Cerebral arrhythmia influencing cardiac rhythm: A case of ictal bradycardia
Almansori M, Ijaz M, and Ahmed SN (2006) Cerebral arrhythmia influencing cardiac rhythm: A case of ictal bradycardia. Seizure 15:6 459–61
Abstract: Partial seizures of temporal origin can be associated with clinically significant tachycardia or bradycardia. Ictal bradycardia and asystole has been implicated in the etiology of sudden unexpected death in epileptic patients (SUDEP). Although symptomatic ictal bradycardia has been relatively well described in the literature; information on asymptomatic ictal bradycardia is scarce. We report a case of asymptomatic ictal bradycardia diagnosed during video EEG telemetry that was subsequently implanted with a cardiac pacemaker.
Article
Introduction
Partial seizures of temporal origin can be associated with clinically significant tachycardia or bradycardia. Ictal bradycardia and asystole has been implicated in the etiology of sudden unexpected death in epileptic patients (SUDEP). Although symptomatic ictal bradycardia has been relatively well described in the literature; information on asymptomatic ictal bradycardia is scarce. We report a case of asymptomatic ictal bradycardia diagnosed during video EEG telemetry that was subsequently implanted with a cardiac pacemaker.
Case Report
A 57-year-old right-handed man presented for a presurgical evaluation for epilepsy surgery at the University of Alberta Hospital. He had experienced complex partial seizures since 19 years of age. MRI was remarkable for left mesial temporal sclerosis. These seizures were not associated with an aura and the patient did not have a recollection of these episodes. Witnesses noted him to stare, be unresponsive and fidget with the left hand. In the past he had been treated with phenytoin, valproate, lamotrigine and clonazepam at maximal tolerated dosage with no significant improvement in his seizures. At the time of presentation he was on lamotrigine and clobazam with a seizure frequency of 3–4 times a week. Past and family history was unremarkable. Neurological examination was unremarkable.
During video-EEG monitoring six stereotypical complex partial seizures were recorded. Seizures were bland consisting of a blank stare, unresponsiveness and minimal motor activity of the right hand. He was sitting upright at the onset during first four seizures and lying supine on the bed during the last two seizures. Ictal recordings were significant for left temporal seizure onset and ictal bradycardia. Three of the six seizures (seizure numbers 2, 5 and 6) had an ictal onset bradycardia at 18, 42 and 36 beats per minute respectively. Seizure 2 occurred while patient was sitting upright reading a book. Electrographic seizure lasted for 30 s. Bradycardia was noted after 15 s of seizure onset and lasted for 17 s. The heart rate ranged from 18 to 36 beats per minute (Fig. 1). Seizure 5 and 6 lasted for 21 and 40 s, respectively, and the duration of bradycardia with these seizures lasted for 12 and 20 s. None of these seizures were associated with syncope. On the basis of the cardiological consultation a ventricle-paced, ventricle-sensed, inhibited, rate-responsive (VVIR) pacemaker was inserted. Patient subsequently underwent left temporal lobectomy and has been seizure free for the past 18 months. One of the antiepileptic medications was tapered off one year after the surgery and the patient elected to continue taking Oxcarbazepine.
Discussion
Cardiac arrhythmias have been implicated as a possible etiology for SUDEP which affects approximately 7–17% of the epileptic population. There is some evidence to suggest a differential response to heart rate based on lateralization to the left or right temporal lobes. Seizures with right temporal onset are considered to cause tachycardia related to sympathetic over activity as compared to the left side causing bradycardia due to a predominantly parasympathetic response. We define “symptomatic ictal bradycardia” as an epileptic seizure associated with bradycardia and clinically manifest signs of syncope and “asymptomatic ictal bradycardia” as an episode of bradycardia during the epileptic seizure with no clinically obvious sign of syncope. Ictal bradycardia with associated syncope (symptomatic ictal bradycardia) is more likely to be noticed and investigated than one that is not (asymptomatic ictal bradycardia). We use the term “asymptomatic” to refer to lack of cardiac but not neurological symptoms. A recent paper published in Lancet where epileptic patients were monitored with insertable loop recorders found a relatively high incidence of cardiac dysrhythmias in epileptic patients, further strengthening the possible relationship of cardiac arrhythmias with SUDEP.
On the basis of the clinical presentation alone we would not have been able to detect the significant bradycardia in our patient. Had it not been for the review of the EKG lead during video-EEG monitoring his condition would have been undiagnosed and untreated. One may argue that none of the published studies such as the one published in Lancet had controls for comparison. How do we know that similar periods of bradycardia or asystole would not be seen in otherwise healthy individuals who are monitored for an extended period of time?
In conclusion, our case adds one more subject to the recently growing literature on autonomic dysregulation during epileptic seizures. The relationship between cardiac arrhythmias and SUDEP at best is still speculative. The authors support the notion of a SUDEP registry as proposed by Dr Andre Kanner. This would require a multicenter study prospectively collecting data related to pulmonary and cardiac functions and postmortem examination of epilepsy patients to help in the identification of risk factors and actual mechanisms of SUDEP.