Evidence map›Paper›PMID 34966269›Full record

ReviewFrontiers in aging neuroscience2021

Inflammation Mediated Epileptogenesis as Possible Mechanism Underlying Ischemic Post-stroke Epilepsy.

Anna Regina Tröscher, Joachim Gruber, Judith N Wagner, Vincent Böhm, Anna-Sophia Wahl, Tim J von Oertzen

Abstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

33 citing papers in PubMed, 3 syntheses or guidelines pooled it.

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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.

Anna Regina TröscherNeurology I, Neuromed Campus, Kepler Universitätsklinikum, Linz, Austria.
Joachim GruberNeurology I, Neuromed Campus, Kepler Universitätsklinikum, Linz, Austria.
Judith N WagnerNeurology I, Neuromed Campus, Kepler Universitätsklinikum, Linz, Austria.
Vincent BöhmNeurology I, Neuromed Campus, Kepler Universitätsklinikum, Linz, Austria.
Anna-Sophia WahlBrain Research Institute, University of Zurich, Zurich, Switzerland.
Tim J von OertzenNeurology I, Neuromed Campus, Kepler Universitätsklinikum, Linz, Austria.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-stroke Epilepsy (PSE) is one of the most common forms of acquired epilepsy, especially in the elderly population. As people get increasingly older, the number of stroke patients is expected to rise and concomitantly the number of people with PSE. Although many patients are affected by post-ischemic epileptogenesis, not much is known about the underlying pathomechanisms resulting in the development of chronic seizures. A common hypothesis is that persistent neuroinflammation and glial scar formation cause aberrant neuronal firing. Here, we summarize the clinical features of PSE and describe in detail the inflammatory changes after an ischemic stroke as well as the chronic changes reported in epilepsy. Moreover, we discuss alterations and disturbances in blood-brain-barrier leakage, astrogliosis, and extracellular matrix changes in both, stroke and epilepsy. In the end, we provide an overview of commonalities of inflammatory reactions and cellular processes in the post-ischemic environment and epileptic brain and discuss how these research questions should be addressed in the future.

Indexed as

BBB leakagegliosisischemianeuroinflammationpost-stroke seizures

Identifiers

PMID34966269
PMCPMC8711648

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Registered trials

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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.