The Open Cardiovascular Medicine Journal




ISSN: 1874-1924 ― Volume 14, 2020

Ictal Cardiac Ryhthym Abnormalities



Rushna Ali*
Henry Ford Hospital, Department of Neurosurgery, 2799 West Grand Blvd. Detroit, MI 48202, USA

Abstract

Cardiac rhythm abnormalities in the context of epilepsy are a well-known phenomenon. However, they are under-recognized and often missed. The pathophysiology of these events is unclear. Bradycardia and asystole are preceded by seizure onset suggesting ictal propagation into the cortex impacting cardiac autonomic function, and the insula and amygdala being possible culprits. Sudden unexpected death in epilepsy (SUDEP) refers to the unanticipated death of a patient with epilepsy not related to status epilepticus, trauma, drowning, or suicide. Frequent refractory generalized tonic-clonic seizures, anti-epileptic polytherapy, and prolonged duration of epilepsy are some of the commonly identified risk factors for SUDEP. However, the most consistent risk factor out of these is an increased frequency of generalized tonic–clonic seizures (GTC). Prevention of SUDEP is extremely important in patients with chronic, generalized epilepsy. Since increased frequency of GTCS is the most consistently reported risk factor for SUDEP, effective seizure control is the most important preventive strategy.

Keywords: Bradycardia, cardiac arrest, epilepsy, sudden unexplained death in epilepsy (SUDEP).


Article Information


Identifiers and Pagination:

Year: 2016
Volume: 10
Issue: Suppl-1, M5
First Page: 105
Last Page: 109
Publisher Id: TOCMJ-10-105
DOI: 10.2174/1874192401610010105

Article History:

Received Date: 22/8/2015
Revision Received Date: 20/9/2015
Acceptance Date: 22/10/2015
Electronic publication date: 27/05/2016
Collection year: 2016

© Rushna Ali; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.


* Address correspondence to this author at the Department of Anatomy, College of Medicine and Health Sciences, Afe Henry Ford Hospital, Department of Neurosurgery, 2799 West Grand Blvd. Detroit, MI 48202, USA; Tel: (313)-400-5520; Email: rali1@hfhs.org





INTRODUCTION

Cardiac rhythm abnormalities in the context of epilepsy are a well-known phenomenon. However, they are under-recognized and often missed [1Schuele SU, Bermeo AC, Alexopoulos AV, et al. Video-electrographic and clinical features in patients with ictal asystole. Neurology 2007; 31; 69(5): 41-434.
[http://dx.doi.org/10.1212/01.wnl.0000266595.77885.7f]
]. Ictal bradycardia and asystole are the most comorbid arrhythmias associated with epilepsy. They are usually triggered by focal seizures with or without secondary generalization. The duration and intensity of these ictal events determine the severity of symptoms associated with these events. Symptomatic events occur infrequently; typically documented in 0.27-0.4% of patients undergoing diagnostic video-electroencephalogram recordings in epilepsy monitoring units (EMU) [1Schuele SU, Bermeo AC, Alexopoulos AV, et al. Video-electrographic and clinical features in patients with ictal asystole. Neurology 2007; 31; 69(5): 41-434.
[http://dx.doi.org/10.1212/01.wnl.0000266595.77885.7f]
-3Rocamora R, Kurthen M, Lickfett L, Von Oertzen J, Elger CE. Cardiac asystole in epilepsy: clinical and neurophysiologic features. Epilepsia 2003; 44(2): 179-85.
[http://dx.doi.org/10.1046/j.1528-1157.2003.15101.x] [PMID: 12558571]
].

However, the incidence may be underestimated given a selection bias of persons referred to epilepsy monitoring units (EMU). Rugg-Gunn et al. reported an incidence of 2.1% of ictal arrhythmias in patients suffering from intractable epilepsy utilizing implantable loop recorders for monitoring these cardiac events [4Rugg-Gunn FJ, Simister RJ, Squirrell M, Holdright DR, Duncan JS. Cardiac arrhythmias in focal epilepsy: a prospective long-term study. Lancet 2004; 364(9452): 2212-9.
[http://dx.doi.org/10.1016/S0140-6736(04)17594-6] [PMID: 15610808]
].

