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昼夜节律性癫痫发作的定时机制。

Timing Mechanisms for Circadian Seizures.

作者信息

Slabeva Kristina, Baud Maxime O

机构信息

Zentrum für Experimentelle Neurologie, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.

Schlaf-Wach Epilepsie Zentrum, Inselspital, Bern University Hospital, University of Bern, 3010 Bern, Switzerland.

出版信息

Clocks Sleep. 2024 Oct 21;6(4):589-601. doi: 10.3390/clockssleep6040040.

DOI:10.3390/clockssleep6040040
PMID:39449314
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11503444/
Abstract

For centuries, epileptic seizures have been noticed to recur with temporal regularity, suggesting that an underlying biological rhythm may play a crucial role in their timing. In this review, we propose to adopt the framework of chronobiology to study the circadian timing of seizures. We first review observations made on seizure timing in patients with epilepsy and animal models of the disorder. We then present the existing chronobiology paradigm to disentangle intertwined circadian and sleep-wake timing mechanisms. In the light of this framework, we review the existing evidence for specific timing mechanisms in specific epilepsy syndromes and highlight that current knowledge is far from sufficient. We propose that individual seizure chronotypes may result from an interplay between independent timing mechanisms. We conclude with a research agenda to help solve the urgency of ticking seizures.

摘要

几个世纪以来,人们注意到癫痫发作会以一定的时间规律反复出现,这表明潜在的生物节律可能在发作时间上起着关键作用。在这篇综述中,我们建议采用生物钟学的框架来研究癫痫发作的昼夜节律时间。我们首先回顾了对癫痫患者和该疾病动物模型的发作时间所做的观察。然后我们介绍现有的生物钟学范式,以厘清相互交织的昼夜节律和睡眠-觉醒时间机制。根据这个框架,我们回顾了特定癫痫综合征中特定时间机制的现有证据,并强调目前的知识还远远不够。我们提出个体发作时型可能是由独立时间机制之间的相互作用导致的。我们最后提出了一个研究议程,以帮助解决癫痫发作定时这一紧迫问题。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb69/11503444/2c947173bf41/clockssleep-06-00040-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb69/11503444/2c947173bf41/clockssleep-06-00040-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eb69/11503444/2c947173bf41/clockssleep-06-00040-g001.jpg

相似文献

1
Timing Mechanisms for Circadian Seizures.昼夜节律性癫痫发作的定时机制。
Clocks Sleep. 2024 Oct 21;6(4):589-601. doi: 10.3390/clockssleep6040040.
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本文引用的文献

1
Clock knockout in inhibitory neurons reduces predisposition to epilepsy and influences anxiety-like behaviors in mice.敲除抑制性神经元中的时钟基因可降低癫痫易感性并影响小鼠的焦虑样行为。
Neurobiol Dis. 2024 Apr;193:106457. doi: 10.1016/j.nbd.2024.106457. Epub 2024 Feb 28.
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Wake slow waves in focal human epilepsy impact network activity and cognition.在人类局灶性癫痫中,慢波觉醒会影响网络活动和认知。
Nat Commun. 2023 Nov 30;14(1):7397. doi: 10.1038/s41467-023-42971-3.
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Sleep and seizure risk in epilepsy: bed and wake times are more important than sleep duration.
癫痫患者的睡眠和癫痫发作风险:卧床和起床时间比睡眠时间更重要。
Brain. 2023 Jul 3;146(7):2803-2813. doi: 10.1093/brain/awac476.
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Desynchronizing the sleep---wake cycle from circadian timing to assess their separate contributions to physiology and behaviour and to estimate intrinsic circadian period.将睡眠-觉醒周期与昼夜节律时间解耦,以评估它们对生理和行为的单独贡献,并估计内在的昼夜周期。
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Photo-Dependent Reflex Seizures-A Scoping Review with Proposal of Classification.光依赖性反射性癫痫——一项分类建议的范围综述
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On the role of REM sleep microstructure in suppressing interictal spikes in Electrical Status Epilepticus during Sleep.在睡眠中电癫痫持续状态下抑制发作间期棘波中 REM 睡眠微观结构的作用。
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Robust chronic convulsive seizures, high frequency oscillations, and human seizure onset patterns in an intrahippocampal kainic acid model in mice.在小鼠海马内海人酸模型中表现出的持久慢性惊厥性发作、高频振荡和人类癫痫发作模式。
Neurobiol Dis. 2022 May;166:105637. doi: 10.1016/j.nbd.2022.105637. Epub 2022 Jan 26.
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Sleep Deprivation Exacerbates Seizures and Diminishes GABAergic Tonic Inhibition.睡眠剥夺可加重癫痫发作并减弱 GABA 能紧张性抑制。
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9
Seizure likelihood varies with day-to-day variations in sleep duration in patients with refractory focal epilepsy: A longitudinal electroencephalography investigation.难治性局灶性癫痫患者的癫痫发作可能性随睡眠时间的每日变化而变化:一项纵向脑电图研究。
EClinicalMedicine. 2021 Jun 5;37:100934. doi: 10.1016/j.eclinm.2021.100934. eCollection 2021 Jul.
10
Slow oscillations open susceptible time windows for epileptic discharges.慢波振荡打开癫痫放电的易损时间窗。
Epilepsia. 2021 Oct;62(10):2357-2371. doi: 10.1111/epi.17020. Epub 2021 Aug 2.