Evidence map›Paper›PMID 40552528›Full record

ArticleAnnals of neurology2025

High-Dose Pulse Glucocorticoid Treatment Prevents White Matter Spinal Cord Pseudoatrophy in Newly Diagnosed Multiple Sclerosis.

Simone Sacco, Nico Papinutto, Vinicius A Schoeps, Shuiting Cheng, William A Stern, Haojun Zhao, Antje Bischof, Eduardo Caverzasi, Manula Dombagahawatta, Jeremy Juwono and 17 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Annals of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Data-Driven Fatigue Trajectories in Multiple Sclerosis and Their Predictors.Neurology(R) neuroimmunology & neuroinflammation · 2026
    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

27 authors.

Simone SaccoWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.ORCID 0000-0001-8789-3099
Nico PapinuttoWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Vinicius A SchoepsWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.ORCID 0000-0001-8875-0567
Shuiting ChengWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
William A SternWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Haojun ZhaoWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Antje BischofDepartment of Neurology, University Hospital of Muenster, Muenster, Germany.ORCID 0000-0003-3862-5738
Eduardo CaverzasiDepartment of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy.
Manula DombagahawattaWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Jeremy JuwonoWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Amit AkulaWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Christian CordanoWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.ORCID 0000-0002-1413-0442
Alexandra Beaudry-RichardDepartment of Microbiology and Immunology, University of Ottawa, Ottawa, Canada.ORCID 0000-0002-5974-8916
Refujia GomezWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Meagan HarmsWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Adam SantanielloWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Riley M BoveWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Jeffrey M GelfandWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Douglas S GoodinWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Ari J GreenWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Jorge R OksenbergWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.
Emmanuelle WaubantWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.ORCID 0000-0001-5188-0157
Michael R WilsonWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.ORCID 0000-0002-8705-5084
Scott S ZamvilWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.ORCID 0000-0003-2720-9915
Bruce A C CreeWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.ORCID 0000-0001-7689-2533
Stephen L HauserWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.ORCID 0000-0002-4932-4001
Roland G HenryWeill Institute for Neurosciences, Department of Neurology, University of California, San Francisco, CA, USA.ORCID 0000-0002-8232-7562

Funding

The Four Repeat Tauopathy Neuroimaging InitiativeR01AG038791 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BOXER, ADAM L. · 2010 to 2020
$18.1M
The Role of B cells in the Origin and Progression of Multiple SclerosisR35NS111644 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI STEPHEN L HAUSER · 2019 to 2026
$9.1M
Tracking longitudinal change in presymptomatic genetic prion disease (TLC-Pre-gPrD)R01AG062562 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GESCHWIND, MICHAEL D · 2019 to 2023
$5.4M
Characterization of T cells in MOG antibody-associated diseaseR01AI170863 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SCOTT S ZAMVIL · 2023 to 2026
$3.2M
Establishing VEP as a quantitative biomarker for remyelination using transgenic models for gain and loss of functionR01NS105741 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GREEN, ARI J · 2018 to 2022
$1.8M
Advanced Research Projects Agency - Energy ARPA-H D24AC00084-00Fondazione Italiana Sclerosi Multipla 2019/BC/002National Multiple Sclerosis Society RG-1707-28564NIAID NIH HHS R01 AI170863NIA NIH HHS R01 AG038791NIA NIH HHS R01 AG062562NIH HHS RO1AI170863NINDS NIH HHS R01AG038791NINDS NIH HHS R01AG062562NINDS NIH HHS R01 NS105741NINDS NIH HHS R01NS105741NINDS NIH HHS R35 NS111644NINDS NIH HHS R35NS111644Race to Erase MS foundationUCSF CTSIValhalla Foundation
6 · The paper itself

Abstract

objectiveSpinal cord (SC) atrophy correlates with and predicts the underlying progressive biology in active and non-active multiple sclerosis (MS), thereby providing a biomarker for clinical trials and patient management. Initiation of disease-modifying therapy (DMT) may be followed by early pronounced central nervous system (CNS) volume loss due to resolution of inflammation (pseudoatrophy) and confounding the interpretation of atrophy. High-dose glucocorticoids (HDGs) reduce inflammation and might therefore modify pseudoatrophy.

methodsOne hundred twenty-three newly diagnosed and DMT-naïve MS participants (relapsing-remitting, 70% female participants, median age = 36 years, Expanded Disability Status Scale [EDSS] 2.0) were followed for up to 3 years. Forty-two participants received HDG before baseline magnetic resonance imaging (MRI; DMT-HDG; median = 52 days, interquartile range [IQR] = 37-71), whereas 60 did not (DMT/no-HDG). Twenty-one participants remained untreated (no-DMT), and 102 started DMT after baseline MRI. SC total cervical cord cross-sectional area (TCA), gray matter area (GMA), and white matter area (WMA) and regional brain volumes were analyzed using mixed effects models.

resultsThe DMT-HDG, DMT/no-HDG, and no-DMT groups had similar demographic, clinical, and radiological features. Pronounced SC pseudoatrophy was observed based on more year 1 versus year 2 volume loss for DMT/no-HDG (-2.06% vs. 0.83%; P = 0.02) but not DMT-HDG (-0.51% vs. 0.66%; P = 0.8) and more year 1 volume loss for DMT/no-HDG compared to DMT-HDG (-2.06% vs. 0.51%; P = 0.02).

interpretationHDG preceding baseline MRI suppresses CNS white matter (WM) pseudoatrophy after DMT initiation, most conspicuously for the SC. Suppression of pseudoatrophy with HDG may improve the fidelity of clinical trials and enhance the feasibility for short-term trials with SC and brain MRI outcomes in active MS by pretreatment with HDG. ANN NEUROL 2025;98:837-850.

Indexed as

GlucocorticoidsMultiple SclerosisMultiple Sclerosis, Relapsing-RemittingSpinal CordWhite MatterAdultAtrophyFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedGlucocorticoids

Identifiers

PMID40552528
PMCPMC12542327

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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.