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Updated: Jan 21, 2026

Motor Dual-Tasks for Gait Analysis and Evaluation in Post-Stroke Patients
Published on: March 11, 2021
Association of systemic inflammatory markers with post-stroke epilepsy after ischemic stroke: A competing risk
Pannaporn Imemkamon1, Somjet Tosamran2, Sununtha Jankaew3
1Division of Neurology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
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.
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