Journal of neuroimaging : official journal of the American Society of Neuroimaging · 2026
Quantitative Choroid Plexus Gadolinium Enhancement Is Related to Diffuse Brain Tissue Injury in Multiple Sclerosis.
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Senthil Sneha, Tagge Ian, Fetco Dumitru, Hsieh Cheng Hsun, Assemlal Haz-Edine, Karimaghaloo Zahra, Fetco Emily, Moore G R Wayne, Arnold Douglas L, Rudko David A, Narayanan Sridar
Аннотация
BACKGROUND: Recent studies suggest that disruptions of the blood-cerebrospinal fluid (CSF) barrier within the choroid plexus (ChP) may contribute to multiple sclerosis (MS) pathogenesis. We investigated the relationship between a quantitative marker of ChP enhancement and markers of focal and diffuse brain tissue injury in MS.
METHODS: A group of 34 MS participants and 21 healthy participants underwent 7T MRI including magnetization prepared 2 rapid acquisition gradient echoes (MP2RAGE) and fluid attenuated inversion recovery (FLAIR) acquisitions. The MS group received contrast, and delta T1 (ΔT1) maps were computed to assess enhancement. ChP, white matter lesions (WML), normal-appearing white matter (NAWM), and gray matter (GM) were segmented. Pre-contrast quantitative T1 (qT1) values were compared between groups, and linear regression with mean ChP ΔT1 was performed for WML volume and pre-gadolinium (Gd) mean qT1 of WML, NAWM, and GM.
RESULTS: Mean qT1 of ChP, NAWM, and GM, as well as ChP volume, were higher in MS compared to controls (p < 0.001). ChP ΔT1 was significantly associated with pre-Gd qT1 of NAWM (β = 0.20, R2 = 0.54, p < 0.001) and GM (β = 0.18, R2 = 0.49, p < 0.001), but not WML volume (p = 0.3) or WML qT1 (p = 0.05).
CONCLUSIONS: The association between ChP enhancement and diffuse tissue injury, together with elevated qT1 values and ChP volumes in MS, supports a mechanism of brain injury involving CSF-mediated toxicity distinct from classic lesion pathology in MS.
METHODS: A group of 34 MS participants and 21 healthy participants underwent 7T MRI including magnetization prepared 2 rapid acquisition gradient echoes (MP2RAGE) and fluid attenuated inversion recovery (FLAIR) acquisitions. The MS group received contrast, and delta T1 (ΔT1) maps were computed to assess enhancement. ChP, white matter lesions (WML), normal-appearing white matter (NAWM), and gray matter (GM) were segmented. Pre-contrast quantitative T1 (qT1) values were compared between groups, and linear regression with mean ChP ΔT1 was performed for WML volume and pre-gadolinium (Gd) mean qT1 of WML, NAWM, and GM.
RESULTS: Mean qT1 of ChP, NAWM, and GM, as well as ChP volume, were higher in MS compared to controls (p < 0.001). ChP ΔT1 was significantly associated with pre-Gd qT1 of NAWM (β = 0.20, R2 = 0.54, p < 0.001) and GM (β = 0.18, R2 = 0.49, p < 0.001), but not WML volume (p = 0.3) or WML qT1 (p = 0.05).
CONCLUSIONS: The association between ChP enhancement and diffuse tissue injury, together with elevated qT1 values and ChP volumes in MS, supports a mechanism of brain injury involving CSF-mediated toxicity distinct from classic lesion pathology in MS.