Evidence map›Paper›PMID 24781079›Full record

Trial reportStroke2014

White matter hyperintensities and their penumbra lie along a continuum of injury in the aging brain.

Pauline Maillard, Evan Fletcher, Samuel N Lockhart, Alexandra E Roach, Bruce Reed, Dan Mungas, Charles DeCarli, Owen T Carmichael

Open access · bronzeAbstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Stroke, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
11.5field-weighted citation impact, top 1% 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

117 citing papers in PubMed, 187 citations in OpenAlex.

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  14. Reduced myelin contributes to cognitive impairment in patients with monogenic small vessel disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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57 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Pauline MaillardFrom the Imaging of Dementia and Aging Laboratory (P.M., E.F., S.N.L., A.E.R., B.R., D.M., C.D., O.T.C.), Department of Neurology (P.M., E.F., B.R., D.M., C.D., O.T.C.), and Center for Neuroscience (S.N.L., A.E.R., C.D.), University of California, Davis.
Evan FletcherFrom the Imaging of Dementia and Aging Laboratory (P.M., E.F., S.N.L., A.E.R., B.R., D.M., C.D., O.T.C.), Department of Neurology (P.M., E.F., B.R., D.M., C.D., O.T.C.), and Center for Neuroscience (S.N.L., A.E.R., C.D.), University of California, Davis.
Samuel N LockhartFrom the Imaging of Dementia and Aging Laboratory (P.M., E.F., S.N.L., A.E.R., B.R., D.M., C.D., O.T.C.), Department of Neurology (P.M., E.F., B.R., D.M., C.D., O.T.C.), and Center for Neuroscience (S.N.L., A.E.R., C.D.), University of California, Davis.
Alexandra E RoachFrom the Imaging of Dementia and Aging Laboratory (P.M., E.F., S.N.L., A.E.R., B.R., D.M., C.D., O.T.C.), Department of Neurology (P.M., E.F., B.R., D.M., C.D., O.T.C.), and Center for Neuroscience (S.N.L., A.E.R., C.D.), University of California, Davis.
Bruce ReedFrom the Imaging of Dementia and Aging Laboratory (P.M., E.F., S.N.L., A.E.R., B.R., D.M., C.D., O.T.C.), Department of Neurology (P.M., E.F., B.R., D.M., C.D., O.T.C.), and Center for Neuroscience (S.N.L., A.E.R., C.D.), University of California, Davis.
Dan MungasFrom the Imaging of Dementia and Aging Laboratory (P.M., E.F., S.N.L., A.E.R., B.R., D.M., C.D., O.T.C.), Department of Neurology (P.M., E.F., B.R., D.M., C.D., O.T.C.), and Center for Neuroscience (S.N.L., A.E.R., C.D.), University of California, Davis.
Charles DeCarliFrom the Imaging of Dementia and Aging Laboratory (P.M., E.F., S.N.L., A.E.R., B.R., D.M., C.D., O.T.C.), Department of Neurology (P.M., E.F., B.R., D.M., C.D., O.T.C.), and Center for Neuroscience (S.N.L., A.E.R., C.D.), University of California, Davis.
Owen T CarmichaelFrom the Imaging of Dementia and Aging Laboratory (P.M., E.F., S.N.L., A.E.R., B.R., D.M., C.D., O.T.C.), Department of Neurology (P.M., E.F., B.R., D.M., C.D., O.T.C.), and Center for Neuroscience (S.N.L., A.E.R., C.D.), University of California, Davis. ocarmichael@ucdavis.edu.
Neurology, Inc · US

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
PRECURSORS OF STROKE INCIDENCE AND PROGNOSISR01NS017950 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Hugo Javier Aparicio, Jose Rafael Romero · 1985 to 2026
$22.9M
Brain pathologies, reserve and cognition in aging and dementiaR01AG031563 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Evan Fletcher, SARAH E TOMASZEWSKI-FARIAS · 2009 to 2026
$8.9M
Heterogeneity of Mild Cognitive Impairment(MCI)R01AG021028 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 2003 to 2014
$4.6M
ENGLISH AND SPANISH ASSESSMENT OF COGNITION IN ELDERLYR01AG010220 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI MUNGAS, DAN M. · 1992 to 2012
$4.5M
NRF2 Anti-Oxidant Systems and White Matter HyperintensitiesR01AG042292 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI DECARLI, CHARLES, SHARP, FRANK R · 2013 to 2017
$3.0M
"MR Morphometrics and Cognitive Decline Rate in Large-Scale Aging Studies"K01AG030514 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARMICHAEL, OWEN T. · 2008 to 2012
$495k
NIA NIH HHS K01 AG030514NIA NIH HHS K01AG030514NIA NIH HHS P30 AG010129NIA NIH HHS P30AG010129NIA NIH HHS R01 AG010220NIA NIH HHS R01AG010220NIA NIH HHS R01 AG021028NIA NIH HHS R01AG021028NIA NIH HHS R01 AG031563NIA NIH HHS R01AG031563NIA NIH HHS R01 AG042292NINDS NIH HHS R01 NS017950
6 · The paper itself

Abstract

background and purposeAging is accompanied by clinically silent cerebral white matter injury identified through white matter hyperintensities (WMHs) on fluid-attenuated inversion recovery (FLAIR)- and diffusion tensor imaging-based measures of white matter integrity. The temporal course of FLAIR and diffusion tensor imaging changes within WMHs and their less-injured periphery (ie, their penumbra), however, has not been fully studied. We used longitudinal diffusion tensor imaging and FLAIR to explore these changes.

methodsOne hundred fifteen participants, aged 73.7±6.7 years, received clinical evaluations and MRIs on 2 dates. WMHs and fractional anisotropy (FA) maps were produced from FLAIR and diffusion tensor imaging and coregistered to a standardized space. Each distinct WMH was categorized as growing, stagnant, or noncontiguous incident. The penumbra of each WMH was similarly categorized as corresponding to a stagnant, growing, or noncontiguous incident WMH. Linear mixed-effect models were used to assess whether FA and FLAIR measurements changed between baseline and follow-up and differed between tissue categories.

resultsBaseline FA differed significantly by tissue category, with the following ordering of categories from highest to lowest FA: penumbra of noncontiguous incident, then stagnant, then growing WMHs; noncontiguous incident, then stagnant, then growing WMHs. Despite differences in baseline values, all tissue categories experienced declines in FA over time. Only noncontiguous incident WMHs showed significant FLAIR signal increases over time, and FLAIR signal significantly decreased in stagnant WMHs.

conclusionsWMHs and their penumbra vary in severity and together span a continuous spectrum of white matter injury that worsens with time. FLAIR fails to capture this continuous injury process fully but does identify a subclass of lesions that seem to improve over time.

Indexed as

Diffusion Tensor ImagingAgedAged, 80 and overAgingCerebral CortexFemaleFollow-Up StudiesHumansMaleRadiographyTime Factorsagingdiffusion tensor imagingmagnetic resonance imagingneuroimaging

Identifiers

PMID24781079
PMCPMC4102626
OpenAlexW2132874104

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Registered trials

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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.