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Ictal central apnea as a predictor for sudden unexpected death in epilepsy
Epilepsy & Behavior 22 (2011) 401–403
Contents lists available at ScienceDirect
Epilepsy & Behavior j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / ye b e h
Case Report
Ictal central apnea as a predictor for sudden unexpected death in epilepsy Stephan U. Schuele a,⁎, Mitra Afshari a, Zahra S. Afshari a, Michael P. Macken a, Jorge Asconape b, Lisa Wolfe a, Elizabeth E. Gerard a a b
Department of Neurology, Northwestern University, Chicago, IL, USA Loyola University Medical Center, Loyola University, Chicago, IL, USA
a r t i c l e
i n f o
Article history: Received 31 May 2011 Revised 24 June 2011 Accepted 28 June 2011 Available online 4 August 2011 Keywords: Sudden unexpected death in epilepsy Central apnea Pulse oximetry Video/EEG monitoring
a b s t r a c t Epidemiological evidence associating ictal hypoventilation during focal seizures with a heightened risk for subsequent sudden unexpected death in epilepsy (SUDEP) is lacking. We describe a patient with temporal lobe epilepsy with two focal seizures recorded in the epilepsy monitoring unit that were associated with central apnea lasting 57 and 58 seconds. During these events, she demonstrated oxygen desaturation down to 68 and 62%. The patient subsequently died at home from autopsy-confirmed SUDEP. The family was not alerted of any seizure activity by the auditory alarm system in her room nor by sleeping in the adjacent room with open doors. This case emphasizes the fact that ictal hypoxia and SUDEP may occur in seizures without noticeable convulsive activity. The report gives credibility to the growing body of literature suggesting that epilepsies affecting the autonomic nervous system may predispose to SUDEP independent of the effects of a secondary generalized convulsion. © 2011 Elsevier Inc. All rights reserved.
1. Introduction Several case reports of sudden unexpected death in epilepsy (SUDEP) in the epilepsy monitoring unit (EMU) support the idea that peri-ictal hypoventilation in a prone position can lead to SUDEP [1–3]. None of these patients had pulse oximetry or airflow recordings, which could have provided respiratory details of the terminal event and prior seizures. The question of whether respiratory failure was triggered by ictal hypoventilation or postictal positioning and suffocation remains unanswered. It is also unclear if ictal hypoventilation indicates a heightened risk for subsequent SUDEP warranting preventive measures [4]. We describe a patient with new-onset temporal lobe epilepsy and ictal apnea and hypoxia documented with multimodality monitoring who subsequently passed away at home from autopsy-confirmed SUDEP. The study was approved by the institutional review board. 2. Case report A 30-year-old right-handed woman with no prior medical history and no known epilepsy risk factors presented to an outside hospital in status epilepticus with seizures arising from both temporal lobes. She had more than 100 focal seizures with alteration of consciousness and several secondarily generalized convulsions within the first 4 days. ⁎ Corresponding author at: Department of Neurology, Northwestern University, Abbott Hall No. 1425, 710 North Lake Shore Drive, Chicago, IL 60611, USA. Fax: + 1 312 926 9089. E-mail address: [email protected] (S.U. Schuele). 1525-5050/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.yebeh.2011.06.036
Extensive laboratory and radiographic evaluation for an autoimmune or neoplastic etiology yielded an elevated thyroid peroxidase antibody level of 354.4 and lymphocytic pleocytosis on cerebrospinal fluid analysis with 7 WBC the first day and 134 the fourth day as the only abnormal laboratory results. Her seizures did not improve with phenytoin, valproic acid, topiramate, and levetiracetam and she was discharged 5 weeks later on carbamazepine and phenobarbital. She was given a 2-week course of prednisone for suspected Hashimoto's encephalopathy. The patient continued to have weekly focal seizures with alteration of consciousness and monthly convulsions. Five months after disease onset, she was admitted for elective video/EEG with concurrent monitoring of ECG and respiratory parameters including chest and abdominal wall excursion, airflow, end-tidal CO2, and oxygen saturation. Her interictal EEG was notable for continuous generalized slowing and independent epileptiform discharges from both temporal lobes, 80% of the discharges arising from the left anterior temporal region, occurring every 5–10 minutes, predominantly during sleep. During the 14-day monitoring admission, she had four of her typical seizures emanating from the left temporal lobe (see Table 1). Archived tracings of her seizures included 2 minutes prior to ictal onset and 5 minutes after onset. The first event occurred during hookup and only video/EEG data were available. The last event was recorded without respiratory monitoring. Seizures 2 and 3 were both focal seizures that occurred from sleep. In both of these seizures respiratory monitoring demonstrated a central apnea with absent chest and abdominal excursion approximately 40 seconds after the onset of the electrographic seizure and 10 seconds prior to contralateral ictal spread on scalp EEG (see Fig. 1).
