Deep grey matter T2 hypo-intensity in patients with paediatric multiple sclerosis

2011 ◽  
Vol 17 (6) ◽  
pp. 702-707 ◽  
Author(s):  
Antonia Ceccarelli ◽  
Maria A Rocca ◽  
Elisabetta Perego ◽  
Lucia Moiola ◽  
Angelo Ghezzi ◽  
...  

Objective: T2 hypo-intensity on magnetic resonance imaging scans is thought to reflect pathological iron deposition in the presence of disease. In this pilot study, we evaluated the utility of the quantification of T2 hypo-intensities in paediatric patients by estimating deep grey matter (DGM) T2 hypo-intensities in paediatric patients with multiple sclerosis (MS) or clinically isolated syndromes (CIS), and their changes over 1 year. Methods: A dual-echo sequence was obtained from 45 paediatric patients (10 with CIS, 35 with relapsing–remitting MS, 8 with an onset of the disease before the age of 10 and 37 during adolescence) and 14 age-matched healthy controls (HC). Eleven patients were reassessed both clinically and with MRI after 1 year. Normalized T2 intensity in the basal ganglia and thalamus was quantified. Results: At baseline, DGM T2 intensity was similar between paediatric patients and HC in all the structures analysed, except for the head of the left caudate nucleus ( p = 0.001). DGM T2 intensity of the head of the left caudate nucleus was similar between paediatric CIS and RRMS patients, but it was reduced in adolescent-onset paediatric patients versus HC ( p = 0.002). In all patients, DGM T2 intensity of the head of the left caudate nucleus was correlated with T2 lesion volume ( r = −0.39, p = 0.007). DGM T2 intensity in all the structures analysed with longitudinal assessment remained stable over the follow-up in the cohort of patients. Conclusions: The quantification of DGM T2 intensity in paediatric patients may provide surrogate markers of neurodegeneration. In paediatric MS, DGM is likely to be affected by iron-related changes, which are likely to be, at least partially, secondary to WM damage.

2007 ◽  
Vol 13 (7) ◽  
pp. 880-883 ◽  
Author(s):  
Y. Zhang ◽  
RK Zabad ◽  
X. Wei ◽  
LM Metz ◽  
MD Hill ◽  
...  

T2 hypointensity (black T2, BT2) in the deep grey matter of multiple sclerosis (MS) patients correlate weakly with disability at 1.5 T. BT2 is likely to be caused by abnormal iron deposition. We compared the correlation between disability and deep grey matter BT2 measured on 3 T MRI and on 1.5 T MRI in 17 MS patients. We observed a significant correlation between expanded disability status scale and signal intensity on 3 T MRI in the globus pallidus and the caudate nucleus ( r = —0.5, P < 0.05). BT2 at 3 T may be a useful MRI measure associated with disability in MS and warrants further study. Multiple Sclerosis 2007; 13: 880—883. http://msj.sagepub.com


2009 ◽  
Vol 16 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Antonia Ceccarelli ◽  
Maria A Rocca ◽  
Mohit Neema ◽  
Vittorio Martinelli ◽  
Ashish Arora ◽  
...  

Gray matter (GM) magnetic resonance imaging (MRI) T2 hypointensity, a putative marker of iron deposition, is a frequent finding in patients with clinically definite (CD) multiple sclerosis (MS). The objective of this study was to assess: (a) how early deep GM T2 hypointensity occurs in MS, by studying patients with clinically isolated syndromes (CIS) suggestive of MS, and (b) whether they contribute to predict subsequent evolution to CDMS. Dual-echo scans using two different acquisition protocols were acquired from 47 CIS patients and 13 healthy controls (HC). Normalized T2-intensity of the basal ganglia and thalamus was quantified. Patients were assessed clinically at the time of MRI acquisition and after three years. During the observation period, 18 patients (38%) evolved to CDMS. At the baseline, only the GM T2-intensity of the left caudate nucleus was significantly reduced in CIS patients in comparison with the HC (p = 0.04). At the baseline, the T2 intensity of the left caudate nucleus was significantly lower (p = 0.01) in CIS patients with disease dissemination in space (DIS), but not in those without DIS, compared to the HC. The baseline T2 lesion volume, but not GM T2 hypointensity, was associated with evolution to CDMS (hazard ratio = 1.60, 95% confidence interval (CI) = 1.05—2.42; p = 0.02). In CIS patients, deep GM is not spared, suggesting that iron-related changes and neurodegeneration occurs early. The magnitude of such damage is only minor and not associated with an increased risk of evolution to CDMS.


