Evidence map›Paper›PMID 35165979›Full record

ArticleJournal of neuroimaging : official journal of the American Society of Neuroimaging2022

Cortical and white matter lesion topology influences focal corpus callosum atrophy in multiple sclerosis.

Michael Platten, Russell Ouellette, Elena Herranz, Valeria Barletta, Constantina A Treaba, Caterina Mainero, Tobias Granberg

Open access · hybridAbstract read
In one paragraph

Article in Journal of neuroimaging : official journal of the American Society of Neuroimaging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 32% of its field
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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Cortical and white matter lesion topology influences focal corpus callosum atrophy in multiple sclerosis.Journal of neuroimaging : official journal of the American Society of Neuroimaging · 2022
    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

7 authors at 2 institutions in 2 countries.

Michael PlattenDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0001-6297-487X
Russell OuelletteDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0001-9217-1445
Elena HerranzDivision of Multiple Sclerosis Imaging Laboratory, Athinoula A. Martinos Center for Biomedical Imaging and Harvard Medical School, Boston, Massachusetts, USA.
Valeria BarlettaDivision of Multiple Sclerosis Imaging Laboratory, Athinoula A. Martinos Center for Biomedical Imaging and Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0003-0655-9406
Constantina A TreabaDivision of Multiple Sclerosis Imaging Laboratory, Athinoula A. Martinos Center for Biomedical Imaging and Harvard Medical School, Boston, Massachusetts, USA.
Caterina MaineroDivision of Multiple Sclerosis Imaging Laboratory, Athinoula A. Martinos Center for Biomedical Imaging and Harvard Medical School, Boston, Massachusetts, USA.
Tobias GranbergDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.ORCID 0000-0001-6700-1022
Harvard University · USKarolinska University Hospital · SE

Funding

Cortical mechanisms of disease progression in early multiple sclerosisR01NS078322 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MAINERO, CATERINA · 2013 to 2017
$1.9M
NIH HHS R01NS078322-01-A1NINDS NIH HHS R01 NS078322
6 · The paper itself

Abstract

background and purposeCorpus callosum (CC) atrophy is a strong predictor of multiple sclerosis (MS) disability but the contributing pathological mechanisms remain uncertain. We aimed to apply advanced MRI to explore what drives the often nonuniform callosal atrophy.

methodsProspective brain 7 Tesla and 3 Tesla Human Connectom Scanner MRI were performed in 92 MS patients. White matter, leukocortical, and intracortical lesions were manually segmented. FreeSurfer was used to segment the CC and topographically classify lesions per lobe or as deep white matter lesions. Regression models were calculated to predict focal CC atrophy.

resultsThe frontal and parietal lobes contained the majority (≥80%) of all lesion classifications in both relapsing-remitting and secondary progressive MS subtypes. The anterior subsection of the CC had the smallest proportional volume difference between subtypes (11%). Deep, temporal, and occipital white matter lesions, and occipital intracortical lesions were the strongest predictors of middle-posterior callosal atrophy (adjusted R

conclusionsBoth white matter and cortical lesions contribute to regional corpus callosal atrophy. The lobe-specific lesion topology does not fully explain the inhomogeneous CC atrophy.

Indexed as

LeukoencephalopathiesMultiple SclerosisMultiple Sclerosis, Relapsing-RemittingWhite MatterAtrophyCorpus CallosumHumansMagnetic Resonance ImagingProspective Studiesatrophycorpus callosummagnetic resonance imagingmultiple sclerosis

Identifiers

PMID35165979
PMCPMC9305945
OpenAlexW4212974504

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.