Evidence map›Paper›PMID 39502073›Full record

ArticleStroke2024

Polygenic Risk of Epilepsy and Poststroke Epilepsy.

Santiago Clocchiatti-Tuozzo, Cyprien A Rivier, Shubham Misra, Johan Zelano, Rajarshi Mazumder, Lauren H Sansing, Adam de Havenon, Lawrence J Hirsch, David S Liebeskind, Emily J Gilmore and 5 more

Abstract read
In one paragraph

Article in Stroke, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Santiago Clocchiatti-Tuozzo *Department of Neurology, University of Gothenburg, Göteborg, Sweden (S.C.-T., C.A.R., S.M., L.H.S., A.d.H., L.J.H., E.J.G., K.N.S., J.A.K., G.J.F., N.K.M.).ORCID 0000-0001-5377-434X
Cyprien A Rivier *Department of Neurology, University of Gothenburg, Göteborg, Sweden (S.C.-T., C.A.R., S.M., L.H.S., A.d.H., L.J.H., E.J.G., K.N.S., J.A.K., G.J.F., N.K.M.).ORCID 0000-0002-1148-1829
Shubham MisraDepartment of Neurology, University of Gothenburg, Göteborg, Sweden (S.C.-T., C.A.R., S.M., L.H.S., A.d.H., L.J.H., E.J.G., K.N.S., J.A.K., G.J.F., N.K.M.).ORCID 0000-0002-4920-2573
Johan ZelanoDepartment of Clinical Neuroscience, University of Gothenburg, Göteborg, Sweden (J.Z.).ORCID 0000-0001-9445-4545
Rajarshi MazumderDepartment of Neurology, The University of California, Los Angeles (R.M., D.S.L.).ORCID 0000-0002-0489-5089
Lauren H SansingDepartment of Neurology, University of Gothenburg, Göteborg, Sweden (S.C.-T., C.A.R., S.M., L.H.S., A.d.H., L.J.H., E.J.G., K.N.S., J.A.K., G.J.F., N.K.M.).ORCID 0000-0002-6898-1680
Adam de HavenonDepartment of Neurology, University of Gothenburg, Göteborg, Sweden (S.C.-T., C.A.R., S.M., L.H.S., A.d.H., L.J.H., E.J.G., K.N.S., J.A.K., G.J.F., N.K.M.).ORCID 0000-0001-8178-8597
Lawrence J HirschDepartment of Neurology, University of Gothenburg, Göteborg, Sweden (S.C.-T., C.A.R., S.M., L.H.S., A.d.H., L.J.H., E.J.G., K.N.S., J.A.K., G.J.F., N.K.M.).ORCID 0000-0002-6333-832X
David S LiebeskindDepartment of Neurology, The University of California, Los Angeles (R.M., D.S.L.).ORCID 0000-0002-5109-8736
Emily J GilmoreDepartment of Neurology, University of Gothenburg, Göteborg, Sweden (S.C.-T., C.A.R., S.M., L.H.S., A.d.H., L.J.H., E.J.G., K.N.S., J.A.K., G.J.F., N.K.M.).ORCID 0000-0002-4659-6861
Kevin N ShethDepartment of Neurology, University of Gothenburg, Göteborg, Sweden (S.C.-T., C.A.R., S.M., L.H.S., A.d.H., L.J.H., E.J.G., K.N.S., J.A.K., G.J.F., N.K.M.).ORCID 0000-0003-2003-5473
Jennifer A KimDepartment of Neurology, University of Gothenburg, Göteborg, Sweden (S.C.-T., C.A.R., S.M., L.H.S., A.d.H., L.J.H., E.J.G., K.N.S., J.A.K., G.J.F., N.K.M.).ORCID 0000-0003-3072-6198
Bradford B WorrallDepartments of Neurology and Public Health Sciences, University of Virginia, Charlottesville (B.B.W.).ORCID 0000-0001-9386-4091
Guido J Falcone *Department of Neurology, University of Gothenburg, Göteborg, Sweden (S.C.-T., C.A.R., S.M., L.H.S., A.d.H., L.J.H., E.J.G., K.N.S., J.A.K., G.J.F., N.K.M.).ORCID 0000-0002-6407-0302
Nishant K Mishra *Department of Neurology, University of Gothenburg, Göteborg, Sweden (S.C.-T., C.A.R., S.M., L.H.S., A.d.H., L.J.H., E.J.G., K.N.S., J.A.K., G.J.F., N.K.M.).ORCID 0000-0002-9327-3707

