Evidence map›Paper›PMID 25158206›Full record

ReviewJournal of neurotrauma2015

Long-Term Consequences of Traumatic Brain Injury: Current Status of Potential Mechanisms of Injury and Neurological Outcomes.

Helen M Bramlett, W Dalton Dietrich

Registry-linked trialAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of neurotrauma, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06337994 (Treatment of Post-traumatic Cognitive Dysfunction With Memantine Hydrochloride, an N-methyl-D-aspartate), which is not on this map. Cited by 286 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
286citing papers in PubMed, 11 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.

NCT06337994 phase3completednot on this mapstarted 2024, after this paper: background citation

Treatment of Post-traumatic Cognitive Dysfunction With Memantine Hydrochloride, an N-methyl-D-aspartate (NMDA)-Type Receptor Blocker: a Clinical Trial

TypeinterventionalSponsorAssiut UniversityRan2024 to 2024Enrolled60ConditionsTreatment of Cognitive Deficits After Traumatic Brain InjuryArmsMemantine Hydrochloride
3 · Its place in the literature

Who cites it

286 citing papers in PubMed, 11 syntheses or guidelines pooled it.

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  12. Article
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  14. Review
  15. Article
  16. Psilocybin restores behavior and 5-HTCell reports. Medicine · 2026
    Article
  17. Pathway-level proteomics identifies subcellular trafficking dysregulation as a molecular signature in severe traumatic brain injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  18. Review
  19. Article
  20. Review

226 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.

Helen M BramlettThe Miami Project to Cure Paralysis/Department of Neurological Surgery, University of Miami Miller School of Medicine , Miami, Florida.
W Dalton DietrichThe Miami Project to Cure Paralysis/Department of Neurological Surgery, University of Miami Miller School of Medicine , Miami, Florida.

Funding

TRAUMATIC BRAIN INJURY INDUCED SEIZURE & SYNAPTIC PLASTICITYP50NS030291 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI HU, BINGREN · 1991 to 2013
$14.8M
The Importance of Temperature on Inflammation after TBIR01NS042133 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI DIETRICH, W DALTON · 2002 to 2020
$5.0M
NINDS NIH HHS NS030291NINDS NIH HHS R01 NS042133
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a significant clinical problem with few therapeutic interventions successfully translated to the clinic. Increased importance on the progressive, long-term consequences of TBI have been emphasized, both in the experimental and clinical literature. Thus, there is a need for a better understanding of the chronic consequences of TBI, with the ultimate goal of developing novel therapeutic interventions to treat the devastating consequences of brain injury. In models of mild, moderate, and severe TBI, histopathological and behavioral studies have emphasized the progressive nature of the initial traumatic insult and the involvement of multiple pathophysiological mechanisms, including sustained injury cascades leading to prolonged motor and cognitive deficits. Recently, the increased incidence in age-dependent neurodegenerative diseases in this patient population has also been emphasized. Pathomechanisms felt to be active in the acute and long-term consequences of TBI include excitotoxicity, apoptosis, inflammatory events, seizures, demyelination, white matter pathology, as well as decreased neurogenesis. The current article will review many of these pathophysiological mechanisms that may be important targets for limiting the chronic consequences of TBI.

Indexed as

Brain Injury, ChronicHumansatrophyinflammationneurogenesisprogressive damageTBIwhite matter

Identifiers

PMID25158206
PMCPMC4677116

What OpenQuestion holds

Textmetadata
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.