PATHOPHYSIOLOGY

The pathophysiology of these events is unclear [5Freeman R. Cardiovascular manifestations of autonomic epilepsy. Clin Auton Res 2006; 16(1): 12-7.
[http://dx.doi.org/10.1007/s10286-006-0278-y] [PMID: 16477490]
]. Bradycardia and asystole are preceded by seizure onset suggesting ictal propagation into cortex impacting cardiac autonomic function - the insular cortex and amygdala are possible culprits in this regard [5Freeman R. Cardiovascular manifestations of autonomic epilepsy. Clin Auton Res 2006; 16(1): 12-7.
[http://dx.doi.org/10.1007/s10286-006-0278-y] [PMID: 16477490]
, 6Tinuper P, Bisulli F, Cerullo A, et al. Ictal bradycardia in partial epileptic seizures: Autonomic investigation in three cases and literature review. Brain 2001; 124(Pt 12): 2361-71.
[http://dx.doi.org/10.1093/brain/124.12.2361] [PMID: 11701591]
]. These events do not seem to have a lateralization bias, with cardiac events occurring equally after seizures originating from either hemisphere [7Stefanidou M, Carlson C, Friedman D. The relationship between seizure onset zone and ictal tachy-cardia: An intracranial EEG study. Clin Neurophysiol 2015; 2457(15)(pii: S1388): 2-77. [Epub ahead of print]
[http://dx.doi.org/10.1016/j.clinph.2015.01.020]
].

In vivo cortical stimulation studies have supported this notion, where stimulation of cortex regulating autonomic networks triggered parasympathetic responses leading to bradyarrhythmias [6Tinuper P, Bisulli F, Cerullo A, et al. Ictal bradycardia in partial epileptic seizures: Autonomic investigation in three cases and literature review. Brain 2001; 124(Pt 12): 2361-71.
[http://dx.doi.org/10.1093/brain/124.12.2361] [PMID: 11701591]
, 8Oppenheimer SM, Wilson JX, Guiraudon C, Cechetto DF. Insular cortex stimulation produces lethal cardiac arrhythmias: a mechanism of sudden death? Brain Res 1991; 550(1): 115-21.
[http://dx.doi.org/10.1016/0006-8993(91)90412-O] [PMID: 1888988]
-11Catenoix H, Mauguière F, Guénot M, Isnard J, Ryvlin P. Recording the insula during ictal asystole. Int J Cardiol 2013; 169(2): e28-30.
[http://dx.doi.org/10.1016/j.ijcard.2013.08.100] [PMID: 24063929]
]. Central nervous system activation induced by seizures may, synergistically, have direct postganglionic effect on the heart as well [12Lathers CM, Schraeder PL, Weiner FL. Synchronization of cardiac autonomic neural discharge with epileptogenic activity: the lockstep phenomenon. Electroencephalogr Clin Neurophysiol 1987; 67(3): 247-59.
[http://dx.doi.org/10.1016/0013-4694(87)90023-X] [PMID: 2441959]
]. However, a vast majority of patients suffering from seizures are not susceptible to these events. Factors predisposing certain individuals to ictal brady-arrhythmia remain unclear [5Freeman R. Cardiovascular manifestations of autonomic epilepsy. Clin Auton Res 2006; 16(1): 12-7.
[http://dx.doi.org/10.1007/s10286-006-0278-y] [PMID: 16477490]
].

SUDDEN UNEXPLAINED DEATH IN EPILEPSY (SUDEP)

Epilepsy is associated with increased mortality [13Devinsky O. Sudden, unexpected death in epilepsy. N Engl J Med 2011; 365(19): 1801-11.
[http://dx.doi.org/10.1056/NEJMra1010481] [PMID: 22070477]
-15Lamberts RJ, Thijs RD, Laffan A, Langan Y, Sander JW. Sudden unexpected death in epilepsy: people with nocturnal seizures may be at highest risk. Epilepsia 2012; 53(2): 253-7.
[http://dx.doi.org/10.1111/j.1528-1167.2011.03360.x] [PMID: 22192074]
]. Sudden unexpected death in epilepsy (SUDEP) refers to the unanticipated death of a patient with epilepsy not related to status epilepticus, trauma, drowning, or suicide. This often occurs following a generalized convulsion in an otherwise healthy individual. SUDEP is the leading cause of death in patients with epilepsy [16Ficker DM, So EL, Shen WK, et al. Population-based study of the incidence of sudden unexplained death in epilepsy. Neurology 1998; 51(5): 1270-4.
[http://dx.doi.org/10.1212/WNL.51.5.1270] [PMID: 9818844]
]. The risk of sudden death can be as high as 24 times in patients with epilepsy compared to people without epilepsy [16Ficker DM, So EL, Shen WK, et al. Population-based study of the incidence of sudden unexplained death in epilepsy. Neurology 1998; 51(5): 1270-4.
[http://dx.doi.org/10.1212/WNL.51.5.1270] [PMID: 9818844]
].

