The effect of seizure spread to the amygdala on respiration and onset of ictal central apnea.
The effect of seizure spread to the amygdala on respiration and onset of ictal central apnea.
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DOI：
10.3171/2019.1.jns183157
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发表时间：
2020-05-01
影响因子：
4.1
通讯作者：
Schuele S
中科院分区：
文献类型：
--
作者：
Nobis WP;González Otárula KA;Templer JW;Gerard EE;VanHaerents S;Lane G;Zhou G;Rosenow JM;Zelano C;Schuele S
癫痫猝死（SUDEP）是难治性癫痫患者死亡的主要原因，越来越多的证据表明中枢介导的呼吸抑制是一种病理生理机制。癫痫发作引起呼吸抑制的大脑区域尚不清楚——脑干中的呼吸核被认为参与其中，但前脑结构的参与尚不清楚。本研究的目的是结合呼吸监测结果分析颅内脑电图，以探讨癫痫发作扩散到特定内侧颞脑区域与呼吸功能障碍和呼吸暂停发作之间的关系。作者回顾了自 2010 年以来在西北纪念医院（芝加哥）进行的所有侵入性脑电图研究，以确定以下病例：1）放置多个内侧颞电极（杏仁核和海马），2）捕获癫痫发作，3）监测患者的呼吸。他们在颞叶癫痫患者中确定了 8 项符合这些标准的调查，这些调查产生了总共 22 次癫痫发作的数据进行分析。与每次癫痫发作相关的发作性呼吸暂停的发作与癫痫发作扩散到杏仁核高度相关。呼吸暂停发生在癫痫发作扩散到杏仁核后 2.7 ± 0.4（平均值 ± SEM）秒，明显早于扩散到海马后（10.2 ± 0.7 秒；p < 0.01）。研究结果表明杏仁核网络的激活与癫痫发作期间的中枢性呼吸暂停相关。这项研究建立在作者之前的工作基础上，该工作证明了杏仁核在自主呼吸控制中的作用，并提出了在癫痫发作期间出现的功能障碍呼吸状态中的进一步作用，对 SUDEP 病理生理学具有影响。
Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death for patients with refractory epilepsy, and there is increasing evidence for a centrally mediated respiratory depression as a pathophysiological mechanism. The brain regions responsible for a seizure’s inducing respiratory depression are unclear—the respiratory nuclei in the brainstem are thought to be involved, but involvement of forebrain structures is not yet understood. The aim of this study was to analyze intracranial EEGs in combination with the results of respiratory monitoring to investigate the relationship between seizure spread to specific mesial temporal brain regions and the onset of respiratory dysfunction and apnea. The authors reviewed all invasive electroencephalographic studies performed at Northwestern Memorial Hospital (Chicago) since 2010 to identify those cases in which 1) multiple mesial temporal electrodes (amygdala and hippocampal) were placed, 2) seizures were captured, and 3) patients’ respiration was monitored. They identified 8 investigations meeting these criteria in patients with temporal lobe epilepsy, and these investigations yielded data on a total of 22 seizures for analysis. The onset of ictal apnea associated with each seizure was highly correlated with seizure spread to the amygdala. Onset of apnea occurred 2.7 ± 0.4 (mean ± SEM) seconds after the spread of the seizure to the amygdala, which was significantly earlier than after spread to the hippocampus (10.2 ± 0.7 seconds; p < 0.01). The findings suggest that activation of amygdalar networks is correlated with central apnea during seizures. This study builds on the authors’ prior work that demonstrates a role for the amygdala in voluntary respiratory control and suggests a further role in dysfunctional breathing states seen during seizures, with implications for SUDEP pathophysiology.