Evidence map›Paper›PMID 29684437›Full record

ArticleNeurobiology of disease2018

Sleep dysfunction following neonatal ischemic seizures are differential by neonatal age of insult as determined by qEEG in a mouse model.

S K Kang, S Ammanuel, S Thodupunuri, D A Adler, M V Johnston, S D Kadam

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Nutrients · 2023
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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

6 authors at 2 institutions in 1 country.

S K KangDepartment of Neuroscience, Hugo Moser Research Institute at Kennedy Krieger, Johns Hopkins University, Baltimore, MD 21205, USA.
S AmmanuelDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21205, USA.
S ThodupunuriDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21205, USA.
D A AdlerDepartment of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21205, USA.
M V JohnstonDepartment of Neuroscience, Hugo Moser Research Institute at Kennedy Krieger, Johns Hopkins University, Baltimore, MD 21205, USA; Departments of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Pediatrics, Johns Hopkins University School of Medicine; Baltimore, MD 21205, USA.
S D KadamDepartment of Neuroscience, Hugo Moser Research Institute at Kennedy Krieger, Johns Hopkins University, Baltimore, MD 21205, USA; Departments of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address: kadam@kennedykrieger.org.
Johns Hopkins University · USKennedy Krieger Institute · US

Funding

Mechanisms regulating KCC2 hypofunction during refractory seizures in a mouse model of ischemic neonatal seizuresR01HD090884 · NICHD · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI SCAFIDI, JOSEPH · 2017 to 2021
$1.9M
NICHD NIH HHS R01 HD090884
6 · The paper itself

Abstract

Neonatal seizures associated with hypoxic-ischemic encephalopathy (HIE) pose a challenge in their acute clinical management and are often followed by long-term neurological consequences. We used a newly characterized CD-1 mouse model of neonatal ischemic seizures associated with age-dependent (P7 vs. P10) seizure severity and phenobarbital efficacy (i.e.; PB-resistant vs. PB-efficacious respectively) following unilateral carotid ligation. The long-term consequences following untreated neonatal seizures in P7 vs. P10 ligated pups were investigated using neurobehavioral testing, 24 h v- quantitative EEG -EMG (qEEG, qEMG), and western blot analyses in adult mice. Significant hyperactivity emerged in a small sub-set of mice in both age-groups associated with a failure to habituate during open-field (OF) testing. 24 h continuous qEEGs detected significantly altered sleep architecture due to long-wake cycles in both age-groups. Delta power (0.5-4 Hz) quantification during slow-wave-sleep (SWS) revealed significant SWS compensation in P10 ligates following periods of increased sleep pressure which the P7 ligate group failed to show. Theta/beta ratios deemed as negative correlation markers of attentional control were significantly higher only in the P10 ligates. These results indicate that neonatal age-dependent differences in the characteristics of ischemic neonatal seizures in CD-1 pups differentially modulate long-term outcomes, when evaluated with v-qEEG/EMG as adults.

Indexed as

Disease Models, AnimalAge FactorsAnimalsAnimals, NewbornBrain IschemiaElectroencephalographyFemaleMaleMaze LearningMiceSeizuresSleep Wake DisordersDelta powerHyperactivityHypoxic-ischemic encephalopathyIschemiaNeonatal seizuresSleep structure

Identifiers

PMID29684437
PMCPMC5995660
OpenAlexW2800840212

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.