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From Cleveland Clinic (S.U.S., A.C.B., A.V.A., E.R.L., R.C.B., D.S.D., N.F.-S.), OH; and Northwestern University (S.U.S.), Chicago, IL.
Address correspondence and reprint requests to Dr. Stephan U. Schuele, Northwestern University, Department of Neurology, Abbott Hall # 1122, 710 North Lake Shore Drive, Chicago, IL 60611 s-schuele{at}northwestern.edu
Objective: Ictal asystole (IA) is a rare event mostly seen in patients with temporal lobe epilepsy (TLE) and a potential contributor to sudden unexplained death in epilepsy (SUDEP). Clinical and video-electroencephalographic findings associated with IA have not been described, and may be helpful in screening for high risk patients.
Methods: A database search was performed of 6,825 patients undergoing long-term video-EEG monitoring for episodes of IA.
Results: IA was recorded in 0.27% of all patients with epilepsy, eight with temporal (TLE), two with extratemporal (XTLE), and none with generalized epilepsy. In 8 out of 16 recorded events, all occurring in patients with TLE, seizures were associated with a sudden atonia on average 42 seconds into the typical semiology of a complex partial seizure. The loss of tone followed after a period of asystole usually lasting longer than 8 seconds and was associated with typical EEG changes seen otherwise with cerebral hypoperfusion. Clinical predisposing factors for IA including cardiovascular risk factors or baseline ECG abnormalities were not identified.
Conclusion: Ictal asystole is a rare feature of patients with focal epilepsy. Delayed loss of tone is distinctly uncommon in patients with temporal lobe seizures, but may inevitably occur in patients with ictal asystole after a critical duration of cardiac arrest and cerebral hypoperfusion. Further cardiac monitoring in patients with temporal lobe epilepsy and a history of unexpected collapse and falls late in the course of a typical seizure may be warranted and can potentially help to prevent sudden unexplained death in epilepsy.
Editorial, see page 423
Supplemental data at www.neurology.org
Disclosure: The authors report no conflicts of interest.
Received October 6, 2006. Accepted in final form March 21, 2007.
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Neurology 2007 69: 423-424.
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