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O’neal, T.B.;  Shrestha, S.;  Singh, H.;  Osagie, I.;  Ben-Okafor, K.;  Cornett, E.M.;  Kaye, A.D. Epidemiology of Sudden Unexpected Death in Epilepsy. Encyclopedia. Available online: https://encyclopedia.pub/entry/25746 (accessed on 30 November 2024).
O’neal TB,  Shrestha S,  Singh H,  Osagie I,  Ben-Okafor K,  Cornett EM, et al. Epidemiology of Sudden Unexpected Death in Epilepsy. Encyclopedia. Available at: https://encyclopedia.pub/entry/25746. Accessed November 30, 2024.
O’neal, Teri B., Sanjay Shrestha, Harsimar Singh, Ihianle Osagie, Kenechukwu Ben-Okafor, Elyse M. Cornett, Alan D. Kaye. "Epidemiology of Sudden Unexpected Death in Epilepsy" Encyclopedia, https://encyclopedia.pub/entry/25746 (accessed November 30, 2024).
O’neal, T.B.,  Shrestha, S.,  Singh, H.,  Osagie, I.,  Ben-Okafor, K.,  Cornett, E.M., & Kaye, A.D. (2022, August 01). Epidemiology of Sudden Unexpected Death in Epilepsy. In Encyclopedia. https://encyclopedia.pub/entry/25746
O’neal, Teri B., et al. "Epidemiology of Sudden Unexpected Death in Epilepsy." Encyclopedia. Web. 01 August, 2022.
Epidemiology of Sudden Unexpected Death in Epilepsy
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This entry is adapted from the peer-reviewed paper 10.3390/neurolint14030048

Epilepsy is a complex neurological condition with numerous etiologies and treatment options. In a subset of these patients, sudden unexpected death can occur, and to date, there are numerous explanations as to the pathophysiological mechanisms and how to mitigate these catastrophic outcomes. Approximately 2.3 million Americans have epilepsy, and nearly 150,000 people develop the condition each year. Sudden unexpected death in epilepsy (SUDEP) accounts for 2–18% of all epilepsy-related deaths and this is equivalent to one death in 1000 person-years of diagnosed epilepsy. It is more common in young adults aged 20–45. Seizures in the past year; the absence of terminal remission in the last five years; increased seizure frequency, particularly GTCS; and nocturnal seizures are the most potent modifiable risk factors for SUDEP. Patients not receiving any antiepileptic drug therapy are at higher risk of SUDEP. Patient education on medication compliance; care plans for seizure clusters (rescue medicines); epilepsy self-management programs; and lifestyle changes to avoid seizure-triggering factors, including avoiding excessive alcohol use and sleep deprivation, should be provided by health care providers. Continued research into SUDEP will hopefully lead to effective interventions to minimize occurrences.

epilepsy sudden death Takotsubo cardiomyopathy

1. Introduction

As one of the most common, chronic, and debilitating neurological conditions, epilepsy is a major problem today. Approximately 2.3 million Americans have epilepsy, and nearly 150,000 people develop the condition each year. Almost half a million children (from 0 to 17 years old) have epilepsy in the United States [1].
The incidence of  Sudden unexpected death in epilepsy (SUDEP) varies greatly depending on the population studied, how epilepsy is recorded and how epilepsy is recognized among the population [2]. A study of the number of people with epilepsy per 1000 per year related to SUDEP found from 6.3 to 9.3 risks for epilepsy surgery candidates, from 1.1 to 5.6 risks for epilepsy clinic populations with a high proportion of refractory epilepsy patients, and from 0.35 to 2.3 risks for community residents with epilepsy (Figure 1A) [3]. SUDEP is estimated to be a lifetime risk of 7 percent overall or 12 percent for those with persistent epilepsy by age 40 [4]. It has been estimated that the cumulative lifetime risk is 35 percent [2].
SUDEP accounts for 2–18% of all epilepsy-related deaths [5]. SUDEP is estimated to occur in approximately 1.2/1000 person-years (PY) [6]. The incidence of SUDEP is low among young children, more prevalent among adolescents, highest in young adults and significantly decreased thereafter (Figure 1B) [7]. In this regard, the estimated incidence of SUDEP in children seems to be significantly lower (0.22/1000 PY) than in adults, but recent studies in children (>12 years) indicated a similar incidence to that of adults.
Neurolint 14 00048 g001 550
Figure 1. Sudden unexpected death in epilepsy epidemiology [7][8] (A) Estimated annual sudden unexpected death in epilepsy incidence in different epilepsy patient populations. (B) Distribution of sudden unexpected death in epilepsy cases by age. Error bars reflect 95% Cis. VNS = vagus nerve stimulation.

