Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 3 complete abstracts (613 words), 9 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Epilepsies; Seizure Disorder; Seizure Disorders; Epilepsy, Cryptogenic; Cryptogenic Epilepsies; Cryptogenic Epilepsy; Epilepsies, Cryptogenic; Aura.
Where it fits in the MeSH classification
- Broader topics
- Brain Diseases
- Narrower topics
- Drug Resistant Epilepsy; Epilepsies, Partial; Epilepsy, Benign Neonatal; Epilepsy, Generalized; Epilepsy, Post-Traumatic; Epilepsy, Reflex; Epileptic Syndromes; Sudden Unexpected Death in Epilepsy
- See also
- Seizures
Research landscape
PubMed indexes 139,261 records tagged with the MeSH heading “Epilepsy” (counts retrieved 2026-10-29). 27,793 of them (20.0%) were published from 2020 onward, and the busiest period so far is through 1999 with 49,090 records.
Reviews account for 20,936 records (15.0%) and meta-analyses for 1,196. Randomized controlled trials number 1,740 (1.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 49,090 |
| 2000-2009 | 27,075 |
| 2010-2019 | 35,303 |
| 2020 onward | 27,793 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 20,936 | 15.0% |
| Meta-analyses | 1,196 | 0.9% |
| Randomized controlled trials | 1,740 | 1.2% |
Method: PubMed query "Epilepsy"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in neuroscience
Neuroscience draws on tools with different strengths: cellular and animal work can manipulate circuits directly, while human imaging and electrophysiology observe the living brain at lower resolution. Small imaging studies are prone to false positives, and findings in animals do not always carry over to people. Clinical neurology and psychiatry rely on trials and cohort studies whose outcomes are often symptom scales. Check the species, the sample size, how the outcome was measured and whether results were replicated.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| Individualized antisense oligonucleotides for SCN2A-related developmental epileptic encephalopathy | 2026 | Research article Design not recorded in structured metadata | 2 | cc by PMID 42481851 · DOI · PMC13472884 |
| Neuroinflammation in Epilepsy: Biochemical and Molecular Mechanisms and Implications for Natural Product-Driven Drug Discovery | 2026 | Review article Design not recorded in structured metadata | 2 | cc by PMID 42450128 · DOI · PMC13362060 |
| Anti-Inflammatory and Antioxidant Strategies in Epilepsy: From Molecular Mechanisms to Threshold Management | 2026 | Review article Design not recorded in structured metadata | 1 | cc by PMID 42589265 · DOI · PMC13466846 |
Individualized antisense oligonucleotides for SCN2A-related developmental epileptic encephalopathy [1]
Abstract reading summary — source excerpts
- Opening excerpt
- SCN2A variants are among the most common genetic causes of developmental and epileptic encephalopathies (DEEs), which can present with uncontrolled seizures at birth and account for 1-2% of all epileptic encephalopathies.
- Closing excerpt
- gov registration: NCT06314490 .
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (240 words)
SCN2A variants are among the most common genetic causes of developmental and epileptic encephalopathies (DEEs), which can present with uncontrolled seizures at birth and account for 1-2% of all epileptic encephalopathies. A substantial fraction of causal variants are gain-of-function or mixed-function variants associated with increased channel open probability or greater sodium current flux. Here two parallel n = 1 clinical studies were conducted in two patients (9-year-old and 14-year-old boys) with SCN2A-related DEE. Individualized allele-selective antisense oligonucleotides (ASOs) were designed to target heterozygous intronic single-nucleotide polymorphisms (SNPs) for decreased expression of mutant SCN2A transcript while preserving the wild-type copy. Primary endpoints included quantitative change from baseline in seizure frequency and neurodevelopment, including motor scores. Efficacy measures were also individualized to each patient's phenotype, including refractory seizures, developmental delay, autism spectrum disorder, choreoathetosis and gastrointestinal dysfunction. Patients experienced a reduction in seizure frequency (26% and 90% in the two patients, respectively), decreased use of concomitant medications and improvement in neurodevelopmental skills. Both ASOs were well tolerated, with no ASO-related serious adverse events. Continued long-term follow-up of these preliminary positive safety and efficacy findings is needed to confirm the disease-modifying potential of these ASOs. Haplotype phasing in a separate cohort of infants with SCN2A-related disorder (SCN2A-RD), diagnosed by rapid whole-genome sequencing, identified 16% of patients with compatible SNPs. These data provide a pathway from n = 1 to n of more patients with SCN2A-RD and other monogenic disorders. ClinicalTrials.gov registration: NCT06314490 .
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42481851 · DOI · PMC13472884
Neuroinflammation in Epilepsy: Biochemical and Molecular Mechanisms and Implications for Natural Product-Driven Drug Discovery [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Epilepsy is a chronic neurological disorder prevalent worldwide, characterized by recurrent episodes of epileptic seizures.
