Ictal asystole: A systematic review

Objective: To comprehensively analyze ictal asystole (IA) on a large number of subjects. Methods: We performed a systematic review of case report studies of patients diagnosed with IA ( 1983- 2016). Each included case was characterized with respect to patient history, IA seizure characteristics, diagnostic workup, and therapy. In addition, comparative analyses were also carried out: two alignments were developed based on the delay between epilepsy onset and IA onset ("new-onset" if < 1 year, "late-onset" if =1 year) and asystole duration (asystole was "very prolonged" if lasted >30 s). Results: One hundred fifty-seven cases were included. All patients had focal epilepsy. In 7% of cases IA developed during a secondary generalized tonic-clonic seizure. Both the seizure- onset zone and the focal seizure activity at asystole beginning were usually temporal ( p < 0.001 and p = 0.001, respectively) and were lateralized to the left hemisphere in 62% (p = 0.005 and p = 0.05, respectively). Asystole duration was 18 +/- 14 s ( mean +/- SD) (range 3- 96 s); 73% of patients had late-onset, 27% had new-onset IA. Compared to late-onset IA, new-onset IA was associated with female gender (p = 0.023), preexisting heart condition (p = 0.014), focal seizure activity at asystole beginning (p = 0.012), normal neuroimaging (p = 0.013), normal interictal EEG (p < 0.001), auditory aura (p = 0.012), and drug-responsive epilepsy (p < 0.001). "Very prolonged" asystole was associated with secondary generalized tonic-clonic seizures (p = 0.003) and tended to occur in extratemporal lobe seizures (p = 0.074). No IArelated death was reported. Significance: Characteristics considered to be typical of IA (focal, left temporal seizures appearing on grounds of a long-lasting, intractable epilepsy) seem only partially legitimate. We suggest that in new-onset IA, female gender and a preexisting heart condition could serve as predispositions in an otherwise benign epilepsy. Wespeculate that in late-onset IA, male-predominant changes in neuronal networks in chronic, intractable epilepsy and an accompanying autonomic dysregulation serve as facilitating factors.