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α-突触核蛋白病体位性低血压患者脑白质变化及其与非运动功能障碍的关联:一项神经突方向离散与密度成像(NODDI)研究

Brain white matter changes and their associations with non-motor dysfunction in orthostatic hypotension in α-synucleinopathy: A NODDI study.

作者信息

Lin Lin, Huang Peilin, Cheng Yingzhe, Jiang Shaofan, Zhang Jiejun, Li Man, Zheng Jiahao, Pan Xiaodong, Wang Yanping

机构信息

Department of Neurology, Center for Cognitive Neurology, Fujian Medical University Union Hospital, Fuzhou City, China.

Fujian Institute of Geriatrics, Fujian Medical University Union Hospital, Fuzhou City, China.

出版信息

CNS Neurosci Ther. 2024 Apr;30(4):e14712. doi: 10.1111/cns.14712.

DOI:10.1111/cns.14712
PMID:38615364
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11016347/
Abstract

BACKGROUND

The specific non-motor symptoms associated with α-synucleinopathies, including orthostatic hypotension (OH), cognitive impairment, and emotional abnormalities, have been a subject of ongoing controversy over the mechanisms underlying the development of a vicious cycle among them. The distinct structural alterations in white matter (WM) in patients with α-synucleinopathies experiencing OH, alongside their association with other non-motor symptoms, remain unexplored. This study employs axial diffusivity and density imaging (NODDI) to investigate WM damage specific to α-synucleinopathies with concurrent OH, delivering fresh evidence to supplement our understanding of the pathogenic mechanisms and pathological rationales behind the occurrence of a spectrum of non-motor functional impairments in α-synucleinopathies.

METHODS

This study recruited 49 individuals diagnosed with α-synucleinopathies, stratified into an α-OH group (n = 24) and an α-NOH group (without OH, n = 25). Additionally, 17 healthy controls were included for supine and standing blood pressure data collection, as well as neuropsychological assessments. Magnetic resonance imaging (MRI) was utilized for the calculation of NODDI parameters, and tract-based spatial statistics (TBSS) were employed to explore differential clusters. The fibers covered by these clusters were defined as regions of interest (ROI) for the extraction of NODDI parameter values and the analysis of their correlation with neuropsychological scores.

RESULTS

The TBSS analysis unveiled specific cerebral regions exhibiting disparities within the α-OH group as compared to both the α-NOH group and the healthy controls. These differences were evident in clusters that indicated a decrease in the acquisition of the neurite density index (NDI), a reduction in the orientation dispersion index (ODI), and an increase in the isotropic volume fraction (FISO) (p < 0.05). The extracted values from these ROIs demonstrated significant correlations with clinically assessed differences in supine and standing blood pressure, overall cognitive scores, and anxiety-depression ratings (p < 0.05).

CONCLUSION

Patients with α-synucleinopathies experiencing OH exhibit distinctive patterns of microstructural damage in the WM as revealed by the NODDI model, and there is a correlation with the onset and progression of non-motor functional impairments.

摘要

背景

与α-突触核蛋白病相关的特定非运动症状,包括体位性低血压(OH)、认知障碍和情绪异常,一直是关于它们之间恶性循环发展机制的持续争议主题。α-突触核蛋白病伴OH患者白质(WM)的明显结构改变,以及它们与其他非运动症状的关联,仍未得到探索。本研究采用轴向扩散率和密度成像(NODDI)来研究α-突触核蛋白病伴OH的WM损伤,为补充我们对α-突触核蛋白病中一系列非运动功能障碍发生的致病机制和病理原理的理解提供新证据。

方法

本研究招募了49名被诊断为α-突触核蛋白病的个体,分为α-OH组(n = 24)和α-NOH组(无OH,n = 25)。此外,纳入17名健康对照者进行仰卧位和站立位血压数据收集以及神经心理学评估。利用磁共振成像(MRI)计算NODDI参数,并采用基于纤维束的空间统计学(TBSS)来探索差异簇。这些簇覆盖的纤维被定义为感兴趣区域(ROI),用于提取NODDI参数值并分析其与神经心理学评分的相关性。

结果

TBSS分析揭示了与α-NOH组和健康对照相比,α-OH组内显示出差异的特定脑区。这些差异在表明神经突密度指数(NDI)获取减少、方向离散指数(ODI)降低和各向同性体积分数(FISO)增加的簇中很明显(p < 0.05)。从这些ROI提取的值与仰卧位和站立位血压的临床评估差异、总体认知评分以及焦虑抑郁评分显示出显著相关性(p < 0.05)。

结论

NODDI模型显示,α-突触核蛋白病伴OH患者的WM存在独特的微观结构损伤模式,并且与非运动功能障碍的发生和进展相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98bd/11016347/4c0e0f625797/CNS-30-e14712-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98bd/11016347/5802938d7b20/CNS-30-e14712-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98bd/11016347/ffb2cebc2f15/CNS-30-e14712-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98bd/11016347/11160382c415/CNS-30-e14712-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98bd/11016347/a9f870cc9625/CNS-30-e14712-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98bd/11016347/4c0e0f625797/CNS-30-e14712-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98bd/11016347/5802938d7b20/CNS-30-e14712-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98bd/11016347/ffb2cebc2f15/CNS-30-e14712-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98bd/11016347/11160382c415/CNS-30-e14712-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98bd/11016347/a9f870cc9625/CNS-30-e14712-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98bd/11016347/4c0e0f625797/CNS-30-e14712-g006.jpg

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