The combined efforts of research teams in the U.S. and Sweden have resulted in a new study showing widespread inflammation in the brains of fibromyalgia patients.
The research is published online in the journal Brain, Behavior and Immunity.
“We don’t have good treatment options for fibromyalgia, so identifying a potential treatment target could lead to the development of innovative, more effective therapies,” said Marco Loggia, Ph.D., of the Massachusetts General Hospital (MGH)-based Martinos Center for Biomedical Imaging, co-senior author of the report.
“And finding objective neurochemical changes in the brains of patients with fibromyalgia should help reduce the persistent stigma that many patients face, often being told their symptoms are imaginary and there’s nothing really wrong with them.”
Fibromyalgia is a chronic condition characterized by widespread pain with associated fatigue, sleep and mood issues. The condition affects around 4 million adults in the U.S., according to the Centers for Disease Control and Prevention.
In a recent study led by Loggia, the researchers combined MR/PET scanning to document neuroinflammation — specifically activation of glial cells — in the brains of patients with chronic back pain. Glial cells surround neurons and are the most abundant cell types in the central nervous system.
The researchers hypothesized that similar glial activation might be found in fibromyalgia patients as well.
In the new study, the team used the same PET radiopharmaceutical, which binds to the translocator protein (TSPO) that is overexpressed by activated glial cells. They enrolled 20 fibromyalgia patients and 14 control volunteers.
Meanwhile, a research team at Karolinska Institutet near Stockholm, Sweden, had also suggested that neuroinflammation might play a role in fibromyalgia, including heightened levels of inflammatory proteins in the cerebrospinal fluid.
The Karolinska team, led by Eva Kosek, M.D., Ph.D., had just enrolled a group of 11 patients and an equal number of control participants to further investigate.
At both centers, participants with fibromyalgia completed questionnaires to assess their symptoms. When the two teams became aware of each other’s work, they decided to combine their data into a single study.
The findings from both centers found that glial activation in several regions of the brains of fibromyalgia patients was significantly greater than in control participants.
Compared to the MGH chronic back pain study, TSPO elevations were even more widespread throughout the brain, which Loggia said corresponds to the more complex symptom patterns of fibromyalgia.
Importantly, TSPO levels in the cingulate gyrus — a brain region associated with emotional processing where neuroinflammation has been reported in patients with chronic fatigue syndrome —corresponded with patients’ reported levels of fatigue.
In the Karolinska study, the researchers used a slightly different method and found little difference between patients and controls, suggesting that microglia were primarily responsible for the increased neuro-inflammation in fibromyalgia patients.
“The activation of glial cells we observed in our studies releases inflammatory mediators that are thought to sensitize pain pathways and contribute to symptoms such as fatigue,” said Loggia, an assistant professor of Radiology at Harvard Medical School.
“The ability to join forces with our colleagues at Karolinska was fantastic, because combining our data and seeing similar results at both sites gives confidence to the reliability of our results.”