Evidence map›Paper›PMID 34556045›Full record

ArticleBMC neurology2021

Response to Sodium Channel blocking Antiseizure medications and coding polymorphisms of Sodium Channel genes in Taiwanese epilepsy patients.

Chih-Hsiang Lin, Chen-Jui Ho, Yan-Ting Lu, Meng-Han Tsai

Open access · goldAbstract read
In one paragraph

Article in BMC neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Lamotrigine Ameliorates Epilepsy during Pregnancy in Rats by Inhibiting Astrocyte Activation via the NLRP3/TXNIP Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
  4. Article
  5. Article
  6. Mechanisms of neurodevelopmental toxicity of topiramate.Critical reviews in toxicology · 2024
    Review
  7. Review
  8. Therapeutic advances in neurological disorders · 2024
    Article
  9. Understanding Lamotrigine's Role in the CNS and Possible Future Evolution.International journal of molecular sciences · 2023
    Review
  10. Polymorphisms Affecting the Response to Novel Antiepileptic Drugs.International journal of molecular sciences · 2023
    Review
  11. 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.

Chih-Hsiang LinDepartment of Neurology, Kaohsiung Chang Gung Memorial Hospital, Colleague of Medicine, Chang Gung University, Kaohsiung, Kaohsiung City, 83301, Taiwan.
Chen-Jui HoDepartment of Neurology, Kaohsiung Chang Gung Memorial Hospital, Colleague of Medicine, Chang Gung University, Kaohsiung, Kaohsiung City, 83301, Taiwan.
Yan-Ting LuDepartment of Neurology, Kaohsiung Chang Gung Memorial Hospital, Colleague of Medicine, Chang Gung University, Kaohsiung, Kaohsiung City, 83301, Taiwan.
Meng-Han TsaiDepartment of Neurology, Kaohsiung Chang Gung Memorial Hospital, Colleague of Medicine, Chang Gung University, Kaohsiung, Kaohsiung City, 83301, Taiwan. menghan@cgmh.org.tw.
Kaohsiung Chang Gung Memorial Hospital · TWChang Gung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMany antiseizure medications (ASMs) control seizures by blocking voltage-dependent sodium channels. Polymorphisms of sodium channel genes may affect the response to ASMs due to altering the effect of ASMs on blocking sodium channels.

methodsWe conducted a retrospective study of epilepsy patients followed up at the Neurological Department of Kaohsiung Chang Gung Memorial Hospital, Taiwan between January 2010 and December 2018. We categorized the patients into response, partial response, and failure to sodium channel blocking ASM groups. Sodium channel blocking ASMs included phenytoin, carbamazepine, lamotrigine, oxcarbazepine, lacosamide, zonisamide, topiramate, and valproic acid. A subgroup of predominant sodium channel blocking ASMs included phenytoin, carbamazepine, lamotrigine, oxcarbazepine, and lacosamide. Associations between the response of ASMs and single-nucleotide polymorphisms of SCN1A, SCN1B, SCN2A, and SCN9A were analyzed.

resultsTwo hundred Taiwanese patients and 21 single-nucleotide polymorphisms among SCN1A, SCN1B, SCN2A, and SCN9A were evaluated. We found allele C of rs55742440 in SCN1B was statistically significantly associated with not achieving seizure-free with sodium channel blocking ASMs. For the predominant sodium channel blocking ASMs group, no SNPs were associated with the response of ASMs.

conclusionSingle-nucleotide polymorphism in SCN1B was associated with the response to sodium channel blocking ASMs. This highlights the possibility that beta subunits may affect the function of sodium channels and resulted in different responsiveness to ASMs.

Indexed as

EpilepsyAnticonvulsantsHumansLamotrigineNAV1.7 Voltage-Gated Sodium ChannelRetrospective StudiesSodium ChannelsAnticonvulsantsLamotrigineNAV1.7 Voltage-Gated Sodium ChannelSCN9A protein, humanSodium ChannelsAntiseizure medicationsDrug resistance epilepsySCN1BSingle-nucleotide polymorphismsSodium channel gene

Identifiers

PMID34556045
PMCPMC8459515
OpenAlexW3200238100

What OpenQuestion holds

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LicenceCC BY
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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.