Evidence map›Paper›PMID 28042008›Full record

ArticleBehavioural brain research2018

Does time heal all wounds? Experimental diffuse traumatic brain injury results in persisting histopathology in the thalamus.

Theresa Currier Thomas, Sarah B Ogle, Benjamin M Rumney, Hazel G May, P David Adelson, Jonathan Lifshitz

Open access · greenAbstract read
In one paragraph

Article in Behavioural brain research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

33 citing papers in PubMed, 47 citations in OpenAlex.

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  13. Drosophila as a model to explore secondary injury cascades after traumatic brain injury.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
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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 5 institutions in 2 countries.

Theresa Currier ThomasBarrow Neurological Institute at Phoenix Children's Hospital, Phoenix, AZ, USA; Department of Child Health, University of Arizona College of Medicine-Phoenix, Phoenix, AZ, USA; Phoenix VA Health Care System, Phoenix, AZ, USA. Electronic address: theresathomas@email.arizona.edu.
Sarah B OgleBarrow Neurological Institute at Phoenix Children's Hospital, Phoenix, AZ, USA; Department of Child Health, University of Arizona College of Medicine-Phoenix, Phoenix, AZ, USA; Phoenix Integrated Surgical Residency, Banner University Medical Center, Phoenix, AZ, USA; Department of Surgery, Banner University Medical Center, Phoenix, AZ, USA. Electronic address: sogle@email.arizona.edu.
Benjamin M RumneyDepartment of Biology and Biochemistry, University of Bath, United Kingdom. Electronic address: ben-rumney@ntlworld.com.
Hazel G MayDepartment of Biology and Biochemistry, University of Bath, United Kingdom. Electronic address: Hazelmay094@gmail.com.
P David AdelsonBarrow Neurological Institute at Phoenix Children's Hospital, Phoenix, AZ, USA; Department of Child Health, University of Arizona College of Medicine-Phoenix, Phoenix, AZ, USA; Neuroscience Program, Arizona State University, Tempe, AZ, USA; School of Biological and Health Systems Engineering, Arizona State University, Tempe, AZ, USA. Electronic address: dadelson@phoenixchildrens.com.
Jonathan LifshitzBarrow Neurological Institute at Phoenix Children's Hospital, Phoenix, AZ, USA; Department of Child Health, University of Arizona College of Medicine-Phoenix, Phoenix, AZ, USA; Phoenix VA Health Care System, Phoenix, AZ, USA; Neuroscience Program, Arizona State University, Tempe, AZ, USA. Electronic address: jlifshitz@email.arizona.edu.
University of Bath · GBArizona State University · USBarrow Neurological Institute · USPhoenix Children's Hospital · USUniversity of Arizona · US

Funding

Neural circuit disruption by diffuse brain injury: basis for morbidity & therapyR01NS065052 · NINDS · UNIVERSITY OF KENTUCKY · PI LIFSHITZ, JONATHAN · 2010 to 2014
$1.7M
Inhibition of synaptogenesis mitigates late-onset post-traumatic morbidity in ratR03NS077098 · NINDS · UNIVERSITY OF ARIZONA · PI LIFSHITZ, JONATHAN · 2012 to 2013
$149k
NINDS NIH HHS R01 NS065052NINDS NIH HHS R03 NS077098
6 · The paper itself

Abstract

backgroundThalamic dysfunction has been implicated in overall chronic neurological dysfunction after traumatic brain injury (TBI), however little is known about the underlying histopathology. In experimental diffuse TBI (dTBI), we hypothesize that persisting histopathological changes in the ventral posteromedial (VPM) nucleus of the thalamus is indicative of progressive circuit reorganization. Since circuit reorganization in the VPM impacts the whisker sensory system, the histopathology could explain the development of hypersensitivity to whisker stimulation by 28days post-injury; similar to light and sound hypersensitivity in human TBI survivors.

methodsAdult, male Sprague-Dawley rats underwent craniotomy and midline fluid percussion injury (FPI) (moderate severity; 1.8-2.0atm) or sham surgery. At 1d, 7d, and 28days post-FPI (d FPI) separate experiments confirmed the cytoarchitecture (Giemsa stain) and evaluated neuropathology (silver stain), activated astrocytes (GFAP), neuron morphology (Golgi stain) and microglial morphology (Iba-1) in the VPM.

resultsCytoarchitecture was unchanged throughout the time course, similar to previously published data; however, neuropathology and astrocyte activation were significantly increased at 7d and 28d and activated microglia were present at all time points. Neuron morphology was dynamic over the time course with decreased dendritic complexity (fewer branch points; decreased length of processes) at 7d FPI and return to sham values by 28d FPI.

conclusionsThese data indicate that dTBI results in persisting thalamic histopathology out to a chronic time point. While these changes can be indicative of either adaptive (recovery) or maladaptive (neurological dysfunction) circuit reorganization, they also provide a potential mechanism by which maladaptive circuit reorganization could contribute to the development of chronic neurological dysfunction. Understanding the processes that mediate circuit reorganization is critical to the development of future therapies for TBI patients.

Indexed as

Acute DiseaseAnimalsAstrocytesBrain Injuries, TraumaticChronic DiseaseDisease Models, AnimalImaging, Three-DimensionalImmunohistochemistryMaleMicrogliaNeuronal PlasticityNeuronsRats, Sprague-DawleySilver StainingThalamusTime FactorsPost-concussive symptomsSomatosensoryThalamusTraumatic brain injuryWhisker-circuit

Identifiers

PMID28042008
PMCPMC5491365
OpenAlexW2562551090

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.