Chang Yan, Zhang Xiwan, Xiao Shaobo, Liu Jiajin, Wang Yuan, Song Jingbin, Fu Huaping, Li Yungang, Su Hui, Yi Huijie, Su Wenjie, Gao Nan, Zhao JinJing, Wang Ruimin, Liu Ruozhuo
Medical School of Chinese PLA, Beijing, 100853, China.
Department of Neurology, International Headache Center, The First Medical Center of Chinese PLA General Hospital, Beijing, 100853, China.
Eur J Nucl Med Mol Imaging. 2025 May 6. doi: 10.1007/s00259-025-07282-3.
Although neuroinflammation may play a key role in the pathology of migraine and its progression to chronic migraine (CM), its specific involvement-particularly the role of microglia- remains unclear. We investigated whether neuroinflammation is involved in the pathophysiology of CM and whether pro-inflammatory signals are associated with its clinical features.
Nineteen individuals with CM and 10 healthy controls (HCs) underwent integrated brain positron emission tomography (PET)/magnetic resonance (MR) using the translocator protein (TSPO) radioligand ([C] PBR28, a marker of glial activation, together with the quantification of blood plasma inflammatory cytokine/chemokine. Volumes in regions of interest (ROI) were calculated based on MRI data and the standardized uptake value ratio (SUVR) for [C] PBR28 was extracted for each ROI. The Spearman's rank correlation coefficient between [C] PBR28 SUVR and changes in plasma factors was calculated.
CM patients had a significantly higher Hamilton Depression Rating Scale (HAMD) and Hamilton Anxiety Rating Scale (HAMA) scores than that in HCs (p < 0.05). Participants with CM also exhibited reduced volume in the thalamus (p = 0.012), compared with HCs. Moreover [11C] PBR28 binding was increased in the midbrain, occipital lobe and vermis, along with increased interictal plasma interleukin-8 (IL-8) and CX3CL1 levels, in individuals with CM compared with HCs. Notably, the midbrain levels of TSPO were negatively correlated with the headache frequency (r=-0.462, p = 0.046).
These findings demonstrate increased central inflammation in CM participants compared to HCs, providing imaging evidence for the potential involvement of neuroinflammation in CM pathophysiology. Additionally, the observed reduction in thalamic volume may contribute to the chronification of migraine.
Not applicable.
尽管神经炎症可能在偏头痛及其向慢性偏头痛（CM）进展的病理过程中起关键作用，但其具体参与情况，尤其是小胶质细胞的作用仍不清楚。我们研究了神经炎症是否参与CM的病理生理学过程，以及促炎信号是否与其临床特征相关。
19例CM患者和10名健康对照者（HCs）接受了整合脑正电子发射断层扫描（PET）/磁共振成像（MR）检查，使用转运蛋白（TSPO）放射性配体（[11C]PBR28，一种神经胶质激活标志物），同时对血浆炎症细胞因子/趋化因子进行定量分析。基于MRI数据计算感兴趣区域（ROI）的体积，并提取每个ROI的[11C]PBR28标准化摄取值比（SUVR）。计算[11C]PBR28 SUVR与血浆因子变化之间的Spearman等级相关系数。
CM患者的汉密尔顿抑郁量表（HAMD）和汉密尔顿焦虑量表（HAMA）得分显著高于HCs（p<0.05）。与HCs相比，CM患者的丘脑体积也减小（p=0.012）。此外，与HCs相比，CM患者中脑、枕叶和小脑蚓部的[11C]PBR28结合增加，发作间期血浆白细胞介素-8（IL-8）和CX3CL1水平升高。值得注意的是，中脑TSPO水平与头痛频率呈负相关（r=-0.462，p=0.046）。
这些发现表明，与HCs相比，CM患者的中枢炎症增加，为神经炎症可能参与CM病理生理学提供了影像学证据。此外，观察到的丘脑体积减小可能导致偏头痛慢性化。
不适用。
