Evidence map›Paper›PMID 42384032›Full record

ArticleMultiple sclerosis (Houndmills, Basingstoke, England)2026

Impact of multiple sclerosis disease-modifying therapies on chronic lesion tissue expansion.

Daniel Guilfoyle, Kayla Ward, Samuel Klistorner, Nathaniel Lizak, Heidi N Beadnall, Robert Zivadinov, Bianca Weinstock-Guttman, Izanne Roos, Helmut Butzkueven, Anneke van der Walt and 11 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Multiple sclerosis (Houndmills, Basingstoke, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

21 authors.

Daniel GuilfoyleBrain and Mind Centre, The University of Sydney, Sydney, NSW, Australia; Royal Prince Alfred Hospital, Sydney, NSW, Australia.ORCID 0009-0004-0028-651X
Kayla WardBrain and Mind Centre, The University of Sydney, Sydney, NSW, Australia; Royal Prince Alfred Hospital, Sydney, NSW, Australia.
Samuel KlistornerBrain and Mind Centre, The University of Sydney, Sydney, NSW, Australia; Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, Australia.ORCID 0000-0001-5761-5178
Nathaniel LizakDepartment of Neurology, Neuroimmunology Centre, The Royal Melbourne Hospital, Melbourne, VIC, Australia; Department of Medicine, CORe, The University of Melbourne, Melbourne, VIC, Australia.ORCID 0009-0009-3213-8390
Heidi N BeadnallBrain and Mind Centre, The University of Sydney, Sydney, NSW, Australia; Royal Prince Alfred Hospital, Sydney, NSW, Australia.
Robert ZivadinovDepartment of Neurology, Buffalo Neuroimaging Analysis Centre, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, USA.ORCID 0000-0002-7799-1485
Bianca Weinstock-GuttmanJacobs MS Center for Treatment and Research, Buffalo, NY, USA.ORCID 0000-0001-6732-151X
Izanne RoosDepartment of Neurology, Neuroimmunology Centre, The Royal Melbourne Hospital, Melbourne, VIC, Australia; Department of Medicine, CORe, The University of Melbourne, Melbourne, VIC, Australia.
Helmut ButzkuevenDepartment of Neurology, The Alfred Hospital, Melbourne, VIC, Australia; Department of Neuroscience, School of Translational Medicine, Monash University, Melbourne, VIC, Australia.ORCID 0000-0003-3940-8727
Anneke van der WaltDepartment of Neurology, The Alfred Hospital, Melbourne, VIC, Australia; Department of Neuroscience, School of Translational Medicine, Monash University, Melbourne, VIC, Australia.ORCID 0000-0002-4278-7003
Katherine BuzzardDepartment of Neurosciences, Box Hill Hospital, Box Hill, VIC, Australia; Eastern Health Clinical School, Monash University, Box Hill, VIC, Australia.
Olga SkibinaDepartment of Neurosciences, Box Hill Hospital, Box Hill, VIC, Australia; Eastern Health Clinical School, Monash University, Box Hill, VIC, Australia.
Mike G DwyerDepartment of Neurology, Buffalo Neuroimaging Analysis Centre, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, NY, USA.
Yael BarnettDepartment of Radiology, St Vincent's Hospital, Sydney, NSW, Australia; Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia.
Elaine LuiDepartment of Medical Imaging, The Royal Melbourne Hospital, Melbourne, VIC, Australia; Department of Radiology, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Melbourne, VIC, Australia.
Meng LawDepartment of Neuroscience, School of Translational Medicine, Monash University, Melbourne, VIC, Australia; Department of Radiology, The Alfred Hospital, Melbourne, VIC, Australia.
Andy ShiehSydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia.
Alexander KlistornerSave Sight Institute, The University of Sydney, Sydney, NSW, Australia.
Chenyu WangBrain and Mind Centre, The University of Sydney, Sydney, NSW, Australia; Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia.ORCID 0000-0001-7135-7662
Tomas KalincikDepartment of Neurology, Neuroimmunology Centre, The Royal Melbourne Hospital, Melbourne, VIC, Australia; Department of Medicine, CORe, The University of Melbourne, Melbourne, VIC, Australia.ORCID 0000-0003-3778-1376
Michael BarnettBrain and Mind Centre, The University of Sydney, Sydney, NSW, Australia; Royal Prince Alfred Hospital, Sydney, NSW, Australia; Sydney Neuroimaging Analysis Centre, Camperdown, NSW, Australia.ORCID 0000-0002-2156-8864

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic lesion tissue expansion (CLTE) reflects slow, concentric growth of established multiple sclerosis (MS) lesions and is linked to central brain atrophy and disability progression. Whether existing MS disease-modifying therapies (DMTs) differentially influence this aspect of progressive MS biology remains unclear.

objectivesTo compare the effect of current DMTs on CLTE in a multicentre, real-world MS cohort.

methodsWe conducted a retrospective, observational study using linked clinical data from MSBase and the MSBase Imaging Repository. Data from patients aged ⩾18 years with ⩾3 longitudinal MRI scans, and 7 therapies with ⩾100 stable treatment epochs were included. Therapy effects on CLTE, new T2 lesions, and brain atrophy were assessed using epoch-based covariate-adjusted generalised estimating equation models, with fingolimod as a comparator.

resultThe cohort included 564 patients contributing 1648 stable treatment epochs. After adjustment for demographic, clinical, and imaging covariates, B-cell depleting therapy was the only DMT associated with significantly lower CLTE (β = -4.03,

conclusionsB-cell depletion is associated with reduced CLTE, a promising biomarker of progressive MS biology.

Indexed as

Disease-modifying therapieslesion expansionmultiple sclerosisprogressivequantitative MRI

Identifiers

PMID42384032
PMCPMC13646398

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.