Autonomic dysfunction in epilepsy mouse models with implications for SUDEP research
Epilepsy has a high prevalence and can severely impair quality of life and increase the risk of premature death. Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in drug-resistant epilepsy and most often results from respiratory and cardiac impairments due to brainstem dysfu...
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Format: | Article |
Language: | English |
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Frontiers Media S.A.
2023-01-01
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Series: | Frontiers in Neurology |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fneur.2022.1040648/full |
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author | Jennifer Bauer Jennifer Bauer Orrin Devinsky Markus Rothermel Henner Koch |
author_facet | Jennifer Bauer Jennifer Bauer Orrin Devinsky Markus Rothermel Henner Koch |
author_sort | Jennifer Bauer |
collection | DOAJ |
description | Epilepsy has a high prevalence and can severely impair quality of life and increase the risk of premature death. Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in drug-resistant epilepsy and most often results from respiratory and cardiac impairments due to brainstem dysfunction. Epileptic activity can spread widely, influencing neuronal activity in regions outside the epileptic network. The brainstem controls cardiorespiratory activity and arousal and reciprocally connects to cortical, diencephalic, and spinal cord areas. Epileptic activity can propagate trans-synaptically or via spreading depression (SD) to alter brainstem functions and cause cardiorespiratory dysfunction. The mechanisms by which seizures propagate to or otherwise impair brainstem function and trigger the cascading effects that cause SUDEP are poorly understood. We review insights from mouse models combined with new techniques to understand the pathophysiology of epilepsy and SUDEP. These techniques include in vivo, ex vivo, invasive and non-invasive methods in anesthetized and awake mice. Optogenetics combined with electrophysiological and optical manipulation and recording methods offer unique opportunities to study neuronal mechanisms under normal conditions, during and after non-fatal seizures, and in SUDEP. These combined approaches can advance our understanding of brainstem pathophysiology associated with seizures and SUDEP and may suggest strategies to prevent SUDEP. |
first_indexed | 2024-04-11T00:36:38Z |
format | Article |
id | doaj.art-148b0209742c425d9e801033d62acd15 |
institution | Directory Open Access Journal |
issn | 1664-2295 |
language | English |
last_indexed | 2024-04-11T00:36:38Z |
publishDate | 2023-01-01 |
publisher | Frontiers Media S.A. |
record_format | Article |
series | Frontiers in Neurology |
spelling | doaj.art-148b0209742c425d9e801033d62acd152023-01-06T16:44:03ZengFrontiers Media S.A.Frontiers in Neurology1664-22952023-01-011310.3389/fneur.2022.10406481040648Autonomic dysfunction in epilepsy mouse models with implications for SUDEP researchJennifer Bauer0Jennifer Bauer1Orrin Devinsky2Markus Rothermel3Henner Koch4Department of Epileptology and Neurology, RWTH Aachen University, Aachen, GermanyInstitute for Physiology and Cell Biology, University of Veterinary Medicine Hannover, Foundation, Hannover, GermanyDepartments of Neurology, Neurosurgery and Psychiatry, NYU Langone School of Medicine, New York, NY, United StatesInstitute for Physiology and Cell Biology, University of Veterinary Medicine Hannover, Foundation, Hannover, GermanyDepartment of Epileptology and Neurology, RWTH Aachen University, Aachen, GermanyEpilepsy has a high prevalence and can severely impair quality of life and increase the risk of premature death. Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death in drug-resistant epilepsy and most often results from respiratory and cardiac impairments due to brainstem dysfunction. Epileptic activity can spread widely, influencing neuronal activity in regions outside the epileptic network. The brainstem controls cardiorespiratory activity and arousal and reciprocally connects to cortical, diencephalic, and spinal cord areas. Epileptic activity can propagate trans-synaptically or via spreading depression (SD) to alter brainstem functions and cause cardiorespiratory dysfunction. The mechanisms by which seizures propagate to or otherwise impair brainstem function and trigger the cascading effects that cause SUDEP are poorly understood. We review insights from mouse models combined with new techniques to understand the pathophysiology of epilepsy and SUDEP. These techniques include in vivo, ex vivo, invasive and non-invasive methods in anesthetized and awake mice. Optogenetics combined with electrophysiological and optical manipulation and recording methods offer unique opportunities to study neuronal mechanisms under normal conditions, during and after non-fatal seizures, and in SUDEP. These combined approaches can advance our understanding of brainstem pathophysiology associated with seizures and SUDEP and may suggest strategies to prevent SUDEP.https://www.frontiersin.org/articles/10.3389/fneur.2022.1040648/fullepilepsySUDEPbrainstemmouse modelscardiorespiratory activity |
spellingShingle | Jennifer Bauer Jennifer Bauer Orrin Devinsky Markus Rothermel Henner Koch Autonomic dysfunction in epilepsy mouse models with implications for SUDEP research Frontiers in Neurology epilepsy SUDEP brainstem mouse models cardiorespiratory activity |
title | Autonomic dysfunction in epilepsy mouse models with implications for SUDEP research |
title_full | Autonomic dysfunction in epilepsy mouse models with implications for SUDEP research |
title_fullStr | Autonomic dysfunction in epilepsy mouse models with implications for SUDEP research |
title_full_unstemmed | Autonomic dysfunction in epilepsy mouse models with implications for SUDEP research |
title_short | Autonomic dysfunction in epilepsy mouse models with implications for SUDEP research |
title_sort | autonomic dysfunction in epilepsy mouse models with implications for sudep research |
topic | epilepsy SUDEP brainstem mouse models cardiorespiratory activity |
url | https://www.frontiersin.org/articles/10.3389/fneur.2022.1040648/full |
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