Evidence map›Paper›PMID 22612806›Full record

ReviewEpilepsia2012

Are you in or out? Leukocyte, ion, and neurotransmitter permeability across the epileptic blood-brain barrier.

Damir Janigro

Abstract readReview
In one paragraph

Review in Epilepsia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
9.0field-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

53 citing papers in PubMed, 115 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Observational
  9. Neuroinflammatory mediators in acquired epilepsy: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Synaptic Reshaping and Neuronal Outcomes in the Temporal Lobe Epilepsy.International journal of molecular sciences · 2021
    Review
  16. Markers in Status Epilepticus Prognosis.Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society · 2020
    Review
  17. Review
  18. Review
  19. Review
  20. Review
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

1 author at 1 institution in 1 country.

Damir JanigroDepartments of Neurological Surgery, Molecular Medicine and Cell Biology, ClevelandClinic Foundation, Euclid Avenue, Cleveland, OH 44195, U.S.A. janigrd@ccf.org
Cleveland Foundation · US

Funding

Neurovascular Unit on a Chip: Regional Chemical Communication, Drug and Toxin ResponsesUH3TR000491 · NCATS · VANDERBILT UNIVERSITY · PI GHOSH, CHAITALI, JANIGRO, DAMIR · 2014 to 2016
$3.8M
Neurovascular Unit on a Chip: Chemical Communication, Drug and Toxin ResponsesUH2TR000491 · NCATS · VANDERBILT UNIVERSITY · PI JANIGRO, DAMIR, NISWENDER, KEVIN D · 2012 to 2013
$2.2M
Development of a BBB model to study transendothelial cell migrationR42MH093302 · NIMH · FLOCEL, INC. · PI JANIGRO, DAMIR · 2012 to 2013
$1.0M
Development of a BBB Model to Study Transendothelial Cell MigrationR41MH093302 · NIMH · FLOCEL, INC. · PI JANIGRO, DAMIR · 2010 to 2011
$158k
NCATS NIH HHS UH2 TR000491NCATS NIH HHS UH3 TR000491NIMH NIH HHS R41 MH093302NIMH NIH HHS R42 MH093302
6 · The paper itself

Abstract

The credo that epileptic seizures can be initiated only by "epileptic" neurons has been recently challenged. The recognition of key astrocytic-neuronal communication, and the close interaction and crosstalk between astrocytes and brain endothelial cells, has shifted attention to the blood-brain barrier (BBB) and the "neurovascular unit." Therefore, the pursuit of mechanisms of seizure generation and epileptogenesis now includes investigations of cerebral blood flow and permeability of cerebral microvessels. For example, leukocyte adhesion molecules at the BBB have been proposed to play a role as an initiating factor for pilocarpine-induced status epilepticus, and a viral infection model with a strong BBB etiology has been used to study epileptogenesis. Finally, the fact that in nonepileptic subjects seizures can be triggered by BBB disruption, together with the antiseizure effects obtained by administration of potent antiinflammatory "BBB repair" drugs, has increased the interest in neuroinflammation; both circulating leukocytes and resident microglia have been studied in this context. The dual scope of this review is the following: (1) outline the proposed role of BBB damage and immune cell activation in seizure disorders; and (2) explain how increased cerebrovascular permeability causes neuronal misfiring. The temporal sequence linking seizures to peripheral inflammation and BBB dysfunction remains to be clarified. For example, it is still debated whether seizures cause systemic inflammation or vice versa. The topographic localization of fundamental triggers of epileptic seizures also remains controversial: Are immunologic mechanisms required for seizure generation brain-specific or is systemic activation of immunity sufficient to alter neuronal excitability? Finally, the causative role of "BBB leakage" remains a largely unresolved issue.

Indexed as

AnimalsBlood-Brain BarrierCell Membrane PermeabilityEpilepsyHumansIonsLeukocytesNervous System DiseasesNeurogliaNeuronsNeurotransmitter AgentsReceptors, MuscarinicSplenectomyT-LymphocytesIonsNeurotransmitter AgentsReceptors, Muscarinic

Identifiers

PMID22612806
PMCPMC4093790
OpenAlexW1813562443

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.