ArticleEpilepsia2025
Acute and persistent changes in neural oscillatory activity predict development of epilepsy following acute organophosphate intoxication in adult rats.
Article in Epilepsia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Seizure and Status Epilepticus in Human Organophosphate Poisoning: A Narrative Review.Neurology international · 2026Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
objectiveAcute organophosphate (OP) intoxication affects a significant number of individuals worldwide. Those who survive OP-induced cholinergic crisis, which includes status epilepticus, often develop neurological morbidities. Here, we provide a rigorous characterization of the acute and delayed electrophysiological responses to OP intoxication with the goal of identifying early electrophysiological changes that predict later brain changes, including spontaneous recurrent seizures (SRS).
methodsMale and female rats were implanted with electroencephalographic (EEG) and intracranial EEG electrodes prior to acute intoxication with diisopropylfluorophosphate (DFP). All animals received standard of care therapeutics and were recorded continuously for 70 min post-DFP, then again for 5 min at 180 min post-DFP, 1 day postexposure (DPE), 3 DPE, and 7 DPE. Between 7 and 14 DPE, animals were recorded continuously.
resultsIn both sexes, acute DFP intoxication produced rapid and robust elevations in broadband power that were reduced but not terminated by midazolam (MDZ). Theta-delta ratio (TDR) was reduced immediately following DFP exposure and was further depressed by MDZ intervention. In the days that followed, broadband power and TDR recovered toward baseline. From 7 to 14 DPE, electrographic spiking was observed in all animals, and 80% developed SRS. Increased broadband power during status epilepticus was positively correlated with spike rate and SRS frequency. Slower recovery of broadband power to baseline in the days following exposure also correlated with increased SRS burden. Finally, a higher acute TDR correlated with increased spike rates at 3 and 7 DPE. SIGNIFICANCE: The data presented in this study provide a rigorous characterization of post-DFP electrographic sequelae that significantly extends the field's current understanding of electrophysiological shifts caused by acute OP intoxication. Critically, we identified potential EEG-based biomarkers that may identify at-risk patients in a clinical setting.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.