Frequent refractory generalized tonic-clonic seizures, antiepileptic polytherapy, and prolonged duration of epilepsy are some of the commonly identified risk factors for SUDEP [17Hesdorffer DC, Tomson T, Benn E, et al. ILAE Commission on epidemiology; subcommission on mortality. Combined analysis of risk factors for SUDEP. Epilepsia 2011; 52(6): 1150-9.
[http://dx.doi.org/10.1111/j.1528-1167.2010.02952.x] [PMID: 21671925]
]. However, the most consistent risk factor out of these is an increased frequency of generalized tonic–clonic seizures (GTC) [16Ficker DM, So EL, Shen WK, et al. Population-based study of the incidence of sudden unexplained death in epilepsy. Neurology 1998; 51(5): 1270-4.
[http://dx.doi.org/10.1212/WNL.51.5.1270] [PMID: 9818844]
].

The cause of SUDEP is unclear but hypothesized to be due to cardiac bradyarrhythmias [17Hesdorffer DC, Tomson T, Benn E, et al. ILAE Commission on epidemiology; subcommission on mortality. Combined analysis of risk factors for SUDEP. Epilepsia 2011; 52(6): 1150-9.
[http://dx.doi.org/10.1111/j.1528-1167.2010.02952.x] [PMID: 21671925]
, 18Surges R, Thijs RD, Tan HL, Sander JW. Sudden unexpected death in epilepsy: risk factors and potential pathomechanisms. Nat Rev Neurol 2009; 5(9): 492-504.
[http://dx.doi.org/10.1038/nrneurol.2009.118] [PMID: 19668244]
]. However, respiratory depression occurring during and after a seizure can be severe enough to cause marked oxygen desaturation and hypoxia [19Nashef L, Walker F, Allen P, Sander JW, Shorvon SD, Fish DR. Apnoea and bradycardia during epileptic seizures: relation to sudden death in epilepsy. J Neurol Neurosurg Psychiatry 1996; 60(3): 297-300.
[http://dx.doi.org/10.1136/jnnp.60.3.297] [PMID: 8609507]
, 20Bateman LM, Li CS, Seyal M. Ictal hypoxemia in localization-related epilepsy: analysis of incidence, severity and risk factors. Brain 2008; 131(Pt 12): 3239-45.
[http://dx.doi.org/10.1093/brain/awn277] [PMID: 18952672]
]. Therefore, it is unclear whether the primary inciting event in the cases of SUDEP is respiratory, cardiac or a combination of both.

CARDIAC DYSFUNTION LEADING TO SUDEP

Impairment of autonomic regulation of cardiac rhythm has been implicated in the development of SUDEP. Hyperactivity of the sympathetic nervous system leads to increased secretion of adrenomedullary catecholamines which facilitates the occurrence of various cardiac arrhythmias that can cause SUDEP [14Ryvlin P, Nashef L, Lhatoo SD, et al. Incidence and mechanisms of cardiorespiratory arrests in epilepsy monitoring units (MORTEMUS): a retrospective study. Lancet Neurol 2013; 12(10): 966-77.
[http://dx.doi.org/10.1016/S1474-4422(13)70214-X] [PMID: 24012372]
]. Studies have shown reduction in cardiac uptake of meta-iodobenzylguanidine (MIBG) during ictal events suggesting a postganglionic cardiac catecholamine disturbance or impaired postganglionic sympathetic cardiac innervation in patients with epilepsy [21Kerling F, Dütsch M, Linke R, Kuwert T, Stefan H, Hilz MJ. Relation between ictal asystole and cardiac sympathetic dysfunction shown by MIBG-SPECT. Acta Neurol Scand 2009; 120(2): 123-9.
[http://dx.doi.org/10.1111/j.1600-0404.2008.01135.x] [PMID: 19154536]
]. Heart rate variability (HRV) is a measure of the beat-to-beat variability of the heart rate and low HRV is a predictor of mortality in patients with heart disease [22Ansakorpi H, Korpelainen JT, Huikuri HV, Tolonen U, Myllylä VV, Isojärvi JI. Heart rate dynamics in refractory and well controlled temporal lobe epilepsy. J Neurol Neurosurg Psychiatry 2002; 72(1): 26-30.
[http://dx.doi.org/10.1136/jnnp.72.1.26] [PMID: 11784820]
]. Similarly, low HRV might be a risk factor for SUDEP [23Mukherjee S, Tripathi M, Chandra PS, et al. Cardiovascular autonomic functions in well-controlled and intractable partial epilepsies. Epilepsy Res 2009; 85(2-3): 261-9.
[http://dx.doi.org/10.1016/j.eplepsyres.2009.03.021] [PMID: 19409754]
]. Studies with larger cohorts are needed to confirm the validity and utility of this variable as a predictor of SUDEP.

