Central sensitisation in chronic fatigue syndrome and fibromyalgia; a case control study, 2021, Bourke, White et al

[Blueskytoo]

White, out of 'retirement' to poke people with FM and CFS until they say it hurts. Not surprised.

I'm not even sure about this idea that people with ME/CFS have lower pain thresholds, let alone the CSS interpretation overlaid on that idea. From memory, the experimental results, even when done by researchers wanting the lower pain threshold idea to be true, have been inconsistent. Certainly I don't think I am unusually sensitive to pain.


Seriously? Would someone really complain that something 22.6°C was causing pain due to it being cold? Or would something 38°C (which is, after all, similar to body temperature) cause someone to report pain due to it being hot? I'd be surprised if this was a reproducible result. If it's true, it certainly deserves a better response than a waving away with some vague theory.

I haven't read the paper.

I actually DO have a lower threshold to pain, or at least an odd reaction to it. I do have a fibromyalgia diagnosis as well as an ME one, but it was one of the first things I noticed was wrong (apart from being exhausted, of course). I had a routine blood pressure test and the pressure of the cuff on my arm brought me to literal tears of pain - previously this was just uncomfortable, as you’d expect, but it’s now agonising and takes me a few days to recover from the after effects. If I stub my toe or bang my elbow into a door frame, for example, (both things which happen way more than they should due to my weird balance issues), I am crippled with pain that leaves me crying and breathless for a good ten to fifteen minutes and I’m left with an echo of the pain for a good half hour or so after that, much longer and much more severe than I would ever have had before. Normally a stubbed toe or bashed elbow makes you hop about and swear a bit, but not to the point of actual tears of agony and prolonged pain afterwards. I don’t bruise easily but even so, these injuries don’t often result in a bruise so they’re clearly not that bad, I just *feel* like they are.

Pain is more acute and lasts longer these days - I have to reassure the poor nurse at the blood pressure clinic who takes my BP that she can safely ignore my reaction as it’s purely how my body reacts to pain. I’ve also found that pain is, for me anyway, a major physical stressor as far as ME goes - poorly controlled pain from my arthritic hips, for example, will bring me out in a hot sweat and pushes me into PEM, and as a severe sufferer this is something that I cannot afford too often.

Of course, this is purely n-1 anecdata, so take it with the grain of salt it probably deserves.

 

[JemPD]

I'd like them to explain the mechanism by which CS is able to fluctuate from day to day & throughout the day..... ie sometimes a certain stimulus will cause me pain, sometimes not.

 

[Mithriel]

I would assume, in my opinion more precisely: ... would imply that all the senses would be potentially effected equally.

In this manner a central sensitisation theory may well be able to explain the range of differences seen in PwME, which is sticking out enough even if it is difficult to deal with it in details (though I have the expectation that scientists are able to put things together).

It also could lead to the question: which structure might be (directly or indirectly) effected so that different sensations (or even deeds) can be bulging high? I think, it could well be a structure responsible for distribution of inputs, or a structure for whole brain homeostasis. Sadly such scope is not seen in any science here.

I could be wrong, but I believe that central sensitisation is a BPS theory which has been stitched on to ME like so many rather than a serious attempt to explain the symptoms we actually have. They use very technical language and methods, but like FND the underlying reasons are assumed to be psychological.

When proper autopsies have been done on ME victims the basal ganglia have been found to be damaged so that inputs have been amplified.

Years ago I read about a type of pain where the nerve had been damaged but when it healed instead of there being a proper nerve there were thin nervelets (think fingers at the end of an arm) Each nervelet carried a pain signal so the pain was amplified.

 

[spinoza577]

I could be wrong, but I believe that central sensitisation is a BPS theory which has been stitched on to ME like so many rather than a serious attempt to explain the symptoms we actually have. They use very technical language and methods, but like FND the underlying reasons are assumed to be psychological.

In my understanding the term doesn´t say anything about the causation, which seems to be right, see the random abstract below.

When I first come about the CS theory for ME, I found it pretty descent. It was by Nijs and as far as I remember nitric oxide was a central feature in the paper. In a paper a few years later though Nijs was focusing on a BPS approach, which I found disappointing, of course. I had a bit the feeling that he might be disappointed by the failure of his approach I first came across, but I still don´t know the research history of Nijs (and might be wrong in both here).

With FND it could be the same, as the term itself doesn´t say anything about the causation and tells only what the theoretical entity is, here a dysfunction of nerves. I am not up to date as to if and how the term is officially used. Even as a replacement for the former conversion disorder it is not wrong, because "conversion" was telling about causation. I know though only too well, that the difference is not liked by scientists to be seen, which shows that some are not all that precise. I remember only one paper mentioning, that the big advantage of "FND" vs "conversion disorder" is that it doesn´t tell anything about the cause. And indeed, otherwise one would not have needed to replace the term (if one is not evil or stupid).


