Evidence map›Paper›PMID 39869436›Full record

ArticleAnnals of clinical and translational neurology2025

An MRI assessment of mechanisms underlying lesion growth and shrinkage in multiple sclerosis.

Ermelinda De Meo, Ferran Prados Carrasco, J William L Brown, Alasdair J Coles, Nick G Cunniffe, Amy E Jolly, Baris Kanber, Rebecca Samson, Frederik Barkhof, Declan Chard

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of clinical and translational neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

10 authors.

Ermelinda De MeoNMR Research Unit, Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.ORCID 0000-0001-5531-1111
Ferran Prados CarrascoNMR Research Unit, Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
J William L BrownDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Alasdair J ColesDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.ORCID 0000-0003-4738-0760
Nick G CunniffeDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Amy E JollyNMR Research Unit, Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Baris KanberNMR Research Unit, Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.ORCID 0000-0003-2443-8800
Rebecca SamsonNMR Research Unit, Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Frederik BarkhofNMR Research Unit, Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Declan ChardNMR Research Unit, Queen Square Multiple Sclerosis Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.

Funding

Cambridge UniversityGrand Charity of the FreemasonsMS Society of the United KingdomNIHR Cambridge Biomedical Research Centre BRC-1215-20014NIHR UCLH Biomedical Research CentreThorne Family Foundation
6 · The paper itself

Abstract

objectiveTo assess the pathological mechanisms contributing to white matter (WM) lesion expansion or contraction and remyelination in multiple sclerosis (MS).

methodsWe assessed 1,613 lesions in 49 people with relapsing-remitting MS in the CCMR-One bexarotene trial (EudraCT 2014-003145-99). We measured lesion orientation relative to WM tracts, surface-in gradients and veins. Jacobian deformation was used to assess lesion expansion over 6 months, while magnetization transfer ratio (MTR) imaging was used to assess remyelination.

resultsAt baseline, 33% of lesions were aligned with veins, 2% along WM tracts, 0% with surface-in gradients, and 4% orthogonal to veins. No significant differences were observed in lesion shape, while lesions aligned with surface-in gradients and with veins had lower volume compared to all remaining orientations. At follow-up, 13% of lesions expanded and 7% contracted. The directions for both expansion and contraction were 18% and 8%, respectively, along WM tracts, 20% and 15% parallel to veins, 22% and 23% orthogonal to veins and 0% and 1% along surface-in gradients. Bexarotene had no effect on lesion expansion or contraction, but MTR significantly increased in lesions aligned with surface-in gradients and veins.

interpretationLesion expansion and shrinkage are affected by venous and WM tract factors, but these do not influence bexarotene's capacity to promote remyelination. This, instead, appears to be affected by surface-in factors. To limit lesion expansion and maximize tissue repair, multiple processes may need to be targeted.

Indexed as

Magnetic Resonance ImagingMultiple Sclerosis, Relapsing-RemittingRemyelinationWhite MatterAdultBexaroteneClinical Trials, Phase II as TopicFemaleHumansMaleMiddle AgedRandomized Controlled Trials as TopicSecondary Data AnalysisBexarotene

Identifiers

PMID39869436
PMCPMC12040513

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.