Thursday, July 23, 2015

A new technique to indicate risk of SUDEP?

[S14.003] Transcutaneous pCO2 and Seizures in the Epilepsy Monitoring Unit: Associations with Markers of Seizure Severity

Derek J. Chong,1Palak S. Patel,1Alla Ahmed,1Nilofer M. Khan,2Bryan J. Still,3Evan Marzouk,4Daniel Friedman,1Orrin Devinsky1
1New York, NY, USA, 2Livingston, NJ, USA, 3Winston-Salem, NC, USA, 4Saratoga Springs, NY, USA.

Transcutaneous pCO2 (TCpCO2) may be an indicator of risk for Sudden Unexpected Death in Epilepsy (SUDEP).
SUDEP is the single largest direct epilepsy-related cause of death, and theories include central or obstructive apneas leading to hypoxemia and hypercapnia and cerebral shutdown. Studies have shown oxygen desaturation <70%, and increases in End-tidal CO2. TCpCO2 is a different technology, is less cumbersome, and its use during seizures has not yet been reported.
The Tosca500 (Radiometer America, Inc) was used in the epilepsy monitoring unit to continuously measure SaO2, heart rate and TCpCO2 in patients at high risk for cardiopulmonary distress during seizures and those undergoing intracranial EEG monitoring. We retrospectively reviewed data from 12 patients who underwent TCpCO2 recording. Seizure type, electro-clinical seizure duration, and the presence of post-ictal generalized electrographic suppression (PGES) were also assessed. PGES was defined as post-ictal EEG suppression <10uV, ending when 15/30 seconds of cerebral activity reached ≥10uV.
Peri-ictal TCpCO2 data were reliable in 15 seizures: 7 GTCs, 3 complex partial, 2 hemiclonic, 2 subclinical and 1 tonic seizure. The average peak increase in TCpCO2 was 8±7.3mmHg, with 7 seizures associated with a ≥20% elevation. TCpCO2 typically peaked several minutes after electrographic offset. Hemiclonic and GTC seizures were also associated with oxygen desaturations and tachycardia, and were left temporal in onset. PGES occurred in 2 GTCs. Seizure duration (p=0.009), seizure type (p=0.029) and PGES (p=0.02) were significantly correlated with ΔTCpCO2 (Spearman correlation). In multivariate analysis using these three variables, only PGES was significantly associated with ΔTCpCO2 (p=0.004).
TCpCO2 elevation was associated with PGES and may denote greater severity and duration of seizure activity. Further study and direct comparison with ETCO2 is required to better understand the cause of hypercapnea, and the potential of this novel modality in identifying SUDEP risks.
Category - Epilepsy and Clinical Neurophysiology (EEG): Co-Morbidities

Session: S14: Platform Session: Epilepsy/Clinical Neurophysiology (EEG): Clinical Epilepsy (3:15 PM-5:00 PM)
Date/Time: Tuesday, April 21, 2015 - 3:45 pm
AAN Annual Meeting 2015  Washington

Courtesy of:

See Respiration and SUDEP 5/18/15


  1. “We have to expand the way we think about SUDEP and go beyond just focusing on the issue of seizure control,” said Lara Jehi, MD, director of the Cleveland Clinic Epilepsy Center, who co-authored, along with Stephen Schuele, MD, a commentary accompanying the study in Neurology. “We know we have to achieve seizure control to reduce the risk of sudden death, but what we learn from this article is that sudden death in patients who have epilepsy is not only related to seizure problems. These patients have a higher prevalence of cardiac problems that can put them at higher risk of sudden death from a cardiac issue. This article suggests that most cases of sudden death that happen in patients with epilepsy may in fact be due to a cardiac problem, rather than the epilepsy triggering sudden death.”

    Practically speaking, what does this mean for the neurologist?

    “We need to be aware that our patients who have seizures are at higher risk of having sudden death, whether it is SUDEP or not,” said Dr. Jehi. “From a practical perspective, if a patient of mine talks about ‘passing out’ events that may not necessarily be corresponding to what their seizures would look like, or if they have an epilepsy that can also involve the heart, such as genetic epilepsies or long QT syndrome, I should at least be cognizant in the setting of my clinic visits with them of problems that could be cardiac and not necessarily epilepsy-related.”

    Selim Benbadis, MD, a professor of neurology and director of the comprehensive epilepsy program at the University of South Florida and Tampa General Hospital, agreed that cardiac risk factors in epilepsy are not sufficiently appreciated by neurologists.

    “That said, we should really distinguish between the ‘run-of-the-mill’ epilepsy patient seen by a neurologist, who is doing well, with seizures that are essentially controlled, and the difficult patients with poorly controlled, convulsive seizures like generalized tonic-clonic and young adults with nocturnal seizures,” he said. “Those are the patients for whom SUDEP is a great risk factor, and they should alert us to doing a full cardiac workup and referring them to a cardiologist for a comprehensive evaluation.”

    Should a cardiac referral for these types of patients be standard of care? “It certainly should be strongly considered,” Dr. Benbadis said. “We need to know more about these patients who are particularly at risk. At most epilepsy centers, at least once or twice a year we have a patient who dies unexpectedly, and far from enough is known.”...

    Managing the risk of SUDEP is primarily the responsibility of the epileptologist, said Dr. Jehi, but they should partner more frequently with cardiologists. “This study is really a step in the right direction, particularly because of the multidisciplinary approach. We don't generally talk about cardiac health as a comorbidity in epilepsy, but this article suggests we should.”

  2. The study in Neurology referred to in the preceding entry.

    Lamberts RJ, Blom MT, Wassenaar M, Bardai A, Leijten FS, de Haan GJ, Sander
    JW, Thijs RD, Tan HL. Sudden cardiac arrest in people with epilepsy in the
    community: Circumstances and risk factors. Neurology. 2015 Jul 21;85(3):212-8.


    To ascertain whether characteristics of ventricular tachycardia/fibrillation (VT/VF) differed between people with epilepsy and those without and which individuals with epilepsy were at highest risk.


    We ascertained 18 people with active epilepsy identified in a community-based registry of sudden cardiac arrest (SCA) with ECG-confirmed VT/VF (cases). We compared them with 470 individuals with VT/VF without epilepsy (VT/VF controls) and 54 individuals with epilepsy without VT/VF (epilepsy controls). Data on comorbidity, epilepsy severity, and medication use were collected and entered into (conditional) logistic regression models to identify determinants of VT/VF in epilepsy.


    In most cases, there was an obvious (10/18) or presumed cardiovascular cause (5/18) in view of preexisting heart disease. In 2 of the 3 remaining events, near-sudden unexpected death in epilepsy (SUDEP) was established after successful resuscitation. Cases had a higher prevalence of congenital/inherited heart disease (17% vs 1%, p = 0.002), and experienced VT/VF at younger age (57 vs 64 years, p = 0.023) than VT/VF controls. VT/VF in cases occurred more frequently at/near home (89% vs 58%, p = 0.009), and was less frequently witnessed (72% vs 89%, p = 0.048) than in VT/VF controls. Cases more frequently had clinically relevant heart disease (50% vs 15%, p = 0.005) and intellectual disability (28% vs 1%, p < 0.001) than epilepsy controls.


    Cardiovascular disease rather than epilepsy characteristics is the main determinant of VT/VF in people with epilepsy in the community. SCA and SUDEP are partially overlapping disease entities.