How did Fibromyalgia become a brain disease? Disentangling conjecture and truth.

[Holinger]

Interesting article on how ‘Central Sensitivity Syndromes’ evolved by Rheumatologists Milton Cohen and John Quintner from 2018. Seems this theory has fallen away somewhat in the last few years.

‘In 2007, Dr Mohammed Yunus from Illinois noted that a number of diverse, medically controversial conditions, such as fibromyalgia, tension type headaches, chronic fatigue syndrome, irritable bowel syndrome had several clinical features in common. He attributed these features to “hyper excitement of the central neurons” which in turn led him to propose the concept of “central sensitivity syndromes (CSS). Yunus 2007.’

How did fibromyalgia ever become a brain disease? Disentangling conjecture and truth

By John Quintner and Milton Cohen Introduction In his seminal book “Propaganda (1928)” Edward Bernays [1891-1995] observed: “The conscious intelligent manipulation of the organized opinions and hab…

blog.apsoc.org.au

 

[Trish]

So they are saying the whole central sensitisation idea started as a metaphor, and, repeated often with confidence, became accepted as fact. The accompanying idea that psychosocial factors contribute to it is also made up and untested.

I wonder if this is an accurate article. I suspect it is.

Yet organisations like BACME state it as established fact.

 

[Utsikt]

These and other statements should be seen for what they are: conjectures that appear plausible until it is recognised that their content is not amenable to hypothesis testing and thus are incapable of leading to the truth.

I think this sums up an important issue with most BPS «hypotheses»: they can’t actually be tested so they are not hypotheses. Yet they are presented as truth, and therefore proven.

 

[MrMagoo]

A candidate for a @ME/CFS Skeptic deep dive hopefully?

 

[Jonathan Edwards]

So they are saying the whole central sensitisation idea started as a metaphor, and, repeated often with confidence, became accepted as fact. The accompanying idea that psychosocial factors contribute to it is also made up and untested.

I wonder if this is an accurate article. I suspect it is.

Yet organisations like BACME state it as established fact.

From my perspective the idea of central sensitization arose from specific neurological findings and the very mechanistic theories of people like Pat Wall in the 1980s or earlier. Rheumatologists probably started bullshitting about it around 1990. I wouldn't trust sources like this.

 

[Jonathan Edwards]

I think this sums up an important issue with most BPS «hypotheses»: they can’t actually be tested so they are not hypotheses. Yet they are presented as truth, and therefore proven.

I actually think the authors of this piece (which I have now read) are talking even more nonsense than those they criticize. The basic central sensitization idea comes from empirical observation using quite clever techniques. The idea that some patients with fibromyalgia have pain largely because of brain signaling patterns is very testable. A GWAS might well show that these people are born with altered neuronal housekeeping. In fact I am fairly sure that something strongly suggesting that has already been reported.

My main grouse would be when it is claimed that 8% of the population have this problem ("FM"). I suspect it is 0.1-0.5% much like MECFS.

 

[ME/CFS Skeptic]

A candidate for a @ME/CFS Skeptic deep dive hopefully?

I once wrote this:

Thread 'Central sensitization: a matter of concern'

Aug 11, 2018

Central sensitization: a matter of concern​

In 1981 Wilbert E. Fordyce challenged conventional wisdom. In one of the most influential findings in modern pain research, he reported a negative relationship between exercise and pain [1]. A subsequent study by Steven Linton confirmed these results. While patients thought their (low back) pain would increase after a cycling test, they themselves reported the exact opposite after the trial [2]. Patients were wrong about their condition...

• ME/CFS Skeptic
• bps catastrophising central sensitivity syndrome central sensitization me/cfs mus pain psychosomatic medicine tack
• Replies: 96
• Forum: Psychosomatic research - ME/CFS and Long Covid

• 

 

[ME/CFS Skeptic]

My main grouse would be when it is claimed that 8% of the population have this problem ("FM"). I suspect it is 0.1-0.5% much like MECFS.

8% seems far too high but my impression is that it is at least double that of ME/CFS.

 

[Jonathan Edwards]

8% seems far too high but my impression is that it is at least double that of ME/CFS.

Well I almost certainly fit the FM criteria and all my pains seem likely to be due to bits falling apart. My job for 35 years was to see people with pain. I never saw anyone whose pain seemed out of proportion, but I am happy to believe there are a few. MECFS I probably didn't see because it was not 'rheumatological' but FM definitely was.

 

[Utsikt]

I actually think the authors of this piece (which I have now read) are talking even more nonsense than those they criticize. The basic central sensitization idea comes from empirical observation using quite clever techniques. The idea that some patients with fibromyalgia have pain largely because of brain signaling patterns is very testable. A GWAS might well show that these people are born with altered neuronal housekeeping. In fact I am fairly sure that something strongly suggesting that has already been reported.

My general impression is that when someone talks about central sensitisation, they talk about pain that is disproportionate and has a strong association with «maladaptive» psychosocial behaviours. And the main treatments are CBT and physical therapy.

So it might be that the authors of this piece are talking about a different concept than what you are, because it has been hijacked by others.

 

[Jonathan Edwards]

So it might be that the authors of this piece are talking about a different concept than what you are, because it has been hijacked by otothers.

They do talk about it as if it were hijacked but their critique is directed against the original biology. Pain arising centrally is a perfectly reasonable and testable idea. They don't criticize the psychologising, which is not the core of the claims of the guy they target as far as I can see. He is still talking biological mechanisms.

 

[rvallee]

Fitting to begin this with a quote by Bernays, who launched the use of propaganda techniques into marketing. And Freud's nephew, not entirely coincidentally.

And how the idea of taking something that seems plausible, seemingly credible but lacking evidence, can be so harmful. Basically the same horrible story as the rehabilitation model. It's just mindless repetition that is indifferent to real life outcomes.

