Abstract
Objective We conducted a nationwide case-control study in Sweden to test the hypothesis that antiepileptic drugs (AEDs) mono- or polytherapy, adherence, antidepressants, neuroleptics, β-blockers, and statins are associated with sudden unexpected death in epilepsy (SUDEP) risk. Methods Included were 255 SUDEP cases and 1,148 matched controls. Information on clinical factors and medications came from medical records and the National Patient and Prescription Registers. The association between SUDEP and medications was assessed by odds ratios (ORs) with 95% confidence intervals (CIs) adjusted for potential risk factors including type of epilepsy, living conditions, comorbidity, and frequency of generalized tonic-clonic seizures (GTCS). Results Polytherapy, especially taking 3 or more AEDs, was associated with a substantially reduced risk of SUDEP (OR 0.31, 95% CI 0.14-0.67). Combinations including lamotrigine (OR 0.55, 95% CI 0.31-0.97), valproic acid (OR 0.53, 95% CI 0.29-0.98), and levetiracetam (OR 0.49, 95% CI 0.27-0.90) were associated with reduced risk. No specific AED was associated with increased risk. Regarding monotherapy, although numbers were limited, the lowest SUDEP risk was seen in users of levetiracetam (0.10, 95% CI 0.02-0.61). Having nonadherence mentioned in the medical record was associated with an OR of 2.75 (95% CI 1.58-4.78). Statin use was associated with a reduced SUDEP risk (OR 0.34, 95% CI 0.11-0.99) but selective serotonin reuptake inhibitor use was not. Conclusion These results provide support for the importance of medication adherence and intensified AED treatment for patients with poorly controlled GTCS in the effort to reduce SUDEP risk and suggest that comedication with statins may reduce risk.
| Original language | English |
|---|---|
| Pages (from-to) | E2509-E2518 |
| Journal | Neurology |
| Volume | 95 |
| Issue number | 18 |
| DOIs | |
| Publication status | Published - 3 Nov 2020 |
Bibliographical note
Funding Information:The study was supported by funding from Stockholm County Council, GlaxoSmithKline, and Citizens United for Research in Epilepsy (CURE). The sponsors had no influence on the conduct of the study, analysis, interpretation, writing of the manuscript, or the decision to publish the results.
Funding Information:
O. Sveinsson has received grants from GSK, personal fees from Biogen, and honoraria to his institution from Biogen and UCB for lectures and advisory board, outside the submitted work. T. Andersson and S. Carlsson report no disclosures. P. Mattsson received research support from the Uppsala County Council, CURE, Epilepsifonden, and Selander Foundation. T. Tomson is an employee of Karolinska Institutet, is associate editor of Epileptic Disorders, has received speaker's honoraria to his institution from Eisai, Sanofi, Sun Pharma, UCB, and Sandoz, and received research support from Stockholm County Council, EU, CURE, GSK, UCB, Eisai, and Bial. Go to Neurology.org/N for full disclosures.
Funding Information:
The Article Processing Charge was funded by Karolinska Institute.
Publisher Copyright:
Copyright © 2020 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology