Postictal EEG Suppression and Peripheral Inflammatory Markers During Electroconvulsive Therapy: Evidence From...

Postictal EEG suppression is considered a key indicator of seizure quality during electroconvulsive therapy (ECT); however, its biological correlates remain incompletely understood. Emerging evidence suggests that systemic inflammatory activity may influence cortical recovery following induced seizures. Whether this neuroimmune interaction differs across psychiatric diagnoses has not been systematically examined.

This retrospective cross-sectional study analyzed EEG parameters recorded during ECT together with peripheral inflammatory markers in 60 patients undergoing ECT. The primary focus was schizoaffective disorder, with bipolar disorder and other diagnoses examined for comparison. EEG indices included tonic and clonic phase durations and postictal suppression. Inflammatory measures comprised C-reactive protein (CRP), neutrophil counts, hemoglobin levels, and composite indices such as the Inflammatory Burden Index (IBI). Associations were evaluated using Spearman correlation analyses with correction for multiple comparisons.

In the schizoaffective disorder subgroup, postictal duration showed strong and biologically coherent associations with inflammatory markers, including a significant inverse correlation with neutrophil count that remained robust after false discovery rate correction. Additional associations with hemoglobin levels and IBI were observed. In contrast, bipolar disorder demonstrated only a limited association between postictal duration and CRP, while other EEG-inflammatory relationships were weak or nonsignificant.

Postictal EEG suppression appears to reflect diagnosis-specific neuroimmune modulation during ECT, with schizoaffective disorder showing particularly pronounced coupling between cortical recovery and systemic inflammatory activity. Postictal EEG features may therefore represent biologically meaningful markers beyond conventional measures of seizure adequacy and contribute to a more mechanistic understanding of ECT response.