Cardiovascular

Systemic inflammatory profiles associated with early EEG abnormalities following ischemic stroke: a cohort study.

TL;DR

Elevated neutrophil count is independently associated with early epileptiform discharges after ischemic stroke, supporting a role for systemic inflammation in acute post-stroke EEG hyperexcitability, while slow-wave activity mainly reflects stroke severity and local complications.

Key Findings

Epileptiform discharges (ED) after ischemic stroke were independently associated with higher white blood cell count, neutrophil count, and neutrophil-to-lymphocyte ratio (NLR).

  • White blood cell count: OR 1.15, 95% CI 1.02–1.31
  • Neutrophil count: OR 1.19, 95% CI 1.05–1.36
  • NLR: OR 1.08, 95% CI 1.01–1.15
  • Associations were identified after adjustment for relevant clinical variables in multivariable logistic regression
  • ED were present in 59 of 307 patients (overall cohort)

Neutrophil count showed the highest discriminative ability for epileptiform discharges and significantly improved model performance when added to clinical predictors.

  • Discriminative ability was assessed using receiver operating characteristic (ROC) analysis
  • Neutrophil count significantly improved model performance beyond clinical variables alone
  • This was the strongest-performing inflammatory biomarker among those tested

No peripheral inflammatory biomarker remained independently associated with slow-wave activity (SA) after multivariable adjustment in patients without epileptiform discharges.

  • Analysis restricted to patients without ED (n = 248)
  • Multivariable logistic regression was used to identify independent predictors of SA
  • Inflammatory biomarkers were measured 24 hours after admission

Stroke severity and hemorrhagic transformation were the main independent predictors of slow-wave activity after ischemic stroke.

  • These clinical variables, not inflammatory markers, drove SA in multivariable analysis
  • SA is interpreted as reflecting stroke severity and local brain complications rather than systemic inflammation
  • Patients without ED (n = 248) formed the subgroup for SA analysis

The study enrolled 307 patients with acute supratentorial ischemic stroke who underwent EEG within 72 hours of admission.

  • Single-center, retrospective observational cohort design
  • Peripheral inflammatory biomarkers were measured 24 hours after admission
  • EEGs were classified according to the presence of slow-wave activity (SA) and/or epileptiform discharges (ED)
  • 59 patients had epileptiform discharges; 248 patients did not

What This Means

This research suggests that after an ischemic stroke, different types of abnormal brain electrical activity (detected by EEG) have different underlying causes. The study followed 307 stroke patients and measured both blood inflammation markers and brain electrical activity within the first 72 hours. Researchers found that epileptiform discharges — abnormal electrical patterns that can signal seizure risk — were linked to higher levels of white blood cells, particularly neutrophils, which are a key part of the body's immune response. This suggests that the body's own inflammatory reaction after a stroke may contribute to the brain becoming electrically overexcitable in some patients. In contrast, slow-wave activity — another common EEG abnormality after stroke that reflects general brain disturbance — was not linked to any inflammation markers. Instead, slow-wave activity was primarily explained by how severe the stroke was and whether bleeding had occurred into the damaged brain tissue (hemorrhagic transformation). This indicates that slow-wave activity reflects direct structural brain damage rather than the body's immune response. These findings matter because they suggest that monitoring neutrophil levels shortly after a stroke might help clinicians identify patients at higher risk of early seizure-related brain activity, potentially informing monitoring strategies. The distinction between the two EEG patterns also highlights that post-stroke brain abnormalities arise through different biological pathways, which could eventually guide more targeted treatment approaches.

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Citation

Prandin G, Furlanis G, Ricci E, Mancinelli L, Vincis E, Quagliotto M, et al.. (2026). Systemic inflammatory profiles associated with early EEG abnormalities following ischemic stroke: a cohort study.. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology. https://doi.org/10.1007/s10072-026-09397-3