ANTI-EPILEPTIC MEDICATION LEADING TO SUDEP

Ionotropic effects of antiepileptic drugs (AEDs) on cardiac musculature have been implicated in the pathophysiology of SUDEP, however there is limited supportive literature. The mechanism of action as phenytoin is central blockade of sodium channels impairing propagation of depolarization. Phenytoin induces similar blockade in cardiac myocytes leading to cardiac rhythm dysfunction [24Nobili L, Proserpio P, Rubboli G, Montano N, Didato G, Tassinari CA. Sudden unexpected death in epilepsy (SUDEP) and sleep. Sleep Med Rev 2011; 15(4): 237-46.
[http://dx.doi.org/10.1016/j.smrv.2010.07.006] [PMID: 20951616]
, 25Randazzo DN, Ciccone A, Schweitzer P, Winters SL. Complete atrioventricular block with ventricular asystole following infusion of intravenous phenytoin. J Electrocardiol 1995; 28(2): 157-9.
[http://dx.doi.org/10.1016/S0022-0736(05)80287-0] [PMID: 7616148]
]. Carbamazepine has also been shown to impair cardiac conduction through its effect on the autonomic nervous system [26Isojärvi JI, Ansakorpi H, Suominen K, Tolonen U, Repo M, Myllylä VV. Interictal cardiovascular autonomic responses in patients with epilepsy. Epilepsia 1998; 39(4): 420-6.
[http://dx.doi.org/10.1111/j.1528-1157.1998.tb01394.x] [PMID: 9578032]
, 27Kennebäck G, Ericson M, Tomson T, Bergfeldt L. Changes in arrhythmia profile and heart rate variability during abrupt withdrawal of antiepileptic drugs. Implications for sudden death. Seizure 1997; 6(5): 369-75.
[http://dx.doi.org/10.1016/S1059-1311(97)80036-2] [PMID: 9663800]
] Lamotrigine may impair repolarization potentials due to its effect on potassium channels leading to comorbid arrhythmias [28Danielsson BR, Lansdell K, Patmore L, Tomson T. Effects of the antiepileptic drugs lamotrigine, topiramate and gabapentin on hERG potassium currents. Epilepsy Res 2005; 63(1): 17-25.
[http://dx.doi.org/10.1016/j.eplepsyres.2004.10.002] [PMID: 15716081]
, 29Aurlien D, Taubøll E, Gjerstad L. Lamotrigine in idiopathic epilepsy - increased risk of cardiac death? Acta Neurol Scand 2007; 115(3): 199-203.
[http://dx.doi.org/10.1111/j.1600-0404.2006.00730.x] [PMID: 17295716]
].

Many persons with epilepsy take multiple anticonvulsants and polypharmacy has also been hypothesized as a risk factor for SUDEP [30Nilsson L, Farahmand BY, Persson PG, Thiblin I, Tomson T. Risk factors for sudden unexpected death in epilepsy: a case-control study. Lancet 1999; 353(9156): 888-93.
[http://dx.doi.org/10.1016/S0140-6736(98)05114-9] [PMID: 10093982]
]. However, this position is controversial as SUDEP appears to have a higher incidence in patients with sub-optimal seizure control [31Langan Y, Nashef L, Sander JW. Case-control study of SUDEP. Neurology 2005; 64(7): 1131-3.
[http://dx.doi.org/10.1212/01.WNL.0000156352.61328.CB] [PMID: 15824334]
, 32Faught E, Duh MS, Weiner JR, Guérin A, Cunnington MC. Nonadherence to antiepileptic drugs and increased mortality: findings from the RANSOM Study. Neurology 2008; 71(20): 1572-8.
[http://dx.doi.org/10.1212/01.wnl.0000319693.10338.b9] [PMID: 18565827]
].

