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Updated: May 7, 2026
3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache
Published on: June 2, 2014
Evidence for brain glial activity in chronic migraine patients: a [11C] PBR28 PET/MR study
Yan Chang1,2, Xiwan Zhang3, Shaobo Xiao4
1Medical School of Chinese PLA, Beijing, 100853, China.
Purpose:
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.
Methods:
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 ([11C] 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 [11C] PBR28 was extracted for each ROI. The Spearman's rank correlation coefficient between [11C] PBR28 SUVR and changes in plasma factors was calculated.
Results:
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).
Conclusions:
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.
Clinical Trial Number:
Not applicable.
Insights
Neuroinflammation is increased in chronic migraine (CM) patients, indicated by glial activation markers and elevated inflammatory signals. These findings suggest neuroinflammation plays a role in CM pathophysiology and headache frequency.
Area of Science:
- Neuroscience
- Immunology
- Radiology
Background:
- Migraine progression to chronic migraine (CM) may involve neuroinflammation, but the specific role of microglia remains unclear.
- Investigating neuroinflammation and its association with clinical features in CM is crucial for understanding disease progression.
Purpose of the Study:
- To investigate the involvement of neuroinflammation in the pathophysiology of chronic migraine (CM).
- To determine if pro-inflammatory signals are associated with the clinical features of CM.
Main Methods:
- Integrated brain positron emission tomography (PET)/magnetic resonance (MR) imaging using the translocator protein (TSPO) radioligand ([11C] PBR28) in 19 CM patients and 10 healthy controls (HCs).
- Quantification of blood plasma inflammatory cytokine/chemokine levels.
- Analysis of brain volumes and correlation between [11C] PBR28 standardized uptake value ratio (SUVR) and plasma factors.
Main Results:
- CM patients showed higher depression and anxiety scores, and reduced thalamic volume compared to HCs.
- [11C] PBR28 binding was increased in the midbrain, occipital lobe, and vermis in CM patients.
- Elevated plasma levels of interleukin-8 (IL-8) and CX3CL1 were observed in CM patients, with midbrain TSPO levels negatively correlated with headache frequency.
Conclusions:
- The study provides imaging evidence of increased central inflammation in CM, supporting the role of neuroinflammation in its pathophysiology.
- Reduced thalamic volume in CM patients may contribute to migraine chronification.
- Elevated inflammatory markers and glial activation are associated with CM.
