Evidence map›Paper›PMID 29194585›Full record

ReviewDevelopmental medicine and child neurology2018

Complex interactions between hypoxia-ischemia and inflammation in preterm brain injury.

Robert Galinsky, Christopher A Lear, Justin M Dean, Guido Wassink, Simerdeep K Dhillon, Mhoyra Fraser, Joanne O Davidson, Laura Bennet, Alistair J Gunn

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Developmental medicine and child neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 2 pooled it
15.8field-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

78 citing papers in PubMed, 2 syntheses or guidelines pooled it, 129 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Perinatal Neuroprotection in Preterm Birth.Geburtshilfe und Frauenheilkunde · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Intra-amniotic infection withBrain communications · 2025
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Observational
  20. Dysmaturation of sleep state and electroencephalographic activity after hypoxia-ischaemia in preterm fetal sheep.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 2 countries.

Robert GalinskyThe Department of Physiology, University of Auckland, Auckland, New Zealand.
Christopher A LearThe Department of Physiology, University of Auckland, Auckland, New Zealand.
Justin M DeanThe Department of Physiology, University of Auckland, Auckland, New Zealand.
Guido WassinkThe Department of Physiology, University of Auckland, Auckland, New Zealand.
Simerdeep K DhillonThe Department of Physiology, University of Auckland, Auckland, New Zealand.
Mhoyra FraserThe Department of Physiology, University of Auckland, Auckland, New Zealand.
Joanne O DavidsonThe Department of Physiology, University of Auckland, Auckland, New Zealand.
Laura BennetThe Department of Physiology, University of Auckland, Auckland, New Zealand.
Alistair J GunnThe Department of Physiology, University of Auckland, Auckland, New Zealand.ORCID 0000-0003-0656-7035
University of Auckland · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Children surviving preterm birth have a high risk of disability, particularly cognitive and learning problems. There is extensive clinical and experimental evidence that disability is now primarily related to dysmaturation of white and gray matter, defined by failure of oligodendrocyte maturation and neuronal dendritic arborization, rather than cell death alone. The etiology of this dysmaturation is multifactorial, with contributions from hypoxia-ischemia, infection/inflammation and barotrauma. Intriguingly, these factors can interact to both increase and decrease damage. In this review we summarize preclinical and clinical evidence that all of these factors trigger secondary or chronic inflammation and gliosis. Thus, we hypothesize that these shared pathological features play a key role in a final common pathway that leads to the impaired neural maturation and connectivity and cognitive/motor impairments that are commonly observed in infants born preterm. This raises the possibility that secondary or chronic inflammation may be a viable therapeutic target for delayed interventions to improve neurodevelopmental outcomes after preterm birth. WHAT THIS PAPER ADDS: Hypoxia-ischemia, infection/inflammation, and barotrauma/volutrauma all contribute to preterm brain injury. Multiple different triggers of preterm brain injury are associated with central nervous system dysmaturation. Secondary brain inflammation may be a viable target to improve neurodevelopment after preterm birth.

Indexed as

AnimalsHumansHypoxia-Ischemia, BrainInfant, Premature, DiseasesInflammation

Identifiers

PMID29194585
OpenAlexW2771122506

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.