2. Risk Factors

Understanding the risk factors for SUDEP is important for clinicians when identifying the patients at high risk. To identify top risk factors associated with SUDEP, DeGiorgio et al. studied the risk factors in studies published in core clinical journals from 1987 to 2017 [9]. Herein, crude and adjusted odds ratios or relative risk ratios (ORs or RRs) were analyzed and the risk factors were ranked using log OR/RR. Figure 2 shows the top ten risk factors using adjusted ORs with corresponding 95% confidence intervals.
Neurolint 14 00048 g002 550
Figure 2. Top ten risk factors using adjusted ORs with corresponding 95% confidence intervals [10].
The frequency of seizures has been consistently identified as the leading risk factor, with the top two risk factors being three or more GTC seizures per year and thirteen or more seizures (any type) in the past year [11][12].
Antiseizure medications (ASM) treatment (previously known as antiepileptic drugs or AEDs) has also been extensively investigated with SUDEP. Patients not receiving any ASM therapy are at higher risk of SUDEP [13]. Polytherapy is another leading risk factor, with three or more ASMs associated with increased risk [12]. However, it is more likely that the risk associated with polytherapy is related to severe drug resistance and high seizure frequency rather than the number of ASMs [14]. Another risk factor is frequent changes in the ASM dose [12].
All these risk factors help clinicians identify the interventions that can help reduce the risk of SUDEP. Clinicians should strive to control GTC seizures aggressively and to make their patients seizure-free whenever possible.

3. Pathophysiology

Any process that affects or diminishes the blood supply to the heart and brain can be potentially fatal. Numerous hypotheses have been put forward to explain SUDEP, including cardiac, respiratory, cerebral, and autonomic dysfunctions.
Many genetic mutations due to their effects on cardiac, respiratory, and nervous system can potentially cause SUDEP. The Table 1 lists the genes associated with SUDEP.
Table 1. Genetic association with SUDEP.
Gene Clinical Condition Function SUDEP Hypothesis
SCN1A Dravet syndrome, generalizedepilepsy with febrile seizures Sodium channel Increases epilepsyseverity by postictal parasympathetichyperactivity
SCN2A Epileptic encephalopathy Sodium channel Increases severity of epilepsy
SCN8A Epileptic encephalopathy Sodium channel Increases severity of epilepsy
PRRT2 Benign familial infantile seizures Proline-rich transmembrane protein 2 Potential interaction withSNAP-25 and presynapticneurotransmitter release
DEPDC5 Focal epilepsy G-protein signaling pathway, inhibits the mTORC1 pathway Potential increase in severity of epilepsy
CSTB Unverricht-Lundborg disease Inhibits intracellular thiol protease, prevents protease leakage from Lysosomes Increases severity of epilepsy and neurological impairment due toprogressive myoclonic epilepsy
TSC1, TSC2 Tuberous sclerosis complex Downregulates mTORC1 pathway Potential increase in severity of epilepsy
HCN2 Generalized epilepsy Contributes to spontaneous rhythmic activity in SA node and brain Potential impairment inbrainstem or cardiac pacemaker cells
KCNQ1 Long QT syndrome Potassium channel; ventricular repolarization Potentialarrhythmogenic effect
KCNH2 Long QT syndrome Potassium channel;repolarization of cardiac action potential Uncertain
SCN5A Long QT syndrome Sodium channel; rapid depolarizing sodium current underlying cardiac action potential upstroke Potential combination of epilepsy and arrhythmia
NOS1AP Long QT syndrome Cytosolic protein that binds to neuronal nitric oxide synthase Potential combination of epilepsy and arrhythmia
RYR2 Sudden cardiac death Cardiac ryanodine receptor 2; intracellular calcium release channel, coupling excitation–contraction Potential combination of epilepsy and arrhythmia
HCN4 Bradycardia, sick sinus syndrome Potassiumchannel; slow kinetics of activation and inactivation, cardiacpacemaker role Variant identified in SUDEP