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S.U. Schuele et al. / Epilepsy & Behavior 22 (2011) 401–403
Table 1 Clinical and neurophysiologic seizure characteristics. Semiology
Seizure 1
Seizure 2
Seizure 3
Staring, R face twitching Awake state EEG Onset Time from onset to contra-lateral spread (s) Seizure duration (s) Apnea Time from seizure onset (s) Duration (s) Oxygen saturation 1 minute preictal Minimum Time to minimum (s) Duration of minimum (s) 5 minutes postonset Heart rate (bpm) 1 minute preictal Maximum Seizure end 1 minute postictal EEG suppression Duration (s) a
Sleep state
Seizure 4 R head version, GTCSa
Sleep state
Sleep state
L temporal L temporal L temporal L temporal 46 52 35 37 70 NA
153
122
41
33
57
58
NA
139 NA
3. Discussion NA
93% 68% 122 27 90%
93% 62% 102 18 87%
60 125 114 81
73 140 117 96
73 109 166 128
None
None
58
NA
None
EEG and her level of alertness improved, but she continued to have biweekly nonconvulsive seizures and monthly convulsions. Five months after the second video/EEG evaluation, her family found her dead in her bed, lying in a prone position. She was last seen alive in the early morning hours when a family member checked up on her. Her bedroom door was kept open and her family slept off the same hallway with open doors. Her husband had installed an auditory monitoring device to capture the noise from her seizures. Despite these precautions, none of the family members were awakened by seizure activity during the night. No signs of convulsive seizure activity were noted when she was found. An autopsy including detailed investigation of her brain for signs of inflammation was performed and no alternative cause of death was found.
Generalized tonic–clonic seizure.
The apneic periods lasted 57 and 58 seconds and were associated with oxygen desaturation to 68 and 62%, respectively. Both seizures were not noticed by a family member sleeping in the same room or by an EEG technologist working in the next room with open doors. The clinical signs were subtle, consisting of a quiet arousal from sleep and stiffening followed by late right face twitching. It is also notable that the patient habitually slept in a prone position, but the hospital bed with headboard elevation forced her to sleep supine. Lamotrigine was added to her existing antiepileptic regimen. The patient was treated with plasmapheresis and immunoglobulin therapy and eventually placed on oral prednisolone for a presumed autoimmune etiology of her epilepsy. The diffuse slowing on the
We have described a patient with temporal lobe epilepsy associated with episodes of central ictal apnea and severe oxygen desaturation during simultaneous video/EEG, ECG, and respiratory monitoring who subsequently died of autopsy-confirmed SUDEP. This case suggests that ictal apnea is not only a potential mechanism but also a risk factor for SUDEP. Epidemiological studies have established a number of risk factors for SUDEP including history and number of generalized tonic–clonic seizures, seizure frequency, subtherapeutic antiepileptic drug levels, young age, long epilepsy duration, antiepileptic polytherapy, and IQ b70. Recently, lamotrigine has been associated with an increased risk of SUDEP in patients with idiopathic generalized epilepsies [5]. However, a significant association between lamotrigine and SUDEP in patients with focal epilepsy has not been established. SUDEP is related to generalization of seizure activity and postictal suppression of brain activity, and prolonged postictal EEG suppression (N50 seconds) may be a neurophysiological risk factor for subsequent SUDEP [6]. Ictal autonomic effects have also been implicated as a cause of SUDEP. A greater heart rate increase with seizures arising from sleep in patients who subsequently died from SUDEP, compared with controls, has been reported (78 bpm vs 52 bpm) [7]. In recent years, it has been recognized that up to one-third of patients with intractable focal seizures with or without secondary generalization experience ictal hypopnea with desaturations below 90%. Only 3.6% show desaturations below 70% [4]. Ictal hypoxemia is associated with temporal lobe epilepsy
