1. Using Generalized Polyspike Train to Predict Drug-Resistant Idiopathic Generalized Epilepsy.
- Author
-
Conrad EC, Chugh N, Ganguly TM, Gugger JJ, Tizazu EF, Shinohara RT, Raghupathi R, Becker DA, Gelfand MA, Omole AT, Decker BM, Pathmanathan JS, Davis KA, and Ellis CA
- Subjects
- Case-Control Studies, Electroencephalography, Humans, Immunoglobulin E, Drug Resistant Epilepsy diagnosis, Drug Resistant Epilepsy drug therapy, Epilepsy, Generalized diagnosis, Epilepsy, Generalized drug therapy
- Abstract
Introduction: The authors tested the hypothesis that the EEG feature generalized polyspike train (GPT) is associated with drug-resistant idiopathic generalized epilepsy (IGE)., Methods: The authors conducted a single-center case-control study of patients with IGE who had outpatient EEGs performed between 2016 and 2020. The authors classified patients as drug-resistant or drug-responsive based on clinical review and in a masked manner reviewed EEG data for the presence and timing of GPT (a burst of generalized rhythmic spikes lasting less than 1 second) and other EEG features. A relationship between GPT and drug resistance was tested before and after controlling for EEG duration. The EEG duration needed to observe GPT was also calculated., Results: One hundred three patients were included (70% drug-responsive and 30% drug-resistant patients). Generalized polyspike train was more prevalent in drug-resistant IGE (odds ratio, 3.8; 95% confidence interval, 1.3-11.4; P = 0.02). This finding persisted when controlling for EEG duration both with stratification and with survival analysis. A median of 6.5 hours (interquartile range, 0.5-12.7 hours) of EEG recording was required to capture the first occurrence of GPT., Conclusions: The findings support the hypothesis that GPT is associated with drug-resistant IGE. Prolonged EEG recording is required to identify this feature. Thus, >24-hour EEG recording early in the evaluation of patients with IGE may facilitate prognostication., Competing Interests: E. C. Conrad received support from Ceribell and NIH R25 NS-065745. J. J. Gugger received support from Ceribell. M. A. Gelfand received research support from Aquestive, Biogen, Cerevel, Eisai, Engage, Otsuka, SK Life Science, and UCB. A. Omole received support from NIH R25 NS-065745. B. M. Decker received support from NIH T32 NS-061779. K. A. Davis received research support from Eisai. The remaining authors have no conflicts of interest to disclose., (Copyright © 2020 by the American Clinical Neurophysiology Society.)
- Published
- 2022
- Full Text
- View/download PDF