Systemic inflammatory profiles associated with early EEG abnormalities following ischemic stroke: a cohort study
Abstract Background Post-stroke inflammation (PSI) contributes to acute brain injury and may influence early electroencephalographic (EEG) abnormalities after ischemic stroke. Although systemic inflammatory biomarkers have prognostic value, their association with specific EEG patterns - slow-wave activity (SA) and epileptiform discharges (ED) - remains unclear. We investigated the relationship between peripheral inflammatory markers and early EEG alterations following ischemic stroke. Methods We conducted a single-center, retrospective observational study including 307 patients with acute supratentorial ischemic stroke who underwent EEG within 72 h from admission. Peripheral inflammatory biomarkers were measured 24 h after admission. EEGs were classified according to the presence of SA and/or ED. Multivariable logistic regression analyses were performed to identify independent predictors of SA and ED. Predictive performance was assessed using receiver operating characteristic (ROC) analysis. Results Among patients without ED ( n = 248), no inflammatory biomarker remained independently associated with SA after multivariable adjustment. Stroke severity and hemorrhagic transformation were the main independent predictors of SA. In the overall cohort, ED ( n = 59) were independently associated with higher white blood cell count (OR 1.15, 95% CI 1.02–1.31), neutrophil count (OR 1.19, 95% CI 1.05–1.36), and NLR (OR 1.08, 95% CI 1.01–1.15), after adjustment for relevant clinical variables. Neutrophil count showed the highest discriminative ability for ED and significantly improved model performance when added to clinical predictors. Conclusions Elevated neutrophil count is independently associated with early ED after ischemic stroke, supporting a role for systemic inflammation in acute post-stroke EEG hyperexcitability. In contrast, SA mainly reflects stroke severity and local complications.
Authors
- Laura Mancinelli
- Paolo Manganotti (ORCID: https://orcid.org/0000-0001-5305-6268)
- Giovanni Furlanis (ORCID: https://orcid.org/0000-0002-9954-0239)
- Giulia Mazzon (ORCID: https://orcid.org/0000-0003-0382-5975)
- Marinella Tomaselli
- Marcello Naccarato (ORCID: https://orcid.org/0000-0002-1825-0126)
- Gabriele Prandin (ORCID: https://orcid.org/0000-0002-5698-4737)
- Emanuele Vincis (ORCID: https://orcid.org/0009-0009-7628-1359)
- Magda Quagliotto
- Michele Malesani
- Edoardo Ricci
- Gianpiero Farina
- Paola Caruso
Institutions
- University of Trieste (IT)
- Ospedale di Cattinara (IT)
Publication Details
- Journal
- Neurological Sciences
- Published
- 2026-09-16
- DOI
- https://doi.org/10.1007/s10072-026-09397-3
- Primary Topic
- Neuroinflammation and Neurodegeneration Mechanisms
- Type
- article
- Field-Weighted Citation Impact
- 0.00