Ictal asystole with convulsive syncope mimicking secondary generalisation: A depth electrode study

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Rossetti AO, Dworetzky BA, Madsen JR, Golub O, Beckman JA, and Bromfield EB (2005) Ictal asystole with convulsive syncope mimicking secondary generalisation: A depth electrode study. J Neurol Neurosurg Psychiatry 76:6 885–7.

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Abstract: Ictal bradycardia is rare and its localising value is debated. Bradyarrhythmias are, however, important because of their potential connection to sudden death and ability to affect clinical seizure manifestations. Cerebral hypoperfusion induces loss of consciousness, at times with myoclonic jerks, whose clinical differentiation from a generalised convulsive seizure may prove difficult. Two invasive and five surface monitored seizures recorded over two years in a 51 year old woman with post-traumatic epilepsy characterised by seizure-triggered asystole were analysed. All seven seizures showed left temporal onset. Both intracranially recorded events started in the left anterior hippocampus/amygdala, spreading to the contralateral hippocampus in 35 and 25 seconds. Within 10 seconds an electrocardiogram showed asystole lasting 21 and 28 seconds, associated with suppression of recorded cerebral electrical activity, except a polyspike suppression pattern remaining in the hippocampi. Clinically, the patient, concomitantly with the cerebral suppression, developed myoclonic twitches of the limbs. A dual chamber cardiac pacemaker was implanted; at 11 months follow up, the patient has experienced only infrequent partial seizures, with none involving falls or shaking. Left temporal lobe seizures produced convulsive syncope initiated by ictal asystole. These observations suggest that intertemporal spread is necessary, though not sufficient, to produce bradycardia and asystole. Furthermore, pacemakers may decrease seizure severity, as well as potentially protect against malignant bradyarrhythmias.

Context

  • Report of a patient with post-traumatic epilepsy who underwent 7 recorded seizures accompanied by asystole. All 7 seizures began in the left temporal lobe, in the anterior hippocampus. Within 10 s of seizure spread to the contralateral hemisphere, asystole began and lasted 20-30 s. During the asystole, the EEG traces were largely suppressed. After pacemaker implantation the patient no longer fell during seizures.

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