Effects of Seizures on Cardiac Function

Schuele, Stephan

doi:10.1097/wnp.0b013e3181b7f13b

Cited by 48 publications

(40 citation statements)

References 116 publications

(148 reference statements)

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“…30 It is likely that some cases of SUDEP primarily resulted from fatal cardiac arrhythmias, while others primarily resulted from respiratory depression and central apnea. 1,31,32 However, SUDEP related to seizure-induced primary cardiorespiratory failures does not reconcile with the high prevalence of a terminal prone position found in our study. Video-EEG-monitored SUDEP cases have provided us with the most valuable insights into the mechanism of SUDEP.…”

Section: Resultscontrasting

confidence: 79%

Association of prone position with sudden unexpected death in epilepsy

et al. 2015

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Section: Resultscontrasting

confidence: 79%

Association of prone position with sudden unexpected death in epilepsy

et al. 2015

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“…Central modulation of the cardiovascular autonomic nervous system involves a complex network, including the anterior insular cortex, anterior cingulate gyrus, amygdala, and ventromedial prefrontal cortex as detailed in previous publications (Moseley et al, 2013;Schuele, 2009;Schuele et al, 2007a;Surges et al, 2009c). These cortical limbic areas are often involved in the generation and propagation of seizures in patients with refractory temporal lobe epilepsy.…”

Section: Other Manifestations Of Autonomic Dysregulationmentioning

confidence: 97%

Cardiac and Autonomic Mechanisms Contributing to SUDEP

Bermeo‐Ovalle

Kennedy

Schuele

2015

Journal of Clinical Neurophysiology

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Sudden unexpected death in epilepsy is likely caused by a cascade of events affecting the vegetative nervous system leading to cardiorespiratory failure and death. Multiple genetic, electrophysiological, neurochemical, and pharmacological cardiac alterations have been associated with epilepsy, which can affect autonomic regulation of the heart and predispose patients to sudden unexpected death in epilepsy. These cardiac and autonomic changes are more frequently seen in patients with longstanding and medication refractory epilepsy and may be a prerequisite for sudden unexpected death in epilepsy. Cardiac changes are also observed within the immediate periictal period in patients with and without preexisting cardiac pathology and could be the tipping point in the cascade of events compromising autonomic, respiratory, and cardiac function during an epileptic convulsion. Better understanding if and how these cardiac alterations can make a particular individual with epilepsy more susceptible to sudden unexpected death in epilepsy will hopefully lead us to more effective preventative strategies.

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“…In 1906, Finny first documented cardiac asystole during a seizure. Since then, a wide range of cardiac arrhythmias have been reported, ranging from atrial fibrillation, supraventricular tachycardia, prolonged QT intervals, and torsades de pointes (Nilsson et al 1997;Nei et al 2004;Schuele 2009;Sevcencu and Struijk 2010). Also, a number of studies have indicated that seizure activity produces cardiac dysfunction and myocardial damage in human patients (Legriel et al 2008;Shimizu et al 2008) as well as animals experiencing seizures that were induced by lethal nerve agents (Tryphonas et al 1996).…”

Section: Introductionmentioning

confidence: 98%

Involvement of cardiomyocyte apoptosis in myocardial injury of hereditary epileptic rats

Chen

Cao

et al. 2013

Can. J. Physiol. Pharmacol.

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Many clinical cases have been reported where epilepsy profoundly influenced the pathophysiological function of the heart; however, the underlying mechanisms were not elucidated. We use the tremor (TRM) rat as an animal model of epilepsy to investigate the potential mechanisms of myocardial injury. Cardiac functions were assessed by arrhythmia score, heart rate, heart:body mass ratio, and hemodynamic parameters including left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), and maximum rate of left ventricular pressure rise and fall (+dp/dtmax and -dp/dtmax). Catecholamine level was detected by HPLC. Apoptotic index was estimated by TUNEL assay. The expressions of Bcl-2, Bax, caspase-3, extracellular signal-regulated protein kinase (ERK), c-Jun NH2-terminal protein kinases (JNK), and p38 were evaluated by Western blot. The results indicated that there existed cardiac dysfunction and cardiomyocyte apoptosis, accompanied by increasing catecholamine levels in TRM rats. Further investigation revealed that apoptosis was mediated by reducing Bcl-2, upregulating Bax, and activating caspase-3. Additional experiments demonstrated that P-ERK1/2 was decreased, whereas P-JNK and P-p38 were up-regulated. Our results suggest that the sympathetic nervous system activation and cardiomyocyte apoptosis are involved in the myocardial injury of TRM rats. The mechanisms of apoptosis might be associated with the activation of the mitochondria-initiated and the mitogen-activated protein kinase pathways.

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Effects of Seizures on Cardiac Function

Cited by 48 publications

References 116 publications

Association of prone position with sudden unexpected death in epilepsy

Association of prone position with sudden unexpected death in epilepsy

Cardiac and Autonomic Mechanisms Contributing to SUDEP

Involvement of cardiomyocyte apoptosis in myocardial injury of hereditary epileptic rats

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