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  1. D. S. Goldstein,
  2. Y. Sharabi,
  3. O. Bentho,
  4. G. Eisenhofer
  1. Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD


All of more than 30 neuroimaging studies and at least 4 postmortem pathology studies have agreed that Parkinson disease entails a loss of myocardial noradrenergic innervation, implying that in addition to being a movement disorder from loss of nigrostriatal dopaminergic neurons, Parkinson disease is also a dysautonomia from loss of postganglionic noradrenergic neurons. Cardiac sympathetic denervation has been reported even in the earliest stages of the disease; however, whether the denervation can actually precede the movement disorder has been unknown. As part of an evaluation of hemodynamic instability suggesting pheochromocytoma, a 52-year-old man underwent 6-[18F]fluorodopamine scanning and other autonomic function tests. Four years later, over the course of 6-12 months, he developed slow movement, limb rigidity, masked face, and small handwriting and was diagnosed with mild Parkinson disease. Review of the earlier 6-[18F]fluorodopamine scan revealed that the patient had had markedly decreased 6-[18F]fluorodopamine-derived radioactivity throughout the left ventricular myocardium, confirmed by follow-up scanning. He also had had evidence of low baroreflex-cardiovagal gain and excessive adrenomedullary secretion, also confirmed at follow-up. In the interval, baroreflex-sympathoneural function declined, as indicated by development of abnormal beat-to-beat blood pressure responses to the Valsalva maneuver; however, the patient did not have orthostatic hypotension. The combination of denervation supersensitivity, baroreflex failure, and increased adrenomedullary secretion may have contributed to the patient's complaints related to neurocirculatory instability. The results lead to the proposition that cardiac sympathetic denervation may be a biomarker of presymptomatic Parkinson disease.

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