Evidence map›Paper›PMID 30398389›Full record

ArticleJournal of neurotrauma2019

Acute Post-Traumatic Sleep May Define Vulnerability to a Second Traumatic Brain Injury in Mice.

Rachel K Rowe, Jordan L Harrison, Helena W Morrison, Vignesh Subbian, Sean M Murphy, Jonathan Lifshitz

Abstract read
In one paragraph

Article in Journal of neurotrauma, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 31 citations in OpenAlex.

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  19. Inflammation in Traumatic Brain Injury.Journal of Alzheimer's disease : JAD · 2020
    Review
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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 4 institutions in 1 country.

Rachel K Rowe1 BARROW Neurological Institute at Phoenix Children's Hospital, Phoenix, Arizona.
Jordan L Harrison4 Department of Basic Medical Sciences, University of Arizona College of Medicine-Phoenix, Phoenix, Arizona.
Helena W Morrison5 University of Arizona College of Nursing, Tucson, Arizona.
Vignesh Subbian6 University of Arizona College of Engineering, Tucson, Arizona.
Sean M Murphy7 Department of Forestry and Natural Resources, University of Kentucky, Lexington, Kentucky.
Jonathan Lifshitz1 BARROW Neurological Institute at Phoenix Children's Hospital, Phoenix, Arizona.
University of Arizona · USPhoenix Children's Hospital · USPhoenix VA Health Care System · USUniversity of Kentucky · 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
Post Traumatic Sleep: An Individualized Indicator of Severity and RecoveryR21NS072611 · NINDS · UNIVERSITY OF KENTUCKY · PI LIFSHITZ, JONATHAN, O'HARA, BRUCE FREDERICK · 2011 to 2012
$408k
Remote ischemic conditioning as a pre-hospital therapeutic intervention for diffuse traumatic brain injuryF31NS090921 · NINDS · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI HARRISON, JORDAN L · 2015 to 2017
$116k
NINDS NIH HHS F31 NS090921NINDS NIH HHS R01 NS065052NINDS NIH HHS R21 NS072611
6 · The paper itself

Abstract

Chronic neurological impairments can manifest from repetitive traumatic brain injury (rTBI), particularly when subsequent injuries occur before the initial injury completely heals. Herein, we apply post-traumatic sleep as a physiological biomarker of vulnerability, hypothesizing that a second TBI during post-traumatic sleep worsens neurological and histological outcomes compared to one TBI or a second TBI after post-traumatic sleep subsides. Mice received sham or diffuse TBI by midline fluid percussion injury; brain-injured mice received one TBI or rTBIs at 3- or 9-h intervals. Over 40 h post-injury, injured mice slept more than shams. Functional assessments indicated lower latencies on rotarod and increased Neurological Severity Scores for mice with rTBIs within 3 h. Anxiety-like behaviors in the open field task were increased for mice with rTBIs at 3 h. Based on pixel density of silver accumulation, neuropathology was greater at 28 days post-injury (DPI) in rTBI groups than sham and single TBI. Cortical microglia morphology was quantified and mice receiving rTBI were de-ramified at 14 DPI compared to shams and mice receiving a single TBI, suggesting robust microglial response in rTBI groups. Orexin-A-positive cells were sustained in the lateral hypothalamus with no loss detected, indicating that loss of wake-promoting neurons did not contribute to post-traumatic sleep. Thus, duration of post-traumatic sleep is a period of vulnerability that results in exacerbated injury from rTBI. Monitoring individual post-traumatic sleep is a potential clinical tool for personalized TBI management, where regular sleep patterns may inform rehabilitative strategies and return-to-activity guidelines.

Indexed as

Brain Injuries, TraumaticAnimalsMaleMiceMice, Inbred C57BLSleepTime Factorsconcussioninflammationpathologyrepetitive TBIsleep

Identifiers

PMID30398389
PMCPMC6479254
OpenAlexW2899813503

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.