The extensive brain inflammation present in patients with fibromyalgia, shows a recent multicenter study

September 28, 2018

A recent collaborative study involving researchers at Massachusetts General Hospital (MGH) and the Karolinska Institutet in Sweden, using PET imaging, revealed signs of widespread brain inflammation in fibromyalgia. This could be extremely important to help identify treatment targets for this condition, which is poorly understood and inadequately addressed.

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Fibromyalgia often presents with chronic pain in many parts of the body, sleep disturbances, persistent fatigue, and cognitive problems involving thinking and memory. About 4 million people in the United States suffer from this disease, reports the Center for Disease Control and Prevention.

An earlier study by researchers at the Karolinska Institutet showed that inflammation of the nervous system could play a role in fibromyalgia, even by detecting high concentrations of inflammatory proteins in the cerebrospinal fluid.

Similarly, previous research conducted by the MGH team in 2015 documented the presence of neuronal inflammation, and in particular glial activation, in patients who complained of chronic back pain. The present study was based on the hypothesis that this result could be replicated in fibromyalgia.

The present study first evaluated the symptoms of fibromyalgia in patients with the help of a questionnaire. A PET tracer was then used, ie a radioactive marker that binds a specific protein called translocative protein (TSPO) expressed at much higher levels than normal in activated glial cells, namely astrocytes. and microglia.

The MGH group of the study included 20 patients with fibromyalgia and 11 controls, while researchers from Karolinska recruited 11 patients and 11 controls. However, the Karolinska study used not only the TEP tracer that binds to TSPO, but also a more specific second-phase tracer for astrocytes. This second tracer was used in 11 patients, six of whom had TSPO imaging and five non-TSPO imaging, as well as 11 controls.

The two teams decided to merge their results when they realized that they were essentially pursuing the same research objectives using a similar methodology.

In both centers, glial activation was present at significantly higher rates in many brain regions in patients with fibromyalgia than in controls. The activation of glial cells causes the release of inflammatory chemicals that make the pain pathways more sensitive to pain and promote fatigue.

Compared to the previous study on pain, elevations of TSPO have occurred in many other brain regions in fibromyalgia, possibly due to greater variations in symptoms. The cingulate gyrus, an area of ​​the brain related to emotional treatment, was one of the areas where the TSPO binding was higher than the level of self-reported fatigue. Previous research has indicated that this area is inflamed with 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 the two centers presented surprisingly similar results gives more credibility to the conclusions.

We do not have good treatment options for fibromyalgia. Identifying a potential treatment target could lead to the development of innovative and more effective therapies, and finding objective neurochemical changes in the brains of patients with fibromyalgia should help reduce persistent stigma in the face, being often told that their symptoms are imaginary and it there is nothing really serious about them. "

Marco Loggia, PhD, co-lead author of the report

Loggia is an assistant professor of radiology at Harvard Medical School and a researcher at MGH-based Martinos Center for Biomedical Imaging.

The main 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.