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多模态 7 特斯拉 MRI 和 C-PBR28 PET 对多发性硬化皮质炎症特征的研究

Profiles of cortical inflammation in multiple sclerosis by C-PBR28 MR-PET and 7 Tesla imaging.

机构信息

Department of Radiology, Massachusetts General Hospital, Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA/ Harvard Medical School, Boston, MA, USA.

Department of Radiology, Massachusetts General Hospital, Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA.

出版信息

Mult Scler. 2020 Oct;26(12):1497-1509. doi: 10.1177/1352458519867320. Epub 2019 Aug 1.

Abstract

BACKGROUND

Neuroinflammation with microglia activation is thought to be closely related to cortical multiple sclerosis (MS) lesion pathogenesis.

OBJECTIVE

Using C-PBR28 and 7 Tesla (7T) imaging, we assessed in 9 relapsing-remitting multiple sclerosis (RRMS) and 10 secondary progressive multiple sclerosis (SPMS) patients the following: (1) microglia activation in lesioned and normal-appearing cortex, (2) cortical lesion inflammatory profiles, and (3) the relationship between neuroinflammation and cortical integrity.

METHODS

Mean C-PBR28 uptake was measured in focal cortical lesions, cortical areas with 7T quantitative T* (q-T*) abnormalities, and normal-appearing cortex. The relative difference in cortical C-PBR28 uptake between patients and 14 controls was used to classify cortical lesions as either active or inactive. Disease burden was investigated according to cortical lesion inflammatory profiles. The relation between q-T* and C-PBR28 uptake along the cortex was assessed.

RESULTS

C-PBR28 uptake was abnormally high in cortical lesions in RRMS and SPMS; in SPMS, tracer uptake was significantly increased also in normal-appearing cortex. C-PBR28 uptake and q-T* correlated positively in many cortical areas, negatively in some regions. Patients with high cortical lesion inflammation had worse clinical outcome and higher intracortical lesion burden than patients with low inflammation.

CONCLUSION

C-PBR28 and 7T imaging reveal distinct profiles of cortical inflammation in MS, which are related to disease burden.

摘要

背景

神经炎症伴小胶质细胞激活被认为与皮质多发性硬化(MS)病变发病机制密切相关。

目的

使用 C-PBR28 和 7 特斯拉(7T)成像,我们评估了 9 例复发缓解型多发性硬化症(RRMS)和 10 例继发进展型多发性硬化症(SPMS)患者:(1)病变和正常皮质的小胶质细胞激活,(2)皮质病变炎症特征,以及(3)神经炎症与皮质完整性之间的关系。

方法

在局灶性皮质病变、7T 定量 T*(q-T*)异常的皮质区域和正常皮质中测量 C-PBR28 的平均摄取量。用患者与 14 名对照者皮质 C-PBR28 摄取量的相对差异,将皮质病变分类为活跃或不活跃。根据皮质病变炎症特征研究疾病负担。评估 q-T*和 C-PBR28 沿皮质摄取量之间的关系。

结果

RRMS 和 SPMS 患者的皮质病变中 C-PBR28 摄取异常升高;SPMS 患者正常皮质中示踪剂摄取也显著增加。C-PBR28 摄取量和 q-T*在许多皮质区域呈正相关,在一些区域呈负相关。皮质病变炎症程度高的患者比炎症程度低的患者临床预后差,皮质内病变负担高。

结论

C-PBR28 和 7T 成像揭示了 MS 皮质炎症的不同特征,与疾病负担有关。

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