What We Can Glean from Glial Cells in Fibromyalgia Fatigue

Not so fast with the psychological stuff.

Posted Dec 04, 2018

Fibromyalgia is the most commonly encountered chronic widespread pain condition in rheumatology. In comparison to well-defined inflammatory conditions such as lupus and rheumatoid arthritis, it can seem ill-defined (or even indefinable), with no clear understanding of the pathology and therefore no specific targeted treatment. This inevitably raises controversies and challenges.

While mounting evidence suggests a role for neuroinflammation, no study has directly provided evidence of brain inflammation activation in fibromyalgia. But some are working to address that piece of the puzzle.

An online version of a study planned for publication in January of 2019 describes the results of a study of a group of patients who met the American College of Rheumatology criteria for fibromyalgia classification and a group of matched patients otherwise healthy and without fibromyalgia who received a hybrid magnetic resonance/positron-emission tomography (MR/PET) brain scan. The study excluded patients with fibromyalgia if they had any pain conditions other than fibromyalgia. The researchers conducted a Positron Emission Tomography (PET) study using [11C]PBR28, which binds to the translocator protein (TSPO), a protein upregulated in activated microglia and astrocytes, which are types of cells in the brain.

Using these imaging results, researchers found higher levels of the glial marker TSPO in several regions of the brain in patients with fibromyalgia relative to healthy control patients. They also found that the degree of glial activation was related to the degree of fatigue the patients reported.

So, perhaps if science could find a way to prevent glial cell activation, there might be less fatigue?

However, while many studies support TSPO as a glial marker in humans, it is important to note that not all studies have detected TSPO upregulation in diseases with a presumed inflammatory component: for example, prior research showed no differences in TSPO PET signal in cocaine addiction and decreased signal in alcohol dependence. In patients with psychosis, initial studies with first generation TSPO tracers showed an increase, whereas recent studies using second-generation radioligands appear to demonstrate the opposite, a decrease in TSPO levels.

Obviously, further work is needed to better assess the potential usefulness of TSPO as a method to demonstrate brain inflammation, and what exactly these TSPO signal changes mean for a given patient, no matter the disease under consideration.

Based on what researchers currently know, the fatigue is all in your head, as well as not just in your head.

References

Brain glial activation in fibromyalgia – A multi-site positron emission tomography investigation; Brain, Behavior, and Immunity Volume 75, January 2019, Pages 72-83

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