3.1. Cardiac Hypothesis

Sudden cardiac arrest has been postulated as one of the mechanisms of SUDEP, and various studies and investigations have been performed to identify specific ECG findings associated with it. Transient prolongation of the QT interval during the peri-ictal state can lead to abnormal cardiac repolarization causing ventricular tachyarrhythmia [15][16][17]. Studies have also detected a shortening of the QT interval during seizures [17][18]. It is of particular interest in people with genetically determined short QT syndrome who have high chances of reentry tachycardia [19]. Another finding is ventricular late potentials associated with seizures, which can cause ventricular tachyarrhythmias [20].
The electrophysiological changes implicated in SUDEP have been linked with many ion channel abnormalities. The mutated SCN1A gene linked with Dravet syndrome is one of the most common gene mutations associated with SUDEP [21][22]. Other mutations include genes associated with long QT syndrome or those involved with controlling cardiac rhythm, such as KCNQ1, LQTS, KCNH2, SCN5A, and ryanodine calcium channels [22][23][24][25][26]. Many of these are expressed in the heart and brain, suggesting that their mutations can predispose an individual to seizure and cardiac arrhythmia [27][28][29].
Contrary to tachyarrhythmias associated with seizures, bradyarrhythmia and asystole have also been described [30]. Ictal bradyarrhythmia is caused by seizure-like activity in both temporal lobes, leading to either deactivation of the sympathetic system or activation of the parasympathetic system [31][32][33]. It is not clear whether this can lead to sudden cardiac death, but a cardiac pacemaker has been advised to manage these patients [34][35].
In some patients with epilepsy, stress-induced Takotsubo cardiomyopathy has been reported, especially after convulsive seizures or status epilepticus. It can impair myocardial contractility, causing cardiogenic shock, cardiac arrhythmias, and SUDEP [36][37].

3.2. Autonomic Dysfunction

It has been established that heart rate increases during seizures due to autonomic system involvement [38]. Autonomic system derangements associated with epilepsy include excessive sympathetic activity, low parasympathetic activity, high vasomotor tone, and severe dysautonomia [10][39]. An important risk factor for sudden cardiac death in intractable epilepsy and antiepileptic usage is decreased heart rate variability [40]. This decrease in heart rate variability is directly related to the duration of seizure disorder, use of antiepileptic drugs, and multiple drug therapy [41][42][43][44].

3.3. Respiratory and Cerebral Dysfunctions

Peri-ictal hypoxemia has been reported in up to 25 percent of patients with SUDEP [17]. It can result from central apnea, airway obstruction, or pulmonary edema [45][46][47][48]. The risk is increased with longer seizure activity, temporal lobe involvement, or contralateral lobe involvement [49][50].
EEG findings suggest that cardiac and respiratory dysfunction are caused by disruptions in the autonomic networks during pathological cerebral activity. A retrospective study of EEG and ECG findings in monitored cardiac arrests revealed central apnea and bradycardia following a generalized tonic-clonic seizure after initial variation of heart and respiratory rates, showing altered cardiorespiratory function leading to SUDEP [51]. Another case–control study suggested a relation between prolonged postictal generalized EEG suppression (PGES) and SUDEP [52]. Although the association between PGES and SUDEP could not be replicated in a subsequent study, still, these studies were able to demonstrate that PGES follows convulsive seizures [53].
Figure 3 is an attempt to show the interactions between different mechanisms and risk factors that can potentially lead to SUDEP.
Neurolint 14 00048 g003 550
Figure 3. Pathophysiology model of SUDEP.