Fig. 1. Seizure 2. Two consecutive 2-minute segments are shown. Broadly distributed left hemispheric sharp wave maximum temporal activity followed by low-amplitude rhythmic activity is seen at EEG onset (see inset). The ictal pattern spreads to the contralateral temporal electrode chain approximately 50 seconds later, coinciding with clinical seizure onset. The clinical symptoms remained unnoticed by a family member sleeping in the same room. On video review, staring and subtle face twitching were observed before the patient went back to sleep. A central apnea lasting 1 minute with absent chest and abdominal excursion preceded clinical seizure onset by 10 seconds, and was associated with a maximum oxygen desaturation to 68%. Her baseline ECG shows normal sinus rhythm at 60 bpm during sleep which increases to sinus tachycardia of maximum 122 bpm during the event. The EEG seizure lasted 153 seconds and was followed by diffuse generalized slowing more prominent over the left hemisphere. The patient's baseline oxygen saturation was 93%, and her ETCO2, 46–47 mm Hg. CO2 measurement dropped to 20 mm Hg during the apnea because of a lack of air exchange. After the patient resumed breathing, ETCO2 increased to 49 mm Hg by the end of the clip, 2.5 minutes after the end of the seizure (not shown).
S.U. Schuele et al. / Epilepsy & Behavior 22 (2011) 401–403
and occurs around the time of EEG seizure spread to the contralateral hemisphere as seen in the patient described [8]. This case illustrates that ictal hypopnea and subsequent SUDEP may occur in patients with focal seizures without noticeable tonic– clonic activity. Prone positioning during sleep may have further contributed to her death [1–3]. The report gives credibility to the growing body of literature suggesting that the autonomic effects of limbic epilepsy, in particular severe ictal hypoxia, may predispose to SUDEP. Epidemiological evidence that peri-ictal oxygen desaturation is related to SUDEP is missing, presumably because of the lack of systematic oxygen monitoring in that patient population. Oxygen desuration may not only indicate a higher risk for SUDEP, but may eventually lend itself to better seizure detection and SUDEP prevention. Simple measures like stimulation of the patient and positioning may already be beneficial and could be supplemented at least in the hospital setting by oxygen administration protocols [9,10]. Obviously, this is a single case report allowing only for limited conclusions. Our patient may still have had a convulsion despite the diligent supervision by her family. Her demise may have been unrelated to the recorded ictal hypoventilation and solely provoked by positioning and postictal cardiorespiratory instability. No evidence of brain inflammation was found on autopsy and her thyroglobulin antibodies had normalized at the time of her death, but a potential impact of her autoimmune disorder cannot be excluded. Conflict of interest statement The study was not industry sponsored. Dr. Schuele has served on the scientific advisory board for Lundbeck Inc. and received honoraria from GlaxoSmithKline and UCB Pharma for speakers’ bureau activities. He received support from Grant NINDS-R37-NS31146. Dr. Macken has
403
served on the scientific advisory board and received honoraria from speakers’ bureau activities for UCB Pharma and Cyberonics Inc. Dr. Asconape serves on the Lundbeck Pharmaceuticals scientific advisory board, receives honoraria from UCB Pharma, GlaxoSmithKline, and Cyberonics. He is the Chief Editor of Frontiers in Epilepsy, and is on the speakers’ bureau for UCB Pharma, GlaxoSmithKline, and Cyberonics. Dr. M. Afshari, Dr. Z. Afshari, Dr. L. Wolf, and Dr, E. Gerard report no disclosures.
