Evidence map›Paper›PMID 22521336›Full record

ReviewNeuropharmacology2013

The role of inflammation in epileptogenesis.

Annamaria Vezzani, Alon Friedman, Raymond J Dingledine

Open access · greenAbstract readReview
In one paragraph

Review in Neuropharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 240 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
240citing papers in PubMed, 2 pooled it
47.7field-weighted citation impact, top 1% 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

240 citing papers in PubMed, 2 syntheses or guidelines pooled it, 480 citations in OpenAlex.

  1. Pooled it
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  9. Observational
  10. Review
  11. Association ofNeurology international · 2026
    Article
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  13. Review
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  18. Review
  19. Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026
    Review
  20. Article

180 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 3 countries.

Annamaria VezzaniLaboratory Experimental Neurology, Department of Neuroscience, Mario Negri Institute for Pharmacological Research, Via G. La Masa 19, 20156 Milano, Italy. vezzani@marionegri.it
Alon Friedman
Raymond J Dingledine
Ben-Gurion University of the Negev · ILEmory University · USMario Negri Institute for Pharmacological Research · IT

Funding

Prostanoid modulators that reduce brain injury and inflammation after seizuresU01NS058158 · NINDS · EMORY UNIVERSITY · PI DINGLEDINE, RAYMOND J · 2006 to 2015
$5.9M
Role of COX2 of Neuronal Origin in Blood-Brain Communication after status epileptR21NS074169 · NINDS · EMORY UNIVERSITY · PI DINGLEDINE, RAYMOND J · 2011 to 2012
$426k
EP2 Allosteric Potentiators for Subarachnoid HemorrhageU01NS074509 · NINDS · EMORY UNIVERSITY · PI DINGLEDINE, RAYMOND J · 2011 to 2012
$226k
NINDS NIH HHS 1 R21 NS074169NINDS NIH HHS 1 U01 NS074509NINDS NIH HHS 2 U01 NS058158NINDS NIH HHS R21 NS074169NINDS NIH HHS U01 NS058158NINDS NIH HHS U01 NS074509
6 · The paper itself

Abstract

One compelling challenge in the therapy of epilepsy is to develop anti-epileptogenic drugs with an impact on the disease progression. The search for novel targets has focused recently on brain inflammation since this phenomenon appears to be an integral part of the diseased hyperexcitable brain tissue from which spontaneous and recurrent seizures originate. Although the contribution of specific proinflammatory pathways to the mechanism of ictogenesis in epileptic tissue has been demonstrated in experimental models, the role of these pathways in epileptogenesis is still under evaluation. We review the evidence conceptually supporting the involvement of brain inflammation and the associated blood-brain barrier damage in epileptogenesis, and describe the available pharmacological evidence where post-injury intervention with anti-inflammatory drugs has been attempted. Our review will focus on three main inflammatory pathways, namely the IL-1 receptor/Toll-like receptor signaling, COX-2 and the TGF-β signaling. The mechanisms underlying neuronal-glia network dysfunctions induced by brain inflammation are also discussed, highlighting novel neuromodulatory effects of classical inflammatory mediators such as cytokines and prostaglandins. The increase in knowledge about a role of inflammation in disease progression, may prompt the use of specific anti-inflammatory drugs for developing disease-modifying treatments. This article is part of the Special Issue entitled 'New Targets and Approaches to the Treatment of Epilepsy'.

Indexed as

AnimalsBiomarkersBlood-Brain BarrierEpilepsyHumansInflammationNeuronal PlasticityNeuronsSignal TransductionTreatment OutcomeBiomarkers

Identifiers

PMID22521336
PMCPMC3447120
OpenAlexW2003646464

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.