Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, NIH, 10 Center Drive MSC-1620, Building 10 Room 5N220, Bethesda, MD 20892-1620, USA.
Neurology. 2010 Jan 19;74(3):245-51. doi: 10.1212/WNL.0b013e3181ca014c.
Olfactory dysfunction and autonomic failure are gaining recognition as nonmotor manifestations of Parkinson disease (PD). This observational study assessed whether in PD anosmia and autonomic failure are related to each other or to neuroimaging evidence of striatal dopamine deficiency.
Olfactory function was assessed by the University of Pennsylvania Smell Identification Test (UPSIT) in 23 patients with sporadic PD. Baroreflex-cardiovagal gain was quantified from the relationship between cardiac interbeat interval and systolic pressure during the Valsalva maneuver and baroreflex-sympathoneural function by responses of systolic pressure to the Valsalva maneuver and of hemodynamics and plasma norepinephrine (NE) and dihydroxyphenylglycol (DHPG) levels to orthostasis. 6-[(18)F]Fluorodopamine PET and plasma and skeletal muscle microdialysate NE and DHPG were used to indicate cardiac and extracardiac noradrenergic innervation and brain 6-[(18)F]fluorodopa PET to indicate striatal dopaminergic innervation. Parkinsonism was assessed by UPDRS scores.
Compared to patients with PD and normal to moderately decreased sense of smell, patients with anosmic PD had lower mean baroreflex-cardiovagal gain (p = 0.04), larger falls in systolic pressure during the Valsalva maneuver and orthostasis (p = 0.04, p = 0.02), smaller orthostatic increments in plasma NE and DHPG (p = 0.003, p = 0.03), lower cardiac septal:hepatic and renal cortical:hepatic ratios of 6-[(18)F]fluorodopamine-derived radioactivity (p = 0.01, p = 0.06), and lower microdialysate NE and DHPG (p = 0.01; p = 0.006). Neither clinical severity of parkinsonism nor the putamen:occipital cortex ratio of 6-[(18)F]fluorodopa-derived radioactivity was related to the UPSIT category.
In Parkinson disease, anosmia is associated with baroreflex failure and cardiac and organ-selective extracardiac noradrenergic denervation, independently of parkinsonism or striatal dopaminergic denervation.
嗅觉功能障碍和自主神经功能衰竭正在被认为是帕金森病（PD）的非运动表现。本观察性研究评估了 PD 患者的嗅觉丧失和自主神经衰竭是否相互关联，或与纹状体多巴胺缺乏的神经影像学证据相关。
23 例散发性 PD 患者接受了宾夕法尼亚大学嗅觉识别测试（UPSIT）的嗅觉功能评估。通过在瓦尔萨尔瓦动作期间心脏间拍间期和收缩压之间的关系来量化压力反射性迷走神经功能，通过收缩压对瓦尔萨尔瓦动作和心血管及血浆去甲肾上腺素（NE）和二羟苯乙二醇（DHPG）水平对直立位的反应来量化压力反射性交感神经功能。使用 6-[（18）F]氟多巴 PET 和血浆及骨骼肌微透析液中的 NE 和 DHPG 来指示心脏和心脏外去甲肾上腺素能神经支配，使用脑 6-[（18）F]氟多巴 PET 来指示纹状体多巴胺能神经支配。UPDRS 评分用于评估帕金森病。
与 PD 患者且嗅觉正常或中度降低的患者相比，嗅觉丧失的 PD 患者的平均压力反射性迷走神经功能降低（p = 0.04），在瓦尔萨尔瓦动作和直立时收缩压下降更大（p = 0.04，p = 0.02），血浆 NE 和 DHPG 的直立位增加较小（p = 0.003，p = 0.03），心脏隔区：肝和肾皮质：肝的 6-[（18）F]氟多巴衍生放射性比值较低（p = 0.01，p = 0.06），微透析液中的 NE 和 DHPG 较低（p = 0.01；p = 0.006）。帕金森病的临床严重程度或 6-[（18）F]氟多巴衍生放射性的纹状体：枕叶皮质比值均与 UPSIT 类别无关。
在帕金森病中，嗅觉丧失与压力反射衰竭以及心脏和器官选择性的心脏外去甲肾上腺素能神经支配有关，与帕金森病或纹状体多巴胺能神经支配无关。
