkel Revere P RP Mainero Caterina C

NeuroImage. Clinical 20161103

Using quantitative T2* at 7 Tesla (T) magnetic resonance imaging, we investigated whether impairment in selective cognitive functions in multiple sclerosis (MS) can be explained by pathology in specific areas and/or layers of the cortex. Thirty-one MS patients underwent neuropsychological evaluation, acquisition of 7 T multi-echo T2* gradient-echo sequences, and 3 T anatomical images for cortical surfaces reconstruction. Seventeen age-matched healthy subjects served as cont ...[more]

PMID: 27872810

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Project description:BackgroundAlthough quantitative measures from research-quality MRI provide a means to study multiple sclerosis (MS) pathology in vivo, these metrics are often unavailable in legacy clinical datasets.ObjectiveTo determine how well an automatically-generated quantitative snapshot of brain pathology, measured only on clinical routine T2-FLAIR MRI, can substitute for more conventional measures on research MRI in terms of capturing multi-factorial disease pathology and providing similar clinical relevance.MethodsMRI with both research-quality sequences and conventional clinical T2-FLAIR was acquired for 172 MS patients at baseline, and neurologic disability was assessed at baseline and five-years later. Five measures (thalamus volume, lateral ventricle volume, medulla oblongata volume, lesion volume, and network efficiency) for quantifying disparate aspects of neuropathology from low-resolution T2-FLAIR were applied to predict standard research-quality MRI measures. They were compared in regard to association with future neurologic disability and disease progression over five years.ResultsThe combination of the five T2-FLAIR measures explained most of the variance in standard research-quality MRI. T2-FLAIR measures were associated with neurologic disability and cognitive function five-years later (R2 = 0.279, p < 0.001; R2 = 0.382, p < 0.001), similar to standard research-quality MRI (R2 = 0.279, p < 0.001; R2 = 0.366, p < 0.001). They also similarly predicted disability progression over five years (%-correctly-classified = 69.8, p = 0.034), compared to standard research-quality MRI (%-correctly-classified = 72.4%, p = 0.022) in relapsing-remitting MS.ConclusionA set of five T2-FLAIR-only measures can substitute for standard research-quality MRI, especially in relapsing-remitting MS. When only clinical T2-FLAIR is available, it can be used to obtain substantially more quantitative information about brain pathology and disability than is currently standard practice.

Project description:We used a surface-based analysis of T2* relaxation rates at 7 T magnetic resonance imaging, which allows sampling quantitative T2* throughout the cortical width, to map in vivo the spatial distribution of intracortical pathology in multiple sclerosis. Ultra-high resolution quantitative T2* maps were obtained in 10 subjects with clinically isolated syndrome/early multiple sclerosis (≤ 3 years disease duration), 18 subjects with relapsing-remitting multiple sclerosis (≥ 4 years disease duration), 13 subjects with secondary progressive multiple sclerosis, and in 17 age-matched healthy controls. Quantitative T2* maps were registered to anatomical cortical surfaces for sampling T2* at 25%, 50% and 75% depth from the pial surface. Differences in laminar quantitative T2* between each patient group and controls were assessed using general linear model (P < 0.05 corrected for multiple comparisons). In all 41 multiple sclerosis cases, we tested for associations between laminar quantitative T2*, neurological disability, Multiple Sclerosis Severity Score, cortical thickness, and white matter lesions. In patients, we measured, T2* in intracortical lesions and in the intracortical portion of leukocortical lesions visually detected on 7 T scans. Cortical lesional T2* was compared with patients' normal-appearing cortical grey matter T2* (paired t-test) and with mean cortical T2* in controls (linear regression using age as nuisance factor). Subjects with multiple sclerosis exhibited relative to controls, independent from cortical thickness, significantly increased T2*, consistent with cortical myelin and iron loss. In early disease, T2* changes were focal and mainly confined at 25% depth, and in cortical sulci. In later disease stages T2* changes involved deeper cortical laminae, multiple cortical areas and gyri. In patients, T2* in intracortical and leukocortical lesions was increased compared with normal-appearing cortical grey matter (P < 10(-10) and P < 10(-7)), and mean cortical T2* in controls (P < 10(-5) and P < 10(-6)). In secondary progressive multiple sclerosis, T2* in normal-appearing cortical grey matter was significantly increased relative to controls (P < 0.001). Laminar T2* changes may, thus, result from cortical pathology within and outside focal cortical lesions. Neurological disability and Multiple Sclerosis Severity Score correlated each with the degree of laminar quantitative T2* changes, independently from white matter lesions, the greatest association being at 25% depth, while they did not correlate with cortical thickness and volume. These findings demonstrate a gradient in the expression of cortical pathology throughout stages of multiple sclerosis, which was associated with worse disability and provides in vivo evidence for the existence of a cortical pathological process driven from the pial surface.

Project description:BACKGROUND:Long acquisition times and motion sensitivity limit T2 mapping in the abdomen. Accelerated mapping at 3 T may allow for quantitative assessment of diffuse pancreatic disease in patients during free-breathing. PURPOSE:To test the feasibility of respiratory-triggered quantitative T2 analysis in the pancreas and correlate T2 -values with age, body mass index, pancreatic location, main pancreatic duct dilatation, and underlying pathology. STUDY TYPE:Retrospective single-center pilot study. POPULATION:Eighty-eight adults. FIELD STRENGTH/SEQUENCE:Ten-fold accelerated multiecho-spin-echo 3 T MRI sequence to quantify T2 at 3 T. ASSESSMENT:Two radiologists independently delineated three regions of interest inside the pancreatic head, body, and tail for each acquisition. Means and standard deviations for T2 values in these regions were determined. T2 -value variation with demographic data, intraparenchymal location, pancreatic duct dilation, and underlying pancreatic disease was assessed. STATISTICAL TESTS:Interreader reliability was determined by calculating the interclass coefficient (ICCs). T2 values were compared for different pancreatic locations by analysis of variance (ANOVA). Interpatient associations between T2 values and demographical, clinical, and radiological data were calculated (ANOVA). RESULTS:The accelerated T2 mapping sequence was successfully performed in all participants (mean acquisition time, 2:48 ± 0:43 min). Low T2 value variability was observed across all patients (intersubject) (head: 60.2 ± 8.3 msec, body: 63.9 ± 11.5 msec, tail: 66.8 ± 16.4 msec). Interreader agreement was good (ICC, 0.82, 95% confidence interval: 0.77-0.86). T2 -values differed significantly depending on age (P < 0.001), location (P < 0.001), main pancreatic duct dilatation (P < 0.001), and diffuse pancreatic disease (P < 0.03). DATA CONCLUSION:The feasibility of accelerated T2 mapping at 3 T in moving abdominal organs was demonstrated in the pancreas, since T2 values were stable and reproducible. In the pancreatic parenchyma, T2 -values were significantly dependent on demographic and clinical parameters. LEVEL OF EVIDENCE:4 Technical Efficacy: Stage 1 J. Magn. Reson. Imaging 2019;50:410-416.

Dataset Information

The association between intra- and juxta-cortical pathology and cognitive impairment in multiple sclerosis by quantitative T2* mapping at 7 T MRI.

Publications

The association between intra- and juxta-cortical pathology and cognitive impairment in multiple sclerosis by quantitative T<sub>2</sub>* mapping at 7 T MRI.

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