Goldstein David S
Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-1620, USA.
Cleve Clin J Med. 2007 Feb;74 Suppl 1:S91-4. doi: 10.3949/ccjm.74.suppl_1.s91.
More than 40 neuroimaging studies have reported evidence for loss of sympathetic noradrenergic nerves in PD. Cardiac sympathetic denervation is virtually universal in patients with PD and neurogenic orthostatic hypotension. About one half of patients with PD who do not have orthostatic hypotension also have evidence for loss of noradrenergic innervation. The loss progresses over years, in a pattern suggesting "dying-back". Because patients with familial PD from mutation of the gene encoding alpha-synuclein or from triplication of the normal gene have low myocardial concentrations of 6-[18F]fluorodopamine-derived radioactivity, cardiac sympathetic denervation seems linked etiologically with alpha-synucleinopathy. Baroreflex-cardiovagal failure and cardiac sympathetic denervation can occur before onset of the movement disorder, suggesting that neurocardiologic testing might provide a biomarker for detecting presymptomatic or early PD and for following responses to putative neuroprotective treatments.
40多项神经影像学研究报告了帕金森病(PD)患者交感去甲肾上腺素能神经缺失的证据。心脏交感神经去神经支配在PD合并神经源性直立性低血压患者中几乎普遍存在。约一半无直立性低血压的PD患者也有去甲肾上腺素能神经支配缺失的证据。这种缺失会在数年内进展,呈“逆行性死亡”模式。由于编码α-突触核蛋白的基因突变或正常基因三倍体导致的家族性PD患者心肌中6-[18F]氟多巴胺衍生的放射性浓度较低,心脏交感神经去神经支配在病因上似乎与α-突触核蛋白病有关。压力反射-心迷走神经功能衰竭和心脏交感神经去神经支配可在运动障碍发作之前出现,这表明神经心脏学检测可能为检测症状前或早期PD以及监测对假定神经保护治疗的反应提供一种生物标志物。