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Mortality and cause of death in childhood onset epilepsy: A population-based cohort study in Finland

Starck, Christian; Helminen, Mika; Nevalainen, Olli P.O.; Eriksson, Kai; Auvinen, Anssi (2026-04)

 
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Mortality_and_cause_of_death_in_childhood_onset_epilepsy.pdf (887.7Kt)
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Starck, Christian
Helminen, Mika
Nevalainen, Olli P.O.
Eriksson, Kai
Auvinen, Anssi
04 / 2026

Seizure
doi:10.1016/j.seizure.2026.03.006
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Julkaisun pysyvä osoite on
https://urn.fi/URN:NBN:fi:tuni-202603233434

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Peer reviewed
Tiivistelmä
Objective To estimate mortality, causes of death, and sudden unexpected death in epilepsy (SUDEP) in childhood onset epilepsy (COE). Methods We identified a population-based cohort of 312 individuals with COE in Tampere University Hospital district with an inception date of December 31, 1992. We gathered death certificates and forensic autopsy records from the Finnish Institute for Health and Welfare and the National Archives of Finland, with follow-up ending in January 2018. Population mortality rates by age and sex were obtained from Statistics Finland for the study period to calculate standardized mortality rates (SMRs). Statistics Finland also provided yearly life expectancy estimates for calculating potential years of life lost (YLL). Results A total of 29 patients died during the follow-up, corresponding to a mortality of 3.9 (2.6–5.6) per 1000 person-years, with a median age at time of death of 22.6 years (IQR 19.4–27.0). We identified ten SUDEP cases (34.5 % of all deaths). All-cause SMR was 6.78 (4.54–9.73). Patients without disabilities had a non-significantly increased SMR (2.56, 0.94–5.58). Patients who were seizure-free for a year or more at baseline had a lower SMR than patients with continued seizures (2.94, 1.18–6.06 vs. 11.59, 7.27–17.55). Symptomatic etiology predicted increased mortality (12.82, 7.6–20.26), whereas genetic etiology was not associated with a significantly increased mortality (3.28, 0.89–8.39). Conclusions COE was associated with increased mortality, with SUDEP accounting a third of all deaths. Seizure freedom at baseline and genetic etiology related to lower mortality than continued seizures or symptomatic etiology.
Kokoelmat
  • TUNICRIS-julkaisut [24189]
Kalevantie 5
PL 617
33014 Tampereen yliopisto
oa[@]tuni.fi | Tietosuoja | Saavutettavuusseloste
 

 

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Kirjaudu sisäänRekisteröidy
Kalevantie 5
PL 617
33014 Tampereen yliopisto
oa[@]tuni.fi | Tietosuoja | Saavutettavuusseloste