4. Treatment for the Prevention of Sudden Unexpected Death in Epilepsy

SUDEP is a devastating cause of premature epilepsy-associated death among children and adult patient populations with epilepsy. The prevention of this enigma is still an arduous task, as the exact pathophysiology of SUDEP is unknown. Measures aimed at reducing the risk of SUDEP largely target postulated theories on its pathophysiology and a few potentially modifiable risk factors in affected patients. These risk factors have been identified from case–control, cohort studies, and systematic reviews. Some of the proposed interventions are highlighted below.

4.1. Counseling and Education

Several societies, including the American Academy of Neurology (AAN), strongly recommend discussing tailored information about SUDEP with patients and their relatives. However, there is no evidence that the disclosure of SUDEP risk to patients is associated with improvements in medication compliance, changes in anxiety levels, or protection from SUDEP [54]. Some experts have opined that it fosters a “truth-telling relationship” between doctors and their patients while helping to define treatment goals.
Additionally, patient education on medication compliance; care plans for seizure clusters (rescue medicines); epilepsy self-management programs; and lifestyle changes to avoid seizure-triggering factors, including avoiding excessive alcohol use and sleep deprivation, should be provided by health care providers [55].

4.2. Optimize Treatment of Drug-Resistant Epilepsy

SUDEP prevention is an important aspect of achieving seizure control with effective epilepsy treatment [56]. The risk of SUDEP is greater in patients with a higher burden of GTCS (generalized tonic-clonic seizures) [57]. Hence, adjunctive anti-seizure medications and referral for surgical evaluation of lesional epilepsy to reduce the frequency of GTCS is protective.

4.3. Seizure-Monitoring Devices

A variety of seizure detection devices (bed sensors, alarms, and heart rate monitors) are currently available for detecting cardiorespiratory distress, thus prompting early intervention when necessary. Their use should be individualized based on a patient’s seizure profile, as evidence to support their effectiveness in preventing SUDEP is lacking. More clinical studies are required to ascertain their role in the SUDEP prevention algorithm [54][56].

4.4. Preventing Airway Obstruction

Safety (ventilated foam) pillows and nocturnal supervision have been hypothesized to reduce the impact of post-ictal airway compromise, especially when sleeping in the prone position. There are no data to support the role of safety pillows, but there is limited low-quality evidence that corroborates the benefit of nocturnal supervision in preventing SUDEP. Hence, timely supervision and prompt administration of emergency treatment post-seizure recovery are advised, especially in patients with frequent nocturnal seizures [54][56].

4.5. Reducing Brain and Brainstem Depression from Endogenous Opioids and Adenosine

The termination of seizures is typically preceded by a surge in endogenous opioids and adenosine, which can lead to postictal apnea when in excess. Medications, including naloxone and caffeine, have been used in a few studies to attenuate the effect of endogenous opioids and adenosine, respectively. However, due to the lack of data on this intervention, there is no compelling evidence to support their benefit or use in preventing SUDEP [55].

4.6. Cardiac and Diaphragmatic Pacing

Standard cardiac and phrenic nerve pacing holds the potential to prevent cardiorespiratory failure. This needs to be explored further as prevention modalities in the SUDEP algorithm.

4.7. Clinical Practice Recommendations

The clinical practice recommendations are presented in Table 2.
Table 2. Clinical practice recommendations for SUDEP treatment.
Grade B Effective epilepsy treatment to decrease the burden of GTCS protects against SUDEP. Providers should use appropriate anti-seizure medications and combine ASM where necessary to achieve seizure control, while actively involving patients in their care and weighing the safety profile of the medications.
Grade C Based on risk profile and psychosocial circumstances, clinicians should selectively counsel patients with frequent uncontrolled nocturnal seizures on nocturnal supervision, as this is protective against SUDEP.
Grade C Prompt referral for surgical evaluation of drug-resistant epilepsy/lesional epilepsy is of paramount importance in reducing the risk of SUDEP.

