Evidence map›Paper›PMID 32286701›Full record

ArticleAnnals of neurology2020

Intrinsic and Extrinsic Mechanisms of Thalamic Pathology in Multiple Sclerosis.

Kedar R Mahajan, Kunio Nakamura, Jeffrey A Cohen, Bruce D Trapp, Daniel Ontaneda

Open access · greenAbstract read
In one paragraph

Article in Annals of neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.5field-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

41 citing papers in PubMed, 66 citations in OpenAlex.

  1. Trial
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  5. Disruption of ClC-3-mediated 2ClScientific reports · 2025
    Article
  6. Article
  7. Article
  8. Claustrum Volume Is Reduced in Multiple Sclerosis and Predicts Disability.Annals of clinical and translational neurology · 2025
    Article
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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

5 authors at 1 institution in 1 country.

Kedar R MahajanMellen Center for MS Treatment and Research, Neurologic Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.ORCID 0000-0002-0339-9876
Kunio NakamuraDepartment of Biomedical Engineering, Lerner Research Institute, Neurologic Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
Jeffrey A CohenMellen Center for MS Treatment and Research, Neurologic Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
Bruce D TrappDepartment of Neuroscience, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
Daniel OntanedaMellen Center for MS Treatment and Research, Neurologic Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
Cleveland Clinic · US

Funding

Pathogenesis of Neurological Disability in Primary Diseases of MyelinR35NS097303 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI TRAPP, BRUCE D · 2017 to 2024
$6.9M
Thalamic MRI, histopathologic, and clinical correlations in multiple sclerosisK23NS109328 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI MAHAJAN, KEDAR · 2018 to 2022
$919k
NINDS NIH HHS K23 NS109328NINDS NIH HHS R35 NS097303
6 · The paper itself

Abstract

objectiveThalamic atrophy is among the earliest brain changes detected in patients with multiple sclerosis (MS) and the degree of thalamic atrophy is a strong predictor of disability progression. The causes of thalamic atrophy are not fully understood. Here, we investigate the contributions of thalamic demyelinated lesions, thalamic neuronal loss, and cerebral white matter (WM) lesions to thalamic volume.

methodsWe used postmortem in situ magnetic resonance imaging (MRI) scans of 95 subjects with MS to correlate thalamic lesion volumes with global MRI metrics. We histologically characterized thalamic demyelination patterns and compared neuronal loss and neuritic pathology in the thalami with the extremes of volume.

resultsGrossly apparent thalamic discolorations in cm-thick brain slices were T2/fluid-attenuated inversion recovery (FLAIR) hyperintense, T1-hypointense, and appeared as perivascular demyelinated lesions with dystrophic neurons/axons. Subependymal demyelinated lesions with axonal loss and microglial/macrophage activation were also observed. The 12 subjects with the least thalamic volume had a 17.6% reduction of median neuronal density in the dorsomedial/ventrolateral and pulvinar nuclei compared with the 14 subjects with the greatest thalamic volume (p = 0.03). After correcting for age, disease duration, sex, and T2 lesion volume, the total (p = 0.20), ovoid (p = 0.31), or subependymal (p = 0.44) MRI thalamic lesion volumes correlated with thalamic volume. Thalamic volume correlated with cerebral T2 lesion volume (Spearman's rho = -0.65, p < 0.001; p < 0.0001 after correcting for age, disease duration, and sex).

interpretationOur findings suggest the degeneration of efferent/afferent thalamic projections and/or a neurodegenerative process as greater contributors to thalamic atrophy than thalamic demyelinating lesions. ANN NEUROL 2020 ANN NEUROL 2020;88:81-92.

Indexed as

AgedAtrophyDisease ProgressionFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedMultiple SclerosisNeuronsPulvinarThalamusWhite Matter

Identifiers

PMID32286701
PMCPMC8291218
OpenAlexW3015988373

What OpenQuestion holds

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LicenceTDM
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.