GENETIC SYNDROMES ASSOCIATED WITH SUDEP

Several genes have been identified which may increase likelihood of SUDEP. A combination of single nucleotide polymorphisms in genes expressed in both neuro-cardiac and respiratory control pathways have been implicated in the development of SUDEP: SCN1A, KCNA1, RYR3, and HTR2C [33Klassen TL, Bomben VC, Patel A, et al. High-resolution molecular genomic autopsy reveals complex sudden unexpected death in epilepsy risk profile. Epilepsia 2014; 55(2): e6-e12.
[http://dx.doi.org/10.1111/epi.12489] [PMID: 24372310]
].

Long QT syndrome is known to cause fatal cardiac arrhythmias [34Goldenberg I, Moss AJ. Long QT syndrome. J Am Coll Cardiol 2008; 51(24): 2291-300.
[http://dx.doi.org/10.1016/j.jacc.2008.02.068] [PMID: 18549912]
]. This syndrome has been attributed to mutations in 13 or more genes that are expressed in the heart. Clinical seizures are observed in upto 29% of these patients, and epileptiform activity on electroencephalography is present in upto 15% of patients with long QT syndrome [35Anderson JH, Bos JM, Cascino GD, Ackerman MJ. Prevalence and spectrum of electroencephalogram-identified epileptiform activity among patients with long QT syndrome. Heart Rhythm 2014; 11(1): 53-7.
[http://dx.doi.org/10.1016/j.hrthm.2013.10.010] [PMID: 24103226]
, 36Johnson JN, Hofman N, Haglund CM, Cascino GD, Wilde AA, Ackerman MJ. Identification of a possible pathogenic link between congenital long QT syndrome and epilepsy. Neurology 2009; 72(3): 224-31.
[http://dx.doi.org/10.1212/01.wnl.0000335760.02995.ca] [PMID: 19038855]
]. Therefore, it is important to evaluate seizures in these patients and effectively treat them to prevent SUDEP.

Dravet syndrome manifests itself in childhood as a severe form of epilepsy progressing from febrile seizures to refractory epilepsy [37Kalume F. Sudden unexpected death in Dravet syndrome: respiratory and other physiological dysfunctions. Respir Physiol Neurobiol 2013; 189(2): 324-8.
[http://dx.doi.org/10.1016/j.resp.2013.06.026] [PMID: 23850567]
]. The genetic cause of Dravet syndrome is a loss-of-function mutation in SCN1A in approximately 80% of cases [38Claes L, Del-Favero J, Ceulemans B, Lagae L, Van Broeckhoven C, De Jonghe P. De novo mutations in the sodium-channel gene SCN1A cause severe myoclonic epilepsy of infancy. Am J Hum Genet 2001; 68(6): 1327-32.
[http://dx.doi.org/10.1086/320609] [PMID: 11359211]
]. Mouse models of Dravet syndrome have revealed cardiac arrhythmias similar to those observed in humans during seizures. These findings support the notion of a channelopathy leading to SUDEP in these patients [37Kalume F. Sudden unexpected death in Dravet syndrome: respiratory and other physiological dysfunctions. Respir Physiol Neurobiol 2013; 189(2): 324-8.
[http://dx.doi.org/10.1016/j.resp.2013.06.026] [PMID: 23850567]
, 39Moseley BD, Ghearing GR, Munger TM, Britton JW. The treatment of ictal asystole with cardiac pacing. Epilepsia 2011; 52(4): e16-9.
[http://dx.doi.org/10.1111/j.1528-1167.2010.02972.x] [PMID: 21463267]
].

