Seizure-related apneas have an inconsistent linkage to amygdala seizure spread
Seizure-related apneas have an inconsistent linkage to amygdala seizure spread
复制标题
DOI：
10.1111/epi.16518
复制
发表时间：
2020-05-11
期刊：
影响因子：
5.6
通讯作者：
Seyal, Masud
中科院分区：
文献类型：
--
作者：
Park, Katherine;Kanth, Kiran;Seyal, Masud
目的 癫痫猝死（SUDEP）是癫痫死亡的常见原因。呼吸功能障碍是 SUDEP 病理生理学的一个关键因素。人体研究表明，电刺激杏仁核会导致呼吸暂停，这表明杏仁核在呼吸控制中发挥着作用。单侧杏仁核刺激导致呼吸功能障碍立即发生，仅在鼻子呼吸时发生。在少数患者中，一些但并非全部自发性癫痫发作导致癫痫发作扩散到杏仁核后不久发生呼吸暂停。通过这项研究，我们旨在确定癫痫发作或扩散到杏仁核是否是引起呼吸暂停所必需和充分的。方法我们研究了植入深度电极的患者呼吸暂停/呼吸不足 (AH) 发作与杏仁核内初始癫痫发作之间的时间关系。结果分析了 17 名患者（11 名女性）47 次癫痫发作的数据。有 7 次癫痫发作（3 名患者），AH 比杏仁核癫痫发作早 2 至 55 秒。没有发生四次癫痫发作（三名患者）涉及杏仁核的 AH。八次癫痫发作（四名患者）在杏仁核癫痫发作后 2 秒内发生 AH。 28 次癫痫发作中，AH 在杏仁核癫痫发作后 2 秒以上开始（范围 3-158 秒）。癫痫发作后，AH 发作时间和杏仁核癫痫发作时间之间存在显着差异 (P < .001)。平均+/-标准差(SD) AH 发作时间为 27.8 +/- 41.06 秒，杏仁核受累的平均时间为 8.83 +/- 20.19 秒。 意义 与杏仁核癫痫发作相关的 AH 发作时间范围很广。对于某些癫痫发作，杏仁核癫痫发作会在没有 AH 的情况下发生。对于其他癫痫发作，AH 先于杏仁核癫痫发作，这表明，对于自发性癫痫发作，杏仁核的参与对于所有癫痫发作诱发 AH 可能并不重要。影响脑干呼吸网络的其他病理生理学可能与癫痫发作引发的呼吸暂停有更大的相关性。
Objective Sudden unexpected death in epilepsy (SUDEP) is a frequent cause of death in epilepsy. Respiratory dysfunction is implicated as a critical factor in SUDEP pathophysiology. Human studies have shown that electrical stimulation of the amygdala resulted in apnea, indicating that the amygdala has a role in respiration control. Unilateral amygdala stimulation resulted in immediate onset of respiratory dysfunction occurring only during nose breathing. In small numbers of patients, some but not all spontaneous seizures resulted in apnea occurring shortly after seizure spread to the amygdala. With this study we aimed to determine whether seizure onset or spread to the amygdala was necessary and sufficient to cause apnea.Methods We investigated the temporal relationship between apnea/hypopnea (AH) onset and initial seizure involvement within the amygdala in patients with implanted depth electrodes.Results Data from 17 patients (11 female) with 47 seizures were analyzed. With seven seizures (three patients), AH preceded amygdala seizure involvement by 2 to 55 seconds. There was no AH with four seizures (three patients) that involved the amygdala. With eight seizures (four patients) AH occurred within 2 seconds following amygdala seizure onset. With 28 seizures, AH started >2 seconds after amygdala seizure onset (range 3-158 seconds). Following seizure onset, there was a significant difference between AH onset time and amygdala seizure onset (P < .001). The mean +/- standard deviation (SD) AH onset was 27.8 +/- 41.06 seconds, and the mean time to amygdala involvement was 8.83 +/- 20.19 seconds.Significance There is a wide range of AH onset times relative to amygdala seizure involvement. With some seizures, amygdala seizure involvement occurs without AH. With other seizures, AH precedes amygdala seizures, suggesting that, with spontaneous seizures, involvement of the amygdala may not be crucial to induction of AH with all seizures. Other pathophysiology impacting brainstem respiratory networks may be of greater relevance to seizure-triggered apneas.