In any case, it is logically a big mistake to do a subordination of nerve-dysfunction under psychology. This is easy to see: Any psychological entity relies on the brain with its nerves. And then there is a machinery in the nerves and between them. And a machinery is vulnerable. An important question could be: Which nerve-structure is flexible enough to get harmed by e.g. viral impacts and is ponderous enough not to readjust itself.
---
random abstract: Harte et al 2018 (my paragraphing)

Central sensitization refers to the amplification of pain by central nervous system mechanisms. Classically described as a consequence of ongoing nociceptive input, it is increasingly recognized that central sensitization also occurs independent of peripheral injury or inflammation.

Features of central sensitization have been identified in nearly all chronic pain conditions, and it is considered the primary underlying cause of pain in conditions such as fibromyalgia. Central sensitization is characterized in these conditions by widespread pain and multisite hyperalgesia/allodynia. Co-occurring symptoms include fatigue, mood and cognitive problems, sleep disturbances, and multisensory hypersensitivity.

Individuals with central sensitization often report previous exposure to psychosocial or physical stressors, and a higher personal lifetime and family history of pain, with the latter findings supported by genetic studies. Neuroimaging studies of central sensitization show evidence of: changes in brain gray matter in pain processing regions; neurochemical imbalances; and altered resting brain-network connectivity between pronociceptive and antinociceptive brain areas. Immune system abnormalities have also been demonstrated in individuals with central sensitization.

The recognition of central sensitization, and whether it is being driven by ongoing nociceptive input or it is occurring in the absence of a peripheral driver, is critical for effective pain management.

The paper might be not that innovative, I would guess from the abstract, but it might be not wrong either, also not for ME. Note that the mentioning of psychological stressors is neither mentioned as a cause nor should indeed imply to be a cause (as Montoya in his paper together with Chu et al 2019, wasn´t it, pointed out).

 

[Hutan]

"Statement of funding
The study was funded by project grants from Barts Charity (470/ 1700), the CFS Research Foundation and Action for ME."

@Action for M.E., could you please explain how a study done by PD White, and on central sensitisation, was funded by an ME/CFS patient charity? Given White's history, no ME/CFS study that includes him as an investigator can be trusted. He simply has too much at stake to achieve the required state of equipoise.

What do we know about the CFS Research Foundation?

 

[Hutan]

Declaration of Competing Interest
JHB, TW, LVC, BK, VM, and EC declare no conflicts of interest.RL has received consultancy and/or speaker fees from: Pfizer, Eli Lilly, Grunenthal GmbH, Grunenthal Ltd., GW, BioQ Pharma, Ipsen, Heron Pharmaceuticals, MedinCell, Compass Pathways; and a study grant from Pfizer.

PDW is a member of the Independent Medical Experts Group, which advises the UK Ministry of Defence about its Armed Forces Compensation Scheme and does consultancy for a re-insurance company.

 

[Ariel]

@Action for M.E., could you please explain how a study done by PD White, and on central sensitisation, was funded by an ME/CFS patient charity? Given White's history, no ME/CFS study that includes him as an investigator can be trusted.

I was very disturbed to see this @Action for M.E.
This is extremely serious. What happened?

 

[Andy]

"Action for M.E. took over the management of this study in July 2014, following the closure of the CFS Research Foundation, which had already secured and allocated funding for it.

• Duration of study: January 2014 to October 2017
• Led by: Prof Peter White and Dr Julius Bourke
• Aims: To discover the physiological and chemical abnormalities underlying pain experienced by people with M.E.

In his report to Action for M.E.'s Research Panel, Dr Julius Bourke says:

"This is the first study, to the authors’ knowledge, that has provided clear and validated evidence of the presence of central sensitisation in both CFS and fibromyalgia. It is also the first study to compare fibromyalgia and chronic fatigue syndrome in this regard [...] The clinical relevance of central sensitisation in CFS and fibromyalgia is twofold – firstly in that QST are essentially bedside tests and can be performed in the clinic; the second is that it may have potential as a therapeutic drug target, defining a physiological abnormality that may be moderated by pharmacological correction."

https://www.actionforme.org.uk/rese...r-projects-and-phds/recently-funded-projects/

 

[rvallee]

Hey smack in the period of time where the BPS gang pretended White was retired and the university literally used this provable lie as a justification for hiding data that made White look like a terrible and biased researcher. As if somehow no one else could do it (and we literally have the notes showing everything was prepared beforehand because they had so much money to use and they just vetoed the data to keep it hidden but whatever).

I really don't see this "taking over an old study that was approved" as a legit argument. So what if that study had been approved and funded? It's a BS study by a charlatan with resources. This is really questionnable behavior given the odd claims of a therapeutic drug target, there is literally zero substance underneath CSS, what possible target could they even hint at here?