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A patient is reported on with habitual episodes of collapse and loss of consciousness associated with EEG evidence of focal epileptiform discharges. Simultaneous ECG recordings disclosed 25 seconds of cardiac ventricular asystole occurring 24 seconds after the onset of electrical seizure activity. After changes to antiepileptic medication and the insertion of a permanent cardiac pacemaker he has had no further episodes. In cases of epileptic cardiac dysrhythmia, isolated EEG or ECG recording may prove insufficient and prolonged simultaneous EEG/ECG monitoring may be required.
Cardiac arrhythmias subsequent to epileptic seizures have been recognised for more than 90 years. They provoke diagnostic confusion and may be a mechanism of sudden unexplained death in epilepsy. Whereas sinus tachycardia was noted to accompany more than 90% of epileptic seizures, isolated bradycardia was seen much less commonly (only 1 of 74 seizures recorded).1 A review in 1996 of the “ictal bradycardia syndrome” showed only 15 documented cases in the literature of either bradycardia or asystole associated with seizures.2 Most patients had temporal lobe seizures. The longest duration of asystole previously reported is in a 17 year old man with temporal lobe epilepsy who sustained a 22 second pause in cardiac output. More typically the asystolic periods in documented cases are in the region of 5–10 seconds.2 Shorter duration asystole may not compromise cerebral function sufficiently to cause loss of consciousness. Implantation of a cardiac pacemaker is advocated but does not ensure that lapses of consciousness are eliminated if these are directly related to the seizure rather than to the secondary asystole. We report on a patient with epileptic cardiac asystole of 25 seconds duration demonstrated by prolonged simultaneous EEG/ECG monitoring which responded well to pacemaker insertion.
A previously well 34 year old right handed builder was referred with a 1 year history of fortnightly episodes of loss of consciousness. There was no associated warning, aura, chest pain, or palpitations and the patient was only aware of the episode once consciousness was restored and he found himself lying on the floor. On recovery there was no confusion, drowsiness, dysphasia, or diuresis. Often, however, he sustained soft tissue injuries to his face and scalp.
Witnesses reported that the patient would, without warning, suddenly collapse to the ground where he would remain unrousable, inaccessible, and motionless for 90 to 120 seconds. On two occasions he appeared confused and disorientated immediately before a collapse. During the period of unconsciousness he would demonstrate no involuntary movements, orofacial automatisms, or cyanosis but he would become pale and “ashen” while staring straight ahead with a glazed look. On resolution of the episode his colour would return to normal and within 2 minutes he would have fully recovered. Unusually during one reported episode of unconsciousness he was seen to briefly extend the fingers of both hands.
He was admitted to his local hospital and CT, MRI, interictal EEG, and 24 hour ECG were normal. No episodes were witnessed while he was an inpatient but they were thought to be epileptic in origin and therefore he was started on phenytoin, with no benefit. Carbamazepine was added, again with minimal effect.
The patient was then referred to the Epilepsy Assessment Centre of The National Society for Epilepsy and National Hospital for Neurology and Neurosurgery for further investigation and management.
Cardiovascular and neurological examination was normal, as were MRI and routine interictal EEG. Sixteen channel ambulatory EEG using an Oxford Instruments digital EEG receiver was performed continuously for 340 hours before an episode was captured. Interictally rare spikes were seen over the right frontocentrotemporal region during sleep. The onset of the episode was not witnessed and the patient was found lying on the floor, regaining consciousness at about 07:06. The event EEG showed a short run of bilateral semirhythmic 2–3 Hz activity at 07:04:34 (figure A), persisting for 8 seconds before being obscured by muscle and movement artefact. Twenty four seconds after the first EEG change, at 07:04:58, the ECG changed from sinus rhythm at 90 bpm to a brief period of sinus bradycardia, followed by a period of asystole with only very occasional ventricular complexes lasting 25–30 seconds (figure B). After a few seconds of bradycardia then tachycardia, sinus rhythm was restored. Throughout the episode the QT interval on the ECG remained within normal limits. The EEG became visible again 16 seconds into the asystolic period, at which time it was dominated by diffuse low amplitude slow activity at <1–2 Hz which persisted for 10 seconds (figure C). This was followed by marked attenuation of the EEG activity over the next 10 seconds before large amplitude generalised rhythmic <1Hz activity became apparent. Diffuse theta activity was seen for a further 15 seconds before the EEG returned to its resting state.
A VVI permanent pacemaker was inserted. The phenytoin was withdrawn and replaced by lamotrigine. Carbamazepine was left unchanged. The patient was discharged, his medication left unaltered, and at follow up 9 months later reported no further episodes.
Cardiac dysrhythmias are an uncommon but serious consequence of partial seizures. Our case is unusual because of the duration of the asystole. In a series of 26 patients with 74 temporal lobe seizures in which simultaneous EEG and ECG recordings were acquired, ictal arrhythmias occurred in 52% of seizures, the commonest being irregular abrupt changes in heart rate, (both acceleration and deceleration) occurring towards the end of the period of EEG abnormality.1 Interictally, patients with epilepsy seem no more likely than age and sex matched healthy subjects to experience arrhythmias although in one study patients with epilepsy had a faster ventricular rate and a longer QT interval than control subjects.3
It has been hypothesised that there is lateralisation with respect to central autonomic cardiac control with an increase in heart rate seen after an intracarotid injection of amobarbital and inactivation of the left hemisphere and a decrease in heart rate on right hemispheric inactivation. Experimental stimulation of the rostral posterior insular cortex in anaesthetised rats has been shown to induce tachycardia and more caudal region stimulation to cause bradycardia.4Additionally, prolonged stimulation resulted in ventricular ectopics, heart block, QT prolongation, and death. In presurgical temporal lobectomy patients stimulation of the left insular cortex (particularly posteriorly) produced bradycardia and a depressor response significantly more often than tachycardia and a pressor effect.5 It was suggested that an epileptic discharge in the insular cortex may result in cardiac arrhythmias.
Recurrent episodes of loss of consciousness are a common clinical problem. An accurate diagnosis relies principally on the patient's and witnesses' accounts of events. Further investigations are frequently required which are often normal unless an episode is captured during monitoring. Recording solely the EEG or the ECG may result in erroneous conclusions being drawn and insufficient or inappropriate therapy being instituted. Distinction between a primary cardiac arrhythmia and a secondary central arrhythmia is possible only with simultaneous EEG/ECG recordings.
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