Multiple sclerosis and related disorders · 2025
Choroid plexus enlargement in secondary progressive MS: phenotype comparison.
СтатьяСравнительное исследованиеНазвание и аннотация: Перевод в очереди
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Klistorner Samuel, Barnett Michael H, Wang Chenyu, Van Der Walt Anneke, Butzkueven Helmut, Gong Zhaoyuan, Bouhrara Mustapha, Parratt John, Yiannikas Con, Klistorner Alexander
Аннотация
BACKGROUND: The choroid plexus (CP) is increasingly recognised as a contributor to chronic inflammation in multiple sclerosis (MS). While CP enlargement is reported in early MS, its role in secondary progressive MS (SPMS) is poorly understood. We aimed to quantify CP volume in SPMS and compare it to relapsing-remitting MS (RRMS) and clinically isolated syndrome (CIS), and to assess associations with disease severity and progression.
METHODS: CP volumes were manually segmented and normalised to intracranial volume in 121 MS patients (32 CIS, 49 RRMS, 39 SPMS). Age correction was applied using a healthy control cohort (n = 109). Cross-sectional and longitudinal analyses were performed to assess associations between baseline CP volume, ventricular size, lesion burden, and brain atrophy.
RESULTS: CP volume increased significantly across MS phenotypes: SPMS patients showed 32 % higher CP volume than CIS (p < 0.001) and 25 % higher than RRMS (p < 0.001). CP enlargement in SPMS was independent of ventricular size, indicating distinct underlying mechanisms. While lesion burden was the primary determinant of brain atrophy in SPMS, longitudinal data revealed significant associations of baseline CP volume with chronic lesion expansion (r²=0.33) and brain volume loss (r²=0.51).
CONCLUSION: CP enlargement is a progressive feature of MS, not driven by ventricular expansion. In SPMS, it may reflect ongoing inflammation contributing to tissue damage, supporting its role as a biomarker.
METHODS: CP volumes were manually segmented and normalised to intracranial volume in 121 MS patients (32 CIS, 49 RRMS, 39 SPMS). Age correction was applied using a healthy control cohort (n = 109). Cross-sectional and longitudinal analyses were performed to assess associations between baseline CP volume, ventricular size, lesion burden, and brain atrophy.
RESULTS: CP volume increased significantly across MS phenotypes: SPMS patients showed 32 % higher CP volume than CIS (p < 0.001) and 25 % higher than RRMS (p < 0.001). CP enlargement in SPMS was independent of ventricular size, indicating distinct underlying mechanisms. While lesion burden was the primary determinant of brain atrophy in SPMS, longitudinal data revealed significant associations of baseline CP volume with chronic lesion expansion (r²=0.33) and brain volume loss (r²=0.51).
CONCLUSION: CP enlargement is a progressive feature of MS, not driven by ventricular expansion. In SPMS, it may reflect ongoing inflammation contributing to tissue damage, supporting its role as a biomarker.