Evidence map›Paper›PMID 36313347›Full record

ReviewFrontiers in pharmacology2022

Antiseizure medication in early nervous system development. Ion channels and synaptic proteins as principal targets.

Patricio A Castro, Ingrid Pinto-Borguero, Gonzalo E Yévenes, Gustavo Moraga-Cid, Jorge Fuentealba

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 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

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. 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

5 authors.

Patricio A CastroLaboratory of Physiology and Pharmacology for Neural Development, LAND, Departamento de Fisiología, Facultad de Ciencias Biológicas, Universidad de Concepción, Concepción, Chile.
Ingrid Pinto-BorgueroLaboratory of Physiology and Pharmacology for Neural Development, LAND, Departamento de Fisiología, Facultad de Ciencias Biológicas, Universidad de Concepción, Concepción, Chile.
Gonzalo E YévenesDepartamento de Fisiología, Facultad de Ciencias Biológicas, Universidad de Concepción, Concepción, Chile.
Gustavo Moraga-CidDepartamento de Fisiología, Facultad de Ciencias Biológicas, Universidad de Concepción, Concepción, Chile.
Jorge FuentealbaDepartamento de Fisiología, Facultad de Ciencias Biológicas, Universidad de Concepción, Concepción, Chile.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The main strategy for the treatment of epilepsy is the use of pharmacological agents known as antiseizure medication (ASM). These drugs control the seizure onset and improves the life expectancy and quality of life of patients. Several ASMs are contraindicated during pregnancy, due to a potential teratogen risk. For this reason, the pharmacological treatments of the pregnant Women with Epilepsy (WWE) need comprehensive analyses to reduce fetal risk during the first trimester of pregnancy. The mechanisms by which ASM are teratogens are still under study and scientists in the field, propose different hypotheses. One of them, which will be addressed in this review, corresponds to the potential alteration of ASM on ion channels and proteins involved in relevant signaling and cellular responses (i.e., migration, differentiation) during embryonic development. The actual information related to the action of ASM and its possible targets it is poorly understood. In this review, we will focus on describing the eventual presence of some ion channels and synaptic proteins of the neurotransmitter signaling pathways present during early neural development, which could potentially interacting as targets of ASM. This information leads to elucidate whether these drugs would have the ability to affect critical signaling during periods of neural development that in turn could explain the fetal malformations observed by the use of ASM during pregnancy.

Indexed as

antiseizure medication (ASM)epilepsyneural developmentpregnancyteratogenicity

Identifiers

PMID36313347
PMCPMC9614143

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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.