Evidence map›Paper›PMID 26519659›Full record

ReviewSeizure2015

Traumatic brain injury and epilepsy: Underlying mechanisms leading to seizure.

Brandon P Lucke-Wold, Linda Nguyen, Ryan C Turner, Aric F Logsdon, Yi-Wen Chen, Kelly E Smith, Jason D Huber, Rae Matsumoto, Charles L Rosen, Eric S Tucker and 1 more

Open access · greenAbstract readReview
In one paragraph

Review in Seizure, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 3 pooled it
6.7field-weighted citation impact, top 2% 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

95 citing papers in PubMed, 3 syntheses or guidelines pooled it, 169 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Synaptic Pathology in Traumatic Brain Injury and Therapeutic Insights.International journal of molecular sciences · 2025
    Review
  14. Review
  15. Review
  16. Review
  17. Mitochondrial Glutamine Metabolism Drives Epileptogenesis in Primary Hippocampal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  18. Article
  19. Article
  20. Article

35 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

11 authors at 1 institution in 1 country.

Brandon P Lucke-WoldDepartment of Neurosurgery, West Virginia University School of Medicine, Morgantown, WV 26506, USA; The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA.
Linda NguyenDepartment of Basic Pharmaceutical Sciences, West Virginia University School of Pharmacy, Morgantown, WV 26506, USA.
Ryan C TurnerDepartment of Neurosurgery, West Virginia University School of Medicine, Morgantown, WV 26506, USA; The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA.
Aric F LogsdonThe Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA; Department of Basic Pharmaceutical Sciences, West Virginia University School of Pharmacy, Morgantown, WV 26506, USA.
Yi-Wen ChenThe Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA.
Kelly E SmithDepartment of Basic Pharmaceutical Sciences, West Virginia University School of Pharmacy, Morgantown, WV 26506, USA.
Jason D HuberThe Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA; Department of Basic Pharmaceutical Sciences, West Virginia University School of Pharmacy, Morgantown, WV 26506, USA.
Rae MatsumotoDepartment of Basic Pharmaceutical Sciences, West Virginia University School of Pharmacy, Morgantown, WV 26506, USA; College of Pharmacy, Touro University California, 1310 Club Drive, Vallejo, CA 94592, USA.
Charles L RosenDepartment of Neurosurgery, West Virginia University School of Medicine, Morgantown, WV 26506, USA; The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA.
Eric S TuckerThe Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA.
Erich RichterDepartment of Neurosurgery, West Virginia University School of Medicine, Morgantown, WV 26506, USA; The Center for Neuroscience, West Virginia University School of Medicine, Morgantown, WV 26506, USA. Electronic address: eorichter@hsc.wvu.edu.
West Virginia University · US

Funding

West Virginia IDEA-CTRU54GM104942 · NIGMS · WEST VIRGINIA UNIVERSITY · PI Laura F. Gibson · 2012 to 2026
$81.0M
NIGMS NIH HHS U54 GM104942
6 · The paper itself

Abstract

Post-traumatic epilepsy continues to be a major concern for those experiencing traumatic brain injury. Post-traumatic epilepsy accounts for 10-20% of epilepsy cases in the general population. While seizure prophylaxis can prevent early onset seizures, no available treatments effectively prevent late-onset seizure. Little is known about the progression of neural injury over time and how this injury progression contributes to late onset seizure development. In this comprehensive review, we discuss the epidemiology and risk factors for post-traumatic epilepsy and the current pharmacologic agents used for treatment. We highlight limitations with the current approach and offer suggestions for remedying the knowledge gap. Critical to this pursuit is the design of pre-clinical models to investigate important mechanistic factors responsible for post-traumatic epilepsy development. We discuss what the current models have provided in terms of understanding acute injury and what is needed to advance understanding regarding late onset seizure. New model designs will be used to investigate novel pathways linking acute injury to chronic changes within the brain. Important components of this transition are likely mediated by toll-like receptors, neuroinflammation, and tauopathy. In the final section, we highlight current experimental therapies that may prove promising in preventing and treating post-traumatic epilepsy. By increasing understanding about post-traumatic epilepsy and injury expansion over time, it will be possible to design better treatments with specific molecular targets to prevent late-onset seizure occurrence following traumatic brain injury.

Indexed as

Brain InjuriesEpilepsyEpilepsy, Post-TraumaticHumansRisk FactorsEpilepsy modelsKetogenic therapyNeuroinflammationPost-traumatic epilepsyTraumatic brain injury

Identifiers

PMID26519659
PMCPMC12767287
OpenAlexW2150484897

What OpenQuestion holds

Textmetadata
LicenceTDM
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.