Evidence map›Paper›PMID 31837825›Full record

ReviewNeuropharmacology2020

Modulating neuroinflammation and oxidative stress to prevent epilepsy and improve outcomes after traumatic brain injury.

Clifford L Eastman, Raimondo D'Ambrosio, Thota Ganesh

Open access · greenAbstract readReview
In one paragraph

Review in Neuropharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
6.1field-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

69 citing papers in PubMed, 133 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Causal correlation between seizure activity and brain damage.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  14. Review
  15. Exploring Molecular Pathways in Exercise-Induced Recovery from Traumatic Brain Injury.Medical science monitor : international medical journal of experimental and clinical research · 2025
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

9 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

3 authors at 3 institutions in 1 country.

Clifford L EastmanDepartment of Neurological Surgery, 325 Ninth Ave., Seattle, WA, 98104, USA. Electronic address: cliff@uw.edu.
Raimondo D'AmbrosioDepartment of Neurological Surgery, 325 Ninth Ave., Seattle, WA, 98104, USA; Regional Epilepsy Center, University of Washington, 325 Ninth Ave., Seattle, WA, 98104, USA.
Thota GaneshDepartment of Pharmacology and Chemical Biology, Emory University School of Medicine, 1510 Clifton Rd, Atlanta, GA, 30322, Georgia. Electronic address: tganesh@emory.edu.
Emory University · USNeurological Surgery · USUniversity of Washington · US

Funding

Development of EP2 receptor antagonists for suppression of Alzheimer's neuropathologyU01AG052460 · NIA · EMORY UNIVERSITY · PI GANESH, THOTA · 2016 to 2020
$3.9M
EP2 antagonists as novel anti-epileptogenic agentsR21NS101167 · NINDS · EMORY UNIVERSITY · PI GANESH, THOTA · 2018 to 2019
$747k
Novel inflammatory targets to prevent posttraumatic epileptogenesisR21NS085459 · NINDS · UNIVERSITY OF WASHINGTON · PI D'AMBROSIO, RAIMONDO · 2014 to 2015
$431k
EP2 antagonists as novel anti-epileptogenic agentsR33NS101167 · NINDS · EMORY UNIVERSITY · PI GANESH, THOTA · 2020 to 2020
$389k
NIA NIH HHS U01 AG052460NINDS NIH HHS R21 NS085459NINDS NIH HHS R21 NS101167NINDS NIH HHS R33 NS101167
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a leading cause of death and disability in young adults worldwide. TBI survival is associated with persistent neuropsychiatric and neurological impairments, including posttraumatic epilepsy (PTE). To date, no pharmaceutical treatment has been found to prevent PTE or ameliorate neurological/neuropsychiatric deficits after TBI. Brain trauma results in immediate mechanical damage to brain cells and blood vessels that may never be fully restored given the limited regenerative capacity of brain tissue. This primary insult unleashes cascades of events, prominently including neuroinflammation and massive oxidative stress that evolve over time, expanding the brain injury, but also clearing cellular debris and establishing homeostasis in the region of damage. Accumulating evidence suggests that oxidative stress and neuroinflammatory sequelae of TBI contribute to posttraumatic epileptogenesis. This review will focus on possible roles of reactive oxygen species (ROS), their interactions with neuroinflammation in posttraumatic epileptogenesis, and emerging therapeutic strategies after TBI. We propose that inhibitors of the professional ROS-generating enzymes, the NADPH oxygenases and myeloperoxidase alone, or combined with selective inhibition of cyclooxygenase mediated signaling may have promise for the treatment or prevention of PTE and other sequelae of TBI. This article is part of the special issue entitled 'New Epilepsy Therapies for the 21st Century - From Antiseizure Drugs to Prevention, Modification and Cure of Epilepsy'.

Indexed as

AnimalsBrain Injuries, TraumaticEncephalitisEpilepsy, Post-TraumaticHumansNADPH OxidasesOxidative StressPeroxidaseNADPH OxidasesPeroxidaseMyeloperoxidase and traumatic brain injuryNADPH oxidaseNeuroinflammationOxidative-stressPosttraumatic epilepsyRedox-signaling

Identifiers

PMID31837825
PMCPMC7274911
OpenAlexW2994514210

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.