Evidence map›Paper›PMID 30525117›Full record

ArticleEpilepsia open2018

Unravelling the brain networks driving spike-wave discharges in genetic generalized epilepsy-common patterns and individual differences.

Silke Klamer, Thomas Ethofer, Franziska Torner, Ashish Kaul Sahib, Adham Elshahabi, Justus Marquetand, Pascal Martin, Holger Lerche, Michael Erb, Niels K Focke

Abstract read
In one paragraph

Article in Epilepsia open, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

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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

13 citing papers in PubMed.

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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

10 authors.

Silke KlamerDepartment of Neurology and Epileptology Hertie-Institute for Clinical Brain Research University of Tübingen Tübingen Germany.
Thomas EthoferDepartment of Biomedical Magnetic Resonance University of Tübingen Tübingen Germany.
Franziska TornerDepartment of Neurology and Epileptology Hertie-Institute for Clinical Brain Research University of Tübingen Tübingen Germany.
Ashish Kaul SahibDepartment of Neurology and Epileptology Hertie-Institute for Clinical Brain Research University of Tübingen Tübingen Germany.
Adham ElshahabiDepartment of Neurology and Epileptology Hertie-Institute for Clinical Brain Research University of Tübingen Tübingen Germany.
Justus MarquetandDepartment of Neurology and Epileptology Hertie-Institute for Clinical Brain Research University of Tübingen Tübingen Germany.
Pascal MartinDepartment of Neurology and Epileptology Hertie-Institute for Clinical Brain Research University of Tübingen Tübingen Germany.
Holger LercheDepartment of Neurology and Epileptology Hertie-Institute for Clinical Brain Research University of Tübingen Tübingen Germany.
Michael ErbDepartment of Biomedical Magnetic Resonance University of Tübingen Tübingen Germany.
Niels K FockeDepartment of Neurology and Epileptology Hertie-Institute for Clinical Brain Research University of Tübingen Tübingen Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGenetic generalized epilepsies (GGEs) are characterized by generalized spike-wave discharges (GSWDs) in electroencephalography (EEG) recordings without underlying structural brain lesions. The origin of the epileptic activity remains unclear, although several studies have reported involvement of thalamus and default mode network (DMN). The aim of the current study was to investigate the networks involved in the generation and temporal evolution of GSWDs to elucidate the origin and propagation of the underlying generalized epileptic activity.

methodsWe examined 12 patients with GGE and GSWDs using EEG-functional magnetic resonance imaging (fMRI) and identified involved brain areas on the basis of a classical general linear model (GLM) analysis. The activation time courses of these areas were further investigated to reveal their temporal sequence of activations and deactivations. Dynamic causal modeling (DCM) was used to determine the generator of GSWDs in GGE.

resultsWe observed activity changes in the thalamus, DMN, dorsal attention network (DAN), salience network (SN), basal ganglia, dorsolateral prefrontal cortex, and motor cortex with supplementary motor area, however, with a certain heterogeneity between patients. Investigation of the temporal sequence of activity changes showed deactivations in the DMN and DAN and activations in the SN and thalamus preceding the onset of GSWDs on EEG by several seconds. DCM analysis indicated that the DMN gates GSWDs in GGE. SIGNIFICANCE: The observed interplay between DMN, DAN, SN, and thalamus may indicate a downregulation of consciousness. The DMN seems to play a leading role as a driving force behind these changes. Overall, however, there were also clear differences in activation patterns between patients, reflecting a certain heterogeneity in this cohort of GGE patients.

Indexed as

Default mode networkDynamic causal modellingGeneralized spike‐wave dischargesGenetic generalized epilepsyThalamus

Identifiers

PMID30525117
PMCPMC6276776

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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.