Letter to the Editor Ictal asystole and syncope Vijairam Selvaraj ⁎, Shanmugam Uthamalingam, James Murphy, Doris Kampe, Marshal T. Fox, William J. House, James R. Cook Baystate Medical Center, Springfield, MA, United States article info Article history: Received 29 October 2014 Accepted 4 November 2014 Available online xxxx Keywords: Syncope Seizures Loss of consciousness SUDEP Asystole To the Editor, Syncope is an abrupt loss of consciousness usually followed by spon- taneous recovery in seconds. In young adults, it is often attributed to va- sovagal or autonomic mechanisms whereas in older patients, cardiac arrhythmias are often implicated. Seizures are always considered in the differential as a neurologic etiology in patients who present with loss of consciousness. Rarely, syncope can be seizure induced. Ictal asystole (IA) is a rare entity that when seen is often in patients with temporal lobe epilepsy, and is one possible mechanism of sudden unex- pected death in epilepsy (SUDEP). IA is noted to occur in 0.3–0.4% of pa- tients during long term video EEG and is believed to be a sinus arrest triggered by an epileptic seizure [1]. We describe a case of a 37 year old woman with multiple syncopal episodes since 2011 characterized by a smell of burning rubber or a sense of drowning followed by a brief loss of consciousness with quick return to baseline. Her husband described cessation of activity and loss of muscle tone. She has no known risk factors for epilepsy. She had an extensive workup done at another hospital with ambiguous re- sults prior to admission here in 2014 including brain MRI, EEGs and Holter monitoring. Her symptoms were attributed to a seizure disorder for which she was placed on Carbamazepine, Levetiracetam and Valproic acid without adequate control. She reported being on a cardiac medication in the past although this was discontinued as there was no benefit. She did not complain of anginal symptoms during any of the episodes. She was admitted with Neurology and Cardiology consulted. Holter tracings showed that patient was in sinus bradycardia followed by runs of intermittent junctional bradycardia at rates of 50 per minute. Howev- er, there were no visible episodes of asystole, pauses, high degree AV block. The patient underwent 4 h of continuous video EEG monitoring that was accompanied by single channel EKG. She had one typical event that began with rhythmic theta activity that started to build in amplitude then slowed in frequency, following which the patient pushed the event button (Fig. 1). Her heart rate in- creased to 84 beats per minute before slowing to 50 beats per minute, and then to 17 s of asystole during which she lost muscle tone and con- sciousness (Fig. 2). She then began to rouse and quickly recovered with EKG showing return of cardiac activity. Her syncopal episodes resolved following implantation of pacemaker although continued to have mild burning in her nose that she associated with previous seizures. It is often challenging to distinguish cardiac from epileptic causes of loss of consciousness. Partial or generalized seizures are more likely known to cause tachycardia and only in rare instances, bradycardia or even asystole [2]. Attacks of IA are noted to be clinically characterized by the loss of muscle tone or brief arrhythmic bilateral upper extremity posturing and jerking distinct from but often confused with the rhyth- mic, tonic–clonic posturing seen typically in epileptic seizures that are not associated with cardiac arrhythmias [3]. There have also been re- ports with stereotypical prodromes that are associated with IA [4]. The pathophysiology, although uncertain, is believed to be related to the cortical control of the autonomic system causing sinus node arrest. It has been studied intra-operatively in humans using intracerebral EEG recording with electrodes in the temporal, frontal and insular regions in addition to the hippocampus, amygdala, orbitofrontal cortex and an- terior cingulate gyrus. Although most studies have documented left hemispheric localization, there is no clear evidence of a lateralization pattern [5]. Activation of the left mesial temporal area and/or ipsilateral posterior gyrus of the insula have been strongly related to effects on the parasympathetic tone [6]. Vagally mediated mechanisms through the left cingular gyrus have also been reported [7] although there is a role of sympathetic inhibition as well [8]. Frontal lobe tumors [9] and certain infectious encephalitis are other causes that have been described in the literature. In our case, our patient described having a characteristic prodrome following by the loss of muscle tone and consciousness with no jerking International Journal of Cardiology xxx (2014) xxx–xxx ⁎ Corresponding author at: 759 Chestnut St S2570, Baystate Medical Center, Springfield, MA 01199, United States. E-mail address: vijairam.selvaraj@bhs.org (V. Selvaraj). IJCA-19196; No of Pages 2 http://dx.doi.org/10.1016/j.ijcard.2014.11.040 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved. Contents lists available at ScienceDirect International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard Please cite this article as: V. Selvaraj, et al., Ictal asystole and syncope, Int J Cardiol (2014), http://dx.doi.org/10.1016/j.ijcard.2014.11.040