Evidence map›Paper›PMID 31827423›Full record

ReviewFrontiers in cellular neuroscience2019

Traumatic Brain Injuries: Pathophysiology and Potential Therapeutic Targets.

Si Yun Ng, Alan Yiu Wah Lee

3 registry-linked trialsAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 3 registered trials, which are not on this map. Cited by 451 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
451citing papers in PubMed, 9 pooled it
–field-weighted citation impact
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.

NCT06163833 phase2recruitingnot on this mapstarted 2023, after this paper: background citation

MATRIx: MesenchymAl Stromal Cells for Traumatic bRain Injury

TypeinterventionalSponsorFondazione IRCCS San Gerardo dei TintoriRan2023 to 2026Enrolled78ConditionsTraumatic Brain Injury With Loss of ConsciousnessArmsMesenchymal stromal cell low dosage-80*10^6 cells, Mesenchymal stromal cell low dosage-160*10^6 cells, Placebo-storage solution
NCT07406555 phase4completednot on this mapstarted 2025, after this paper: background citation

Differences in C-Reactive Protein Levels Between Traumatic Brain Injury Patients Receiving Dexmedetomidine and Those Not Receiving Dexmedetomidine Undergoing Craniotomy at Prof. Dr. Margono Soekarjo Regional General Hospital, Purwokerto

TypeinterventionalSponsorUniversitas Jenderal SoedirmanRan2025 to 2025Enrolled25ConditionsTraumatic Brain InjuryArmsDexmedetomidine, Sufentanyl
NCT07535736 not yet recruitingnot on this mapstarted 2026, after this paper: background citation

Role of Prophylactic Anti-epileptic Regimen in Traumatic Brain Injury

TypeobservationalSponsorAssiut UniversityRan2026 to 2027Enrolled70ConditionsAntiepileptic Efficacy and Safety, Brain InjuriesArmsAnti-Epileptic
3 · Its place in the literature

Who cites it

451 citing papers in PubMed, 9 syntheses or guidelines pooled it.

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  6. Accuracy of GFAP and UCH-L1 in predicting brain abnormalities on CT scans after mild traumatic brain injury: a systematic review and meta-analysis.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025
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391 more citing papers are in PubMed but not listed here.

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

2 authors.

Si Yun NgNeurobiology/Ageing Program, Centre for Life Sciences, Department of Physiology, Yong Loo Lin School of Medicine, Life Sciences Institute, National University of Singapore, Singapore, Singapore.
Alan Yiu Wah LeeNeurobiology/Ageing Program, Centre for Life Sciences, Department of Physiology, Yong Loo Lin School of Medicine, Life Sciences Institute, National University of Singapore, Singapore, Singapore.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) remains one of the leading causes of morbidity and mortality amongst civilians and military personnel globally. Despite advances in our knowledge of the complex pathophysiology of TBI, the underlying mechanisms are yet to be fully elucidated. While initial brain insult involves acute and irreversible primary damage to the parenchyma, the ensuing secondary brain injuries often progress slowly over months to years, hence providing a window for therapeutic interventions. To date, hallmark events during delayed secondary CNS damage include Wallerian degeneration of axons, mitochondrial dysfunction, excitotoxicity, oxidative stress and apoptotic cell death of neurons and glia. Extensive research has been directed to the identification of druggable targets associated with these processes. Furthermore, tremendous effort has been put forth to improve the bioavailability of therapeutics to CNS by devising strategies for efficient, specific and controlled delivery of bioactive agents to cellular targets. Here, we give an overview of the pathophysiology of TBI and the underlying molecular mechanisms, followed by an update on novel therapeutic targets and agents. Recent development of various approaches of drug delivery to the CNS is also discussed.

Indexed as

biopolymerscell penetrating proteinsCNS traumacontrolled drug releaseneuronal regenerationsecondary injuries

Identifiers

PMID31827423
PMCPMC6890857

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.