References

  1. Collazo, I.V.M.; Tatum, W.O. Sudden Unexpected Death in Epilepsy (SUDEP): Are All Your Patients Informed? Neurologist 2016, 21, 66–71.
  2. Graber, K.D.; Buchhalter, J.; So, E.; Surges, R.; Boison, D.; Kalume, F.; Wright, C.; Gehlbach, B.; Noebels, J.; Whittemore, V.; et al. Summary of the 2016 Partners Against Mortality in Epilepsy (PAME) Conference. Epilepsy Curr. 2016, 16, 1–17.
  3. Devinsky, O.; Hesdorffer, D.C.; Thurman, D.J.; Lhatoo, S.; Richerson, G. Sudden unexpected death in epilepsy: Epidemiology, mechanisms, and prevention. Lancet Neurol. 2016, 5, 1075–1088.
  4. Sillanpää, M.; Shinnar, S. Long-term mortality in childhood-onset epilepsy. N. Engl. J. Med. 2010, 363, 2522–2529.
  5. Mohanraj, R.; Norrie, J.; Stephen, L.J.; Kelly, K.; Hitiris, N.; Brodie, M.J. Mortality in adults with newly diagnosed and chronic epilepsy: A retrospective comparative study. Lancet Neurol. 2006, 5, 481–487.
  6. May, T.W.; Israel, C.W. Sudden unexpected death in epilepsy (SUDEP): Epidemiology, cardiac and other risk factors. Herzschrittmacherther. Elektrophysiol. 2019, 30, 274–286.
  7. Tomson, T.; Nashef, L.; Ryvlin, M. Sudden unexpected death in epilepsy: Current knowledge and future directions. Lancet Neurol. 2008, 7, 1021–1031.
  8. Thurman, D.J.; Hesdorffer, D.C.; French, J.A. Sudden unexpected death in epilepsy: Assessing the public health burden. Epilepsia 2014, 55, 1479–1485.
  9. DeGiorgio, C.M.; Markovic, D.; Mazumder, R.; Moseley, B.D. Ranking the Leading Risk Factors for Sudden Unexpected Death in Epilepsy. Front. Neurol. 2017, 8, 473.
  10. Sathyaprabha, T.N.; Satishchandra, P.; Netravathi, K.; Sinha, S.; Thennarasu, K.; Raju, T.R. Cardiac autonomic dysfunctions in chronic refractory epilepsy. Epilepsy Res. 2006, 72, 49–56.
  11. Hesdorffer, D.C.; Tomson, T.; Benn, E.; Sander, J.W.; Nilsson, L.; Langan, Y.; Walczak, T.S.; Beghi, E.; Brodie, M.J.; Hauser, A.; et al. Combined analysis of risk factors for SUDEP. Epilepsia 2011, 52, 1150–1159.
  12. Nilsson, L.; Farahmand, B.Y.; Persson, P.G.; Thiblin, I.; Tomson, T. Risk factors for sudden unexpected death in epilepsy: A case-control study. Lancet Lond. Engl. 1999, 353, 888–893.
  13. Langan, Y.; Nashef, L.; Sander, J.W. Case-control study of SUDEP. Neurology 2005, 64, 1131–1133.
  14. Hesdorffer, D.C.; Tomson, T.; Benn, E.; Sander, J.W.; Nilsson, L.; Langan, Y.; Walczak, T.S.; Beghi, E.; Brodie, M.J.; Hauser, W.A. Do antiepileptic drugs or generalized tonic-clonic seizure frequency increase SUDEP risk? A combined analysis. Epilepsia 2012, 53, 249–252.
  15. Surges, R.; Adjei, P.; Kallis, C.; Erhuero, J.; Scott, C.A.; Bell, G.S.; Sander, J.W.; Walker, M.C. Pathologic cardiac repolarization in pharmacoresistant epilepsy and its potential role in sudden unexpected death in epilepsy: A case-control study. Epilepsia 2010, 51, 233–242.
  16. Brotherstone, R.; Blackhall, B.; McLellan, A. Lengthening of corrected QT during epileptic seizures. Epilepsia 2010, 51, 221–232.