Nothing surprising to most of us here, but still shocking. Worth reading, it's shorter than the page length makes it seem, and very accessible.

Although the consequences of the Lancet MMR paper are much more profound, the mistreatment of chronic health conditions under the psychobehavioral ideology is a much more serious scandal. So much more devious, malicious, even. Probably top 5 in the history of medicine. A history filled to the brim with horror.

Yup:

‘But the facts don’t exactly matter: people repeat them so often that you believe them. Welcome to the “illusory truth effect,” is a glitch in the human psyche that equates repetition with truth [Dreyfuss 2017]’.

The oddest thing about so-called evidence-based medicine is that evidence is entirely irrelevant. Not somewhat, or mostly, entirely, because it mostly applies to issues where evidence is lacking, and is itself unable to produce any.

 

[Utsikt]

They do talk about it as if it were hijacked but their critique is directed against the original biology. Pain arising centrally is a perfectly reasonable and testable idea. They don't criticize the psychologising, which is not the core of the claims of the guy they target as far as I can see. He is still talking biological mechanisms.

The psychologising is here:

secondly it was stated that the biology of CSS is “based on neuroendocrine aberrations (including CS) that interact with psychosocial factors to cause a number of symptoms”. How these undefined biochemical aberrations within the body “interact” with such extra-corporeal “factors” was never clarified.

They also critique the use of rule in signs of pain being centralised based on the presence of other symptoms:

But just how is pain to be “centralised” – and who or what does the “centralising”? Apparently “centralised” pain can be identified “when multifocal pain occurs in conjunction with other centrally mediated symptoms, such as fatigue, insomnia, memory difficulties, and mood disturbances.” Such individuals are then said to“have centralized their pain” [Phillips and Clauw, 2013].

This implies that polysymptomatic distress in association with (multifocal) pain defines that pain as “centralized”. This diagnostic methodology could be termed “guilt by association”, which is a recognised logical fallacy.

Then there is this argument:

Returning to his dial-on-the-radio metaphor, Clauw [2015] asserted, “the pathophysiological hallmark is a sensitized or hyperactive central nervous system that leads to an increased volume control or gain on pain and sensory processing.”

Translated, that statement can be written as, “Increased CNS activity leads to increased pain and sensory processing”, which is a circular and tautological conjecture.

To me, it seems like they are going after the circular or otherwise flawed reasoning and descriptions by the people they critique.

And the conclusion is quite clear that the biology might be tested, as you say. The issue is that they don’t bother testing it and instead use circular reasoning to propagate an unevidenced narrative or tautological statements.

There may be validity in the proposition that the phenomenon of central sensitisation of nociception could be relevant to the pain experienced by patients who have been labeled with “fibromyalgia”. That is a theory from which testable hypotheses might be generated. Such an approach stands in marked contrast to statements such as “the brain turns up the volume of pain processing”, as if pain is a “thing” that can be “processed” including being “centralised”, or that “neuroendocrine aberrations interact with psychosocial factors” without outlining the biochemical basis of psychosocial factors, or that “chronic pain [is] caused by alterations in sensory processing in the CNS” which is equivalent to saying that the central nervous system is integral to the experience of chronic pain.

 

[Jonathan Edwards]

But they spoil it all by arguing that the biology cannot be tested when it can. Most of the things they call circular are not.

 

[ME/CFS Skeptic]

Well I almost certainly fit the FM criteria and all my pains seem likely to be due to bits falling apart. My job for 35 years was to see people with pain. I never saw anyone whose pain seemed out of proportion, but I am happy to believe there are a few. MECFS I probably didn't see because it was not 'rheumatological' but FM definitely was.

I meant chronic unexplained widespread pain which I think is what the fibromyalgia diagnosis is mostly used for (this may differ pre region though). Seems to occur in a similar population to ME/CFS (mostly adult females), and shows some overlap in symptoms but the energy limitations, PEM, POTS, and other symptoms such as light sensitivity are not present or much less common.

 

[Utsikt]

But they spoil it all by arguing that the biology cannot be tested when it can. Most of the things they call circular are not.

Where do they say that the biology can’t be tested? They say this as the end:

There may be validity in the proposition that the phenomenon of central sensitisation of nociception could be relevant to the pain experienced by patients who have been labeled with “fibromyalgia”. That is a theory from which testable hypotheses might be generated.

Most of the things they call circular are not.

There are two argument they say are circular:

Returning to his dial-on-the-radio metaphor, Clauw [2015] asserted, “the pathophysiological hallmark is a sensitized or hyperactive central nervous system that leads to an increased volume control or gain on pain and sensory processing.”

Translated, that statement can be written as, “Increased CNS activity leads to increased pain and sensory processing”, which is a circular and tautological conjecture.

The first one is because they say that A leads to B, but A = B and A isn’t proven.

According to Sluka and Clauw [2016], the overlapping conditions drawn together as CSS by Yunus [2007] are in fact manifestations of an underlying brain disorder with “similar underlying pathology with alterations in central nervous system function leading to augmented nociceptive processing and the development of central nervous system (CNS)-mediated somatic symptoms of fatigue, sleep, memory and mood difficulties.”

Translated, that statement can be written as, “Central sensitisation syndromes are characterised by the development of CNS-mediated symptoms attributable to altered brain function”. Or, to put it another way, a cluster of “CNS-mediated symptoms” allows the inference of a brain disorder called “central sensitisation”. This is yet another circular and self-fulfilling argument.

For the second one, I think the issue is that they say that all of these condition are CSS because the symptoms are mediated by the CNS, without actually proving that there is central sensitisation involved. So it’s another case of your proof for your conclusion not actually being proved.