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Review Article
Published online: 2019-09-26
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Epilepsy and hypertension: The possible link for SUDEP?

Patrycja J. Szczurkowska, Katarzyna Polonis, Christiane Becari, Michał Hoffmann, Krzysztof Narkiewicz, Marzena Chrostowska
DOI: 10.5603/CJ.a2019.0095
·
Pubmed: 31565791

open access

Ahead of print
Review articles
Published online: 2019-09-26

Abstract

Epilepsy affects about 50 million people worldwide. Sudden unexpected death in epilepsy (SUDEP) is the main cause of death in epilepsy accounting for up to 17% of all deaths in epileptic patients, and therefore remains a major public health problem. SUDEP likely arises from a combination and interaction of multiple risk factors (such as being male, drug resistance, frequent generalized tonic-clonic seizures) making risk prediction and mitigation challenging. While there is a general understanding of the physiopathology of SUDEP, mechanistic hypotheses linking risk factors with a risk of SUDEP are still lacking. Identifying cross-talk between biological systems implicated in SUDEP may facilitate the development of improved models for SUDEP risk assessment, treatment and clinical management. In this review, the  aim was to explore an overlap between the pathophysiology of hypertension, cardiovascular disease and epilepsy, and discuss its implication for SUDEP. Presented herein, evidence in literature in support of a cross-talk between the renin–angiotensin system (RAS) and sympathetic nervous system (SNS), both known to be involved in the development of hypertension and cardiovascular disease, and as one of the underlying mechanisms of SUDEP. This article also provides a brief description of local RAS in brain neuroinflammation and the role of centrally acting RAS inhibitors in epileptic seizure alleviation.

Abstract

Epilepsy affects about 50 million people worldwide. Sudden unexpected death in epilepsy (SUDEP) is the main cause of death in epilepsy accounting for up to 17% of all deaths in epileptic patients, and therefore remains a major public health problem. SUDEP likely arises from a combination and interaction of multiple risk factors (such as being male, drug resistance, frequent generalized tonic-clonic seizures) making risk prediction and mitigation challenging. While there is a general understanding of the physiopathology of SUDEP, mechanistic hypotheses linking risk factors with a risk of SUDEP are still lacking. Identifying cross-talk between biological systems implicated in SUDEP may facilitate the development of improved models for SUDEP risk assessment, treatment and clinical management. In this review, the  aim was to explore an overlap between the pathophysiology of hypertension, cardiovascular disease and epilepsy, and discuss its implication for SUDEP. Presented herein, evidence in literature in support of a cross-talk between the renin–angiotensin system (RAS) and sympathetic nervous system (SNS), both known to be involved in the development of hypertension and cardiovascular disease, and as one of the underlying mechanisms of SUDEP. This article also provides a brief description of local RAS in brain neuroinflammation and the role of centrally acting RAS inhibitors in epileptic seizure alleviation.

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Keywords

hypertension, epilepsy, SUDEP, cardiovascular diseases, renin angiotensin system, neuroinflammation

About this article
Title

Epilepsy and hypertension: The possible link for SUDEP?

Journal

Cardiology Journal

Issue

Ahead of print

Article type

Review Article

Published online

2019-09-26

DOI

10.5603/CJ.a2019.0095

Pubmed

31565791

Keywords

hypertension
epilepsy
SUDEP
cardiovascular diseases
renin angiotensin system
neuroinflammation

Authors

Patrycja J. Szczurkowska
Katarzyna Polonis
Christiane Becari
Michał Hoffmann
Krzysztof Narkiewicz
Marzena Chrostowska

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