Abstracts

Unlike tachycardia, ictal bradycardia is rare, and its localizing value is debated. Bradyarrythmias are clinically important because of their potential morbidity, and ability to affect clinical seizure manifestations. Cerebral hypoperfusion induces loss of consciousness, at times with myoclonic jerks, whose clinical differentiation from a generalized convulsive seizure may prove difficult. We compared 2 invasive to 5 surface monitored seizures recorded over 2 years in a 49-year-old woman with post-traumatic epilepsy. Phase II recording included bilateral medial temporal depth and right frontal subdural electrodes. Seizures involved somatosensory phenomena and altered awareness, with occasional [ldquo]generalization[rdquo] described as diffuse limb jerks and prolonged unresponsiveness. All 7 seizures showed left temporal onset. Both intracranially recorded events appeared to start in the left amygdala and rapidly involved the adjacent hippocampus. They spread to the contralateral hippocampus in 35 and 25 seconds respectively; then, within 10 seconds, EKG showed asystole lasting 22 and 28 seconds, associated with loss of all recorded cerebral electric activity, apart from a polyspike-suppression pattern in the left hippocampus. Clinically, the patient was motionless until 20 and 8 seconds after the beginning of asystole, and then, concomitantly with cerebral suppression, had myoclonic twitches of the limbs. 4/5 surface recorded seizures showed bradycardia, with pauses of 2-4 seconds; mild tachycardia to 100-130 BPM preceded the bradycardia in 2/5 seizures.
Interictal EKG and echocardiography were normal. A dual chamber cardiac pacemaker was implanted. After seven months, the patient has experienced only infrequent partial seizures, with none involving falls or shaking. Left temporal lobe seizures produced apparent convulsions that most likely represented convulsive syncope initiated by ictal asystole, which occurred shortly after the seizure had spread from the left to the right hippocampus. Similar spread was briefly mentioned in two previous reports of intracranial recordings, although the exact timing was not specified. These observations suggest that intertemporal spread is necessary, though probably not sufficient, to produce asystole. While intracranial recording is needed to precisely analyze EEG/EKG relationships, our surface recorded seizures demonstrate how variable ictal arrythmias may be, even in electrographically and clinically similar seizures. Furthermore, pacemaker implantation may be not only potentially life-saving, but also may decrease seizure severity. (Supported by the Swiss National Science Foundation and the SICPA Foundation.)