Evidence map›Paper›PMID 28347765›Full record

ArticleExperimental neurology2017

Spinal cord injury in hypertonic newborns after antenatal hypoxia-ischemia in a rabbit model of cerebral palsy.

Alexander Drobyshevsky, Katharina A Quinlan

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.7field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Modeling cerebral palsy in animals.Developmental medicine and child neurology · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Inhibitory Synaptic Influences on Developmental Motor Disorders.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Maturation of the Locomotor Circuitry in Children With Cerebral Palsy.Frontiers in bioengineering and biotechnology · 2020
    Review
  12. Article
  13. Article
  14. Article
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 1 country.

Alexander DrobyshevskyDepartment of Pediatric, NorthShore University HealthSystem Research Institute, Evanston, IL, United States. Electronic address: adrobyshevsky@northshore.org.
Katharina A QuinlanDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States.
NorthShore University HealthSystem · USNorthwestern University · US

Funding

Spinal serotonin in cerebral palsyR01NS091278 · NINDS · ENDEAVOR HEALTH CLINICAL OPERATIONS · PI DROBYSHEVSKY, ALEXANDER · 2015 to 2019
$1.7M
NINDS NIH HHS R01 NS091278
6 · The paper itself

Abstract

While antenatal hypoxia-ischemia (H-I) is a well-established cause of brain injury, the effects of H-I on the spinal cord remain undefined. This study examined whether hypertonia in rabbits was accompanied by changes in spinal architecture. Rabbit dams underwent global fetal H-I at embryonic day 25 for 40min. High resolution diffusion tensor imaging was performed on fixed neonatal CNS. Fractional anisotropy (FA) and regional volumetric measurements were compared between kits with and without hypertonia after H-I and sham controls using Tract Based Spatial Statistics. Hypertonic kits showed evidence of damage from hypoxia not only in the brain, but in spinal cord as well. Hypertonic kits showed reduced FA and thickness in corticospinal tracts, external capsule, fimbria, and in white and gray matter of both cervical and lumbar spinal cord. Dorsal white matter of the spinal cord was the exception, where there was thickening and increased FA in hypertonic kits. Direct damage to the spinal cord was demonstrated in a subset of dams imaged during H-I with a 3T magnetic resonance scanner, where apparent diffusion coefficient in fetal spinal cords acutely decreased during hypoxia. Hypertonic kits showed subsequent decreases in lumbar motoneuron counts and extensive TUNEL- and Fluoro-Jade C-positive labeling was present in the spinal cord 48h after H-I, demonstrating spinal neurodegeneration. We speculate that global H-I causes significant loss of both spinal white and gray matter in hypertonic newborns due to direct H-I injury to the spinal cord as well as due to upstream brain injury and consequent loss of descending projections.

Indexed as

AnimalsAnimals, NewbornCentral Nervous SystemCerebral PalsyDiffusion Tensor ImagingDisease Models, AnimalFemaleFetal HypoxiaFluoresceinsGlial Fibrillary Acidic ProteinGliosisImage Processing, Computer-AssistedIn Situ Nick-End LabelingMuscle HypertoniaNeural PathwaysPregnancyFluoresceinsfluoro jadeGlial Fibrillary Acidic ProteinCerebral palsyDiffusion tensor imagingHypoxia-ischemiaPerinatal brain injury

Identifiers

PMID28347765
PMCPMC5509441
OpenAlexW2601111930

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.