In both centers glial activation was found to be present at significantly higher levels in multiple brain areas in patients who had fibromyalgia than in controls. Glial cell activation causes inflammatory chemicals to be released, which cause the pain pathways to be more sensitive to pain, and promote fatigue.
When compared with the earlier back pain study, TSPO elevations occurred in many more regions of the brain in fibromyalgia, probably because of greater symptom variations in this condition. One area showing higher TSPO binding in direct proportion to the self-reported level of fatigue was the cingulate gyrus, an area of the brain linked to emotional processing. Previous research has reported that this area is inflamed in chronic fatigue syndrome.
The second astrocyte-binding tracer showed no major differences between patients and controls, indicating that microglia rather than astrocytes were responsible for the inflammation seen in the brain in fibromyalgia.
The fact that both centers came up with strikingly similar results lends greater credibility to the findings.
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,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.”
Marco Loggia, PhD, co-senior author of the report
Loggia is assistant professor of Radiology at Harvard Medical School and a researcher at the MGH-based Martinos Center for Biomedical Imaging.
The lead authors of the study published in the journal “Brain, Behavior and Immunity” are Daniel Albrecht, PhD, MGH Martinos Center and Department of Radiology, and Anton Forsberg, PhD, Karolinska Institutet.