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Updated: Jan 21, 2026
Magnetic Resonance Imaging of Multiple Sclerosis at 7.0 Tesla
Published on: February 19, 2021
Profiles of cortical inflammation in multiple sclerosis by 11C-PBR28 MR-PET and 7 Tesla imaging
Elena Herranz1, Céline Louapre1, Constantina Andrada Treaba1
1Department of Radiology, Massachusetts General Hospital, Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA/ Harvard Medical School, Boston, MA, USA.
Background:
Neuroinflammation with microglia activation is thought to be closely related to cortical multiple sclerosis (MS) lesion pathogenesis.
Objective:
Using 11C-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 11C-PBR28 uptake was measured in focal cortical lesions, cortical areas with 7T quantitative T2* (q-T2*) abnormalities, and normal-appearing cortex. The relative difference in cortical 11C-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-T2* and 11C-PBR28 uptake along the cortex was assessed.
Results:
11C-PBR28 uptake was abnormally high in cortical lesions in RRMS and SPMS; in SPMS, tracer uptake was significantly increased also in normal-appearing cortex. 11C-PBR28 uptake and q-T2* 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:
11C-PBR28 and 7T imaging reveal distinct profiles of cortical inflammation in MS, which are related to disease burden.
Insights
Neuroinflammation in multiple sclerosis (MS) is linked to cortical lesions. Advanced imaging shows distinct inflammation patterns in MS patients, correlating with disease severity and burden.
Area of Science:
- Neuroimaging
- Neuroinflammation
- Multiple Sclerosis Pathogenesis
Background:
- Neuroinflammation and microglia activation are implicated in cortical multiple sclerosis (MS) lesion development.
- Understanding cortical inflammation is crucial for MS progression insights.
Purpose of the Study:
- Assess microglia activation in lesioned and normal-appearing cortex in MS patients using 11C-PBR28 and 7T imaging.
- Characterize cortical lesion inflammatory profiles and their relationship with cortical integrity.
- Investigate the link between neuroinflammation and clinical outcomes in MS.
Main Methods:
- Utilized 11C-PBR28 PET and 7 Tesla (7T) MRI to evaluate neuroinflammation in 9 relapsing-remitting MS (RRMS) and 10 secondary progressive MS (SPMS) patients.
- Measured 11C-PBR28 uptake in focal cortical lesions, areas with quantitative T2* (q-T2*) abnormalities, and normal-appearing cortex.
- Correlated imaging findings with clinical data to assess disease burden and outcome.
Main Results:
- Elevated 11C-PBR28 uptake was observed in cortical lesions across both RRMS and SPMS patients.
- SPMS patients showed increased tracer uptake in normal-appearing cortex as well.
- Higher cortical lesion inflammation correlated with worse clinical outcomes and increased intracortical lesion burden.
Conclusions:
- 11C-PBR28 and 7T imaging demonstrate distinct cortical inflammation profiles in MS.
- These inflammation patterns are associated with the overall disease burden in multiple sclerosis.
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