Evidence map›Paper›PMID 15563512›Full record

ArticleBrain : a journal of neurology2005

Progression from frontal-parietal to mesial-temporal epilepsy after fluid percussion injury in the rat.

Raimondo D'Ambrosio, Jason S Fender, Jared P Fairbanks, Ednea A Simon, Donald E Born, Dana L Doyle, John W Miller

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain : a journal of neurology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

76 citing papers in PubMed, 174 citations in OpenAlex.

  1. Article
  2. Safety and efficacy of Igk-TATk-CDKL5 gene therapy in mosaic CDKL5 deficiency.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Novel Approaches to Prevent Epileptogenesis After Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Review

16 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

7 authors at 1 institution in 1 country.

Raimondo D'AmbrosioDepartment of Neurological Surgery, Center on Human Development and Disability, University of Washington, School of Medicine, Harborview Medical Center, Box 359915, 325 Ninth Avenue, Seattle, WA 98104, USA. raid@u.washington.edu
Jason S Fender
Jared P Fairbanks
Ednea A Simon
Donald E Born
Dana L Doyle
John W Miller
University of Washington · US

Funding

Pathophysiology of glia following traumatic brain injuryR01NS040823 · NINDS · UNIVERSITY OF WASHINGTON · PI D'AMBROSIO, RAIMONDO · 2002 to 2005
$1.4M
NINDS NIH HHS NS040823NINDS NIH HHS R01 NS040823
6 · The paper itself

Abstract

We recently described an in vivo model of post-traumatic epilepsy (PTE) in the rat where chronic spontaneous recurrent seizures appear following a single episode of fluid percussion injury (FPI). PTE, studied during the first 2 months post-injury, was focal and seizures originated predominantly from the frontal-parietal neocortex at or around the injury site. However, rarer bilateral seizures originating from a different and undefined focus were also observed. To shed light on the Posttraumatic Epileptogenic mechanisms and on the generation of bilateral seizures, we studied rats up to 7 months post-injury. In vivo paired epidural and depth-electrode recordings indicated that the anterior hippocampus evolves into an epileptic focus which initiates bilateral seizures. The rate of frontal-parietal seizures remained constant over time after 2 weeks post-injury, while the rate of hippocampal seizures greatly increased over time, suggesting that different mechanisms mediate neocortical and hippocampal post-traumatic epileptogenesis. Because of different temporal evolution of these foci, the epileptic syndrome was characterized by predominant frontal-parietal seizures early after injury, but by predominant mesio-temporal seizures at later time points. Pathological analysis demonstrated progressive hippocampal and temporal cortex pathology that paralleled the increase in frequency and duration of bilateral seizures. These results demonstrate that FPI-induced frontal-parietal epilepsy (FPE) progresses to mesial-temporal lobe epilepsy (MTLE) with dual pathology. These observations establish numerous similarities between FPI-induced and human PTE and further validate it as a clinically relevant model of PTE.

Indexed as

AnimalsAnimals, Outbred StrainsBrain InjuriesElectroencephalographyEpilepsy, Frontal LobeEpilepsy, Post-TraumaticEpilepsy, Temporal LobeMaleNeocortexRatsRats, Sprague-DawleySeizuresTime Factors

Identifiers

PMID15563512
PMCPMC2696356
OpenAlexW2171468307

What OpenQuestion holds

Textmetadata
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.