Evidence map›Paper›PMID 37463748›Full record

ArticleNeurology2023

Association of Circumscribed Subcortical Gray and White Matter Lesions With Apraxic Deficits in Patients With Left Hemisphere Stroke.

Claudia C Schmidt, Elisabeth I S Achilles, Katharina Bolte, Nina N Kleineberg, Monika K Richter, Natalie Schloss, Gereon R Fink, Peter H Weiss

Open access · greenAbstract read
In one paragraph

Article in Neurology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
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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

8 authors at 1 institution in 1 country.

Claudia C SchmidtFrom the Cognitive Neuroscience (C.C.S., E.I.S.A., N.N.K., M.K.R., G.R.F., P.H.W.), Institute of Neuroscience and Medicine (INM-3), Forschungszentrum Jülich, Germany; and Department of Neurology (E.I.S.A., K.B., N.N.K., M.K.R., N.S., G.R.F., P.H.W.), Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany. c.schmidt@fz-juelich.de.ORCID 0000-0002-1296-577X
Elisabeth I S AchillesFrom the Cognitive Neuroscience (C.C.S., E.I.S.A., N.N.K., M.K.R., G.R.F., P.H.W.), Institute of Neuroscience and Medicine (INM-3), Forschungszentrum Jülich, Germany; and Department of Neurology (E.I.S.A., K.B., N.N.K., M.K.R., N.S., G.R.F., P.H.W.), Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany.
Katharina BolteFrom the Cognitive Neuroscience (C.C.S., E.I.S.A., N.N.K., M.K.R., G.R.F., P.H.W.), Institute of Neuroscience and Medicine (INM-3), Forschungszentrum Jülich, Germany; and Department of Neurology (E.I.S.A., K.B., N.N.K., M.K.R., N.S., G.R.F., P.H.W.), Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany.
Nina N KleinebergFrom the Cognitive Neuroscience (C.C.S., E.I.S.A., N.N.K., M.K.R., G.R.F., P.H.W.), Institute of Neuroscience and Medicine (INM-3), Forschungszentrum Jülich, Germany; and Department of Neurology (E.I.S.A., K.B., N.N.K., M.K.R., N.S., G.R.F., P.H.W.), Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany.
Monika K RichterFrom the Cognitive Neuroscience (C.C.S., E.I.S.A., N.N.K., M.K.R., G.R.F., P.H.W.), Institute of Neuroscience and Medicine (INM-3), Forschungszentrum Jülich, Germany; and Department of Neurology (E.I.S.A., K.B., N.N.K., M.K.R., N.S., G.R.F., P.H.W.), Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany.
Natalie SchlossFrom the Cognitive Neuroscience (C.C.S., E.I.S.A., N.N.K., M.K.R., G.R.F., P.H.W.), Institute of Neuroscience and Medicine (INM-3), Forschungszentrum Jülich, Germany; and Department of Neurology (E.I.S.A., K.B., N.N.K., M.K.R., N.S., G.R.F., P.H.W.), Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany.
Gereon R FinkFrom the Cognitive Neuroscience (C.C.S., E.I.S.A., N.N.K., M.K.R., G.R.F., P.H.W.), Institute of Neuroscience and Medicine (INM-3), Forschungszentrum Jülich, Germany; and Department of Neurology (E.I.S.A., K.B., N.N.K., M.K.R., N.S., G.R.F., P.H.W.), Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany.ORCID 0000-0002-8230-1856
Peter H WeissFrom the Cognitive Neuroscience (C.C.S., E.I.S.A., N.N.K., M.K.R., G.R.F., P.H.W.), Institute of Neuroscience and Medicine (INM-3), Forschungszentrum Jülich, Germany; and Department of Neurology (E.I.S.A., K.B., N.N.K., M.K.R., N.S., G.R.F., P.H.W.), Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany.ORCID 0000-0002-5230-9080
University Hospital Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesApraxia is commonly attributed to left hemisphere (LH) lesions of the cortical fronto-temporo-parietal praxis networks or white matter lesions causing disconnections between cortical nodes. By contrast, the contribution of lesions to the subcortical gray matter, that is, basal ganglia or thalamus, to apraxic deficits remains controversial. Here, we investigate whether damage to these subcortical gray matter structures (i.e., caudate nucleus, putamen, globus pallidus, and thalamus) or the adjacent white matter tracts was associated with apraxic deficits.

methodsWe identified patients with distinct subcortical lesions with and without apraxia from a large retrospective sample of subacute LH ischemic stroke patients (n = 194). To test which subcortical structures (caudate nucleus, putamen, globus pallidus, thalamus, and adjacent white matter tracts), when lesioned, contributed to apraxic deficits, we statistically compared the proportion of lesioned voxels within subcortical gray and white matter structures between the apraxic and nonapraxic patients.

resultsOf the 194 stroke patients screened, 39 (median age = 65 years, range 30-82 years; median time poststroke at the apraxia assessment = 7 days, range 1-44 days) had lesions confined to subcortical regions (gray and white matter). Eleven patients showed apraxic deficits when imitating gestures or pantomiming object use. Region-wise statistical lesion comparison (controlled for lesion size) revealed a more significant proportion of damage ('lesion load') in the caudate nucleus in apraxic stroke patients (mean difference = 6.9%, 95% CI 0.4-13.3, DISCUSSION: These findings provide new insights into the subcortical anatomy of apraxia after LH stroke, suggesting a specific contribution of caudate nucleus lesions to apraxic deficits.

Indexed as

ApraxiasStrokeWhite MatterAdultAgedAged, 80 and overGray MatterHumansMagnetic Resonance ImagingMiddle AgedRetrospective Studies

Identifiers

PMID37463748
PMCPMC10513893
OpenAlexW4384664814

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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.