Research teams find widespread neuroinflammation in the brains of fibromyalgia patients

Jackb23

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PET imaging studies reveal elevated glial activation, correlation with fatigue levels

The results from both centers found that glial activation in several regions of the brains of fibromyalgia patients was significantly greater than it was in control participants. Compared to the MGH team's chronic back pain study, TSPO elevations were more widespread throughout the brain, which Loggia indicates corresponds to the more complex symptom patterns of fibromyalgia. TSPO levels in a structure called the cingulate gyrus -- an area associated with emotional processing where neuroinflammation has been reported in patients with chronic fatigue syndrome -- corresponded with patients reported levels of fatigue. The Karolinska team's studies with the astrocyte-binding tracer found little difference between patients and controls, suggesting that microglia were primarily responsible for the increased neuro-inflammation in fibromyalgia patients.




https://www.sciencedaily.com/releases/2018/09/180927122946.htm
 

percyval577

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Microglia account for 10-15% of all brain cells. They are quite small though.


(Their production of nitric oxide responds to the level of manganese, eg Filipov, Seegal et al 2004)
 
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Countrygirl

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Here is a similar article on ME:


https://www.prohealth.com/library/invasion-source-neuroinflammation-chronic-fatigue-syndrome-86580


Invasion: The Source Of The Neuroinflammation In Chronic Fatigue Syndrome?

Younger hypothesizes that T and B-cell infiltration play a key role in both MS and ME/CFS
By Cort Johnson • ProHealth.com • October 1, 2018

If T and B-cells can cause so much damage, why would they ever show up in the brain? Younger reported it’s possible that the microglia are actually asking them in. Ordinarily, this would only happen in the most extreme of circumstances – if the brain is in danger from an infection or a tumor which the microglia can’t handle. In that situation, calling in these A A A carpet bombers may be the only way to save the brain.

Another possibility is that hypersensitized microglia are opening the door for the T and B cells. A strong immune insult, a series of illnesses, a massive infection like Lyme disease, exposure to environmental toxins (diesel can do it), even obesity through its production of leptin, can lead to hypersensitized microglia and a traumatized, sensitized immune response in the brain. With the microglia responding to every little stressor, they simply go into overwhelm and call the big guns in. This may be the most likely model for chronic fatigue syndrome (ME/CFS).
If Younger can show that ME/CFS patients’ brains have been invaded by immune cells from the body he’ll have evidence that ME/CFS is an immune disease which attacks the central nervous system. His heat map /spectroscopy study already suggests that ME/CFS is an encephalomyelitis – an inflammatory brain condition with metabolic issues. The PET scan study showing how the inflammation is occurring is the next step.

This one-two punch – showing that neuroinflammation and the immune cells that may be causing it are present in the brain -would clearly make it much harder not to take this condition seriously. These are the same general processes, after all, that are occurring in some of our most devastating neurodegenerative diseases.
 
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Brain glial activation in fibromyalgia – A multi-site positron emission tomography investigation (Albrecht et al. 2019)

Here are the highlights:
Albrecht et al 2019 said:
Highlights
• Fibromyalgia patients exhibit elevated cortical levels of [11C]PBR28 signal.
• [11C]PBR28 signal was correlated with subjective fatigue in patients.
• Results from [11C]PBR28 SUVR and VT analyses show strong regional overlap.
• No differences in [11C]-L-deprenyl-D2 signal implicate microglia, not astrocytes.
• Our data support glial modulation as a potential therapeutic strategy for FM.

And here is the full abstract:
Albrecht et al 2019 said:
Fibromyalgia (FM) is a poorly understood chronic condition characterized by widespread musculoskeletal pain, fatigue, and cognitive difficulties. While mounting evidence suggests a role for neuroinflammation, no study has directly provided evidence of brain glial activation in FM. In this study, we 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. To enhance statistical power and generalizability, we combined datasets collected independently at two separate institutions (Massachusetts General Hospital [MGH] and Karolinska Institutet [KI]). In an attempt to disentangle the contributions of different glial cell types to FM, a smaller sample was scanned at KI with [11C]-L-deprenyl-D2 PET, thought to primarily reflect astrocytic (but not microglial) signal.

Thirty-one FM patients and 27 healthy controls (HC) were examined using [11C]PBR28 PET. 11 FM patients and 11 HC were scanned using [11C]-L-deprenyl-D2 PET. Standardized uptake values normalized by occipital cortex signal (SUVR) and distribution volume (VT) were computed from the [11C]PBR28 data. [11C]-L-deprenyl-D2 was quantified using λ k3. PET imaging metrics were compared across groups, and when differing across groups, against clinical variables.

Compared to HC, FM patients demonstrated widespread cortical elevations, and no decreases, in [11C]PBR28 VT and SUVR, most pronounced in the medial and lateral walls of the frontal and parietal lobes. No regions showed significant group differences in [11C]-L-deprenyl-D2 signal, including those demonstrating elevated [11C]PBR28 signal in patients (p’s ≥ 0.53, uncorrected). The elevations in [11C]PBR28 VT and SUVR were correlated both spatially (i.e., were observed in overlapping regions) and, in several areas, also in terms of magnitude. In exploratory, uncorrected analyses, higher subjective ratings of fatigue in FM patients were associated with higher [11C]PBR28 SUVR in the anterior and posterior middle cingulate cortices (p’s < 0.03). SUVR was not significantly associated with any other clinical variable.

Our work provides the first in vivo evidence supporting a role for glial activation in FM pathophysiology. Given that the elevations in [11C]PBR28 signal were not also accompanied by increased [11C]-L-deprenyl-D2 signal, our data suggests that microglia, but not astrocytes, may be driving the TSPO elevation in these regions. Although [11C]-L-deprenyl-D2 signal was not found to be increased in FM patients, larger studies are needed to further assess the role of possible astrocytic contributions in FM. Overall, our data support glial modulation as a potential therapeutic strategy for FM.
(emphasis added)
 
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And here is a related study:

Fibromyalgia Is Correlated with Retinal Nerve Fiber Layer Thinning (Garcia-Martin et al. 2016)
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0161574
Main points:
  • The optic nerve that connects the eye to the thalamus in the brain can be examined with noninvasive eye scan technology.
  • People with fibromyalgia appear to have damaged optic nerves.
  • People with severe fibromyalgia appeared to have more optic nerve damage than milder patients.
  • Damage to the optic nerve could be a sign of inflammation in the brain, especially in the thalamus.
Excerpt:
Garcia-Martin et al 2016 said:
A significant decrease in the [Retinal Nerve Fiber Layer (RNFL)] was detected in fibromyalgia patients compared with controls [...] RNFL thickness was significantly reduced in patients with severe fibromyalgia (FIQ≥60) compared with patients with mild fibromyalgia [...] Fibromyalgia causes subclinical axonal damage in the RNFL that can be detected using innocuous and non-invasive OCT, even in the early disease stages.
 
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