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale Study Support Suite (YES3): Dashboard and Web Portal Software Supporting Research Workflow through integrated, customizable REDCap External ModulesP30AG021342 · NIA · YALE UNIVERSITY · PI Lauren Ferrante · 2002 to 2026
$37.9M
Yale Training Program in Geriatric Clinical Epidemiology and Aging-Related ResearchT32AG019134 · NIA · YALE UNIVERSITY · PI Terri R. Fried · 2001 to 2026
$7.5M
Etiological Role of Parasitic Exposure and Familial Susceptibility in Nodding Syndrome-Related EpilepsiesK01TW012178 · FIC · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Rajarshi Mazumder · 2022 to 2026
$957k
Intensive Blood Pressure Reduction in Deep Intracerebral HemorrhageR03NS112859 · NINDS · YALE UNIVERSITY · PI FALCONE, GUIDO JOSE, SHETH, KEVIN NAVIN · 2019 to 2020
$84k
FIC NIH HHS K01 TW012178NCATS NIH HHS UL1 TR001863NIA NIH HHS K76 AG059992NIA NIH HHS P30 AG021342NIA NIH HHS T32 AG019134NINDS NIH HHS R03 NS112859
6 · The paper itself

Abstract

backgroundEpilepsy is highly heritable, with numerous known genetic risk loci. However, the genetic predisposition's role in poststroke epilepsy (PSE) remains understudied. This study assesses whether a higher genetic predisposition to epilepsy raises poststroke survivor's risk of PSE.

methodsWe conducted a case-control genetic association study nested within the UK Biobank, a large UK-based prospective cohort. Our exposures of interest were 2 distinct polygenic risk scores-generalized and focal epilepsy-modeled as deciles and constructed using genetic variants identified in the latest International League Against Epilepsy genome-wide association study meta-analysis. We aimed to evaluate the association between these polygenic risk scores and their corresponding subtype of PSE-generalized and focal. In sensitivity analyses, we evaluated participants of European ancestry separately and considered focal and generalized epilepsy outcomes in participants without a history of stroke. In secondary analyses, we evaluated the polygenic risk of PSE by stroke subtype (ischemic, hemorrhagic, or any stroke). Multivariable logistic regression models were fitted, adjusting for age, sex, genetic ancestry, and the first 5 principal genetic components.

resultsAmong 17 549 UK Biobank stroke survivors with available genetic information (mean age, 61; 43% female), 185 (1%) developed generalized PSE, while 124 (0.7%) developed focal PSE. Multivariable logistic regression results showed that, when compared against the lowest decile, participants within the highest PRS decile for generalized PSE had 5-fold higher odds of developing generalized PSE (OR, 5.05 [95% CI, 2.37-12.5];

conclusionsOur findings suggest that, like other forms of epilepsy, genetic predisposition plays an essential role in PSE. These results underscore the need for future studies to elucidate the mechanisms underlying PSE development and to identify novel therapeutic avenues.

Indexed as

Genetic Predisposition to DiseaseMultifactorial InheritanceStrokeAgedCase-Control StudiesEpilepsies, PartialEpilepsyFemaleGenome-Wide Association StudyHumansMaleMiddle AgedProspective StudiesRisk FactorsUnited Kingdomepilepsygenetic risk scoregeneticspoststroke epilepsystroke

Identifiers

PMID39502073
PMCPMC11653790

What Socratic holds

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Registered trials

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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 Socratic graph.