Natelson B H, Chang Q
Department of Neuroscience, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark.
Neurol Clin. 1993 May;11(2):293-308.
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.
在过去二十年中，已有确凿证据表明，自主神经功能失衡时的大脑激活与以心源性猝死（SCD）告终的心律失常之间存在紧密联系。脑岛和边缘下皮质在调节心脏交感 - 副交感神经相互作用时，对下丘脑和其他脑干核团产生直接和间接影响。具体而言，交感神经过度活跃有利于危及生命的心律失常的发生，而迷走神经激活通常发挥相对的保护和抗纤颤作用。皮质脑区的癫痫激活可启动该系统，这可能部分解释了该患者群体意外死亡发生率增加的原因。环境压力在心律失常发生和心源性猝死中的作用对心脏病的转归至关重要。
