ArticleEpilepsia2018
Modeling pathogenesis and treatment response in childhood absence epilepsy.
Article in Epilepsia, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Topological Organization Alterations of Whole-Brain Functional Networks in Patients with Childhood Absence Epilepsy: Associations with Treatment Effects.Disease markers · 2021Trial
- Modelling the effect of allopregnanolone on the resolution of spike-wave discharges.Journal of computational neuroscience · 2025Article
- Genotype-function-phenotype correlations for SCN1A variants identified by clinical genetic testing.Annals of clinical and translational neurology · 2025Article
- Computational modeling of resistance to hormone-mediated remission in childhood absence epilepsy.Frontiers in computational neuroscience · 2025Article
- Article
- Degeneracy in epilepsy: multiple routes to hyperexcitable brain circuits and their repair.Communications biology · 2023Review
- Modelling novelty detection in the thalamocortical loop.PLoS computational biology · 2023Article
- Pareto optimality, economy-effectiveness trade-offs and ion channel degeneracy: improving population modelling for single neurons.Open biology · 2022Review
- The Transcription Factor Shox2 Shapes Neuron Firing Properties and Suppresses Seizures by Regulation of Key Ion Channels in Thalamocortical Neurons.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- Computational Evidence for a Competitive Thalamocortical Model of Spikes and Spindle Activity in Rolandic Epilepsy.Frontiers in computational neuroscience · 2021Article
- The absence of NIPA2 enhances neural excitability through BK (big potassium) channels.CNS neuroscience & therapeutics · 2019Article
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveChildhood absence epilepsy (CAE) is a genetic generalized epilepsy syndrome with polygenic inheritance, with genes for γ-aminobutyric acid (GABA) receptors and T-type calcium channels implicated in the disorder. Previous studies of T-type calcium channel electrophysiology have shown genetic changes and medications have multiple effects. The aim of this study was to use an established thalamocortical computer model to determine how T-type calcium channels work in concert with cortical excitability to contribute to pathogenesis and treatment response in CAE.
methodsThe model is comprised of cortical pyramidal, cortical inhibitory, thalamocortical relay, and thalamic reticular single-compartment neurons, implemented with Hodgkin-Huxley model ion channels and connected by AMPA, GABA
resultsDecreasing cortical GABA SIGNIFICANCE: These results provide a window into mechanisms underlying polygenic inheritance in CAE, as well as a mechanism for treatment effects and failures mediated by these channels. Although the model is a simplification of the human thalamocortical network, it serves as a useful starting point for predicting the implications of ion channel electrophysiology in polygenic epilepsy such as CAE.
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Registered trials
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.