Evidence map›Paper›PMID 27306624›Full record

ArticleNeurology2016

Autism and epilepsy: A population-based nationwide cohort study.

Heléne E K Sundelin, Henrik Larsson, Paul Lichtenstein, Catarina Almqvist, Christina M Hultman, Torbjörn Tomson, Jonas F Ludvigsson

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.0field-weighted citation impact, top 3% of its field
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

31 citing papers in PubMed, 83 citations in OpenAlex.

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  6. Epilepsy and childhood psychiatric disorders: a two-sample bidirectional Mendelian randomization study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Heléne E K SundelinFrom the Department of Pediatrics (H.E.K.S.), University Hospital, Linköping; Departments of Medical Epidemiology and Biostatistics (H.L., P.L., C.A., C.M.H., J.F.L.) and Clinical Neuroscience (T.T.), Karolinska Institutet; Astrid Lindgren Children's Hospital (C.A.), Karolinska University Hospital, Stockholm; Department of Pediatrics (J.F.L.), University Hospital, Örebro, Sweden; and Division of Epidemiology and Public Health (J.F.L.), School of Medicine, University of Nottingham, UK. helene.sundelin@hotmail.com.
Henrik LarssonFrom the Department of Pediatrics (H.E.K.S.), University Hospital, Linköping; Departments of Medical Epidemiology and Biostatistics (H.L., P.L., C.A., C.M.H., J.F.L.) and Clinical Neuroscience (T.T.), Karolinska Institutet; Astrid Lindgren Children's Hospital (C.A.), Karolinska University Hospital, Stockholm; Department of Pediatrics (J.F.L.), University Hospital, Örebro, Sweden; and Division of Epidemiology and Public Health (J.F.L.), School of Medicine, University of Nottingham, UK.
Paul LichtensteinFrom the Department of Pediatrics (H.E.K.S.), University Hospital, Linköping; Departments of Medical Epidemiology and Biostatistics (H.L., P.L., C.A., C.M.H., J.F.L.) and Clinical Neuroscience (T.T.), Karolinska Institutet; Astrid Lindgren Children's Hospital (C.A.), Karolinska University Hospital, Stockholm; Department of Pediatrics (J.F.L.), University Hospital, Örebro, Sweden; and Division of Epidemiology and Public Health (J.F.L.), School of Medicine, University of Nottingham, UK.
Catarina AlmqvistFrom the Department of Pediatrics (H.E.K.S.), University Hospital, Linköping; Departments of Medical Epidemiology and Biostatistics (H.L., P.L., C.A., C.M.H., J.F.L.) and Clinical Neuroscience (T.T.), Karolinska Institutet; Astrid Lindgren Children's Hospital (C.A.), Karolinska University Hospital, Stockholm; Department of Pediatrics (J.F.L.), University Hospital, Örebro, Sweden; and Division of Epidemiology and Public Health (J.F.L.), School of Medicine, University of Nottingham, UK.
Christina M HultmanFrom the Department of Pediatrics (H.E.K.S.), University Hospital, Linköping; Departments of Medical Epidemiology and Biostatistics (H.L., P.L., C.A., C.M.H., J.F.L.) and Clinical Neuroscience (T.T.), Karolinska Institutet; Astrid Lindgren Children's Hospital (C.A.), Karolinska University Hospital, Stockholm; Department of Pediatrics (J.F.L.), University Hospital, Örebro, Sweden; and Division of Epidemiology and Public Health (J.F.L.), School of Medicine, University of Nottingham, UK.
Torbjörn TomsonFrom the Department of Pediatrics (H.E.K.S.), University Hospital, Linköping; Departments of Medical Epidemiology and Biostatistics (H.L., P.L., C.A., C.M.H., J.F.L.) and Clinical Neuroscience (T.T.), Karolinska Institutet; Astrid Lindgren Children's Hospital (C.A.), Karolinska University Hospital, Stockholm; Department of Pediatrics (J.F.L.), University Hospital, Örebro, Sweden; and Division of Epidemiology and Public Health (J.F.L.), School of Medicine, University of Nottingham, UK.
Jonas F LudvigssonFrom the Department of Pediatrics (H.E.K.S.), University Hospital, Linköping; Departments of Medical Epidemiology and Biostatistics (H.L., P.L., C.A., C.M.H., J.F.L.) and Clinical Neuroscience (T.T.), Karolinska Institutet; Astrid Lindgren Children's Hospital (C.A.), Karolinska University Hospital, Stockholm; Department of Pediatrics (J.F.L.), University Hospital, Örebro, Sweden; and Division of Epidemiology and Public Health (J.F.L.), School of Medicine, University of Nottingham, UK.
Karolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the risk of autism spectrum disorder (ASD) in individuals with epilepsy and in their first-degree relatives to determine shared etiology.

methodsThrough the Swedish Patient Register, we identified 85,201 individuals with epilepsy, as well as all their siblings (n = 80,511) and offspring (n = 98,534). Each individual with epilepsy was compared with 5 controls, matched for age, sex, calendar period, and county, while siblings and offspring were compared with siblings and offspring of controls. We excluded siblings and offspring with epilepsy. Using Cox regression, we calculated hazard ratios (HRs) for future diagnosis of ASD. Logistic regression was applied to calculate odds ratios (ORs) for prior diagnosis of ASD.

resultsDuring follow-up, 1,381 (1.6%) individuals with epilepsy and 700 (0.2%) controls were diagnosed with ASD. Individuals with epilepsy were therefore at increased risk of future ASD (HR 10.49, 95% confidence interval [CI] 9.55-11.53), with the highest risk seen in individuals diagnosed with epilepsy in childhood. Both siblings (HR 1.62, 95% CI 1.43-1.83) and offspring (HR 1.64, 95% CI 1.46-1.84) of epilepsy patients were at increased risk of ASD. The risk in the offspring was particularly high in mothers with epilepsy (HR 1.91; 95% CI 1.63-2.23). Epilepsy was also associated with a prior diagnosis of ASD (OR 4.56, 95% CI 4.02-5.18).

conclusionsIndividuals with epilepsy are at increased risk of ASD, especially if epilepsy appears in childhood. Further, ASD is more common in the siblings and offspring of individuals with epilepsy, suggesting shared etiology.

Indexed as

AdolescentAdultAgedAged, 80 and overAutism Spectrum DisorderChildChild, PreschoolEpilepsyFamilyFemaleFollow-Up StudiesGenetic Predisposition to DiseaseHumansInfantInfant, NewbornMale

Identifiers

PMID27306624
PMCPMC4940061
OpenAlexW2420966984

What OpenQuestion holds

Textmetadata
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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 OpenQuestion graph.