Evidence map›Paper›PMID 24615937›Full record

ArticleAnnals of neurology2014

Brain injury in premature neonates: A primary cerebral dysmaturation disorder?

Stephen A Back, Steven P Miller

Open access · greenAbstract read
In one paragraph

Article in Annals of neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 190 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
190citing papers in PubMed, 1 pooled it
56.7field-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

190 citing papers in PubMed, 1 synthesis or guideline pooled it, 343 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Observational
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Commentary on: "Delayed necrostatin-1s infusion attenuates cystic white matter injury in preterm fetal sheep."Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

130 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

Stephen A BackDepartments of Pediatrics, Oregon Health and Science University, Portland; Departments of Neurology, Oregon Health and Science University, Portland.
Steven P Miller
Oregon Health & Science University · USUniversity of Toronto · CA

Funding

Ultrastructure and Single Particle Microscopy CoreP30NS061800 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI AICHER, SUE A · 2009 to 2020
$6.6M
Role of Extracellular Matrix in Hypoxic-Ischemic Perinatal White Matter InjuryR01NS054044 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2006 to 2021
$4.8M
Cellular Mechanisms of Fetal White Matter InjuryR01NS045737 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2003 to 2019
$3.7M
Cellular mechanisms of fetal white matter injuryR37NS045737 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2007 to 2013
$2.7M
AGING AND THE MUCOSAL IMMUNE RESPONSER01AG003189 · NIA · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI KAGNOFF, MARTIN FREDERICK · 1985 to 1985
–
CIHR MOP-79262NIA NIH HHS 1R01AG03189NINDS NIH HHS 1R01NS054044NINDS NIH HHS P30 NS061800NINDS NIH HHS P30NS061800NINDS NIH HHS R01 NS045737NINDS NIH HHS R01 NS054044NINDS NIH HHS R37 NS045737NINDS NIH HHS R37NS045737-06S1/06S2
6 · The paper itself

Abstract

With advances in neonatal care, preterm neonates are surviving with an evolving constellation of motor and cognitive disabilities that appear to be related to widespread cellular maturational disturbances that target cerebral gray and white matter. Whereas preterm infants were previously at high risk for destructive brain lesions that resulted in cystic white matter injury and secondary cortical and subcortical gray matter degeneration, contemporary cohorts of preterm survivors commonly display less severe injury that does not appear to involve pronounced glial or neuronal loss. Nevertheless, these milder forms of injury are also associated with reduced cerebral growth. Recent human and experimental studies support that impaired cerebral growth is related to disparate responses in gray and white matter. Myelination disturbances in cerebral white matter are related to aberrant regeneration and repair responses to acute death of premyelinating late oligodendrocyte progenitors (preOLs). In response to preOL death, early oligodendrocyte progenitors rapidly proliferate and differentiate, but the regenerated preOLs fail to normally mature to myelinating cells required for white matter growth. Although immature neurons appear to be more resistant to cell death from hypoxia-ischemia than glia, they display widespread disturbances in maturation of their dendritic arbors, which further contribute to impaired cerebral growth. These complex and disparate responses of neurons and preOLs thus result in large numbers of cells that fail to fully mature during a critical window in development of neural circuitry. These recently recognized forms of cerebral gray and white matter dysmaturation raise new diagnostic challenges and suggest new therapeutic directions centered on reversal of the processes that promote dysmaturation.

Indexed as

Infant, PrematureBrain InjuriesCognition DisordersDevelopmental DisabilitiesHumansInfant, NewbornNerve DegenerationNerve Fibers, Myelinated

Identifiers

PMID24615937
PMCPMC5989572
OpenAlexW1556848471

What OpenQuestion holds

Textmetadata
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.