No Signs of Neuroinflammation in Women With Chronic Fatigue Syndrome or Q Fever Fatigue Syndrome Using the TSPO Ligand [<sup>11</sup>C]-PK11195. — ME/CFS Atlas
E3 PreliminaryPreliminaryPEM not requiredCross-SectionalPeer-reviewedReviewed
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No Signs of Neuroinflammation in Women With Chronic Fatigue Syndrome or Q Fever Fatigue Syndrome Using the TSPO Ligand [11C]-PK11195.
Raijmakers, Ruud, Roerink, Megan, Keijmel, Stephan et al. · Neurology(R) neuroimmunology & neuroinflammation · 2022 · DOI
Quick Summary
Researchers used a specialized brain scan to look for signs of inflammation in the brains of women with ME/CFS and Q fever fatigue syndrome, compared to healthy women. The scan didn't find evidence of the type of brain inflammation they were looking for, which contradicts some earlier research suggesting inflammation might play a role in these conditions.
Why It Matters
This study directly tests a leading neurobiological hypothesis in ME/CFS—that brain inflammation drives symptoms. Understanding whether neuroinflammation is actually present helps researchers identify the true mechanisms of disease and could guide development of targeted treatments. The negative finding also suggests researchers should investigate other biological pathways.
Observed Findings
No statistically significant differences in [11C]-PK11195 binding potential between CFS patients and healthy controls
No statistically significant differences in [11C]-PK11195 binding potential between QFS patients and healthy controls
Negative correlation between binding potential and symptom severity in CFS patients
Positive correlation between binding potential and symptom severity in QFS patients
Findings contradict previous reports suggesting elevated neuroinflammation in CFS
Inferred Conclusions
Neuroinflammation as measured by TSPO ligand binding may not be a primary feature of CFS and QFS in this population
The relationship between TSPO expression and symptoms differs between CFS and QFS, suggesting distinct pathophysiological mechanisms
Previous findings of elevated neuroinflammation in CFS may not be universally replicated or may depend on patient selection factors
Remaining Questions
Why do previous studies report neuroinflammation in CFS while this study does not? Could differences in patient characteristics, disease duration, or disease stage explain the discrepancy?
Is neuroinflammation present only in subgroups of ME/CFS patients rather than uniformly across the diagnosis?
What This Study Does Not Prove
This study does not prove that neuroinflammation is absent in all ME/CFS patients; the small sample size (n=9) limits generalizability, and it examined only women of specific ages without recent vaccination. The study also does not exclude other forms of inflammation or immune dysfunction outside the brain, nor does it rule out neuroinflammation in subgroups defined by disease onset or duration.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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What alternative biological mechanisms (mitochondrial dysfunction, autonomic dysfunction, metabolic abnormalities) might be more central to ME/CFS pathophysiology?
Do men with ME/CFS or patients with different disease onset patterns show different neuroinflammatory signatures?