Difference between revisions of "Ictal asystole: A benign condition?"
(Created page with "''Schuele SU, Bermeo AC, Locatelli E, Burgess RC, and Lüders HO (2008) Ictal asystole: A benign condition? Epilepsia 49:1 168–71.'' '''[http://onlinelibrary.wiley.com/doi/...") |
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| − | + | Schuele SU, Bermeo AC, Locatelli E, Burgess RC, and Lüders HO (2008) Ictal asystole: A benign condition? Epilepsia 49:1 168–71. | |
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| + | Ictal asystole (IA) has been implicated as a preventable cause of sudden unexplained death in epilepsy presumably provoked by a direct autonomic effect of the electrical stimulus on the heart. An electronic database search of patients with IA was performed comparing heart rate (HR) characteristics to a group of patients with vasovagal asystole. IA was seen in eight patients, all with temporal lobe epilepsy. No statistical difference was found in duration of asystole, bradycardia, and baseline HR characteristics except of a higher HR acceleration postasystole in the controls. None of the six patients with IA who underwent pacemaker implantation had recurrence of asystolic events during mean follow-up of 5 years. This study in a small group of patients suggests that the epileptic activation leading to IA is possibly mediated through a transient increase in vagal tone and not by a direct autonomic effect on the heart. | ||
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| + | Ictal asystole, Syncope, Sudden unexplained death in epilepsy, SUDEP | ||
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*Comparison of baseline EKG parameters in ictal asystole and vaso-vagal asystole. The only difference identified was more rapid acceleration in HR after asystole among vasovagal patients than among ictal patients, and the authors argue that because of the similarity in heart rate patterns in the two groups in most metrics assessed, ictal asystole is likely mediated by the same vagal mechanisms that underlie vasovagal asystole. The cases reported here were also reported in Schuele et al. | *Comparison of baseline EKG parameters in ictal asystole and vaso-vagal asystole. The only difference identified was more rapid acceleration in HR after asystole among vasovagal patients than among ictal patients, and the authors argue that because of the similarity in heart rate patterns in the two groups in most metrics assessed, ictal asystole is likely mediated by the same vagal mechanisms that underlie vasovagal asystole. The cases reported here were also reported in Schuele et al. | ||
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Latest revision as of 13:34, 17 June 2019
Schuele SU, Bermeo AC, Locatelli E, Burgess RC, and Lüders HO (2008) Ictal asystole: A benign condition? Epilepsia 49:1 168–71.
Abstract: Ictal asystole (IA) has been implicated as a preventable cause of sudden unexplained death in epilepsy presumably provoked by a direct autonomic effect of the electrical stimulus on the heart. An electronic database search of patients with IA was performed comparing heart rate (HR) characteristics to a group of patients with vasovagal asystole. IA was seen in eight patients, all with temporal lobe epilepsy. No statistical difference was found in duration of asystole, bradycardia, and baseline HR characteristics except of a higher HR acceleration postasystole in the controls. None of the six patients with IA who underwent pacemaker implantation had recurrence of asystolic events during mean follow-up of 5 years. This study in a small group of patients suggests that the epileptic activation leading to IA is possibly mediated through a transient increase in vagal tone and not by a direct autonomic effect on the heart.
Keywords: Ictal asystole, Syncope, Sudden unexplained death in epilepsy, SUDEP
Context
- Comparison of baseline EKG parameters in ictal asystole and vaso-vagal asystole. The only difference identified was more rapid acceleration in HR after asystole among vasovagal patients than among ictal patients, and the authors argue that because of the similarity in heart rate patterns in the two groups in most metrics assessed, ictal asystole is likely mediated by the same vagal mechanisms that underlie vasovagal asystole. The cases reported here were also reported in Schuele et al.