Type, Etiology, and Duration of Epilepsy as Risk Factors for SUDEP: Further Analyses of a Population-Based Case-Control Study.


Journal

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

Informations de publication

Date de publication:
27 Nov 2023
Historique:
received: 08 05 2023
accepted: 28 08 2023
medline: 29 11 2023
pubmed: 10 10 2023
entrez: 9 10 2023
Statut: epublish

Résumé

We conducted a nationwide case-control study in Sweden to investigate the risk of sudden unexpected death in epilepsy (SUDEP) in relation to epilepsy duration, epilepsy type, and etiology in combination with occurrence and frequency of tonic-clonic seizures (TCS) and nocturnal TCS. The study comprised 255 SUDEP cases and 1,148 epilepsy controls. Clinical information was obtained from medical records. The association between SUDEP and risk factors was estimated by odds ratios (ORs) with 95% CIs calculated by conditional logistic regression to account for matching by sex and calendar time. The risk of SUDEP was elevated in people with focal (OR 1.48, 95% CI 1.00-2.20), generalized and focal (OR 3.51, 95% CI 1.55-7.96), or unknown (OR 2.43, 95% CI 1.29-4.57) vs generalized epilepsy type. Increased risk of SUDEP was also observed in relation to epilepsy with traumatic causes (OR 2.27, 95% CI 1.33-3.89 vs genetic etiology) or short duration (OR 1.71, 95% CI 1.01-2.87 for 0-5 vs 6-15 years duration). Among those with 1-3 TCS during the preceding year, structural epilepsy etiology was associated with a more than 10-fold increase 10.84 (4.85-24.27) in SUDEP risk compared with people with genetic epilepsy without TCS. The risk with ≥4 TCS the preceding year was similar among those with generalized and focal epilepsies. Those with ≥4 TCS had an OR of 210.73 (95% CI 28.40-∞) during years 0-5 compared with those free from TCS and an epilepsy duration of 6-15 years. The combination of short epilepsy duration (0-5 years) and nocturnal TCS conferred an OR of 45.99 (95% CI 12.19-173.61) compared with having longer duration (6-15 years) and being free from nocturnal TCS. Although certain etiologies, such as post-traumatic epilepsy, seem to entail a higher SUDEP risk, our data indicate that frequent and nocturnal TCS carry a similar level of risk whether focal or generalized from onset. The tonic-clonic part of the seizure seems to be decisive for the fatal outcome. SUDEP risk associated with TCS is highest during the first years after the epilepsy diagnosis which calls for effective TCS treatment and vigilance from the onset of diagnosis.

Sections du résumé

BACKGROUND AND OBJECTIVES OBJECTIVE
We conducted a nationwide case-control study in Sweden to investigate the risk of sudden unexpected death in epilepsy (SUDEP) in relation to epilepsy duration, epilepsy type, and etiology in combination with occurrence and frequency of tonic-clonic seizures (TCS) and nocturnal TCS.
METHODS METHODS
The study comprised 255 SUDEP cases and 1,148 epilepsy controls. Clinical information was obtained from medical records. The association between SUDEP and risk factors was estimated by odds ratios (ORs) with 95% CIs calculated by conditional logistic regression to account for matching by sex and calendar time.
RESULTS RESULTS
The risk of SUDEP was elevated in people with focal (OR 1.48, 95% CI 1.00-2.20), generalized and focal (OR 3.51, 95% CI 1.55-7.96), or unknown (OR 2.43, 95% CI 1.29-4.57) vs generalized epilepsy type. Increased risk of SUDEP was also observed in relation to epilepsy with traumatic causes (OR 2.27, 95% CI 1.33-3.89 vs genetic etiology) or short duration (OR 1.71, 95% CI 1.01-2.87 for 0-5 vs 6-15 years duration). Among those with 1-3 TCS during the preceding year, structural epilepsy etiology was associated with a more than 10-fold increase 10.84 (4.85-24.27) in SUDEP risk compared with people with genetic epilepsy without TCS. The risk with ≥4 TCS the preceding year was similar among those with generalized and focal epilepsies. Those with ≥4 TCS had an OR of 210.73 (95% CI 28.40-∞) during years 0-5 compared with those free from TCS and an epilepsy duration of 6-15 years. The combination of short epilepsy duration (0-5 years) and nocturnal TCS conferred an OR of 45.99 (95% CI 12.19-173.61) compared with having longer duration (6-15 years) and being free from nocturnal TCS.
DISCUSSION CONCLUSIONS
Although certain etiologies, such as post-traumatic epilepsy, seem to entail a higher SUDEP risk, our data indicate that frequent and nocturnal TCS carry a similar level of risk whether focal or generalized from onset. The tonic-clonic part of the seizure seems to be decisive for the fatal outcome. SUDEP risk associated with TCS is highest during the first years after the epilepsy diagnosis which calls for effective TCS treatment and vigilance from the onset of diagnosis.

Identifiants

pubmed: 37813583
pii: WNL.0000000000207921
doi: 10.1212/WNL.0000000000207921
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

e2257-e2265

Informations de copyright

© 2023 American Academy of Neurology.

Auteurs

Olafur Sveinsson (O)

From the Faculty of Medicine (O.S.), University of Iceland, Reykjavik; Department of Neurology (O.S., T.T.), Karolinska University Hospital; Department of Clinical Neuroscience (O.S., T.T.), and Institute of Environmental Medicine (T.A., S.C.), Karolinska Institutet, Stockholm; and Center for Occupational and Environmental Medicine (T.A.), Stockholm County Council, Sweden. olafursv@landspitali.is.

Tomas Andersson (T)

From the Faculty of Medicine (O.S.), University of Iceland, Reykjavik; Department of Neurology (O.S., T.T.), Karolinska University Hospital; Department of Clinical Neuroscience (O.S., T.T.), and Institute of Environmental Medicine (T.A., S.C.), Karolinska Institutet, Stockholm; and Center for Occupational and Environmental Medicine (T.A.), Stockholm County Council, Sweden.

Sofia Carlsson (S)

From the Faculty of Medicine (O.S.), University of Iceland, Reykjavik; Department of Neurology (O.S., T.T.), Karolinska University Hospital; Department of Clinical Neuroscience (O.S., T.T.), and Institute of Environmental Medicine (T.A., S.C.), Karolinska Institutet, Stockholm; and Center for Occupational and Environmental Medicine (T.A.), Stockholm County Council, Sweden.

Torbjörn Tomson (T)

From the Faculty of Medicine (O.S.), University of Iceland, Reykjavik; Department of Neurology (O.S., T.T.), Karolinska University Hospital; Department of Clinical Neuroscience (O.S., T.T.), and Institute of Environmental Medicine (T.A., S.C.), Karolinska Institutet, Stockholm; and Center for Occupational and Environmental Medicine (T.A.), Stockholm County Council, Sweden.

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