  17. Moseley, B.D.; Wirrell, E.C.; Nickels, K.; Johnson, J.N.; Ackerman, M.J.; Britton, J. Electrocardiographic and oximetric changes during partial complex and generalized seizures. Epilepsy Res. 2011, 95, 237–245.
  18. Surges, R.; Scott, C.A.; Walker, M.C. Enhanced QT shortening and persistent tachycardia after generalized seizures. Neurology 2010, 74, 421–426.
  19. Surges, R.; Taggart, P.; Sander, J.W.; Walker, M.C. Too long or too short? New insights into abnormal cardiac repolarization in people with chronic epilepsy and its potential role in sudden unexpected death. Epilepsia 2010, 51, 738–744.
  20. Rejdak, K.; Rubaj, A.; Głowniak, A.; Furmanek, K.; Kutarski, A.; Wysokiński, A.; Stelmasiak, Z. Analysis of ventricular late potentials in signal-averaged ECG of people with epilepsy. Epilepsia 2011, 52, 2118–2124.
  21. Le Gal, F.; Korff, C.M.; Monso-Hinard, C.; Mund, M.T.; Morris, M.; Malafosse, A.; Schmitt-Mechelke, T. A case of SUDEP in a patient with Dravet syndrome with SCN1A mutation. Epilepsia 2010, 51, 1915–1918.
  22. Aurlien, D.; Leren, T.P.; Taubøll, E.; Gjerstad, L. New SCN5A mutation in a SUDEP victim with idiopathic epilepsy. Seizure 2009, 18, 158–160.
  23. Tu, E.; Bagnall, R.D.; Duflou, J.; Semsarian, C. Post-mortem review and genetic analysis of sudden unexpected death in epilepsy (SUDEP) cases. Brain Pathol. Zur. Switz. 2011, 21, 201–208.
  24. Johnson, J.N.; Tester, D.J.; Bass, N.E.; Ackerman, M.J. Cardiac channel molecular autopsy for sudden unexpected death in epilepsy. J. Child Neurol. 2010, 25, 916–921.
  25. Tu, E.; Waterhouse, L.; Duflou, J.; Bagnall, R.D.; Semsarian, C. Genetic analysis of hyperpolarization-activated cyclic nucleotide-gated cation channels in sudden unexpected death in epilepsy cases. Brain Pathol. Zur. Switz. 2011, 21, 692–698.
  26. Glasscock, E. Genomic biomarkers of SUDEP in brain and heart. Epilepsy Behav. EB 2014, 38, 172–179.
  27. Lehnart, S.E.; Mongillo, M.; Bellinger, A.; Lindegger, N.; Chen, B.; Hsueh, W.; Reiken, S.; Wronska, A.; Drew, L.J.; Ward, C.W.; et al. Leaky Ca2+ release channel/ryanodine receptor 2 causes seizures and sudden cardiac death in mice. J. Clin. Investig. 2008, 118, 2230–2245.
  28. Goldman, A.M.; Glasscock, E.; Yoo, J.; Chen, T.T.; Klassen, T.L.; Noebels, J.L. Arrhythmia in heart and brain: KCNQ1 mutations link epilepsy and sudden unexplained death. Sci. Transl. Med. 2009, 1, 2ra6.
  29. Nagrani, T.; Siyamwala, M.; Vahid, G.; Bekheit, S. Ryanodine calcium channel: A novel channelopathy for seizures. Neurologist 2011, 17, 91–94.
  30. Rugg-Gunn, F.J.; Simister, R.J.; Squirrell, M.; Holdright, D.R.; Duncan, J.S. Cardiac arrhythmias in focal epilepsy: A prospective long-term study. Lancet Lond. Engl. 2004, 364, 2212–2219.
  31. Britton, J.W.; Ghearing, G.R.; Benarroch, E.E.; Cascino, G.D. The ictal bradycardia syndrome: Localization and lateralization. Epilepsia 2006, 47, 737–744.
