Evidence map›Paper›PMID 39666315›Full record

ArticleEpilepsia2025

Neuronal complexity tracks changes of epileptic activity and identifies epilepsy patients independent of interictal epileptiform discharges.

Ricardo Kienitz, Michael Strüber, Nina Merkel, Annika Süß, Andrea Spyrantis, Adam Strzelczyk, Felix Rosenow

Abstract read
In one paragraph

Article in Epilepsia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Ricardo KienitzGoethe University Frankfurt, Epilepsy Center Frankfurt Rhine-Main, Department of Neurology, University Hospital Frankfurt, Frankfurt, Germany.ORCID https://orcid.org/0000-0003-2328-3413
Michael StrüberGoethe University Frankfurt, Epilepsy Center Frankfurt Rhine-Main, Department of Neurology, University Hospital Frankfurt, Frankfurt, Germany.ORCID https://orcid.org/0000-0002-3478-0848
Nina MerkelGoethe University Frankfurt, Epilepsy Center Frankfurt Rhine-Main, Department of Neurology, University Hospital Frankfurt, Frankfurt, Germany.
Annika SüßGoethe University Frankfurt, Epilepsy Center Frankfurt Rhine-Main, Department of Neurology, University Hospital Frankfurt, Frankfurt, Germany.
Andrea SpyrantisGoethe University Frankfurt, Epilepsy Center Frankfurt Rhine-Main, Department of Neurosurgery, University Hospital Frankfurt, Frankfurt, Germany.ORCID https://orcid.org/0000-0002-7635-6295
Adam StrzelczykGoethe University Frankfurt, Epilepsy Center Frankfurt Rhine-Main, Department of Neurology, University Hospital Frankfurt, Frankfurt, Germany.ORCID https://orcid.org/0000-0001-6288-9915
Felix RosenowGoethe University Frankfurt, Epilepsy Center Frankfurt Rhine-Main, Department of Neurology, University Hospital Frankfurt, Frankfurt, Germany.ORCID https://orcid.org/0000-0002-3989-7471

Funding

LOEWE Center for Personalized Translational Epilepsy Research (CePTER), III L6-519/03/03.001-(0007)
6 · The paper itself

Abstract

objectiveTo date, the identification of objective biomarkers of neural epileptic activity (EA) remains challenging. We therefore investigated whether neuronal complexity could serve as an interictal electroencephalographic measure of EA, independent of interictal epileptiform discharges (IEDs). By tapering anti-seizure medication (ASM) during video-EEG (electroencephalography) monitoring (VEM), we studied whether changes in neuronal complexity could reliably indicate the increase in EA and identify patients with epilepsy.

methodsThe study included 27 patients with unilateral mesial temporal lobe epilepsy (TLE) and 24 control patients with non-epileptic episodes (NEEs) only, each undergoing ASM reduction during VEM. Thirteen additional patients undergoing intracranial recordings during VEM were included to study the relation of surface EEG complexity to intracranial IED. Neuronal complexity was quantified using sample entropy. Delta power served as a control parameter. Receiver-operating characteristic (ROC) analysis was used to evaluate diagnostic performance.

resultsAs ASM was reduced, patients with epilepsy showed a significant decrease in neuronal complexity over consecutive days (p = .0008). In contrast, patients with NEE showed no significant change in neuronal complexity (p = .78). Delta power in contrast increased and did not differ significantly between patients with TLE and patients with NEE (p = 1). ROC analysis demonstrated that neuronal complexity effectively distinguished between patients with epilepsy and patients with NEE (area under the curve [AUC] = .76), whereas delta power performed at chance level (AUC = .5). Analysis of simultaneously recorded surface and intracranial EEG showed that hippocampal IEDs are followed by an increase in surface EEG delta power (p = 1.8 × 10 SIGNIFICANCE: An increase in EA caused by ASM reduction resulted in a loss of neuronal complexity in surface EEG recordings of patients with epilepsy, independent of IEDs. These findings suggest that neuronal complexity could serve as a potential biomarker to differentiate between epilepsy patients and those with NEEs only. This holds promise for improving the clinical evaluation of EA in epilepsy, addressing the limitations of seizure frequency and IED identification.

Indexed as

EpilepsyEpilepsy, Temporal LobeNeuronsAdolescentAdultAnticonvulsantsElectroencephalographyFemaleHumansMaleMiddle AgedYoung AdultAnticonvulsantsanti‐seizure medicationcomplexityEEGinterictal epileptiform dischargestemporal lobe epilepsy

Identifiers

PMID39666315
PMCPMC11908660

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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.