Brain seizes, heart ceases: a case of ictal asystole

Lim, Erle C.H.; Lim, Shih-Hui; Wilder-Smith, Einar

doi:10.1136/jnnp.69.4.557

Cited by 25 publications

(16 citation statements)

References 14 publications

(9 reference statements)

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“…The AV conduction blocks and bradycardias observed during seizures in Kcna1 -null mice are consistent with ictal cardiac bradyarrhythmias present in humans, where they have been reported in up to 21% of epilepsy patients (Rugg-Gunn et al, 2004; Leung et al, 2006) and more than 60 cases have been described with potentially life-threatening AV block, bradycardia, and asystole associated with seizures (Wilder-Smith, 1992; Reeves et al, 1996; Devinsky et al, 1997; Lim et al, 2000; Tinuper et al, 2001; Tigaran et al, 2002; Zubair et al, 2009). At least one report describes an instance of seizure-provoked asystole that actually progressed to SUDEP (Dasheiff and Dickinson, 1986).…”

Section: Discussionsupporting

confidence: 75%

Kv1.1 Potassium Channel Deficiency Reveals Brain-Driven Cardiac Dysfunction as a Candidate Mechanism for Sudden Unexplained Death in Epilepsy

Glasscock¹,

Yoo²,

Chen³

et al. 2010

J. Neurosci.

199

233

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Mice lacking Kv1.1 Shaker-like potassium channels encoded by the Kcna1 gene exhibit severe seizures and die prematurely. The channel is widely expressed in brain but only minimally, if at all, in mouse myocardium. To test whether Kv1.1-potassium deficiency could underlie primary neurogenic cardiac dysfunction, we performed simultaneous video EEG-ECG recordings and found that Kcna1-null mice display potentially malignant interictal cardiac abnormalities, including a fivefold increase in atrioventricular (AV) conduction blocks, as well as bradycardia and premature ventricular contractions. During seizures the occurrence of AV conduction blocks increased, predisposing Kv1.1-deficient mice to sudden unexplained death in epilepsy (SUDEP), which we recorded fortuitously in one animal. To determine whether the interictal AV conduction blocks were of cardiac or neural origin, we examined their response to selective pharmacological blockade of the autonomic nervous system. Simultaneous administration of atropine and propranolol to block parasympathetic and sympathetic branches, respectively, eliminated conduction blocks. When administered separately, only atropine ameliorated AV conduction blocks, indicating that excessive parasympathetic tone contributes to the neurocardiac defect. We found no changes in Kv1.1-deficient cardiac structure, but extensive Kv1.1 expression in juxtaparanodes of the wild-type vagus nerve, the primary source of parasympathetic input to the heart, suggesting a novel site of action leading to Kv1.1-associated cardiac bradyarrhythmias. Together, our data suggest that Kv1.1 deficiency leads to impaired neural control of cardiac rhythmicity due in part to aberrant parasympathetic neurotransmission, making Kcna1 a strong candidate gene for human SUDEP.

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Section: Discussionsupporting

confidence: 75%

Kv1.1 Potassium Channel Deficiency Reveals Brain-Driven Cardiac Dysfunction as a Candidate Mechanism for Sudden Unexplained Death in Epilepsy

Glasscock¹,

Yoo²,

Chen³

et al. 2010

J. Neurosci.

199

233

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“…The walls of these lesions are thin, fragile, and easily lacerated during surgery. 1,3,4,6 Pathologically, the blister-like aneurysms appear to be lacerations of the carotid wall caused by degeneration of the internal elastic lamina, a situation similar to that of intracranial arterial dissections. 2 …”

Section: Introductionmentioning

confidence: 97%

Intravascular lymphoma presenting as progressive paraparesis

Grove¹,

Robbins²,

Kermode³

2008

Journal of Clinical Neuroscience

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“…Cardiac and respiratory changes could possibly contribute to SUDEP (12) and it is known that ECG abnormalities occur often during or after seizures (1,2,13). Cardiac arrests and severe bradyarrhythmias during seizures have been described often in case reports (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25) and ECG abnormalities appear to occur more often during generalized seizures and within seizures of longer duration (1,2). We describe the occurrence of ECG abnormalities in a large group of patients and in several seizures per patient and evaluate the possible risk factors for the occurrence of ECG abnormalities.…”

mentioning

confidence: 99%

Heart Rate Changes and ECG Abnormalities During Epileptic Seizures: Prevalence and Definition of an Objective Clinical Sign

2002

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Summary:Purpose: To determine the prevalence of heart rate changes and ECG abnormalities during epileptic seizures and to determine the timing of heart rate changes compared to the first electrographic and clinical signs. To assess the risk factors for the occurrence of ECG abnormalities.Methods: We analyzed retrospectively 281 seizures in 81 patients with intractable epilepsy who had prolonged video-EEG and two-channel ECG. The nature and timing of heart rate changes compared to the electrographic and clinical seizure onset was determined. The ictal period (including one minute preictally and three minutes postictally) was analyzed for cardiac arrhythmias, conduction and repolarization abnormalities. Risk factors for cardiac abnormalities were investigated using parametric and non-parametric statistics.Results: There was an increase in heart rate of at least 10 beats/minute in 73% of seizures (93% of patients) and this occurred most often around seizure onset. In 23% of seizures (49% of patients) the rate increase preceded both the electrographic and the clinical onset. ECG abnormalities were found in 26% of seizures (44% of patients). One patient had an asystole for 30 seconds. Long seizure duration increased the occurrence of ECG abnormalities. No other risk factor was found.Conclusions: Heart rate changes occur frequently and occur around the time or even before the earliest electrographic or clinical change. The change can clarify the timing of seizure onset and the specific rate pattern may be useful for seizure diagnosis and for automatic seizure detection. ECG abnormalities occur often and repeatedly in several seizures of the same patient. Key Words: Heart rate-ECG-Epilepsy-Seizure onset-Asystole.Heart rate changes at the onset of epileptic seizures are often overlooked as a clinical sign. An increase in heart rate has been described in a high proportion of seizures (1-7) and the timing of these changes may provide useful clinical information. The purpose of our study is to describe the timing of changes in heart rate compared to the electrographic and clinical seizure onset. Although heart rate changes have often been described in seizures, the specific timing of these changes has not been reported. If the increase is at the onset or even before a seizure, it could be a helpful additional clinical sign in determining seizure onset. The prevalence of heart rate changes and their timing might also suggest uses for ECG detectors in the effort to detect seizures automatically.While most studies have noted increases in heart rate around some seizures, there are also instances of decreased heart rate, and an increased occurrence of serious ECG abnormalities (1,2,8). Sudden unexpected death in epilepsy (SUDEP) is a major cause of death in patients with epilepsy, especially in patients with intractable epilepsy (9,10) and SUDEP occurs much more when patients are having seizures (11). Cardiac and respiratory changes could possibly contribute to SUDEP (12) and it is known that ECG abnormalities occur often durin...

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Brain seizes, heart ceases: a case of ictal asystole

Cited by 25 publications

References 14 publications

Kv1.1 Potassium Channel Deficiency Reveals Brain-Driven Cardiac Dysfunction as a Candidate Mechanism for Sudden Unexplained Death in Epilepsy

Kv1.1 Potassium Channel Deficiency Reveals Brain-Driven Cardiac Dysfunction as a Candidate Mechanism for Sudden Unexplained Death in Epilepsy

Intravascular lymphoma presenting as progressive paraparesis

Heart Rate Changes and ECG Abnormalities During Epileptic Seizures: Prevalence and Definition of an Objective Clinical Sign

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