2021 ◽  
pp. 135245852110189
Author(s):  
Silvia Messina ◽  
Romina Mariano ◽  
Adriana Roca-Fernandez ◽  
Ana Cavey ◽  
Maciej Jurynczyk ◽  
...  

Background: Identifying magnetic resonance imaging (MRI) markers in myelin-oligodendrocytes-glycoprotein antibody-associated disease (MOGAD), neuromyelitis optica spectrum disorder-aquaporin-4 positive (NMOSD-AQP4) and multiple sclerosis (MS) is essential for establishing objective outcome measures. Objectives: To quantify imaging patterns of central nervous system (CNS) damage in MOGAD during the remission stage, and to compare it with NMOSD-AQP4 and MS. Methods: 20 MOGAD, 19 NMOSD-AQP4, 18 MS in remission with brain or spinal cord involvement and 18 healthy controls (HC) were recruited. Volumetrics, lesions and cortical lesions, diffusion-imaging measures, were analysed. Results: Deep grey matter volumes were lower in MOGAD ( p = 0.02) and MS ( p = 0.0001), compared to HC and were strongly correlated with current lesion volume (MOGAD R = −0.93, p < 0.001, MS R = −0.65, p = 0.0034). Cortical/juxtacortical lesions were seen in a minority of MOGAD, in a majority of MS and in none of NMOSD-AQP4. Non-lesional tissue fractional anisotropy (FA) was only reduced in MS ( p = 0.01), although focal reductions were noted in NMOSD-AQP4, reflecting mainly optic nerve and corticospinal tract pathways. Conclusion: MOGAD patients are left with grey matter damage, and this may be related to persistent white matter lesions. NMOSD-AQP4 patients showed a relative sparing of deep grey matter volumes, but reduced non-lesional tissue FA. Observations from our study can be used to identify new markers of damage for future multicentre studies.


2015 ◽  
Vol 234 (3) ◽  
pp. 352-361 ◽  
Author(s):  
Laëtitia Debernard ◽  
Tracy R. Melzer ◽  
Sridhar Alla ◽  
Jane Eagle ◽  
Saskia Van Stockum ◽  
...  

2017 ◽  
Vol 89 (2) ◽  
pp. 205-210 ◽  
Author(s):  
Kim A Meijer ◽  
Anand J C Eijlers ◽  
Jeroen J G Geurts ◽  
Menno M Schoonheim

ObjectiveFunctional connectivity is known to increase as well as decrease throughout the brain in multiple sclerosis (MS), which could represent different stages of the disease. In addition, functional connectivity changes could follow the atrophy pattern observed with disease progression, that is, moving from the deep grey matter towards the cortex. This study investigated when and where connectivity changes develop and explored their clinical and cognitive relevance across different MS stages.MethodsA cohort of 121 patients with early relapsing–remitting MS (RRMS), 122 with late RRMS and 53 with secondary progressive MS (SPMS) as well as 96 healthy controls underwent MRI and neuropsychological testing. Functional connectivity changes were investigated for (1) within deep grey matter connectivity, (2) connectivity between the deep grey matter and cortex and (3) within-cortex connectivity. A post hoc regional analysis was performed to identify which regions were driving the connectivity changes.ResultsPatients with late RRMS and SPMS showed increased connectivity of the deep grey matter, especially of the putamen and palladium, with other deep grey matter structures and with the cortex. Within-cortex connectivity was decreased, especially for temporal, occipital and frontal regions, but only in SPMS relative to early RRMS. Deep grey matter connectivity alterations were related to cognition and disability, whereas within-cortex connectivity was only related to disability.ConclusionIncreased connectivity of the deep grey matter became apparent in late RRMS and further increased in SPMS. The additive effect of cortical network degeneration, which was only seen in SPMS, may explain the sudden clinical deterioration characteristic to this phase of the disease.


2020 ◽  
Vol 267 (12) ◽  
pp. 3541-3554 ◽  
Author(s):  
Alexandra de Sitter ◽  
◽  
Tom Verhoeven ◽  
Jessica Burggraaff ◽  
Yaou Liu ◽  
...  

