Evidence map›Paper›PMID 31795040›Full record

ReviewNeuroImage. Clinical2019

Role of cerebral glutamate in post-stroke epileptogenesis.

John-Paul Nicolo, Terence J O'Brien, Patrick Kwan

Open access · goldAbstract readReview
In one paragraph

Review in NeuroImage. Clinical, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Convulsive Status Epilepticus in IndonesiaBalkan medical journal · 2024
    Article
  8. Observational
  9. Review
  10. Article
  11. The lactate metabolism and protein lactylation in epilepsy.Frontiers in cellular neuroscience · 2024
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Seizures and epilepsy in patients with ischaemic stroke.Neurological research and practice · 2021
    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

3 authors at 2 institutions in 1 country.

John-Paul NicoloDepartment of Neurology, Royal Melbourne Hospital, 300 Grattan Street Parkville Victoria Australia; Department of Neurology, Alfred Hospital, 55 Commercial Road, Melbourne Victoria Australia. Electronic address: JohnPaul.Nicolo@mh.org.au.
Terence J O'BrienDepartment of Neuroscience, Monash University, Alfred Hospital, 55 Commercial Road, Melbourne Victoria Australia; Department of Medicine (The Royal Melbourne Hospital), The University of Melbourne, Royal Parade, Parkville Victoria Australia. Electronic address: te.obrien@alfred.org.au.
Patrick KwanDepartment of Neurology, Royal Melbourne Hospital, 300 Grattan Street Parkville Victoria Australia; Department of Neuroscience, Monash University, Alfred Hospital, 55 Commercial Road, Melbourne Victoria Australia. Electronic address: patrick.kwan@monash.edu.
The Royal Melbourne Hospital · AUThe Alfred Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is one of the most important causes of acquired epilepsy in the adult population. While factors such as cortical involvement and haemorrhage have been associated with increased seizure risk, the mechanisms underlying the development of epilepsy after stroke remain unclear. One hypothesised mechanism is an excitotoxic effect of abnormal glutamate release following a stroke. Cerebral extracellular glutamate levels are known to rise in the setting of acute stroke, and numerous studies have implicated glutamate in the pathogenesis of seizures and epilepsy, both through direct measurement of glutamate from the epileptic brain and by analysis of receptors and transporters central to glutamate homeostasis. While experimental evidence suggests the cellular injury induced by glutamate exposure may lead to development of an epileptic phenotype, there is little direct data linking the rise in glutamate during stroke with the later development of epilepsy. Clinical research in this field has been hampered by the lack of non-invasive methods to measure cerebral glutamate. However, with the increasing availability of 7T MRI technology, Magnetic Resonance Spectroscopy is able to better resolve glutamate from other chemical species at this field strength, and Glutamate Chemical Exchange Saturation Transfer (GluCEST) imaging has been applied to localise epileptic foci in non-lesional focal epilepsy. This review outlines the evidence implicating a pivotal role for cerebral glutamate in the development of post-stroke epilepsy, and exploring the role of MRI in studying glutamate as a biomarker and therefore its suitability as a molecular target for anti-epileptogenic therapies. We hypothesise that the rise in glutamate levels in the setting of acute stroke is a clinically relevant biomarker for the development of post-stroke epilepsy.

Indexed as

AnimalsBrainEpilepsyGlutamic AcidHumansMagnetic Resonance ImagingMagnetic Resonance SpectroscopyStrokeGlutamic AcidEpilepsyglutamateMRIMRSStroke

Identifiers

PMID31795040
PMCPMC6883323
OpenAlexW2986932146

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.