  32. Lanz, M.; Oehl, B.; Brandt, A.; Schulze-Bonhage, A. Seizure induced cardiac asystole in epilepsy patients undergoing long term video-EEG monitoring. Seizure 2011, 20, 167–172.
  33. Kerling, F.; Dütsch, M.; Linke, R.; Kuwert, T.; Stefan, H.; Hilz, M.J. Relation between ictal asystole and cardiac sympathetic dysfunction shown by MIBG-SPECT. Acta Neurol. Scand. 2009, 120, 123–129.
  34. Strzelczyk, A.; Cenusa, M.; Bauer, S.; Hamer, H.M.; Mothersill, I.W.; Grunwald, T.; Hillenbrand, B.; Ebner, A.; Steinhoff, B.J.; Krämer, G.; et al. Management and long-term outcome in patients presenting with ictal asystole or bradycardia. Epilepsia 2011, 52, 1160–1167.
  35. Moseley, B.D.; Ghearing, G.R.; Munger, T.M.; Britton, J.W. The treatment of ictal asystole with cardiac pacing. Epilepsia 2011, 52, e16–e19.
  36. Stöllberger, C.; Wegner, C.; Finsterer, J. Seizure-associated Takotsubo cardiomyopathy. Epilepsia 2011, 52, e160–e167.
  37. Dupuis, M.; van Rijckevorsel, K.; Evrard, F.; Dubuisson, N.; Dupuis, F.; van Robays, P. Takotsubo syndrome (TKS): A possible mechanism of sudden unexplained death in epilepsy (SUDEP). Seizure 2012, 21, 51–54.
  38. Zijlmans, M.; Flanagan, D.; Gotman, J. Heart rate changes and ECG abnormalities during epileptic seizures: Prevalence and definition of an objective clinical sign. Epilepsia 2002, 43, 847–854.
  39. Mukherjee, S.; Tripathi, M.; Chandra, P.S.; Yadav, R.; Choudhary, N.; Sagar, R.; Bhore, R.; Pandey, R.M.; Deepak, K.K. Cardiovascular autonomic functions in well-controlled and intractable partial epilepsies. Epilepsy Res. 2009, 85, 261–269.
  40. Lotufo, P.A.; Valiengo, L.; Benseñor, I.M.; Brunoni, A.R. A systematic review and meta-analysis of heart rate variability in epilepsy and antiepileptic drugs. Epilepsia 2012, 53, 272–282.
  41. Lossius, M.I.; Erikssen, J.E.; Mowinckel, P.; Gulbrandsen, P.; Gjerstad, L. Changes in autonomic cardiac control in patients with epilepsy after discontinuation of antiepileptic drugs: A randomized controlled withdrawal study. Eur. J. Neurol. 2007, 14, 1022–1028.
  42. Suorsa, E.; Korpelainen, J.T.; Ansakorpi, H.; Huikuri, H.V.; Suorsa, V.; Myllylä, V.V.; Isojärvi, J.I.T. Heart rate dynamics in temporal lobe epilepsy-A long-term follow-up study. Epilepsy Res. 2011, 93, 80–83.
  43. Yildiz, G.U.; Apaydın, E.; Umuttan, D.; Tokgoz, D.O.S.; Ozdemir, K.; Genca, B.O.; İlhana, N. Analysis of 24-hour heart rate variations in patients with epilepsy receiving antiepileptic drugs. Epilepsy Behav. EB 2011, 20, 349–354.
  44. Rauscher, G.; DeGiorgio, A.C.; Miller, P.R.; De Giorgio, C.M. Sudden unexpected death in epilepsy associated with progressive deterioration in heart rate variability. Epilepsy Behav. EB 2011, 21, 103–105.
  45. So, E.L.; Sam, M.C.; Lagerlund, T.L. Postictal central apnea as a cause of SUDEP: Evidence from near-SUDEP incident. Epilepsia 2000, 41, 1494–1497.
