Evidence map›Paper›PMID 19187292›Full record

ReviewEpilepsia2009

Epilepsy following cortical injury: cellular and molecular mechanisms as targets for potential prophylaxis.

David A Prince, Isabel Parada, Karina Scalise, Kevin Graber, Xiaoming Jin, Fran Shen

Open access · bronzeAbstract readReview
In one paragraph

Review in Epilepsia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
7.5field-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

67 citing papers in PubMed, 141 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Posttraumatic epilepsy in critically ill children with traumatic brain injury.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2023
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Epilepsy-on-a-Chip System for Antiepileptic Drug Discovery.IEEE transactions on bio-medical engineering · 2019
    Article
  17. Article
  18. Review
  19. Article
  20. Article

7 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

6 authors at 1 institution in 1 country.

David A PrinceDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, USA. daprince@stanford.edu
Isabel Parada
Karina Scalise
Kevin Graber
Xiaoming Jin
Fran Shen
Stanford University · US

Funding

REGULATION OF NEURONAL EXCITABILITY IN CHRONIC EPILEPTOGENESISP50NS012151 · NINDS · STANFORD UNIVERSITY · PI BUCKMASTER, PAUL S. · 1985 to 2007
$9.1M
NEUROBIOLOGY AND BEHAVIOR RESEARCH TRAINING PROGRAMT32HD007430 · NICHD · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GRUEBER, WESLEY B · 1999 to 2017
$6.8M
Epilepsy Research ProgramP01NS012151 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 2008 to 2011
$4.4M
MODULATION OF NEOCORTICAL INTERNEURONAL FUNCTIONR01NS039579 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R, PRINCE, DAVID ALLAN · 2000 to 2013
$4.3M
Modulation of Neocortical Interneuronal FunctionR56NS039579 · NINDS · STANFORD UNIVERSITY · PI PRINCE, DAVID ALLAN · 2014 to 2014
$402k
Excitatory and Inhibitory Synaptic Connectivity in Posttraumatic EpileptogenesisK99NS057940 · NINDS · STANFORD UNIVERSITY · PI JIN, XIAOMING · 2007 to 2008
$180k
NICHD NIH HHS T32 HD007430NINDS NIH HHS K99 NS057940NINDS NIH HHS NS02167NINDS NIH HHS NS12151NINDS NIH HHS P01 NS012151NINDS NIH HHS P50 NS012151NINDS NIH HHS R01 NS039579NINDS NIH HHS R56 NS039579
6 · The paper itself

Abstract

The sequelae of traumatic brain injury, including posttraumatic epilepsy, represent a major societal problem. Significant resources are required to develop a better understanding of the underlying pathophysiologic mechanisms as targets for potential prophylactic therapies. Posttraumatic epilepsy undoubtedly involves numerous pathogenic factors that develop more or less in parallel. We have highlighted two potential "prime movers": disinhibition and development of new functional excitatory connectivity, which occur in a number of animal models and some forms of epilepsy in humans. Previous experiments have shown that tetrodotoxin (TTX) applied to injured cortex during a critical period early after lesion placement can prevent epileptogenesis in the partial cortical ("undercut") model of posttraumatic epilepsy. Here we show that such treatment markedly attenuates histologic indices of axonal and terminal sprouting and presumably associated aberrant excitatory connectivity. A second finding in the undercut model is a decrease in spontaneous inhibitory events. Current experiments show that this is accompanied by regressive alterations in fast-spiking gamma-aminobutyric acid (GABA)ergic interneurons, including shrinkage of dendrites, marked decreases in axonal length, structural changes in inhibitory boutons, and loss of inhibitory synapses on pyramidal cells. Other data support the hypothesis that these anatomic abnormalities may result from loss of trophic support normally provided to interneurons by brain-derived neurotrophic factor (BDNF). Approaches that prevent these two pathophysiologic mechanisms may offer avenues for prophylaxis for posttraumatic epilepsy. However, major issues such as the role of these processes in functional recovery from injury and the timing of the critical period(s) for application of potential therapies in humans need to be resolved.

Indexed as

AnimalsAnticonvulsantsBrain InjuriesCerebral CortexDisease Models, AnimalEpilepsy, Post-Traumaticgamma-Aminobutyric AcidHumansInterneuronsNerve NetNerve RegenerationNeural InhibitionNeuronal PlasticityPyramidal CellsTetrodotoxinAnticonvulsantsgamma-Aminobutyric AcidTetrodotoxin

Identifiers

PMID19187292
PMCPMC2710960
OpenAlexW2033320602

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.