Abstracts

Rationale: IA has been described in a small number of patients predominantly with temporal lobe epilepsy (TLE) and has been implicated as a potential cause of sudden unexplained death in epilepsy (SUDEP). However, it is unclear if the mechanism leading to ictal asystole is sustained and able to lead to permanent cessation of heart rate. Ictal asystole invariably leads to cerebral anoxia-ischemia which might act as a mechanism for seizure termination and abolish the ictal autonomic activation which initially led to the ictal asystole. Methods: Electronic database search of patients with recorded IA between 1994 and 2006. Ictal events in the same patient population not associated with IA or signs of cerebral anoxia-ischemia were used as internal controls. Results: IA was seen in eight patients (0.12% of all patients monitored) and in 17 out of their 34 recorded events. Six patients had right and two left TLE. Agre range: 15 to 68 yrs, five patients were female and three male. Sixteen asystolic events were available for review lasting on average 15.7 ± 8.2s with three patients having multiple events. EEG onset preceded the asystole by 31.4s ± 21.9. At time of the asystole, an ictal EEG pattern was seen in all events, in 11 still restricted to the temporal region. A bilateral hypersynchronous slowing (BHS) typical for cerebral hypoperfusion was seen in 10 events with an asystole duration of 17.6 ± 8.5s, in half of the patients followed by a diffuse background suppression. In all 10 events, the BHS terminated the ictal pattern. In six events with an asystole duration of 12.6 ± 7.1s, BHS was not noted and the ictal pattern persisted after heart rate recovery. Time from IA onset to seizure end in the 10 seizures associated with BHS was 10.5 ± 2.3s compared to 41.0 ± 23.6s of ictal activity between onset of IA and EEG seizure end in the six events not leading to BHS (p<0.005). Total seizure duration of the 10 events with IA associated with BHS was 46.6 ± 25.1s compared to a total seizure duration of 94.6 ± 71.0s in the 18 seizures (6 with and 12 without IA) not associated with BHS (p<0.05). Conclusions: Prolonged asystole triggered by an epileptic discharge predictably leads to anoxia/ischemia associated with generalized slowing and burst suppression on EEG. In our series of patients, this effect terminates the ictal discharge and seems to shorten the total seizure duration. Anoxia-ischemia may represent an effective mechanism for seizure termination. Without triggering ictal stimulus on the autonomic nervous system, the heart in epileptic patients with IA may recover spontaneously similar to patients with vasovagal asystole.