Association of systemic inflammatory markers with post-stroke epilepsy after ischemic stroke: A competing risk analysis
Issued Date
2026-02-01
Resource Type
ISSN
10591311
eISSN
15322688
Scopus ID
2-s2.0-105027658781
Pubmed ID
41554232
Journal Title
Seizure
Volume
135
Start Page
11
End Page
18
Rights Holder(s)
SCOPUS
Bibliographic Citation
Seizure Vol.135 (2026) , 11-18
Suggested Citation
Imemkamon P., Tosamran S., Jankaew S., Unwanatham N., Limotai C. Association of systemic inflammatory markers with post-stroke epilepsy after ischemic stroke: A competing risk analysis. Seizure Vol.135 (2026) , 11-18. 18. doi:10.1016/j.seizure.2026.01.004 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/114724
Title
Association of systemic inflammatory markers with post-stroke epilepsy after ischemic stroke: A competing risk analysis
Author(s)
Corresponding Author(s)
Other Contributor(s)
Abstract
Purpose Post-stroke epilepsy (PSE) is a serious long-term complication of ischemic stroke, yet early identification of patients at risk remains challenging. Systemic inflammatory biomarkers may reflect underlying epileptogenic processes. This study explored the association between neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and hemoglobin-to-lymphocyte ratio (HLR) and the subsequent development of PSE in a large, long-term cohort. Methods We retrospectively analyzed 1445 adult patients hospitalized for acute ischemic stroke between 2014 and 2017 at a university-affiliated center. Patients with prior epilepsy were excluded. Blood counts within 2 days of admission were used to calculate NLR, PLR, and HLR. PSE was defined as the occurrence of at least one unprovoked seizure beyond 7 days post-stroke. A competing risk model was used to assess associations, accounting for death as a competing event. Results Over a median follow-up of nearly 7 years, 43 patients (2.98 %) developed PSE. Median NLR was higher in the PSE group than in the non-PSE group (3.45 vs. 2.94; nominal p = 0.036). In multivariable competing risk analysis, continuous NLR was nominally associated with PSE (subdistribution hazard ratio [SHR] = 1.048, 95 % CI 1.002–1.100; p = 0.040). As an exploratory sensitivity analysis, NLR > 7 was also associated with increased PSE incidence (SHR = 2.20, 95 % CI 1.11–4.35; p = 0.024). PLR and HLR did not show associations with PSE. The PSE group also experienced higher mortality and longer hospital stays. Conclusion NLR, an inexpensive and readily available inflammatory marker, was nominally associated with the development of PSE after ischemic stroke. These findings are exploratory and hypothesis-generating, supporting further investigation into the role of systemic inflammation in post-stroke epileptogenesis.