Risk of poststroke epilepsy after reperfusion therapies: A national cohort study.


Journal

European journal of neurology
ISSN: 1468-1331
Titre abrégé: Eur J Neurol
Pays: England
ID NLM: 9506311

Informations de publication

Date de publication:
05 2023
Historique:
revised: 13 01 2023
received: 22 09 2022
accepted: 18 01 2023
medline: 6 4 2023
pubmed: 25 1 2023
entrez: 24 1 2023
Statut: ppublish

Résumé

The risk of poststroke epilepsy (PSE) after endovascular treatment (EVT) is not well characterized. In this nationwide study, we assessed the risk of PSE after EVT and identified associated predictors. We included all individuals (n = 3319) treated with EVT (±intravenous thrombolysis [IVT]) between 2015 and 2019 in the Swedish National Quality Register for EVT. Two control groups were identified from the Swedish Stroke Register: the first treated with IVT alone (n = 3132) and the second with no treatment (n = 3184), both matched for age, sex, stroke severity, and time of stroke. PSE developed in 7.9% (n = 410). The survival-adjusted 2-year risk was 6.5% (95% confidence interval [CI] = 5.28-7.70) after EVT, 10.0% (95% CI = 8.25-11.75) after IVT, and 12.3% after no revascularization (95% CI = 10.33-14.25). The hazard ratio (HR) of PSE after EVT was almost half compared to no treatment (HR = 0.51, 95% CI = 0.41-0.64). The risk of PSE after EVT was lower compared to no treatment in a multivariable Cox model that adjusted for age, sex, hemicraniectomy, and stroke severity (HR = 0.76, 95% CI = 0.60-0.96). Multivariable predictors of PSE after EVT were large infarction on computed tomography Day 1, high posttreatment National Institutes of Health Stroke Scale score, and need of assistance 3 months after stroke. IVT before EVT was associated with a lower risk of PSE (HR = 0.66, 95% CI = 0.46-0.94). This nationwide study identified a reduced risk of PSE after EVT. Markers of severe infarction after EVT were associated with PSE, whereas IVT given before EVT was protective.

Sections du résumé

BACKGROUND AND PURPOSE
The risk of poststroke epilepsy (PSE) after endovascular treatment (EVT) is not well characterized. In this nationwide study, we assessed the risk of PSE after EVT and identified associated predictors.
METHODS
We included all individuals (n = 3319) treated with EVT (±intravenous thrombolysis [IVT]) between 2015 and 2019 in the Swedish National Quality Register for EVT. Two control groups were identified from the Swedish Stroke Register: the first treated with IVT alone (n = 3132) and the second with no treatment (n = 3184), both matched for age, sex, stroke severity, and time of stroke.
RESULTS
PSE developed in 7.9% (n = 410). The survival-adjusted 2-year risk was 6.5% (95% confidence interval [CI] = 5.28-7.70) after EVT, 10.0% (95% CI = 8.25-11.75) after IVT, and 12.3% after no revascularization (95% CI = 10.33-14.25). The hazard ratio (HR) of PSE after EVT was almost half compared to no treatment (HR = 0.51, 95% CI = 0.41-0.64). The risk of PSE after EVT was lower compared to no treatment in a multivariable Cox model that adjusted for age, sex, hemicraniectomy, and stroke severity (HR = 0.76, 95% CI = 0.60-0.96). Multivariable predictors of PSE after EVT were large infarction on computed tomography Day 1, high posttreatment National Institutes of Health Stroke Scale score, and need of assistance 3 months after stroke. IVT before EVT was associated with a lower risk of PSE (HR = 0.66, 95% CI = 0.46-0.94).
CONCLUSIONS
This nationwide study identified a reduced risk of PSE after EVT. Markers of severe infarction after EVT were associated with PSE, whereas IVT given before EVT was protective.

Identifiants

pubmed: 36692236
doi: 10.1111/ene.15695
doi:

Substances chimiques

Fibrinolytic Agents 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1303-1311

Informations de copyright

© 2023 The Authors. European Journal of Neurology published by John Wiley & Sons Ltd on behalf of European Academy of Neurology.

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Auteurs

Hanna Eriksson (H)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Wallenberg Center for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden.

Annika Nordanstig (A)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Alexandros Rentzos (A)

Department of Interventional and Diagnostic Neuroradiology, Institute of Clinical Sciences, Sahlgrenska University Hospital, Gothenburg, Sweden.
Department of Radiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.

Johan Zelano (J)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Wallenberg Center for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden.
Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden.

Petra Redfors (P)

Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Department of Neurology, Sahlgrenska University Hospital, Gothenburg, Sweden.

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