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Olfactory dysfunction in Parkinson disease

机译:帕金森氏病的嗅觉功能障碍

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Olfactory dysfunction is among the earliest nonmotor features of Parkinson disease (PD). Such dysfunction is present in approximately 90% of early-stage PD cases and can precede the onset of motor symptoms by years. The mechanisms responsible for olfactory dysfunction are currently unknown. As equivalent deficits are observed in Alzheimer disease, Down syndrome, and the Parkinson - dementia complex of Guam, a common pathological substrate may be involved. Given that olfactory loss occurs to a lesser extent or is absent in disorders such as multiple system atrophy, corticobasal degeneration, and progressive supranuclear palsy, olfactory testing can be useful in differential diagnosis. The olfactory dysfunction in PD and a number of related diseases with smell loss correlates with decreased numbers of neurons in structures such as the locus coeruleus, the raphe nuclei, and the nucleus basalis of Meynart. These neuroanatomical findings, together with evidence for involvement of the autonomic nervous system in numerous PD-related symptoms, suggest that deficits in cholinergic, noradrenergic and serotonergic function may contribute to the olfactory loss. This Review discusses the current understanding of olfactory dysfunction in PD, including factors that may be related to its cause.
机译:嗅觉功能障碍是帕金森病(PD)最早的非运动功能之一。大约90%的早期PD患者存在这种功能障碍,并且可以提前几年出现运动症状。目前尚不清楚导致嗅觉功能障碍的机制。由于在关岛的阿尔茨海默病,唐氏综合症和帕金森-痴呆症复合物中观察到同等的缺陷,可能涉及一种常见的病理学底物。鉴于嗅觉损失较少发生或在多系统萎缩,皮质基底变性和进行性核上性麻痹等疾病中不存在,嗅觉测试可用于鉴别诊断。帕金森氏症的嗅觉功能障碍和许多有嗅觉丧失的相关疾病与结构中的神经元数量减少有关,这些神经元的结构例如是蓝斑核,网状核和Meynart的基底核。这些神经解剖学发现,以及涉及许多PD相关症状的自主神经系统的证据表明,胆碱能,去甲肾上腺素能和血清素能功能的缺陷可能导致嗅觉丧失。这篇综述讨论了对PD嗅觉功能障碍的当前理解,包括可能与其原因有关的因素。

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