  46. Pezzella, M.; Striano, P.; Ciampa, C.; Errichiello, L.; Penza, P.; Striano, S. Severe pulmonary congestion in a near miss at the first seizure: Further evidence for respiratory dysfunction in sudden unexpected death in epilepsy. Epilepsy Behav. EB 2009, 14, 701–702.
  47. Tao, J.X.; Qian, S.; Baldwin, M.; Chen, X.J.; Rose, S.; Ebersole, S.H.; Ebersole, J.S. SUDEP, suspected positional airway obstruction, and hypoventilation in postictal coma. Epilepsia 2010, 51, 2344–2347.
  48. Tavee, J.; Morris, H. Severe postictal laryngospasm as a potential mechanism for sudden unexpected death in epilepsy: A near-miss in an EMU. Epilepsia 2008, 49, 2113–2117.
  49. Bateman, L.M.; Li, C.-S.; Seyal, M. Ictal hypoxemia in localization-related epilepsy: Analysis of incidence, severity and risk factors. Brain J. Neurol. 2008, 131, 3239–3245.
  50. Seyal, M.; Bateman, L.M. Ictal apnea linked to contralateral spread of temporal lobe seizures: Intracranial EEG recordings in refractory temporal lobe epilepsy. Epilepsia 2009, 50, 2557–2562.
  51. Ryvlin, P.; Nashef, L.; Lhatoo, S.D.; Bateman, L.M.; Bird, J.; Bleasel, A.; Boon, P.; Crespel, A.; Dworetzky, B.A.; Høgenhaven, H.; et al. Incidence and mechanisms of cardiorespiratory arrests in epilepsy monitoring units (MORTEMUS): A retrospective study. Lancet Neurol. 2013, 12, 966–977.
  52. Lhatoo, S.D.; Faulkner, H.J.; Dembny, K.; Trippick, K.; Johnson, C.; Bird, J.M. An electroclinical case-control study of sudden unexpected death in epilepsy. Ann. Neurol. 2010, 68, 787–796.
  53. Surges, R.; Strzelczyk, A.; Scott, C.A.; Walker, M.C.; Sander, J.W. Postictal generalized electroencephalographic suppression is associated with generalized seizures. Epilepsy Behav. EB 2011, 21, 271–274.
  54. Maguire, M.J.; Jackson, C.F.; Marson, A.G.; Nevitt, S.J. Treatments for the prevention of Sudden Unexpected Death in Epilepsy (SUDEP). Cochrane Database Syst. Rev. 2020, 4, CD011792.
  55. Bhasin, H.; Sharma, S.; Ramachandrannair, R. Can We Prevent Sudden Unexpected Death in Epilepsy (SUDEP)? Can. J. Neurol. Sci. J. Can. Sci. Neurol. 2021, 48, 464–468.
  56. Pensel, M.C.; Nass, R.D.; Taubøll, E.; Aurlien, D.; Surges, R. Prevention of sudden unexpected death in epilepsy: Current status and future perspectives. Expert Rev. Neurother. 2020, 20, 497–508.
  57. Sveinsson, O.; Andersson, T.; Mattsson, P.; Carlsson, S.; Tomson, T. Clinical risk factors in SUDEP: A nationwide population-based case-control study. Neurology 2020, 94, e419–e429.
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Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Teri B. O’Neal
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Sanjay Shrestha
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Harsimar Singh
,
Ihianle Osagie
,
Kenechukwu Ben-Okafor
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Elyse M. Cornett
,
Alan D. Kaye
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