What Is the Clinical Correlation of Cardiac Noradrenergic Denervation in Parkinson Disease?

Abstract

The autonomic nervous system controls cardiac performance on a beat-to-beat basis in order to match regional blood flow demand. To that end, there is continuous interaction among central autonomic areas (anterior insula, anterior cingulate cortex, amygdala, hypothalamus, periaqueductal gray matter, parabrachial nucleus, and medulla), preganglionic sympathetic and parasympathetic efferent neurons, and intrinsic cardiac ganglia.1,2 Cardiac sympathetic and parasympathetic outputs have been classically thought to act in a reciprocal antagonistic fashion, whereby sympathetic stimulation increases heart rate (chronotropy), atrioventricular conduction (dromotropy), and myocardial contractility (inotropy), whereas parasympathetic stimulation reduces heart rate and atrioventricular conduction. There is evidence, however, for a complex and redundant organization, as cardiac control is mediated by feedback loops organized at 3 main levels: the intrinsic cardiac nervous system, the intrathoracic extracardiac ganglia, and the central autonomic nervous system. These systems are in constant communication, and at each level, afferent signals provide feedback information to neurons that in turn affect efferent control of the heart.1,3