References [1] Bateman LM, Spitz M, Seyal M. Ictal hypoventilation contributes to cardiac arrhythmia and SUDEP: report on two deaths in video-EEG-monitored patients. Epilepsia 2010;51:916–20. [2] Tao JX, Qian S, Baldwin M, et al. SUDEP, suspected positional airway obstruction, and hypoventilation in postictal coma. Epilepsia 2010;51:2344–7. [3] So EL, Sam MC, Lagerlund TL. Postictal central apnea as a cause of SUDEP: evidence from near-SUDEP incident. Epilepsia 2000;41:1494–7. [4] Bateman 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. [5] Hesdorffer DC, Tomson T, Benn E, et al. Combined analysis of risk factors for SUDEP. Epilepsia 2011;52:1150–9. [6] Lhatoo SD, Faulkner HJ, Dembny K, Trippick K, Johnson C, Bird JM. An electroclinical case–control study of sudden unexpected death in epilepsy. Ann Neurol 2010;68:787–96. [7] Nei M, Ho RT, Abou-Khalil BW, et al. EEG and ECG in sudden unexplained death in epilepsy. Epilepsia 2004;45:338–45. [8] Seyal M, Bateman LM. Ictal apnea linked to contralateral spread of temporal lobe seizures: intracranial EEG recordings in refractory temporal lobe epilepsy. Epilepsia 2009;50:2557–62. [9] Nashef L, Fish DR, Garner S, Sander JW, Shorvon SD. Sudden death in epilepsy: a study of incidence in a young cohort with epilepsy and learning difficulty. Epilepsia 1995;36:1187–94. [10] Yung I, Rose S, Hawes-Ebersole S, Ebersole J, Tao J. Convergence of ictal hypoxia and postictal hypoventilation as a potential mechanism of SUDEP [abstract]. Epilepsia 2010:A1.098.
Contents lists available at ScienceDirect
Epilepsy & Behavior j o u r n a l h o m e p a g e : w w w. e l s ev i e r. c o m / l o c a t e / ye b e h
Case Report
Ictal central apnea as a predictor for sudden unexpected death in epilepsy Stephan U. Schuele a,⁎, Mitra Afshari a, Zahra S. Afshari a, Michael P. Macken a, Jorge Asconape b, Lisa Wolfe a, Elizabeth E. Gerard a a b
Department of Neurology, Northwestern University, Chicago, IL, USA Loyola University Medical Center, Loyola University, Chicago, IL, USA
a r t i c l e
i n f o
Article history: Received 31 May 2011 Revised 24 June 2011 Accepted 28 June 2011 Available online 4 August 2011 Keywords: Sudden unexpected death in epilepsy Central apnea Pulse oximetry Video/EEG monitoring
a b s t r a c t Epidemiological evidence associating ictal hypoventilation during focal seizures with a heightened risk for subsequent sudden unexpected death in epilepsy (SUDEP) is lacking. We describe a patient with temporal lobe epilepsy with two focal seizures recorded in the epilepsy monitoring unit that were associated with central apnea lasting 57 and 58 seconds. During these events, she demonstrated oxygen desaturation down to 68 and 62%. The patient subsequently died at home from autopsy-confirmed SUDEP. The family was not alerted of any seizure activity by the auditory alarm system in her room nor by sleeping in the adjacent room with open doors. This case emphasizes the fact that ictal hypoxia and SUDEP may occur in seizures without noticeable convulsive activity. The report gives credibility to the growing body of literature suggesting that epilepsies affecting the autonomic nervous system may predispose to SUDEP independent of the effects of a secondary generalized convulsion. © 2011 Elsevier Inc. All rights reserved.
