EBioMedicine · 2025
Paroxysmal cortical slowing linked to drug-resistant epilepsy.
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Serlin Yonatan, Imtiaz Hamza, Avigdor Tamir, Minarik Anna, Lash Sina, Bardouille Timothy, Whatley Ben, Ikeda Kristin M, Milikovsky Dan Z, Inati Sara K, Rüber Theodor, Surges Rainer, Rácz Attila, Friedman Alon
Аннотация
BACKGROUND: Paroxysmal slow wave events (PSWEs), defined as electroencephalography (EEG) segments where the median power frequency falls below 6 Hz for ≥5 s, have been shown to predict epilepsy in patients with a first seizure. We evaluated the prevalence and localisation of PSWEs in large independent EEG datasets, exploring their potential as biomarkers for drug-resistant epilepsy (DRE).
METHODS: An exploratory analysis used 1064 participants from the Temple University EEG corpus, comparing patients with epilepsy (N = 903) with participants with seizure-mimics and normal EEGs (N = 161). Validation analysis used an independent cohort from Bonn University, comprising drug-responsive (N = 51) and patients with DRE (N = 44).
FINDINGS: In the exploratory analysis, the proportion of time PSWEs were detected was longer in epilepsy compared with participants without epilepsy (P < 0.0001). Analyses of aetiology and EEG localisation revealed that PSWEs were most prolonged in patients with reported focal epilepsy (P = 0.004), particularly with temporal lobe involvement (P = 0.005). Patients with DRE had prolonged time in PSWEs (P = 0.005), corresponding with an increased risk of refractoriness (OR = 1.9; 95% CI 1.2-2.9). Validation analysis confirmed these findings, with prolonged PSWEs in DRE vs. drug-responsive patients (P < 0.0001, AUC = 0.829). Based on the cutoff established in the exploratory cohort, prolonged time in PSWEs in the validation cohort was associated with increased DRE risk (OR = 5.14, 95% CI 2.1-12.3). In patients with poor surgical outcomes (Engel IB-IV, N = 13), pre-surgical EEGs showed prolonged time in PSWEs compared with Engel IA (N = 24, P = 0.038).
INTERPRETATION: Analysis of 1159 EEGs from two independent cohorts demonstrated that PSWEs are more prevalent and prolonged in patients with focal epilepsy and may indicate a lack of therapeutic response.
FUNDING: The Canadian Institutes of Health Research (168164, 180636).
METHODS: An exploratory analysis used 1064 participants from the Temple University EEG corpus, comparing patients with epilepsy (N = 903) with participants with seizure-mimics and normal EEGs (N = 161). Validation analysis used an independent cohort from Bonn University, comprising drug-responsive (N = 51) and patients with DRE (N = 44).
FINDINGS: In the exploratory analysis, the proportion of time PSWEs were detected was longer in epilepsy compared with participants without epilepsy (P < 0.0001). Analyses of aetiology and EEG localisation revealed that PSWEs were most prolonged in patients with reported focal epilepsy (P = 0.004), particularly with temporal lobe involvement (P = 0.005). Patients with DRE had prolonged time in PSWEs (P = 0.005), corresponding with an increased risk of refractoriness (OR = 1.9; 95% CI 1.2-2.9). Validation analysis confirmed these findings, with prolonged PSWEs in DRE vs. drug-responsive patients (P < 0.0001, AUC = 0.829). Based on the cutoff established in the exploratory cohort, prolonged time in PSWEs in the validation cohort was associated with increased DRE risk (OR = 5.14, 95% CI 2.1-12.3). In patients with poor surgical outcomes (Engel IB-IV, N = 13), pre-surgical EEGs showed prolonged time in PSWEs compared with Engel IA (N = 24, P = 0.038).
INTERPRETATION: Analysis of 1159 EEGs from two independent cohorts demonstrated that PSWEs are more prevalent and prolonged in patients with focal epilepsy and may indicate a lack of therapeutic response.
FUNDING: The Canadian Institutes of Health Research (168164, 180636).