Evidence map›Paper›PMID 36054439›Full record

ArticleEpilepsia2022

Functional neuropathology of neonatal hypoxia-ischemia by single-mouse longitudinal electroencephalography.

Kevin J Johnson, Brianna Moy, Nicholas Rensing, Alexia Robinson, Michael Ly, Ramya Chengalvala, Michael Wong, Rafael Galindo

Open access · greenAbstract read
In one paragraph

Article in Epilepsia, 2022. 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
0.8field-weighted citation impact, top 25% 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, 2 citations in OpenAlex.

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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.

Kevin J JohnsonDepartment of Neurology, Division of Pediatric & Developmental Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Brianna MoyDepartment of Neurology, Division of Pediatric & Developmental Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Nicholas RensingDepartment of Neurology, Division of Pediatric & Developmental Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Alexia RobinsonDepartment of Neurology, Division of Pediatric & Developmental Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Michael LyDepartment of Neurology, Division of Pediatric & Developmental Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Ramya ChengalvalaDepartment of Neurology, Division of Pediatric & Developmental Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.
Michael WongDepartment of Neurology, Division of Pediatric & Developmental Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.ORCID 0000-0002-3796-743X
Rafael GalindoDepartment of Neurology, Division of Pediatric & Developmental Neurology, Washington University School of Medicine, St. Louis, Missouri, USA.ORCID 0000-0002-0913-2435
Washington University in St. Louis · US

Funding

Neuroprotective Actions of hCG in a Mouse Model of Term and Preterm Brain InjuryR01NS112234 · NINDS · WASHINGTON UNIVERSITY · PI GALINDO, RAFAEL · 2019 to 2023
$1.7M
NIH HHS R01 NS112234NINDS NIH HHS R01 NS112234
6 · The paper itself

Abstract

objectiveNeonatal cerebral hypoxia-ischemia (HI) results in symptomatic seizures and long-term neurodevelopmental disability. The Rice-Vannucci model of rodent neonatal HI has been used extensively to examine and translate the functional consequences of acute and chronic HI-induced encephalopathy. Yet, longitudinal electrophysiological characterization of this brain injury model has been limited by the size of the neonatal mouse's head and postnatal maternal dependency. We overcome this challenge by employing a novel method of longitudinal single-mouse electroencephalography (EEG) using chronically implanted subcranial electrodes in the term-equivalent mouse pup. We characterize the neurophysiological disturbances occurring during awake and sleep states in the acute and chronic phases following newborn brain injury.

methodsC57BL/6 mice underwent long-term bilateral subcranial EEG and electromyographic electrode placement at postnatal day 9 followed by unilateral carotid cauterization and exposure to 40 minutes of hypoxia the following day. EEG recordings were obtained prior, during, and intermittently after the HI procedure from postnatal day 10 to weaning age. Quantitative EEG and fast Fourier transform analysis were used to evaluate seizures, cortical cerebral dysfunction, and disturbances in vigilance states.

resultsWe observed neonatal HI-provoked electrographic focal and bilateral seizures during or immediately following global hypoxia and most commonly contralateral to the ischemic injury. Spontaneous chronic seizures were not seen. Injured mice developed long-term asymmetric EEG background attenuation in all frequencies and most prominently during non-rapid eye movement (NREM) sleep. HI mice also showed transient impairments in vigilance state duration and transitions during the first 2 days following injury. SIGNIFICANCE: The functional burden of mouse neonatal HI recorded by EEG resembles closely that of the injured human newborn. The use of single-mouse longitudinal EEG in this immature model can advance our understanding of the developmental and pathophysiological mechanisms of neonatal cerebral injury and help translate novel therapeutic strategies against this devastating condition.

Indexed as

Brain InjuriesIschemiaAnimalsHumansHypoxiaMiceMice, Inbred C57BLSeizuresbrain injurydevelopmentEEGneonatal encephalopathynewbornseizuressleep

Identifiers

PMID36054439
PMCPMC10176800
OpenAlexW4293758713

What OpenQuestion holds

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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.