Risk of Autism After Pediatric Ischemic Stroke: A Nationwide Cohort Study.


Journal

Neurology
ISSN: 1526-632X
Titre abrégé: Neurology
Pays: United States
ID NLM: 0401060

Informations de publication

Date de publication:
10 05 2022
Historique:
received: 06 09 2021
accepted: 04 02 2022
pubmed: 23 3 2022
medline: 12 5 2022
entrez: 22 3 2022
Statut: ppublish

Résumé

Ischemic stroke increases the risk of neurodevelopmental disorders; however, the risk of autism is not thoroughly explored. Our aim was to evaluate risk of autism and risk factors for autism in children with pediatric ischemic stroke and in their first-degree relatives. In this cohort study, individuals with ischemic stroke from 1969 to 2016, <18 years of age, alive 1 week after stroke, and without prior autism were identified in Swedish national registers. Ten matched controls per index individual and all first-degree relatives of index individuals and controls were identified. Conditional Cox regression was used to calculate the risk of autism. Unconditional logistic regression was performed to analyze sex, gestational age, age at stroke diagnoses, comorbid adverse motor outcome, comorbid epilepsy, and a sibling with autism as risk factors for autism in children with ischemic stroke. Of the 1,322 index individuals, 46 (3.5%) were diagnosed with autism compared to 161 (1.2%) controls (adjusted hazard ratio [aHR] 3.02, 95% CI 2.15-4.25). There was no significant difference in risk of autism according to age at stroke: perinatal (aHR 2.69, 95% CI 1.44-5.03) and childhood stroke (aHR 3.18, 95% CI 2.12-4.78). The increased risk remained after exclusion of children born preterm or small for gestational age (aHR 3.78, 95% CI 2.55-5.60) and when children with stroke diagnosed from 1997 to 2014 were analyzed (aHR 2.91, 95% CI = 1.95-4.35). Compared to controls, the risk of autism was increased in individuals with ischemic stroke and comorbid epilepsy (aHR 7.05, 95% CI 3.74-13.30), as well as adverse motor outcome (aHR 4.28, 95% CI 2.44-7.51). When individuals with adverse motor outcome and epilepsy were censored, the risk of autism was still increased (aHR 2.37, 95% CI 1.45-3.85). Sex, gestational age, and having a sibling with autism were not associated with autism in individuals with pediatric ischemic stroke. An increased risk of autism was seen after pediatric ischemic stroke, particularly in individuals with comorbid epilepsy, and could not be explained by being born preterm or small for gestational age. The risk was increased also in individuals free from epilepsy and adverse motor outcome, implying that all children with ischemic stroke should be readily screened for autism if the disorder is suspected.

Sections du résumé

BACKGROUND AND OBJECTIVES
Ischemic stroke increases the risk of neurodevelopmental disorders; however, the risk of autism is not thoroughly explored. Our aim was to evaluate risk of autism and risk factors for autism in children with pediatric ischemic stroke and in their first-degree relatives.
METHODS
In this cohort study, individuals with ischemic stroke from 1969 to 2016, <18 years of age, alive 1 week after stroke, and without prior autism were identified in Swedish national registers. Ten matched controls per index individual and all first-degree relatives of index individuals and controls were identified. Conditional Cox regression was used to calculate the risk of autism. Unconditional logistic regression was performed to analyze sex, gestational age, age at stroke diagnoses, comorbid adverse motor outcome, comorbid epilepsy, and a sibling with autism as risk factors for autism in children with ischemic stroke.
RESULTS
Of the 1,322 index individuals, 46 (3.5%) were diagnosed with autism compared to 161 (1.2%) controls (adjusted hazard ratio [aHR] 3.02, 95% CI 2.15-4.25). There was no significant difference in risk of autism according to age at stroke: perinatal (aHR 2.69, 95% CI 1.44-5.03) and childhood stroke (aHR 3.18, 95% CI 2.12-4.78). The increased risk remained after exclusion of children born preterm or small for gestational age (aHR 3.78, 95% CI 2.55-5.60) and when children with stroke diagnosed from 1997 to 2014 were analyzed (aHR 2.91, 95% CI = 1.95-4.35). Compared to controls, the risk of autism was increased in individuals with ischemic stroke and comorbid epilepsy (aHR 7.05, 95% CI 3.74-13.30), as well as adverse motor outcome (aHR 4.28, 95% CI 2.44-7.51). When individuals with adverse motor outcome and epilepsy were censored, the risk of autism was still increased (aHR 2.37, 95% CI 1.45-3.85). Sex, gestational age, and having a sibling with autism were not associated with autism in individuals with pediatric ischemic stroke.
DISCUSSION
An increased risk of autism was seen after pediatric ischemic stroke, particularly in individuals with comorbid epilepsy, and could not be explained by being born preterm or small for gestational age. The risk was increased also in individuals free from epilepsy and adverse motor outcome, implying that all children with ischemic stroke should be readily screened for autism if the disorder is suspected.

Identifiants

pubmed: 35314504
pii: WNL.0000000000200253
doi: 10.1212/WNL.0000000000200253
pmc: PMC9141625
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1953-e1963

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.

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Auteurs

Heléne Sundelin (H)

From the Department of Women's and Children's Health (H.S.), Neuropediatric Unit, Karolinska University Hospital; Department of Medicine Solna (J.S., J.B.), Clinical Epidemiology Division, Karolinska Institutet, Stockholm; Department of Biomedical and Clinical Sciences (H.S., P.B.), Division of Children's and Women's Health, Linköping University; Department of Clinical Science and Education Södersjukhuset (J.B.); and Sachs' Children and Youth Hospital (J.B.), Stockholm, Sweden.

Jonas Söderling (J)

From the Department of Women's and Children's Health (H.S.), Neuropediatric Unit, Karolinska University Hospital; Department of Medicine Solna (J.S., J.B.), Clinical Epidemiology Division, Karolinska Institutet, Stockholm; Department of Biomedical and Clinical Sciences (H.S., P.B.), Division of Children's and Women's Health, Linköping University; Department of Clinical Science and Education Södersjukhuset (J.B.); and Sachs' Children and Youth Hospital (J.B.), Stockholm, Sweden.

Peter Bang (P)

From the Department of Women's and Children's Health (H.S.), Neuropediatric Unit, Karolinska University Hospital; Department of Medicine Solna (J.S., J.B.), Clinical Epidemiology Division, Karolinska Institutet, Stockholm; Department of Biomedical and Clinical Sciences (H.S., P.B.), Division of Children's and Women's Health, Linköping University; Department of Clinical Science and Education Södersjukhuset (J.B.); and Sachs' Children and Youth Hospital (J.B.), Stockholm, Sweden.

Jenny Bolk (J)

From the Department of Women's and Children's Health (H.S.), Neuropediatric Unit, Karolinska University Hospital; Department of Medicine Solna (J.S., J.B.), Clinical Epidemiology Division, Karolinska Institutet, Stockholm; Department of Biomedical and Clinical Sciences (H.S., P.B.), Division of Children's and Women's Health, Linköping University; Department of Clinical Science and Education Södersjukhuset (J.B.); and Sachs' Children and Youth Hospital (J.B.), Stockholm, Sweden.

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