1. Introduction Several case reports of sudden unexpected death in epilepsy (SUDEP) in the epilepsy monitoring unit (EMU) support the idea that peri-ictal hypoventilation in a prone position can lead to SUDEP [1–3]. None of these patients had pulse oximetry or airflow recordings, which could have provided respiratory details of the terminal event and prior seizures. The question of whether respiratory failure was triggered by ictal hypoventilation or postictal positioning and suffocation remains unanswered. It is also unclear if ictal hypoventilation indicates a heightened risk for subsequent SUDEP warranting preventive measures [4]. We describe a patient with new-onset temporal lobe epilepsy and ictal apnea and hypoxia documented with multimodality monitoring who subsequently passed away at home from autopsy-confirmed SUDEP. The study was approved by the institutional review board. 2. Case report A 30-year-old right-handed woman with no prior medical history and no known epilepsy risk factors presented to an outside hospital in status epilepticus with seizures arising from both temporal lobes. She had more than 100 focal seizures with alteration of consciousness and several secondarily generalized convulsions within the first 4 days. ⁎ Corresponding author at: Department of Neurology, Northwestern University, Abbott Hall No. 1425, 710 North Lake Shore Drive, Chicago, IL 60611, USA. Fax: + 1 312 926 9089. E-mail address: [email protected] (S.U. Schuele). 1525-5050/$ – see front matter © 2011 Elsevier Inc. All rights reserved. doi:10.1016/j.yebeh.2011.06.036
Extensive laboratory and radiographic evaluation for an autoimmune or neoplastic etiology yielded an elevated thyroid peroxidase antibody level of 354.4 and lymphocytic pleocytosis on cerebrospinal fluid analysis with 7 WBC the first day and 134 the fourth day as the only abnormal laboratory results. Her seizures did not improve with phenytoin, valproic acid, topiramate, and levetiracetam and she was discharged 5 weeks later on carbamazepine and phenobarbital. She was given a 2-week course of prednisone for suspected Hashimoto's encephalopathy. The patient continued to have weekly focal seizures with alteration of consciousness and monthly convulsions. Five months after disease onset, she was admitted for elective video/EEG with concurrent monitoring of ECG and respiratory parameters including chest and abdominal wall excursion, airflow, end-tidal CO2, and oxygen saturation. Her interictal EEG was notable for continuous generalized slowing and independent epileptiform discharges from both temporal lobes, 80% of the discharges arising from the left anterior temporal region, occurring every 5–10 minutes, predominantly during sleep. During the 14-day monitoring admission, she had four of her typical seizures emanating from the left temporal lobe (see Table 1). Archived tracings of her seizures included 2 minutes prior to ictal onset and 5 minutes after onset. The first event occurred during hookup and only video/EEG data were available. The last event was recorded without respiratory monitoring. Seizures 2 and 3 were both focal seizures that occurred from sleep. In both of these seizures respiratory monitoring demonstrated a central apnea with absent chest and abdominal excursion approximately 40 seconds after the onset of the electrographic seizure and 10 seconds prior to contralateral ictal spread on scalp EEG (see Fig. 1).
402
S.U. Schuele et al. / Epilepsy & Behavior 22 (2011) 401–403
Table 1 Clinical and neurophysiologic seizure characteristics. Semiology
Seizure 1
Seizure 2
Seizure 3
Staring, R face twitching Awake state EEG Onset Time from onset to contra-lateral spread (s) Seizure duration (s) Apnea Time from seizure onset (s) Duration (s) Oxygen saturation 1 minute preictal Minimum Time to minimum (s) Duration of minimum (s) 5 minutes postonset Heart rate (bpm) 1 minute preictal Maximum Seizure end 1 minute postictal EEG suppression Duration (s) a
Sleep state
Seizure 4 R head version, GTCSa
Sleep state
Sleep state
L temporal L temporal L temporal L temporal 46 52 35 37 70 NA
153
122
41
33
57
58
NA
139 NA
3. Discussion NA
93% 68% 122 27 90%
93% 62% 102 18 87%
60 125 114 81
73 140 117 96
73 109 166 128
None
None
58
NA
None
EEG and her level of alertness improved, but she continued to have biweekly nonconvulsive seizures and monthly convulsions. Five months after the second video/EEG evaluation, her family found her dead in her bed, lying in a prone position. She was last seen alive in the early morning hours when a family member checked up on her. Her bedroom door was kept open and her family slept off the same hallway with open doors. Her husband had installed an auditory monitoring device to capture the noise from her seizures. Despite these precautions, none of the family members were awakened by seizure activity during the night. No signs of convulsive seizure activity were noted when she was found. An autopsy including detailed investigation of her brain for signs of inflammation was performed and no alternative cause of death was found.
