Evidence map›Paper›PMID 32252390›Full record

ReviewAntioxidants (Basel, Switzerland)2020

Management of Traumatic Brain Injury: From Present to Future.

Rosalia Crupi, Marika Cordaro, Salvatore Cuzzocrea, Daniela Impellizzeri

Open access · goldAbstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Effects of poloxamer 188 on traumatic brain injury.Brain, behavior, & immunity - health · 2024
    Review
  11. Calcified apoptotic vesicles from PROCRJournal of extracellular vesicles · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Tanshinone-IIA mediated neuroprotection by modulating neuronal pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Review
  16. Article
  17. Article
  18. P188 Therapy in In Vitro Models of Traumatic Brain Injury.International journal of molecular sciences · 2023
    Review
  19. Article
  20. Review
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

4 authors at 1 institution in 2 countries.

Rosalia CrupiDepartment of Veterinary Science, University of Messina, 98168 Messina, Italy.ORCID 0000-0002-7629-3132
Marika CordaroDepartment of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Via Consolare Valeria 1, 98100 Messina, Italy.ORCID 0000-0002-3980-0043
Salvatore CuzzocreaDepartment of Chemical, Biological, Pharmacological and Environmental Sciences, Messina University, Viale F. Stagno D'Alcontres 31, 98166 Messina, Italy.ORCID 0000-0001-6131-3690
Daniela ImpellizzeriDepartment of Chemical, Biological, Pharmacological and Environmental Sciences, Messina University, Viale F. Stagno D'Alcontres 31, 98166 Messina, Italy.
University of Messina · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TBI (traumatic brain injury) is a major cause of death among youth in industrialized societies. Brain damage following traumatic injury is a result of direct and indirect mechanisms; indirect or secondary injury involves the initiation of an acute inflammatory response, including the breakdown of the blood-brain barrier (BBB), brain edema, infiltration of peripheral blood cells, and activation of resident immunocompetent cells, as well as the release of numerous immune mediators such as interleukins and chemotactic factors. TBI can cause changes in molecular signaling and cellular functions and structures, in addition to tissue damage, such as hemorrhage, diffuse axonal damages, and contusions. TBI typically disturbs brain functions such as executive actions, cognitive grade, attention, memory data processing, and language abilities. Animal models have been developed to reproduce the different features of human TBI, better understand its pathophysiology, and discover potential new treatments. For many years, the first approach to manage TBI has been treatment of the injured tissue with interventions designed to reduce the complex secondary-injury cascade. Several studies in the literature have stressed the importance of more closely examining injuries, including endothelial, microglia, astroglia, oligodendroglia, and precursor cells. Significant effort has been invested in developing neuroprotective agents. The aim of this work is to review TBI pathophysiology and existing and potential new therapeutic strategies in the management of inflammatory events and behavioral deficits associated with TBI.

Indexed as

neuroinflammationoxidative stress.palmitoylethanolamide (PEA)therapeutic strategiestraumatic brain injury

Identifiers

PMID32252390
PMCPMC7222188
OpenAlexW3014932431

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.