Quantitative Susceptibility Mapping of the Thalamus: Relationships with Thalamic Volume, Total Gray Matter Volume, and T2 Lesion Burden

Both thalamic iron deposition and atrophy have been reported in patients with multiple sclerosis compared with healthy controls, but how they are related is unclear. The purpose of this study was to understand the pathophysiologic basis for this iron deposition. Ninety-five patients with relapsing-r...

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Veröffentlicht in:American journal of neuroradiology : AJNR 2018-03, Vol.39 (3), p.467-472
Hauptverfasser: Chiang, G C, Hu, J, Morris, E, Wang, Y, Gauthier, S A
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Sprache:eng
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Zusammenfassung:Both thalamic iron deposition and atrophy have been reported in patients with multiple sclerosis compared with healthy controls, but how they are related is unclear. The purpose of this study was to understand the pathophysiologic basis for this iron deposition. Ninety-five patients with relapsing-remitting multiple sclerosis underwent 3T MR imaging with a standardized protocol that included quantitative susceptibility mapping to measure iron concentration and a 3D T1 echo-spoiled gradient-echo sequence to obtain thalamic volumes. Volumes of interest were manually delineated on the quantitative susceptibility map to encompass both thalami. Multivariate regression analyses were performed to identify the association between thalamic susceptibility and volume. Associations between thalamic susceptibility and total gray matter volume, cortical thickness, and T2 lesion volume were also assessed. The relative susceptibility of the thalamus was associated with T2 lesion volume ( = .015) and was higher in the presence of enhancing lesions ( = .013). The relative susceptibility of the thalami was not associated with thalamic volumes, total gray matter volumes, or cortical thickness ( > .05). Iron levels in the thalami are associated with T2 lesion burden and the presence of enhancing lesions, but not with thalamic or gray matter volumes, suggesting that iron accumulation is associated with white matter inflammation rather than gray matter neurodegeneration.
ISSN:0195-6108
1936-959X
DOI:10.3174/ajnr.A5537