Generalized tonic–clonic seizure.
The apneic periods lasted 57 and 58 seconds and were associated with oxygen desaturation to 68 and 62%, respectively. Both seizures were not noticed by a family member sleeping in the same room or by an EEG technologist working in the next room with open doors. The clinical signs were subtle, consisting of a quiet arousal from sleep and stiffening followed by late right face twitching. It is also notable that the patient habitually slept in a prone position, but the hospital bed with headboard elevation forced her to sleep supine. Lamotrigine was added to her existing antiepileptic regimen. The patient was treated with plasmapheresis and immunoglobulin therapy and eventually placed on oral prednisolone for a presumed autoimmune etiology of her epilepsy. The diffuse slowing on the
We have described a patient with temporal lobe epilepsy associated with episodes of central ictal apnea and severe oxygen desaturation during simultaneous video/EEG, ECG, and respiratory monitoring who subsequently died of autopsy-confirmed SUDEP. This case suggests that ictal apnea is not only a potential mechanism but also a risk factor for SUDEP. Epidemiological studies have established a number of risk factors for SUDEP including history and number of generalized tonic–clonic seizures, seizure frequency, subtherapeutic antiepileptic drug levels, young age, long epilepsy duration, antiepileptic polytherapy, and IQ b70. Recently, lamotrigine has been associated with an increased risk of SUDEP in patients with idiopathic generalized epilepsies [5]. However, a significant association between lamotrigine and SUDEP in patients with focal epilepsy has not been established. SUDEP is related to generalization of seizure activity and postictal suppression of brain activity, and prolonged postictal EEG suppression (N50 seconds) may be a neurophysiological risk factor for subsequent SUDEP [6]. Ictal autonomic effects have also been implicated as a cause of SUDEP. A greater heart rate increase with seizures arising from sleep in patients who subsequently died from SUDEP, compared with controls, has been reported (78 bpm vs 52 bpm) [7]. In recent years, it has been recognized that up to one-third of patients with intractable focal seizures with or without secondary generalization experience ictal hypopnea with desaturations below 90%. Only 3.6% show desaturations below 70% [4]. Ictal hypoxemia is associated with temporal lobe epilepsy
Fig. 1. Seizure 2. Two consecutive 2-minute segments are shown. Broadly distributed left hemispheric sharp wave maximum temporal activity followed by low-amplitude rhythmic activity is seen at EEG onset (see inset). The ictal pattern spreads to the contralateral temporal electrode chain approximately 50 seconds later, coinciding with clinical seizure onset. The clinical symptoms remained unnoticed by a family member sleeping in the same room. On video review, staring and subtle face twitching were observed before the patient went back to sleep. A central apnea lasting 1 minute with absent chest and abdominal excursion preceded clinical seizure onset by 10 seconds, and was associated with a maximum oxygen desaturation to 68%. Her baseline ECG shows normal sinus rhythm at 60 bpm during sleep which increases to sinus tachycardia of maximum 122 bpm during the event. The EEG seizure lasted 153 seconds and was followed by diffuse generalized slowing more prominent over the left hemisphere. The patient's baseline oxygen saturation was 93%, and her ETCO2, 46–47 mm Hg. CO2 measurement dropped to 20 mm Hg during the apnea because of a lack of air exchange. After the patient resumed breathing, ETCO2 increased to 49 mm Hg by the end of the clip, 2.5 minutes after the end of the seizure (not shown).
