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使用动脉自旋标记(ASL)和功能磁共振成像(fMRI)方法研究糖尿病视网膜病变中的异常神经血管耦合。

Aberrant Neurovascular Coupling in Diabetic Retinopathy Using Arterial Spin Labeling (ASL) and Functional Magnetic Resonance Imaging (fMRI) methods.

作者信息

Zhong Yu-Lin, Hu Rui-Yang, Huang Xin

机构信息

Department of Ophthalmology, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, 330006, People's Republic of China.

School of Ophthalmology and Optometry, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, 330006, People's Republic of China.

出版信息

Diabetes Metab Syndr Obes. 2024 Jul 26;17:2809-2822. doi: 10.2147/DMSO.S465103. eCollection 2024.

DOI:10.2147/DMSO.S465103
PMID:39081370
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11288319/
Abstract

BACKGROUND

Previous imaging studies have demonstrated that diabetic retinopathy (DR) is linked to structural and functional abnormalities in the brain. However, the extent to which DR patients exhibit abnormal neurovascular coupling remains largely unknown.

METHODS

Thirty-one patients with DR and 31 sex- and age-matched healthy controls underwent resting-state functional magnetic resonance imaging (rs-fMRI) to calculate functional connectivity strength (FCS) and arterial spin-labeling imaging (ASL) to calculate cerebral blood flow (CBF). The study compared CBF-FCS coupling across the entire grey matter and CBF/FCS ratios (representing blood supply per unit of connectivity strength) per voxel between the two groups. Additionally, a support vector machine (SVM) method was employed to differentiate between diabetic retinopathy (DR) patients and healthy controls (HC).

RESULTS

In DRpatients compared to healthy controls, there was a reduction in CBF-FCS coupling across the entire grey matter. Specifically, DR patients exhibited elevated CBF/FCS ratios primarily in the primary visual cortex, including the right calcarine fissure and surrounding cortex. On the other hand, reduced CBF/FCS ratios were mainly observed in premotor and supplementary motor areas, including the left middle frontal gyrus.

CONCLUSION

An elevated CBF/FCS ratio suggests that patients with DR may have a reduced volume of gray matter in the brain. A decrease in its ratio indicates a decrease in regional CBF in patients with DR. These findings suggest that neurovascular decoupling in the visual cortex, as well as in the supplementary motor and frontal gyrus, may represent a neuropathological mechanism in diabetic retinopathy.

摘要

背景

先前的影像学研究表明,糖尿病视网膜病变(DR)与大脑的结构和功能异常有关。然而,DR患者神经血管耦合异常的程度在很大程度上仍不清楚。

方法

31例DR患者和31例年龄、性别匹配的健康对照者接受静息态功能磁共振成像(rs-fMRI)以计算功能连接强度(FCS),并接受动脉自旋标记成像(ASL)以计算脑血流量(CBF)。该研究比较了两组之间全脑灰质的CBF-FCS耦合以及每个体素的CBF/FCS比率(代表单位连接强度的血液供应)。此外,采用支持向量机(SVM)方法区分糖尿病视网膜病变(DR)患者和健康对照者(HC)。

结果

与健康对照者相比,DR患者全脑灰质的CBF-FCS耦合降低。具体而言,DR患者主要在初级视觉皮层,包括右侧距状裂和周围皮层,表现出升高的CBF/FCS比率。另一方面,CBF/FCS比率降低主要见于运动前区和辅助运动区,包括左侧额中回。

结论

CBF/FCS比率升高表明DR患者脑灰质体积可能减小。其比率降低表明DR患者局部脑血流量减少。这些发现表明,视觉皮层以及辅助运动区和额回中的神经血管解耦可能是糖尿病视网膜病变的一种神经病理机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/5ea72a999a18/DMSO-17-2809-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/a722846cbd3e/DMSO-17-2809-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/17b640a0c1a1/DMSO-17-2809-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/5b1dfd01d308/DMSO-17-2809-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/b87828b897fc/DMSO-17-2809-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/42c45fdd61c1/DMSO-17-2809-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/5ea72a999a18/DMSO-17-2809-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/a722846cbd3e/DMSO-17-2809-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/a0f392a60cf3/DMSO-17-2809-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/17b640a0c1a1/DMSO-17-2809-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/5b1dfd01d308/DMSO-17-2809-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/b87828b897fc/DMSO-17-2809-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/42c45fdd61c1/DMSO-17-2809-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4c3d/11288319/5ea72a999a18/DMSO-17-2809-g0007.jpg

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