ReviewEpileptic seizures associated with syncope: Ictal bradycardia and ictal asystole
Introduction
In 1906, before the introduction of electroencephalography (EEG), Russell described the cessation of the pulse during a seizure in a young man [1]. Since then, different anecdotal cases have been reported in which ictal episodes were accompanied by a decrease of the heart rate or even asystole. In 1996, Reeves described the ictal bradycardia syndrome as “a syndrome that occurs when epileptic discharges profoundly disrupt normal cardiac rhythm, resulting in cardiogenic syncope during the ictal event” [2].
Although ictal tachycardia is very frequent (70–90%), ictal bradycardia is considered a rare event, which affects < 5% of patients with epilepsy [3], [4]. Asystolic episodes following ictal bradycardia seem to occur even less frequent (0.3-0.4%) [5], [6]. Since these studies were typically based on relatively short-term monitoring, the incidence of ictal asystole could have been underestimated.
The recognition of ictal bradycardia is important. Documenting ictal arrhythmias during epileptic seizures is relevant in patient management to avoid undesirable complications. Insertion of a cardiac pacemaker should be considered in case of asystoles. Different authors argued that ictal bradycardia and subsequent asystole are potentially life-threatening and might be a possible explanation for sudden unexpected death in epilepsy (SUDEP). The mortality in epilepsy monitoring units study (MORTEMUS), however, showed that in cases of witnessed SUDEP, the asystole is a terminal event after a long period of central apnea [7].
Reeves concluded that the ictal bradycardia syndrome should be considered in patients with unusual or refractory episodes of syncope or in patients with a history suggestive of both epilepsy and syncope. He found an association between seizure onset in the temporal lobe and male gender [2]. Tinuper found that in the majority (31 out of 46) of patients, the epileptic seizures originated from the temporal lobe and the left hemisphere (20 versus 12, 15 unknown). Furthermore, a male/female ratio of 20:10 was found [8].
The pathophysiology of ictal bradycardia is not known. Seizure discharges may activate sympathetic or parasympathetic centers, which result in ictal tachycardia or ictal bradycardia [4]. Parasympathetic activation may exert a strong influence on the atrioventricular (AV) node.
We systematically reviewed the literature to better understand the clinical signs and risk factors of ictal bradycardia.
Section snippets
Literature search
We performed a systematic review from the first date available to February 2018 and searched Pubmed by queries containing the terms “ictal bradycardia” and “ictal asystole”. We also checked the references of these papers we added from our personal archives. One author (CM) screened all full texts.
Articles relating to animal studies, seizures without ictal decrease of heart rate, cases without simultaneous EEG and electrocardiography (ECG), convulsive syncopes, or cases with bradycardia before
Included cases
Based on our queries containing the terms “ictal bradycardia” and “ictal asystole”, we found 218 different papers (Supplement 1). One paper was missing, and 114 were excluded resulting in 75 case reports and 28 case series for further analysis.
We collected 289 cases and excluded 70 cases who were reported more than once and 55 cases not fitting our quality score which resulted in 174 different cases for this analysis (Fig. 1).
“Ictal bradycardia” vs “ictal asystole”
Between the groups “ictal bradycardia” and “ictal asystole”,
General
Ictal bradycardia and ictal asystole predominantly occurred during focal seizures with loss of awareness in people with mainly left lateralized temporal lobe epilepsy. Seizures with ictal asystole typically started with a heart rate decrease. During ictal asystole in the majority of cases, not only the clinical signs of syncope occurred, which interrupted the seizure semiology, but also the characteristic EEG signs. Occurrence of signs of syncope was statistically associated with the presence
Acknowledgments
We are grateful to Dr. R. Thijs for critically reviewing this manuscript.
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