Abstract Background Deep grey matter (DGM) atrophy in multiple sclerosis (MS) and its relation to cognitive and clinical decline requires accurate measurements. MS pathology may deteriorate the performance of automated segmentation methods. Accuracy of DGM segmentation methods is compared between MS and controls, and the relation of performance with lesions and atrophy is studied. Methods On images of 21 MS subjects and 11 controls, three raters manually outlined caudate nucleus, putamen and thalamus; outlines were combined by majority voting. FSL-FIRST, FreeSurfer, Geodesic Information Flow and volBrain were evaluated. Performance was evaluated volumetrically (intra-class correlation coefficient (ICC)) and spatially (Dice similarity coefficient (DSC)). Spearman's correlations of DSC with global and local lesion volume, structure of interest volume (ROIV), and normalized brain volume (NBV) were assessed. Results ICC with manual volumes was mostly good and spatial agreement was high. MS exhibited significantly lower DSC than controls for thalamus and putamen. For some combinations of structure and method, DSC correlated negatively with lesion volume or positively with NBV or ROIV. Lesion-filling did not substantially change segmentations. Conclusions Automated methods have impaired performance in patients. Performance generally deteriorated with higher lesion volume and lower NBV and ROIV, suggesting that these may contribute to the impaired performance.


2020 ◽  
Author(s):  
Silvia Messina ◽  
Romina Mariano ◽  
Adriana Roca-Fernandez ◽  
Ana Cavey ◽  
Maciej Jurynczyk ◽  
...  

Neuromyelitis optica associated with aquaporin-4-antibodies (NMOSD-AQP4) and myelin oligodentrocyte-glycoprotein antibody-associated disorder (MOGAD) have been recently recognised as different from multiple sclerosis. Although conventional MRI may help distinguish multiple sclerosis from antibody-mediated diseases, the use of quantitative and non-conventional imaging may give more pathological information and explain the clinical differences. We compared, using non-conventional imaging, brain MRI findings in 75 subjects in remission with NMOSD-AQP4, MOGAD, multiple sclerosis or healthy controls (HC). Volumetrics, white matter and cortical lesions, and tissue integrity measures using diffusion imaging, were analysed in the four groups along with their association with disability (expanded disability status scale [EDSS] and visual acuity). The volumetric analysis showed that, deep grey matter volumes were significantly lower in multiple sclerosis (p=0.0001) and MOGAD (p=0.02), compared to HC. Relapsing MOGAD had lower white matter, pallidus and hippocampus volumes than in monophasic (p<0.05). Optic chiasm volume was reduced only in NMOSD-AQP4 who had at least one episode of optic neuritis (ON) (NMOSD-AQP4-ON vs NMOSD-AQP4 p<0.001, HC p<0.001, MOGAD-ON p=0.04, multiple sclerosis-ON p=0.02) likely reflecting the recognised posterior location of NMOSD-AQP4-ON and its severity. Lesion volume was greatest in multiple sclerosis followed by MOGAD and in these two diseases, the lesion volume correlated with disease duration (multiple sclerosis R=0.46, p=0.05, MOGAD R=0.81, p<0.001), cortical thickness (multiple sclerosis R=-0.64, p=0.0042, MOGAD=-0.71, p=0.005) and deep grey matter volumes (multiple sclerosis R=-0.65, p=0.0034, MOGAD R=-0.93, p<0.001). Lesional-fractional anisotropy (FA) was reduced and mean diffusivity increased in all patients, but overall, FA was only reduced in the non-lesional tissue in multiple sclerosis (p=0.01), although focal reductions were noted in NMOSD-AQP4, reflecting mainly optic nerve and corticospinal tract pathways. Cortical/juxtacortical lesions were seen in a minority of MOGAD, while cortical/juxtacortical and purely cortical lesions were identified in the majority of multiple sclerosis and in none of the NMOSD-AQP4. Non-lesional FA in NMOSD-AQP4, lower white-matter volume and female sex in multiple sclerosis, and lower brainstem volume in MOGAD were the best predictors of EDSS disability (accounting for 46%, 49% and 19% respectively). Worse visual acuity associated with lower optic chiasm volume in NMOSD-AQP4 and lower thalamus volume in MOGAD (accounting for 58% and 35% respectively). Although MOGAD patients had good outcomes, deep grey matter atrophy was present. In contrast, NMOSD-AQP4 patients showed a relative sparing of deep grey matter volumes, despite greater residual disability as compared with MOGAD patients. NMOSD-AQP4 but not MOGAD patients showed reduced FA in non-lesional tissue.


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