Characterization of seizure‐induced syncopes:EEG,ECG, and clinical features

Abstract

SUMMARYObjective: 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. Methods: Among 828 patients with epilepsy who were admitted for presurgical videoelectroencephalogram (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. Results: Nine (1.08%) of 828 patients (four men, mean age 43 AE 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 AE 18 s after the onset of the seizure, the HR decreased progressively during 11 AE 6 s, reaching a sinusal pause for 13 AE 7 s. The duration of the IA was strongly correlated with electroclinical consequences. IA was longer in patients with atonia (14.8 AE 7 vs. 5.7 AE 3 s), late myoclonic jerks (15.8 AE 7 vs. 8 AE 6 s), hypertonia (19 AE 4.5 vs. 8.3 AE 5 s), and EEG hypoperfusion changes (16 AE 5.6 vs. 6.9 AE 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. Significance: 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.

Ictal Asystole and Ictal Syncope

“…14 Nguyen-Michel et al similarly reported that ictal asystole duration was longer in patients with hypoperfusion changes on EEG. 15 …”

Progressive development of cardiomyopathy following altered autonomic activity in status epilepticus

“…Within the different seizure classifications, status epilepticus has the highest mortality risk, with death generally occurring within 30 days of the initial convulsant activity (39). Death often occurs in the absence of seizures and is believed to be due to an imbalance in autonomic function, resulting in altered cardiac control, electrical instability, and increased risk of lethal cardiac arrhythmias (46,51).…”

Curious turns in the night-time

“…One small study of seven people with ictal asystole found that none required cardiac resuscitation despite ictal asystole episodes lasting up to 25 s; only one person opted to have a permanent pacemaker; all patients were alive after 4 years of follow-up 2. However, this small cohort study does not refute the need for pacemaker insertion.…”

“…Video EEG–ECG monitoring can distinguish syncope from ictal asystole. There are two distinct EEG patterns2: type 1 comprises persistent ictal discharges while type 2 comprises ictal discharges interrupted by EEG features of cerebral hypoperfusion (as in this case).…”