Evidence map›Paper›PMID 26920497›Full record

ArticleHuman brain mapping2016

Early silent microstructural degeneration and atrophy of the thalamocortical network in multiple sclerosis.

Michael Deppe, Julia Krämer, Jan-Gerd Tenberge, Jasmin Marinell, Wolfram Schwindt, Katja Deppe, Sergiu Groppa, Heinz Wiendl, Sven G Meuth

Open access · greenAbstract read
In one paragraph

Article in Human brain mapping, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
7.4field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 63 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Michael DeppeDepartment of Neurology, Westfälische Wilhelms University, Münster, Germany.
Julia KrämerDepartment of Neurology, Westfälische Wilhelms University, Münster, Germany.
Jan-Gerd TenbergeDepartment of Neurology, Westfälische Wilhelms University, Münster, Germany.
Jasmin MarinellDepartment of Neurology, Westfälische Wilhelms University, Münster, Germany.
Wolfram SchwindtDepartment of Clinical Radiology, Westfälische Wilhelms University, Münster, Germany.
Katja DeppeRadiologische Praxis Göb & Hovestadt, Coesfeld, Germany.
Sergiu GroppaDepartment of Neurology, University Medical Center, Johannes Gutenberg University, Mainz, Germany.
Heinz WiendlDepartment of Neurology, Westfälische Wilhelms University, Münster, Germany.
Sven G MeuthDepartment of Neurology, Westfälische Wilhelms University, Münster, Germany.
University of Münster · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies on patients with clinically isolated syndrome (CIS) and multiple sclerosis (MS) demonstrated thalamic atrophy. Here we addressed the following question: Is early thalamic atrophy in patients with CIS and relapsing-remitting MS (RRMS) mainly a direct consequence of white matter (WM) lesions-as frequently claimed-or is the atrophy stronger correlated to "silent" (nonlesional) microstructural thalamic alterations? One-hundred and ten patients with RRMS, 12 with CIS, and 30 healthy controls were admitted to 3 T magnetic resonance imaging. Fractional anisotropy (FA) was computed from diffusion tensor imaging (DTI) to assess thalamic and WM microstructure. The relative thalamic volume (RTV) and thalamic FA were significantly reduced in patients with CIS and RRMS relative to healthy controls. Both measures were also correlated. The age, gender, WM lesion load, thalamic FA, and gray matter volume-corrected RTV were reduced even in the absence of thalamic and extensive white matter lesions-also in patients with short disease duration (≤24 months). A voxel-based correlation analysis revealed that the RTV reduction had a significant effect on local WM FA-in areas next to the thalamus and basal ganglia. These WM alterations could not be explained by WM lesions, which had a differing spatial distribution. Early thalamic atrophy is mainly driven by silent microstructural thalamic alterations. Lesions do not disclose the early damage of thalamocortical circuits, which seem to be much more affected in CIS and RRMS than expected. Thalamocortical damage can be detected by DTI in normal appearing brain tissue. Hum Brain Mapp 37:1866-1879, 2016. © 2016 Wiley Periodicals, Inc.

Indexed as

Brain MappingAdolescentAdultAgedAnisotropyAtrophyDemyelinating DiseasesDiffusion Tensor ImagingFemaleHumansImaging, Three-DimensionalImmunologic FactorsInterferon-betaMaleMiddle AgedMultiple SclerosisImmunologic FactorsInterferon-betaatrophyclinically isolated syndromeDTIfractional anisotropyMRImultiple sclerosisneurodegenerationsilent disease activitythalamocortical networkthalamus

Identifiers

PMID26920497
PMCPMC6867391
OpenAlexW2282300175

What OpenQuestion holds

Textmetadata
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.