RESPIRATORY DYSFUNCTION LEADING TO SUDEP

Respiratory dysfunction is well documented during seizures [19Nashef L, Walker F, Allen P, Sander JW, Shorvon SD, Fish DR. Apnoea and bradycardia during epileptic seizures: relation to sudden death in epilepsy. J Neurol Neurosurg Psychiatry 1996; 60(3): 297-300.
[http://dx.doi.org/10.1136/jnnp.60.3.297] [PMID: 8609507]
, 20Bateman LM, Li CS, Seyal M. Ictal hypoxemia in localization-related epilepsy: analysis of incidence, severity and risk factors. Brain 2008; 131(Pt 12): 3239-45.
[http://dx.doi.org/10.1093/brain/awn277] [PMID: 18952672]
, 39Moseley BD, Ghearing GR, Munger TM, Britton JW. The treatment of ictal asystole with cardiac pacing. Epilepsia 2011; 52(4): e16-9.
[http://dx.doi.org/10.1111/j.1528-1167.2010.02972.x] [PMID: 21463267]
]. Apnea, severe oxygen desaturation and pulmonary edema has been observed in patients during and after ictal events [19Nashef L, Walker F, Allen P, Sander JW, Shorvon SD, Fish DR. Apnoea and bradycardia during epileptic seizures: relation to sudden death in epilepsy. J Neurol Neurosurg Psychiatry 1996; 60(3): 297-300.
[http://dx.doi.org/10.1136/jnnp.60.3.297] [PMID: 8609507]
, 20Bateman LM, Li CS, Seyal M. Ictal hypoxemia in localization-related epilepsy: analysis of incidence, severity and risk factors. Brain 2008; 131(Pt 12): 3239-45.
[http://dx.doi.org/10.1093/brain/awn277] [PMID: 18952672]
, 39Moseley BD, Ghearing GR, Munger TM, Britton JW. The treatment of ictal asystole with cardiac pacing. Epilepsia 2011; 52(4): e16-9.
[http://dx.doi.org/10.1111/j.1528-1167.2010.02972.x] [PMID: 21463267]
]. Consequently, respiratory depression is hypothesized to lead to SUDEP.

The Mortality in Epilepsy Monitoring Units Study (MORTEMUS) is a landmark study aimed at evaluating the cardiorespiratory mechanism involved in SUDEP. The patients were enrolled from multiple epilepsy monitoring units (EMU) internationally. Interestingly, all the SUDEPs were preceded by a GTC and, the majority, occurring at night while patients were prone. Cardiopulmonary resuscitation (CPR) was only successful when started immediately after the event. Post-ictal tachypnea near 18-50 breaths per minute seemed to progress to apnea, bradycardia and cardiac arrest. This study improved our understanding of SUDEP and physicians began to understand it as a combination of cardio-respiratory dysfunction which is centrally mediated [14Ryvlin P, Nashef L, Lhatoo SD, et al. Incidence and mechanisms of cardiorespiratory arrests in epilepsy monitoring units (MORTEMUS): a retrospective study. Lancet Neurol 2013; 12(10): 966-77.
[http://dx.doi.org/10.1016/S1474-4422(13)70214-X] [PMID: 24012372]
].

CONCLUSION

Prevention of SUDEP is extremely important in patients with chronic, generalized epilepsy. Since increased frequency of GTCS is the most consistently reported risk factor for SUDEP, effective seizure control is the most important preventive strategy. Non-pharmacological approaches such as nocturnal checks and supervision, as well as family or care-giver CPR training have the potential to decrease the incidence of SUDEP. Cardiac monitoring with routine, as well as, long term holter monitors is suggested in high risk epilepsy patients to prevent SUDEP. Pacemakers have been implanted to prevent death in high-risk epilepsy patients but the clinical utility of this is currently controversial [39Moseley BD, Ghearing GR, Munger TM, Britton JW. The treatment of ictal asystole with cardiac pacing. Epilepsia 2011; 52(4): e16-9.
[http://dx.doi.org/10.1111/j.1528-1167.2010.02972.x] [PMID: 21463267]
] Vagus nerve stimulation (VNS) has the potential to reduce the incidence of SUDEP by decreasing seizure frequency [39Moseley BD, Ghearing GR, Munger TM, Britton JW. The treatment of ictal asystole with cardiac pacing. Epilepsia 2011; 52(4): e16-9.
[http://dx.doi.org/10.1111/j.1528-1167.2010.02972.x] [PMID: 21463267]
]. Therefore, it should be considered in patients with medically intractable, non-lesional epilepsy [39Moseley BD, Ghearing GR, Munger TM, Britton JW. The treatment of ictal asystole with cardiac pacing. Epilepsia 2011; 52(4): e16-9.
[http://dx.doi.org/10.1111/j.1528-1167.2010.02972.x] [PMID: 21463267]
].

CONFLICT OF INTEREST

The author confirms that this article content has no conflict of interest.

ACKNOWLEDGEMENTS

Declared none.

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