Epileptology Unit, Department of Neurology and Neurophysiology, Assistance Publique-Hôpitaux de Paris, Pitié-Salpêtrière Hospital and Pierre et Marie Curie (Paris 6) University, CRICM, Paris, France.
Epilepsia. 2014 Jan;55(1):146-55. doi: 10.1111/epi.12482. Epub 2013 Dec 20.
Ictal bradycardia and ictal asystole (IA) are rare but severe complications of epileptic seizures. They are difficult to recognize within a seizure and their consequences remain unclear. Herein we aimed to extend the description of electrical and clinical features of seizures with IA and/or syncope.
Among 828 patients with epilepsy who were admitted for presurgical video-electroencephalogram (EEG) monitoring evaluation between 2003 and 2012, we selected those presenting IA and/or syncope. We studied the electroclinical sequence of these manifestations and their correlation with electrocardiogram (ECG), and we compared seizures with or without IA among the same patients.
Nine (1.08%) of 828 patients (four men, mean age 43 ± 6 years) showed IA. Six patients had temporal lobe epilepsy and the others had frontal, temporooccipital, or occipital epilepsy, demonstrated by intracranial EEG in two. In these patients, 59 of 103 recorded seizures induced a reduction of heart rate (HR), leading to IA in 26. IAs were mostly (80%) symptomatic, whereas ictal HR decreases alone were not. In seizures with IA, we identified usual ictal symptoms, and then symptoms related primarily to cerebral hypoperfusion (pallor, atonia, early myoclonic jerks, loss of consciousness, hypertonia, and fall) and secondarily to cerebral reperfusion (skin flushing, late myoclonic jerks). At 32 ± 18 s after the onset of the seizure, the HR decreased progressively during 11 ± 6 s, reaching a sinusal pause for 13 ± 7 s. The duration of the IA was strongly correlated with electroclinical consequences. IA was longer in patients with atonia (14.8 ± 7 vs. 5.7 ± 3 s), late myoclonic jerks (15.8 ± 7 vs. 8 ± 6 s), hypertonia (19 ± 4.5 vs. 8.3 ± 5 s), and EEG hypoperfusion changes (16 ± 5.6 vs. 6.9 ± 5.5 s). IA may induce a fall during atonia or hypertonia. Surface and intracerebral EEG recordings showed that ictal HR decrease and IA often occurred when seizure activity became bilateral. Finally, we identified one patient with ictal syncopes but without IA, presumably related to vasoplegia.
We provide a more complete description of the electroclinical features of seizures with IA, of the mechanism of falls, and distinguish between hypoperfusion and reperfusion symptoms of syncope. Identification of the mechanisms of syncope may improve management of patients with epilepsy. A pacemaker can be proposed, when parasympathetic activation provokes a negative chronotropic effect that leads to asystole. It is less likely to be useful when vasoplegic effects predominate.
癫痫发作时的心动过缓和心动停止（IA）是癫痫发作的罕见但严重的并发症。它们在癫痫发作期间很难识别，其后果仍不清楚。在此，我们旨在扩展具有 IA 和/或晕厥的癫痫发作的电和临床特征的描述。
在 2003 年至 2012 年间因术前视频脑电图（EEG）监测评估而入院的 828 例癫痫患者中，我们选择了出现 IA 和/或晕厥的患者。我们研究了这些表现的电临床序列及其与心电图（ECG）的相关性，并比较了同一患者中有无 IA 的癫痫发作。
828 例患者中有 9 例（1.08%）出现 IA（4 例男性，平均年龄 43 ± 6 岁）。6 例患者患有颞叶癫痫，其余患者患有额颞叶、颞枕叶或枕叶癫痫，其中 2 例通过颅内 EEG 显示。在这些患者中，103 次记录的癫痫发作中有 59 次导致心率（HR）降低，导致 26 次 IA。IA 大多（80%）是有症状的，而单纯的癫痫发作时 HR 降低则不是。在具有 IA 的癫痫发作中，我们确定了通常的癫痫发作症状，然后是主要与脑灌注不足相关的症状（苍白、弛缓、早期肌阵挛性抽搐、意识丧失、强直和跌倒），其次是与脑再灌注相关的症状（皮肤潮红、晚期肌阵挛性抽搐）。在癫痫发作开始后 32 ± 18 s，HR 在 11 ± 6 s 期间逐渐下降，达到窦性暂停 13 ± 7 s。IA 的持续时间与电临床后果密切相关。伴有弛缓（14.8 ± 7 比 5.7 ± 3 s）、晚期肌阵挛性抽搐（15.8 ± 7 比 8 ± 6 s）、强直（19 ± 4.5 比 8.3 ± 5 s）和脑电图低灌注变化（16 ± 5.6 比 6.9 ± 5.5 s）的患者，IA 持续时间更长。IA 可能在弛缓和强直期间引起跌倒。表面和颅内 EEG 记录显示，当癫痫活动变得双侧时，癫痫发作时 HR 降低和 IA 通常发生。最后，我们发现了一名患有癫痫性晕厥但无 IA 的患者，可能与血管扩张有关。
我们提供了更完整的具有 IA 的癫痫发作的电临床特征描述，包括跌倒机制，并区分晕厥的低灌注和再灌注症状。识别晕厥的机制可能会改善癫痫患者的管理。当副交感神经激活引起负变时，可以提出起搏器，导致心动过缓。当血管扩张作用占主导地位时，它不太可能有用。
