Evidence map›Paper›PMID 41932958›Full record

ArticleScientific reports2026

Qualitative EEG abnormalities in ASD reflect inhibition-dominated brain dynamics.

Arthur-Ervin Avramiea, Erika L Juarez-Martinez, Pilar Garcés, Joerg F Hipp, Simon-Shlomo Poil, Marina Diachenko, Huibert D Mansvelder, Emily Jones, Luke Mason, Declan Murphy and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–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

1 citing paper in PubMed.

  1. Diverse excess GABA modes drive autism and epilepsy-autism comorbidity.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Article
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

18 authors.

Arthur-Ervin AvramieaDepartment of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research, (CNCR), Amsterdam Neuroscience, VU Amsterdam, De Boelelaan 1100, 1081 HV, Amsterdam, The Netherlands.
Erika L Juarez-MartinezDepartment of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research, (CNCR), Amsterdam Neuroscience, VU Amsterdam, De Boelelaan 1100, 1081 HV, Amsterdam, The Netherlands.
Pilar GarcésRoche Pharma Research and Early Development, Neuroscience and Rare Diseases, Roche Innovation Center Basel, Basel, Switzerland.
Joerg F HippRoche Pharma Research and Early Development, Neuroscience and Rare Diseases, Roche Innovation Center Basel, Basel, Switzerland.
Simon-Shlomo PoilAspect Neuroprofiles BV, Amsterdam, The Netherlands.
Marina DiachenkoDepartment of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research, (CNCR), Amsterdam Neuroscience, VU Amsterdam, De Boelelaan 1100, 1081 HV, Amsterdam, The Netherlands.
Huibert D MansvelderDepartment of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research, (CNCR), Amsterdam Neuroscience, VU Amsterdam, De Boelelaan 1100, 1081 HV, Amsterdam, The Netherlands.
Emily JonesDepartment of Psychological Sciences, Centre for Brain and Cognitive Development, Birkbeck, University of London, London, UK.
Luke MasonDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Declan MurphyDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Eva LothDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Bethany OakleyDepartment of Forensic and Neurodevelopmental Sciences, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Tony CharmanDepartment of Psychology, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Tobias BanaschewskiDepartment of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, University of Heidelberg, German Center for Mental Health (DZPG), Partner Site Mannheim-Heidelberg-Ulm, Mannheim, Germany.
Bob OranjeCenter for Neuropsychiatric Schizophrenia Research (CNSR), Psychiatric Center Glostrup, Copenhagen University Hospital, Copenhagen, Denmark.
Jan BuitelaarDepartment of Medical Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboudumc, Nijmegen, The Netherlands.
Hilgo Bruining *Child and Adolescent Psychiatry and Psychosocial Care, Emma Children's Hospital, Amsterdam UMC, Vrije Universiteit Amsterdam, Meibergdreef 5, 1105 AZ, Amsterdam, The Netherlands. h.bruining@amsterdamumc.nl.
Klaus Linkenkaer-Hansen *Department of Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research, (CNCR), Amsterdam Neuroscience, VU Amsterdam, De Boelelaan 1100, 1081 HV, Amsterdam, The Netherlands. klaus.linkenkaer@cncr.vu.nl.

Funding

Amsterdam UMC TKI grant BRAINinBALANCE project number 31556-2012377H2020 Society 604102Nederlandse Organisatie voor Wetenschappelijk Onderzoek 10250022110003Nederlandse Organisatie voor Wetenschappelijk Onderzoek 406-15-256Nederlandse Organisatie voor Wetenschappelijk Onderzoek 612.001.123NWA NWA.1160.18.200
6 · The paper itself

Abstract

Qualitative EEG abnormalities are common in Autism Spectrum Disorder (ASD) and hypothesized to reflect disrupted excitation/inhibition (E/I) balance. To test this, we recently introduced a functional measure of network-level E/I ratio (fE/I). Here, we applied fE/I and other EEG measures to alpha oscillations from source-reconstructed data in the EU-AIMS dataset (267 ASD, 209 controls). We analyzed these measures alongside qualitative EEG abnormalities ranging from slowing of activity to epileptiform patterns, aiming to replicate the findings from the SPACE-BAMBI study. Contrary to our previous report, we did not observe increased fE/I variability in ASD compared to controls. EEG abnormalities were rare in adults and could not be statistically assessed. ASD children-adolescents with EEG abnormalities exhibited lower relative alpha power and fE/I compared to those without. However, EEG-abnormality scoring did not stratify the behavioral heterogeneity of ASD using clinical measures. Surprisingly, several controls also exhibited qualitative EEG abnormalities with a strikingly similar anatomical distribution of reduced fE/I, reflecting inhibition-dominated network dynamics in sensory processing regions. The robustness of this association between EEG abnormalities and reduced fE/I was further supported by re-analysis of the SPACE-BAMBI study in source space. Stratification by the presence of EEG abnormalities and their effects on network activity may help understand neurodevelopmental physiological heterogeneity and the difficulties in implementing E/I targeting treatments in unselected cohorts.

Indexed as

Autism Spectrum DisorderBrainElectroencephalographyAdolescentChildFemaleHumansMaleAutism spectrum disorderEEGExcitation-inhibition balance

Identifiers

PMID41932958
PMCPMC13199430

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