Sudden death. A neurocardiologic phenomenon
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Updated: Oct 12, 2026

Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus
Published on: April 5, 2011
1Department of Neuroscience, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark.
Abstract:
During the last two decades compelling evidence has been provided for the existence of a tight relation between brain activation of unbalanced autonomic function and arrhythmias ending in SCD. Insular and infralimbic cortex exert direct and indirect effects on hypothalamus and other brain stem nuclei in modulating cardiac sympathetic-parasympathetic interactions. Specifically, sympathetic hyperactivity favors the onset of life-threatening cardiac arrhythmias, whereas vagal activation usually exerts relatively protective and antifibrillatory effects. Epileptic activation of cortical brain sites can turn this system on and probably is responsible partially for the increased incidence of unexpected death in this patient population. The role of environmental stress in arrhythmogenesis and SCD is of great importance in the outcome of heart disease.
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