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复发缓解型多发性硬化症患者丘脑神经递质水平降低与感觉运动束损伤的关联

Association of decreased thalamic neurotransmitter level with sensorimotor tract damage in patients with relapsing-remitting multiple sclerosis.

作者信息

Xie Yan, Ding Yujie, Wu Shaolong, Zhang Yan, Zhu Hongquan, Li Yuanhao, Zhang Xiaoxiao, Zhu Wenzhen

机构信息

Department of Radiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Clinical Technical Solutions, Philips Healthcare, Beijing, China.

出版信息

Quant Imaging Med Surg. 2025 Sep 1;15(9):8040-8054. doi: 10.21037/qims-2025-219. Epub 2025 Aug 12.

DOI:10.21037/qims-2025-219
PMID:40893569
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12397645/
Abstract

BACKGROUND

Thalamic microstructural damage and neurotransmission dysfunction are present in patients with multiple sclerosis (MS). The aim of this study was to investigate the relationship of altered γ-aminobutyric acid (GABA) and glutamate + glutamine (Glx) levels in the thalamus with the white-matter (WM) microstructural damage of the sensorimotor tract in patients with relapsing-remitting MS (RRMS).

METHODS

In this cross-sectional study, 50 patients with RRMS and 43 healthy controls (HCs) were scanned using Mescher-Garwood point resolved spectroscopy (MEGA-PRESS) to quantify the GABA+ and Glx level of the thalamus. Metrics derived from diffusion tensor imaging (DTI) were calculated to reflect the degree of WM microstructural damage of the sensorimotor tract. The correlation between neurotransmitter level and diffusion metrics was determined in patients with RRMS and HCs, respectively.

RESULTS

Thalamic GABA+ and Glx levels were significantly decreased in patients with RRMS as compared with HCs (GABA+: 2.859±0.451 3.092±0.283 IU, P=0.002; Glx: 5.787±1.307 6.439±0.680 IU, P=0.002), and the neurotransmitter levels were significantly and negatively correlated with total lesion volume and disease duration in patients with RRMS (P<0.05). With the exception of the tract of right supplementary motor area, other sensorimotor tracts of patients with RRMS showed extensive WM microstructural damage. In addition, there was a significant correlation between decreased thalamic GABA+ and Glx levels and sensorimotor tract damage in patients with RRMS (corrected P<0.05). Analysis in HCs showed that the thalamic neurotransmitter level was not correlated with diffusion metrics in any of the sensorimotor tracts.

CONCLUSIONS

Neurotransmitters may play an important role in the pathophysiologic mechanisms of MS. Our study suggests an association between altered GABA and glutamate levels in deep gray-matter and WM microstructural damage in the sensorimotor tract.

摘要

背景

多发性硬化症(MS)患者存在丘脑微观结构损伤和神经传递功能障碍。本研究旨在探讨复发缓解型多发性硬化症(RRMS)患者丘脑中γ-氨基丁酸(GABA)和谷氨酸+谷氨酰胺(Glx)水平改变与感觉运动传导通路白质(WM)微观结构损伤之间的关系。

方法

在这项横断面研究中,对50例RRMS患者和43名健康对照者(HCs)进行了Mescher-Garwood点分辨波谱(MEGA-PRESS)扫描,以量化丘脑的GABA+和Glx水平。计算扩散张量成像(DTI)得出的指标,以反映感觉运动传导通路WM微观结构损伤的程度。分别在RRMS患者和HCs中确定神经递质水平与扩散指标之间的相关性。

结果

与HCs相比,RRMS患者丘脑GABA+和Glx水平显著降低(GABA+:2.859±0.451对3.092±0.283 IU,P=0.002;Glx:5.787±1.307对6.439±0.680 IU,P=0.002),并且RRMS患者的神经递质水平与总病变体积和病程显著负相关(P<0.05)。除右侧辅助运动区传导束外,RRMS患者的其他感觉运动传导束均显示出广泛的WM微观结构损伤。此外,RRMS患者丘脑中GABA+和Glx水平降低与感觉运动传导束损伤之间存在显著相关性(校正P<0.05)。对HCs的分析表明,丘脑神经递质水平与任何感觉运动传导束的扩散指标均无相关性。

结论

神经递质可能在MS的病理生理机制中起重要作用。我们的研究表明,深部灰质中GABA和谷氨酸水平的改变与感觉运动传导通路的WM微观结构损伤之间存在关联。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/6c27260f9ba7/qims-15-09-8040-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/a10542e4a952/qims-15-09-8040-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/5505b1ae1a98/qims-15-09-8040-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/d548c48b09eb/qims-15-09-8040-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/62f930c8a6a0/qims-15-09-8040-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/6c27260f9ba7/qims-15-09-8040-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/a10542e4a952/qims-15-09-8040-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/f533c00d36d9/qims-15-09-8040-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/c38b79049d03/qims-15-09-8040-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/96f47569200e/qims-15-09-8040-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/5505b1ae1a98/qims-15-09-8040-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/d548c48b09eb/qims-15-09-8040-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/62f930c8a6a0/qims-15-09-8040-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1ca3/12397645/6c27260f9ba7/qims-15-09-8040-f8.jpg

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