Evidence map›Paper›PMID 18226499›Full record

ReviewEpilepsy research2008

Pathology and pathophysiology of the amygdala in epileptogenesis and epilepsy.

Vassiliki Aroniadou-Anderjaska, Brita Fritsch, Felicia Qashu, Maria F M Braga

Open access · greenAbstract readReview
In one paragraph

Review in Epilepsy research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

95 citing papers in PubMed, 220 citations in OpenAlex.

  1. Article
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  9. Article
  10. Review
  11. Article
  12. Posterior Basolateral Amygdala is a Critical Amygdaloid Area for Temporal Lobe Epilepsy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  13. Adeno-Associated Viral Vectors in the Treatment of Epilepsy.International journal of molecular sciences · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

35 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

4 authors at 1 institution in 1 country.

Vassiliki Aroniadou-AnderjaskaDepartment of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Brita Fritsch
Felicia Qashu
Maria F M Braga
Uniformed Services University of the Health Sciences · US

Funding

Efficacy of GluR5 Antogonists Against Soman-Induced Seizures and NeuropathologyU01NS058162 · NINDS · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI BRAGA, MARIA F. · 2006 to 2016
$4.5M
Antiglutamatergic Therapy to Protect the Immature Brain Against Nerve AgentsU01NS102135 · NINDS · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI BRAGA, MARIA F. · 2018 to 2020
$1.3M
Targeting the Glutamatergic System to Counteract Soman Toxicity in Immature RatsR21NS094131 · NINDS · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI BRAGA, MARIA F. · 2015 to 2016
$744k
NINDS NIH HHS R21 NS094131NINDS NIH HHS U01 NS058162NINDS NIH HHS U01 NS102135
6 · The paper itself

Abstract

Acute brain insults, such as traumatic brain injury, status epilepticus, or stroke are common etiologies for the development of epilepsy, including temporal lobe epilepsy (TLE), which is often refractory to drug therapy. The mechanisms by which a brain injury can lead to epilepsy are poorly understood. It is well recognized that excessive glutamatergic activity plays a major role in the initial pathological and pathophysiological damage. This initial damage is followed by a latent period, during which there is no seizure activity, yet a number of pathophysiological and structural alterations are taking place in key brain regions, that culminate in the expression of epilepsy. The process by which affected/injured neurons that have survived the acute insult, along with well-preserved neurons are progressively forming hyperexcitable, epileptic neuronal networks has been termed epileptogenesis. Understanding the mechanisms of epileptogenesis is crucial for the development of therapeutic interventions that will prevent the manifestation of epilepsy after a brain injury, or reduce its severity. The amygdala, a temporal lobe structure that is most well known for its central role in emotional behavior, also plays a key role in epileptogenesis and epilepsy. In this article, we review the current knowledge on the pathology of the amygdala associated with epileptogenesis and/or epilepsy in TLE patients, and in animal models of TLE. In addition, because a derangement in the balance between glutamatergic and GABAergic synaptic transmission is a salient feature of hyperexcitable, epileptic neuronal circuits, we also review the information available on the role of the glutamatergic and GABAergic systems in epileptogenesis and epilepsy in the amygdala.

Indexed as

AmygdalaAnimalsEpilepsygamma-Aminobutyric AcidGlutamic AcidHumansgamma-Aminobutyric AcidGlutamic Acid

Identifiers

PMID18226499
PMCPMC2272535
OpenAlexW1994308963

What OpenQuestion holds

Textmetadata
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.