C-reactive protein and seizures in focal epilepsy: a video-electroencephalographic study

Purpose: C‐reactive protein (CRP) has been studied extensively in many noninflammatory neurologic conditions, but there has been little study of CRP in the context of seizures or epilepsy. The purpose of this study was to examine CRP concentrations in patients with refractory focal epilepsy who were undergoing video‐electroencephalography (EEG) monitoring compared with healthy controls, and CRP change during 24 h after a seizure. Methods: CRP levels were measured in serum at the onset of video‐EEG recording (CRP‐0h) and at 3, 6, 12, and 24 h after index seizure (the first verified localized‐onset seizure) in 31 patients during inpatient video‐EEG monitoring by using high sensitivity measurement of CRP concentration. The patients were categorized into two groups: temporal lobe epilepsy (TLE; n = 15) and extratemporal lobe epilepsy (XLE; n = 16). Eighty healthy volunteers served as controls. Key Findings: CRP‐0h concentration was significantly higher in patients with refractory focal epilepsy than in controls (3.5 vs. 0.7 mg/ml, p < 0.001). All five patients with elevated CRP‐0h (>mean + 2 standard deviations in controls) had TLE (vs. none in XLE; p = 0.018). Index seizure type was associated with CRP increase from baseline to maximum level after index seizure (p = 0.005). The most important predictor of increase in CRP level was secondarily generalized tonic–clonic seizure (SGTCS; p = 0.030). Significance: The higher baseline levels in patients with epilepsy compared with healthy controls demonstrates that CRP concentrations are also affected in refractory epilepsy. Our data suggest that SGTCS stimulates CRP production. These results emphasize the association between inflammation and refractory epilepsy.