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帕金森病患者嗅觉功能障碍与大脑代谢的相关性研究。

Association of olfactory dysfunction and brain. Metabolism in Parkinson's disease.

机构信息

Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan.

出版信息

Mov Disord. 2011 Mar;26(4):621-8. doi: 10.1002/mds.23602. Epub 2011 Jan 31.

Abstract

Hyposmia is one of the cardinal early symptoms of Parkinson disease (PD). Accumulating clinical and pathological evidence suggests that dysfunction of the olfactory-related cortices may be responsible for the impaired olfactory processing observed in PD; however, there are no clear data showing a direct association between altered brain metabolism and hyposmia in PD. In this study, we evaluated brain glucose metabolism and smell-identification ability in 69 Japanese patients with nondemented PD. Olfactory function was assessed using the Odor Stick Identification Test for Japanese. The regional cerebral metabolic rate of glucose consumption at rest was measured using (18)F-fluorodeoxyglucose positron emission tomography and was analyzed using SPM-based group comparisons and the brain-behavior partial least-squares method. We found that olfactory dysfunction was closely related to cognitive dysfunction, including memory impairment. Moreover, brain-behavior partial least-squares analysis revealed that odor-identification performance was closely associated with broad cortical dysfunction, including dysfunction of the piriform cortex and amygdala. Our results suggest that the cognitive deficit in olfactory perception is an important aspect of hyposmia in PD and that this deficit is caused by altered brain metabolism in the amygdala and piriform cortex.

摘要

嗅觉减退是帕金森病 (PD) 的早期主要症状之一。越来越多的临床和病理学证据表明,嗅觉相关皮质的功能障碍可能是 PD 患者嗅觉处理受损的原因;然而,目前尚无明确的数据显示 PD 患者的大脑代谢改变与嗅觉减退之间存在直接关联。在这项研究中,我们评估了 69 例非痴呆 PD 日本患者的大脑葡萄糖代谢和嗅觉识别能力。使用日本的 Odor Stick 识别测试评估嗅觉功能。使用(18)F-氟脱氧葡萄糖正电子发射断层扫描测量静息状态下的局部脑葡萄糖代谢率,并使用基于 SPM 的组间比较和脑-行为偏最小二乘法进行分析。我们发现嗅觉功能障碍与认知功能障碍密切相关,包括记忆障碍。此外,脑-行为偏最小二乘法分析表明,气味识别性能与广泛的皮质功能障碍密切相关,包括梨状皮层和杏仁核功能障碍。我们的研究结果表明,嗅觉感知认知缺陷是 PD 嗅觉减退的一个重要方面,这种缺陷是由杏仁核和梨状皮层的大脑代谢改变引起的。

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