- Closing excerpt
- In this context, natural products stand out as promising therapeutic alternatives, given their multitarget mechanisms of action, potential to attenuate neuroinflammation and neuronal hyperexcitability.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
Epilepsy is a chronic neurological disorder prevalent worldwide, characterized by recurrent episodes of epileptic seizures. The primary current treatment approach is pharmacological, aimed at reducing the intensity and frequency of seizures, though it does not provide a cure. Neuroinflammation plays a central role in epilepsy by activating glial cells and stimulating the release of inflammatory mediators, further disrupting the balance between excitation and inhibition, thereby promoting the onset and recurrence of seizures. Furthermore, persistent inflammatory processes induce synaptic remodeling and the formation of dysfunctional neural circuits, establishing a pathological cycle in which inflammation and epileptic activity feed into each other. In this regard, natural products represent an important avenue for the discovery of new treatments. Thus, this review aimed to relate the role of the main inflammatory targets (Inflammasome/NLRP3, NF-κB, MAPK, mTOR, COX-2/PGE2, and TLR4/HMGB1) to epilepsy and to investigate in the literature natural products acting through these pathways in the treatment of epileptic seizures. Consequently, inflammatory pathways have emerged as critical targets in epilepsy, highlighting the importance of strategies capable of modulating neuroinflammatory processes. In this context, natural products stand out as promising therapeutic alternatives, given their multitarget mechanisms of action, potential to attenuate neuroinflammation and neuronal hyperexcitability.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42450128 · DOI · PMC13362060
Anti-Inflammatory and Antioxidant Strategies in Epilepsy: From Molecular Mechanisms to Threshold Management [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Epilepsy is a multifactorial disorder, yet routine management still focuses on neuronal excitation and insufficient inhibition, with antiseizure medications (ASMs) as the primary therapeutic strategy.
- Closing excerpt
- Together, these proposals reframe epilepsy management from sequential pharmacological trials toward coordinated optimization of the full seizure threshold landscape.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (174 words)
Epilepsy is a multifactorial disorder, yet routine management still focuses on neuronal excitation and insufficient inhibition, with antiseizure medications (ASMs) as the primary therapeutic strategy. This approach fails in roughly one-third of patients who develop drug-resistant epilepsy (DRE). Converging evidence links DRE with neuroinflammation, oxidative stress (OS), and mitochondrial dysfunction-an interconnected distal pathophysiological triad that progressively lowers seizure thresholds yet remains peripheral to clinical epilepsy management. We map this triad mechanistically and show that ASMs modulate it beyond their anticonvulsant activity, while triad-targeting pharmacological, dietary, and botanical interventions independently reduce seizure susceptibility. Common precipitants are reinterpreted as acute activators of the distal triad, linking precipitant identification and patient agency to threshold elevation. Integrating these elements, we propose a threshold management framework for DRE, built on a revised reservoir model, and translate it into three structural priorities: mechanistic phenotyping to stratify patients by pathophysiological domain, dual-mechanism drug development, and trial designs suited to multicomponent, context-dependent interventions. Together, these proposals reframe epilepsy management from sequential pharmacological trials toward coordinated optimization of the full seizure threshold landscape.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42589265 · DOI · PMC13466846
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Incidence and Prevalence of Drug-Resistant Epilepsy: A Systematic Review and Meta-analysis [4]
- Research article GWAS meta-analysis of over 29,000 people with epilepsy identifies 26 risk loci and subtype-specific genetic architecture [5]
- Research article Treatment of seizures in the neonate: Guidelines and consensus-based recommendations-Special report from the ILAE Task Force on Neonatal Seizures [6]
- Research article Genetic testing and counseling for the unexplained epilepsies: An evidence-based practice guideline of the National Society of Genetic Counselors [7]
- Research article Prevalence of epilepsy in autism spectrum disorders: A systematic review and meta-analysis [8]
- Research article Ketogenic diet for epilepsy: an overview of systematic review and meta-analysis [9]
References
- Kim-McManus O, Mignon L, Douville J, Pu H, Parisien C, Glass S, et al.. Individualized antisense oligonucleotides for SCN2A-related developmental epileptic encephalopathy. . 2026. PMID 42481851 · DOI · PMC13472884
- Dias AL, da Silva PR, Souza LRP, Pires HFO, Gonçalves MCF, Neri LCD, et al.. Neuroinflammation in Epilepsy: Biochemical and Molecular Mechanisms and Implications for Natural Product-Driven Drug Discovery. . 2026. PMID 42450128 · DOI · PMC13362060
- Trofimov A, Shcherbakova K, Schwarz A, Akbay B, Karapina O, Myrkhiyeva Z, et al.. Anti-Inflammatory and Antioxidant Strategies in Epilepsy: From Molecular Mechanisms to Threshold Management. . 2026. PMID 42589265 · DOI · PMC13466846
- Sultana B, Panzini MA, Veilleux Carpentier A, Comtois J, Rioux B, Gore G, et al.. Incidence and Prevalence of Drug-Resistant Epilepsy: A Systematic Review and Meta-analysis. Neurology. 2021. PMID 33722992 · DOI
- International League Against Epilepsy Consortium on Complex Epilepsies. GWAS meta-analysis of over 29,000 people with epilepsy identifies 26 risk loci and subtype-specific genetic architecture. Nat Genet. 2023. PMID 37653029 · DOI · PMC10484785
- Pressler RM, Abend NS, Auvin S, Boylan G, Brigo F, Cilio MR, et al.. Treatment of seizures in the neonate: Guidelines and consensus-based recommendations-Special report from the ILAE Task Force on Neonatal Seizures. Epilepsia. 2023. PMID 37655702 · DOI
- Smith L, Malinowski J, Ceulemans S, Peck K, Walton N, Sheidley BR, et al.. Genetic testing and counseling for the unexplained epilepsies: An evidence-based practice guideline of the National Society of Genetic Counselors. J Genet Couns. 2023. PMID 36281494 · DOI
- Liu X, Sun X, Sun C, Zou M, Chen Y, Huang J, et al.. Prevalence of epilepsy in autism spectrum disorders: A systematic review and meta-analysis. Autism. 2022. PMID 34510916 · DOI
- Ruan Y, Chen L, She D, Chung Y, Ge L, Han L. Ketogenic diet for epilepsy: an overview of systematic review and meta-analysis. Eur J Clin Nutr. 2022. PMID 35027683 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.