Evidence map›Paper›PMID 25404064›Full record

ReviewCNS neuroscience & therapeutics2015

Basic mechanisms of epileptogenesis in pediatric cortical dysplasia.

Sara Abdijadid, Gary W Mathern, Michael S Levine, Carlos Cepeda

Open access · bronzeAbstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 18% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.

  1. GABAFrontiers in neural circuits · 2022
    Pooled it
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  19. Clinical and Surgical Approach for Cerebral Cortical Dysplasia.Advances and technical standards in neurosurgery · 2023
    Article
  20. Article
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 2 institutions in 1 country.

Sara AbdijadidIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, Los Angeles, CA, USA.
Gary W Mathern
Michael S Levine
Carlos Cepeda
Intel (United States) · USUniversity of California, Los Angeles · US

Funding

PATHOPHYSIOLOGY OF DEVELOPING DYSPLASTIC HUMAN CORTEXR01NS038992 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CEPEDA, CARLOS T, MATHERN, GARY W. · 1999 to 2013
$3.3M
Molecular characterization of HemimegalencephalyR01NS083823 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLEESON, JOSEPH G, MATHERN, GARY W. · 2013 to 2017
$3.1M
NINDS NIH HHS NS 38992NINDS NIH HHS R01 NS038992NINDS NIH HHS R01 NS083823
6 · The paper itself

Abstract

Cortical dysplasia (CD) is a neurodevelopmental disorder due to aberrant cell proliferation and differentiation. Advances in neuroimaging have proven effective in early identification of the more severe lesions and timely surgical removal to treat epilepsy. However, the exact mechanisms of epileptogenesis are not well understood. This review examines possible mechanisms based on anatomical and electrophysiological studies. CD can be classified as CD type I consisting of architectural abnormalities, CD type II with the presence of dysmorphic cytomegalic neurons and balloon cells, and CD type III which occurs in association with other pathologies. Use of freshly resected brain tissue has allowed a better understanding of basic mechanisms of epileptogenesis and has delineated the role of abnormal cells and synaptic activity. In CD type II, it was demonstrated that balloon cells do not initiate epileptic activity, whereas dysmorphic cytomegalic and immature neurons play an important role in generation and propagation of epileptic discharges. An unexpected finding in pediatric CD was that GABA synaptic activity is not reduced, and in fact, it may facilitate the occurrence of epileptic activity. This could be because neuronal circuits display morphological and functional signs of dysmaturity. In consequence, drugs that increase GABA function may prove ineffective in pediatric CD. In contrast, drugs that counteract depolarizing actions of GABA or drugs that inhibit the mammalian target of rapamycin (mTOR) pathway could be more effective.

Indexed as

AnimalsBrainEpilepsygamma-Aminobutyric AcidHumansMalformations of Cortical Development, Group IINeuronsSignal TransductionSirolimusgamma-Aminobutyric AcidSirolimusBalloon cellsCortical dysplasiaDysmorphic neuronsEpileptogenesismTOR pathway

Identifiers

PMID25404064
PMCPMC4442638
OpenAlexW1972225310

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.