Purpose The top citation article reflects the developmental milestone of a given field. The purpose of this bibliometric analysis was to identify and assess the 100 most-cited (T100) articles on the epigenetics mechanism of epilepsy. Methods The Web of Science Core Collection (WoSCC) database was used to investigate, and search terms related to epilepsy epigenetics were compiled. Results were ranked according to citation number. The publication year, citation density, authorship, journal, country, institution, manuscript type, theme, and clinical topics were further evaluated. Results The Web of Science search returned a total of 1231 manuscripts. The number of citations for a manuscript ranges from 739 to 75. The greatest number of manuscripts in the top 100 was published in the Human Molecular Genetics and Neurobiology of Disease (n = 4). The journal with the highest 2021 impact factor was Nature Medicine (IF = 87.244). The most-cited paper by Aid et al. reported a new nomenclature for mouse and rat BDNF gene and its expression profiles. Most manuscripts were original articles (n = 69), of which 52 (75.4%) report findings of basic scientific work. The most prevalent theme was microRNA (n = 29), and the most popular clinical topic was temporal lobe epilepsy (n = 13). Conclusions The research on the epigenetics mechanism of epilepsy was in its infancy but full of potential. The developmental history and current achievements of hot themes, including microRNA, DNA methylation, and temporal lobe epilepsy, were overviewed. This bibliometric analysis provides useful information and insight for researchers when launching new projects.

The genetic generalized epilepsies (GGEs) have been proved to generate from genetic impact by twin studies and family studies. The genetic mechanisms of generalized epilepsies are always updating over time. Although the genetics of GGE is complex, there are always new susceptibility genes coming up as well as copy number variations which can lead to important breakthroughs in exploring the problem. At the same time, the development of ClinGen fades out some of the candidate genes. This means we have to figure out what accounts for a reliable gene for GGE, in another word, which gene has sufficient evidence for GGE. This will improve our understanding of the genetic mechanisms of GGE. In this review, important up-to-date genetic mechanisms of GGE were discussed.