Cardiac arrest: it's all in the head

Abstract

In May, 2007, a 59-year-old man lost consciousness twice in 4 days. The fi rst episode occurred while he was watching a fi lm, and the second episode while he was at work, laying a carpet. Each episode started and ended abruptly, without warning or apparent triggers, and lasted less than 15 s. He did not bite his tongue or leak urine. After each episode, he was lucid, and felt well. He had no past history of loss of consciousness. He did, however, have diabetes and hypercholesterolaemia, for which he was being treated with miglitol and atorvastatin, respectively. The patient’s general practitioner provi sionally diagnosed syncope, and referred him to us. Cardiovascular and neurological examinations showed nothing abnormal; notably, the patient had no orthostatic hypotension. Blood tests, an electrocardiogram (ECG), transthoracic echocardiography, an exercise stress test, a 24 h ECG, and tilt-table testing also showed no abnormality. However, the day after the patient was admitted, he abruptly lost consciousness. Nurses observed tonic-clonic movements. The ECG monitor showed asystole, lasting 12 s. We provisionally diagnosed epilepsy. 5 days later, the patient lost consciousness again, during video-electroencephalography (video-EEG) monitoring. EEG showed ictal activity in the anterior part of the left temporal lobe, which became generalised. The seizure lasted 35 s. 10 s after the seizure began, the ECG monitor showed a sinus arrest, lasting 4·3 s (fi gure). Asystole was succeeded by sinus bradycardia (36 beats per min); the heart rate increased steadily thereafter, until it reached the pre-ictal rate of 66 beats per min; the heart rate was 47 beats per min when the seizure ceased. CT of the brain showed no abnormality. MRI showed sporadic bilateral white-matter changes, located near the insular cortex on both sides. These lesions were of vascular origin, but non-specifi c. Doppler ultrasonography of the carotid arteries showed no atherosclerosis. We prescribed levetiracetam, at a dose of 1000 mg per day. The patient remained in hospital for another week, during which time he did not lose consciousness; a further 24 h of combined videoEEG and ECG monitoring showed nothing abnormal. However, 4 months after discharge, the patient had another seizure, with bradycardia. We therefore implanted a cardiac pacemaker. When last seen, in March, 2008, the patient had not had a fi t or faint since the pacemaker was fi tted. Sinus tachycardia is common during epileptic fi ts. In one case series, 13 (30%) of 43 patients with intractable partial epilepsy had cardiac dysrhythmias, other than sinus tachycardia, during, or immediately after, fi ts. Ictal bradycardia tends to occur in (perhaps especially left) temporal-lobe epilepsy. The mechanism may be parasympathetic activation. Our patient had a seizure of the left temporal lobe, with secondary generalisation. Ictal bradycardia is rare, especially in women. However, it is likely to be substantially underdiagnosed. Moreover, it may be a major cause of sudden unexpected death in epilepsy, which kills an estimated 0·12% of people with epilepsy per year. This case illustrates that cardiac arrest can occur during the fi rst epileptic seizure. Pacemaker implantation can prevent death and disability.