ArticleEBioMedicine2025
Paroxysmal cortical slowing linked to drug-resistant epilepsy.
Article in EBioMedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Paroxysmal slow waves mark ictal networks.Epilepsia · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundParoxysmal 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).
methodsAn 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).
findingsIn 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).
interpretationAnalysis 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.
fundingThe Canadian Institutes of Health Research (168164, 180636).
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.