No signs of neuroinflammation in women with [CFS] or Q fever fatigue syndrome using the TSPO ligand [11C]-PK11195, 2021, Raijmakers, Knoop et al

Had another look at the results.

Nakatomi et al. reported huge differences in BPND of [11C]-PK11195 between ME/CFS and controls, for example an effect size of 2.4 standard deviations for the midbrain. In all brain regions, ME/CFS patients had much higher values.

In the study by Raijmakers et al. ME/CFS patients had lower values in all brain regions. These differences were not statistically significant but this could be due to the low sample size. The figure that reports standard deviations shows that the differences weren't exactly small either.

So the results are directly opposite.

 

Surely the selection of 'CFS' patients who can get by on only paracetamol to control their pain is going to mean the results are not going to be transferable to the majority of moderate or severe ME sufferers? I've had to take prescription meds for my headaches since I first developed ME 30 years ago...

 

Pain is not a required element to meet the CCC case definition; i am not entirely sure we can assume that Tylenol= mild ME and morphine =moderate and severe. It’s just plain wrong.

 

It is important to remember that the BPS lobby is particularly powerful in the Netherlands and that many professionals active in the field of CFS have a vested interest in finding negative or null biomedical results.

 

The point is they are excluding those who use stronger pain meds to control neurological pain and severe headaches. Maybe that is the group with possible neuroinflammation, since ME/CFS is likely to have several subgroups.

 

But that sounds like you did try stronger pain medication, but discontinued it because of side effects?

 

It is possible but i would suspect that linking neuroinflammation with headaches may be simplistic and possibly inaccurate. It goes back to past discussions we’ve had on this forum with the concept of ‘neuroinflammation’ and what it means.

 

All the more reason to ensure that this type of research is done on a large representative group of patients with the full range of severity and symptoms, without which any conclusions about the nonexistence of neuroinflammation in ME drawn would be very questionable.

 

No Signs of Neuroinflammation in Women With Chronic Fatigue Syndrome or Q Fever Fatigue Syndrome Using the TSPO Ligand [11C]-PK11195
https://research.rug.nl/en/publicat...lammation-in-women-with-chronic-fatigue-syndr

 

The neurological symptoms we experience don't necessarily have to be caused by (neuro)inflammation, there could well be hundreds of other possible mechanisms that could trigger them. I am glad they did this study, even if the result is not what some hoped. I'd say a few more studies like this and it's time to move on from the neuroinflammation hypothesis. It always seemed a bit too simplistic to me anyway.

 

These studies done with very low numbers of patients who are selected by the fukuda definition are dangerous to the community.

Over the years there have been many of this sort of studies done. They were criticised at the time and all the limitations of small sample numbers and insecure disease selection were known, but as time passed the results would be quoted as if they were definitive. The BPS were happy to see study after study give no evidence of physical disease but new patients and researchers would also take the results as proven and all the limitations forgotten.

In a few years we will be hearing that neuroinflammation has been found not to happen in ME so that avenue will be closed off. New people will assume that someone has tried to replicate the original finding but been unable to do so yet nothing can be concluded by looking at 9 people.

Yet another piece of research will disappear without us knowing if it was important or not.

 

With regards to:

https://research.rug.nl/en/publicat...lammation-in-women-with-chronic-fatigue-syndr

This study was funded by the Q-support Foundation
(UMCN-140928-00). The was no role for the funding body
in the design of the study, collection of data, analysis, in-
terpretation of data, or writing of the manuscript.

 

It may not be as simple as standard neuroinflammation, but I'm still convinced that it's part of my ME. My ME symptoms always increased with infections or exertions that would produce IFN-g, which would in turn activate glial cells.

So far there's no definitive study (large, proper controls, proper selection, etc) to determine whether or to what degree neuroinflammation is involved in ME.