By John Quintner and Milton Cohen
In his seminal book “Propaganda (1928)” Edward Bernays [1891-1995] observed:
“The conscious intelligent manipulation of the organized opinions and habits of the masses is an important element in a democratic society. Those who manipulate this unseen mechanism of society constitute an invisible government which is the ruling power in our society.”
As this article will show, his words still ring true in the field of Rheumatology. That which commenced as conjecture on fibromyalgia has been repeatedly embellished to a stage where it has assumed the status of established knowledge or truth.
“Central sensitivity syndromes”
In 2007, Dr Muhammad Yunus from Illinois noted that a number of diverse medically controversial conditions, such as fibromyalgia, irritable bowel syndrome, tension-type headaches and chronic fatigue syndrome, had several clinical features in common. He attributed these features to “hyperexcitement of the central neurons”, which in turn led him to propose the “concept of central sensitivity syndromes (CSS)” [Yunus 2007].
A closer examination of this proposition reveals two assertions: firstly, central sensitisation (CS) of nociception was taken as the model from which a generalisation to “central sensitisation” was made; 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.
This concept of “central sensitivity syndromes” should be seen as a bold proposition that there may be a common pathogenesis for the symptom clusters (technically not syndromes) under consideration. Although at that time “evidence for CS is not present in all patients of the CSS family”, the proposition was plausible and indeed the author stated explicitly, “The concept of CSS seems viable”. This can be seen as an example of a conjecture being raised to the status of a truth simply because if it were true so much that is currently not understood may become so [Lipton, 2005]. But is it true?
Rheumatologist Dr Dan Clauw and his colleagues at the University of Michigan not only championed the cause of CSS around the world, but also have gone much further than Yunus by introducing the concept of “centralised” pain.
In their paper with a tantalising title – “maybe it (pain) is all in their head – Phillips and Clauw  likened “augmented pain transmission” and “sensory amplification” to the volume control on a radio dial. They suggested that individuals might have different “volume control settings” on “their pain and central processing”. This is an attractive metaphor, perhaps, but one that suggests lack of understanding of contemporary concepts of nociception and pain.
They followed up this paper by defining their concept of “centralised” pain [Phillips & Clauw, 2013]:
For clarity, we will use terms such as central augmentation or amplification to refer more broadly to central mechanisms that enhance perception or modulation of pain differentially between individuals. We will use the term “centralization” of pain to refer to a common process that seems to occur to a vulnerable subset of individuals with any chronic pain state, wherein pain primarily due to peripheral nociceptive input is subsequently amplified by central factors, such that both peripheral and central factors are then contributing to the perception of pain by an individual.
In this assertion, note the language: “centralization of pain … seems to occur … with any chronic pain state…” and “… pain primarily due to peripheral nociceptive input is … amplified by central factors, such that both peripheral and central factors … [contribute] to … pain”? Did they not notice the tautology inherent in these statements? Is not the experience of pain itself the “perception”, not a thing that is “perceived”? And is not “perception” an emergent function of the brain? “Modulation” of nociception may be analogous to a volume control; “amplification” of the experience of pain is not quite so linear.
The paragraph quoted above could be restated simply as, “Any chronic pain state is a function of the brain and may be influenced by many factors”.
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.
Clauw  then proclaimed:
“Fibromyalgia can be thought of as a centralized pain state. Centralized pain is a lifelong disorder beginning in adolescence or young adulthood manifested by pain experienced in different body regions at different times. “Centralized” refers to central nervous system origins of or amplification of pain. This term does not imply that peripheral nociceptive input (i.e. damage or inflammation of body regions) is not contributing to these individuals’ pain but rather that they feel more pain than would normally be expected based on the degree of nociceptive input.”
How is it known that this is a “lifelong disorder”? How can it be determined that any one feels “more pain than normally would be expected …”? How would an observer be able to determine this [Cronje & Williamson 2006]?
A “white paper” [Arnold et al. 2016] then appeared in which fibromyalgia was said to exemplify “centralized” pain and to result from “persistent neuronal dysfunction” (See their Fig 1). Here is their argument:
“Aberrant neurochemical processing of sensory signals in the CNS may lower the threshold of pain, amplify normal sensory signals, and alter gene expression, thereby leading to hypersensitivity and central sensitization that result in chronic pain. [Arnold et al. 2016]”
In this context, what is the “threshold of pain”? And how might “alter[ed] gene expression” lead to “hypersensitivity”. Of what and to what do “hypersensitivity and central sensitization” refer?
Returning to his dial-on-the-radio metaphor, Clauw  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.
FM as a brain disorder/disease
According to Sluka and Clauw , the overlapping conditions drawn together as CSS by Yunus  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.
In 2017 the National Institute of Health awarded Michigan Medical School researchers, Drs Chad Brummett and Dan Clauw, funding of US $7.5 million to expand their work on the metaphor of the radio dial.
As Dr Clauw explained:
“For those with fibromyalgia, it’s like the brain turns up the volume control on pain processing. The high volume is often the underlying problem, more than damage or inflammation in the region of the body that hurts.”
In terms of contemporary neuroscientific knowledge of brain function, this comment makes no sense. Our brains are much more complex than are radio transmitters or receivers.
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.
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.
‘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]’.
Such an effect is all too evident in this discourse where the main agenda is to promote fibromyalgia as a brain disease.
Arnold LM, Choy E, Clauw DJ, et al. Fibromyalgia and chronic pain syndromes: a white paper detailing current challenges in the field. Clin J Pain 2016; 32(9): 737-746.
Clauw DJ. Fibromyalgia: a clinical review. JAMA 2014; 311(15): 1547-1555.
Clauw DJ. Fibromyalgia and related disorders. Mayo Clin Proc 2015; 90(5): 680-692.
Cronje RJ, Williamson OD. Is pain ever “normal”? Clin J Pain 2006; 22: 692–699
Dreyfuss E. “Want to make a lie seem true? Say it again. And again. And again.” WIRED 11 February 2017. Link: https://www.wired.com/2017/02/dont-believe-lies-just-people-repeat/
Lipton P. The Medawar Lecture 2004: The truth about science. Philos Trans R Soc Lond B Biol Sci 2005; 360: 1259–69.
Phillips K, Clauw DJ. Central pain mechanisms in chronic pain states – maybe it is all in their head. Best Pract Res Clin Rheumatol 2011; 25(2): 141-154.
Phillips K, Clauw DJ. Central pain mechanisms in rheumatic diseases: future directions. Arthritis Rheum 2013; 65(2): 291-302.
Sluka KA, Clauw DJ. Neurobiology of fibromyalgia and chronic widespread pain. Neuroscience 2016; 338: 114-129.
Yunus M. Fibromyalgia and overlapping disorders: the unifying concept of central sensitivity syndromes. Semin Arthritis Rheum 2007; 36(6): 339-356.