S.U. Schuele et al. / Epilepsy & Behavior 22 (2011) 401–403
and occurs around the time of EEG seizure spread to the contralateral hemisphere as seen in the patient described [8]. This case illustrates that ictal hypopnea and subsequent SUDEP may occur in patients with focal seizures without noticeable tonic– clonic activity. Prone positioning during sleep may have further contributed to her death [1–3]. The report gives credibility to the growing body of literature suggesting that the autonomic effects of limbic epilepsy, in particular severe ictal hypoxia, may predispose to SUDEP. Epidemiological evidence that peri-ictal oxygen desaturation is related to SUDEP is missing, presumably because of the lack of systematic oxygen monitoring in that patient population. Oxygen desuration may not only indicate a higher risk for SUDEP, but may eventually lend itself to better seizure detection and SUDEP prevention. Simple measures like stimulation of the patient and positioning may already be beneficial and could be supplemented at least in the hospital setting by oxygen administration protocols [9,10]. Obviously, this is a single case report allowing only for limited conclusions. Our patient may still have had a convulsion despite the diligent supervision by her family. Her demise may have been unrelated to the recorded ictal hypoventilation and solely provoked by positioning and postictal cardiorespiratory instability. No evidence of brain inflammation was found on autopsy and her thyroglobulin antibodies had normalized at the time of her death, but a potential impact of her autoimmune disorder cannot be excluded. Conflict of interest statement The study was not industry sponsored. Dr. Schuele has served on the scientific advisory board for Lundbeck Inc. and received honoraria from GlaxoSmithKline and UCB Pharma for speakers’ bureau activities. He received support from Grant NINDS-R37-NS31146. Dr. Macken has
403
served on the scientific advisory board and received honoraria from speakers’ bureau activities for UCB Pharma and Cyberonics Inc. Dr. Asconape serves on the Lundbeck Pharmaceuticals scientific advisory board, receives honoraria from UCB Pharma, GlaxoSmithKline, and Cyberonics. He is the Chief Editor of Frontiers in Epilepsy, and is on the speakers’ bureau for UCB Pharma, GlaxoSmithKline, and Cyberonics. Dr. M. Afshari, Dr. Z. Afshari, Dr. L. Wolf, and Dr, E. Gerard report no disclosures.
References [1] Bateman LM, Spitz M, Seyal M. Ictal hypoventilation contributes to cardiac arrhythmia and SUDEP: report on two deaths in video-EEG-monitored patients. Epilepsia 2010;51:916–20. [2] Tao JX, Qian S, Baldwin M, et al. SUDEP, suspected positional airway obstruction, and hypoventilation in postictal coma. Epilepsia 2010;51:2344–7. [3] So EL, Sam MC, Lagerlund TL. Postictal central apnea as a cause of SUDEP: evidence from near-SUDEP incident. Epilepsia 2000;41:1494–7. [4] Bateman 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. [5] Hesdorffer DC, Tomson T, Benn E, et al. Combined analysis of risk factors for SUDEP. Epilepsia 2011;52:1150–9. [6] Lhatoo SD, Faulkner HJ, Dembny K, Trippick K, Johnson C, Bird JM. An electroclinical case–control study of sudden unexpected death in epilepsy. Ann Neurol 2010;68:787–96. [7] Nei M, Ho RT, Abou-Khalil BW, et al. EEG and ECG in sudden unexplained death in epilepsy. Epilepsia 2004;45:338–45. [8] Seyal M, Bateman LM. Ictal apnea linked to contralateral spread of temporal lobe seizures: intracranial EEG recordings in refractory temporal lobe epilepsy. Epilepsia 2009;50:2557–62. [9] Nashef L, Fish DR, Garner S, Sander JW, Shorvon SD. Sudden death in epilepsy: a study of incidence in a young cohort with epilepsy and learning difficulty. Epilepsia 1995;36:1187–94. [10] Yung I, Rose S, Hawes-Ebersole S, Ebersole J, Tao J. Convergence of ictal hypoxia and postictal hypoventilation as a potential mechanism of SUDEP [abstract]. Epilepsia 2010:A1.098.