Central sensitization: a matter of concern

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 and this provided new therapeutic opportunities.

An innovative hypothesis was formed, called the fear-avoidance model [3]. Central to this model was the idea that some (chronic) pain patients catastrophize their bodily sensations. This lead to hypervigilance, fear and avoidance of activities patients mistakenly thought would worsen their condition [4]. Pain patients were said to suffer from kinesiophobia, an “irrational, weakening and devastating fear of movement and activity stemming from the belief of fragility and susceptibility to injury” [5]. Avoidance behavior resulted in a vicious cycle of hopelessness, depression and deconditioning which was thought to explain the chronicity of symptoms. Inspired by the treatment of phobia [6], the model proposed graded exposure to threatening activities. Cognitive behavioral therapy (CBT) was promoted to tackle ‘myths about pain’ [7]; false illness beliefs patients held about pain and its relation to exercise.

Substitute pain with fatigue and you get the biopsychosocial model that has been imposed on patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) for almost thirty years [8, 9]. Only recently has this model begun to dissolve. Instead of an irrational fear of movement, ME/CFS patients are now known to suffer from an “exertion intolerance disease” [10]. Instead of catastrophic and somatic attributions, ME/CFS patients display “multiple pathophysiological changes that affect multiple systems” [11]. But just as the deconditioning-hypothesis begins to crumble, a new pain paradigm is ready to take its place.

Central sensitization (CS) originally referred to an increase in excitability of the central nervous system in response to a peripheral noxious stimulus [12]. Its influence was mostly confined to the area surrounding the site of injury, where a heightened sensitivity to heat and pressure was observed [13]. Since then the concept has gone through a significant expansion. CS became the supposed mechanism behind chronic, widespread pain, unrelated to an identifiable injury. Its effects were extended beyond the somatosensory system to include sensitivity to light, sounds and chemical substances [14]. The main rationale behind this inflation of the term was that some researchers thought CS could explain various medically unexplained syndromes, particularly those that have chronic pain as their dominant feature. In 2000 Muhammad Yunus proposed to group these disorders under the unifying concept of ‘central sensitivity syndromes (CSS)’ [15]. ME/CFS was one of them [16].

There are some valid arguments supporting this hypothesis. First of all the symptomatology matches the theory. Widespread pain can be a severely debilitating aspect of ME/CFS and many patients display an increased sensitivity to light, sounds or chemical substances [17]. Some studies [18, 19] have shown a generalized hyperalgesia (increased sensitivity to pain) in ME/CFS patients that was not present in controls. And while pain thresholds rise after exercise in healthy people, they seem to drop in ME/CFS-patients (i.e. patients experience more pain after exercise while they should be feeling less) [20-22]. These findings suggest that there is something wrong with pain modulation in ME/CFS. Given that the theory of central sensitization offers specific therapeutic options [23], this is definitely a direction future research should explore.

It is however a different matter to tout central sensitization as a fact in ME/CFS. Too many studies exploring the CS-hypothesis have reported negative findings for this to be accurate. Several of the mechanisms researchers use to evaluate the presence of CS (such as ‘conditioned pain modulation’ or ‘temporal summation’) have shown conflicting results in ME/CFS [24-28]. Increased levels of substance P, a neuropeptide involved in the transmission of pain signals, have been found in fibromyalgia (the ‘prototype’ of central sensitivity syndromes) but not in ME/CFS [29]. Nitric oxide (NO), another substance involved in neuronal excitability, instigated the initial research on central sensitization in ME/CFS [30] but has since proven to be a dead end [31]. These negative results have pressed Muhammad Yunus to remove ME/CFS from his central sensitivity syndromes-hypothesis, stating:

“Despite the fact that chronic fatigue syndrome (CFS) (systemic exertion intolerance disease) clinically overlaps with other members of the CSS family, definitive evidence of CS in this disease (excluding those having pain) is lacking, and was, therefore, not included.” [32]​

Despite this lack of evidence for central sensitization in ME/CFS, the theory has been put forward as a rationale for behavioral therapies associated with the fear-avoidance model [33]. Clinical guidelines in Australia [34, 35], Denmark [36], Belgium [37] and the US [38] refer to central sensitization to promote the use of graded exercise therapy (GET), claiming it can “desensitize the nervous system”. This is an extraordinary claim to make, since there is simply no scientific evidence to support it [39]. In fact, those diseases where the hypothesis of CS stands strongest like fibromyalgia and whiplash-related disorders, are also those where exercise therapy is most controversial. Ironically, “the presence of central sensitization may reduce the effectiveness of exercise interventions” [40]. As a 2014 review on the treatment of CS explained:

“Some patients with CS pain, including those with chronic whiplash associated disorders, chronic fatigue syndrome and fibromyalgia, are unable to activate endogenous analgesia following exercise. It remains to be established whether long-term exercise therapy accounting for the dysfunctional endogenous analgesia is able to ‘treat’ CS in these patients.”[41]​

So why is central sensitization being promoted as a rationale for GET?

It is no secret that some researchers hope central sensitization might revitalize the biopsychosocial model in the field of ME/CFS. Now that even the CDC explicitly warns this is a “biological illness, not a psychologic disorder” a new paradigm is needed that can point to pathophysiological abnormalities without breaking with the core tenet of the fear-avoidance model: ‘patients are mistaken about their own condition’. Central sensitization fits those needs rather well. Post-exertional malaise is no longer seen as a consequence of deconditioning but as the result of an excitatory central nervous system that sensitizes patients to the feeling of pain and fatigue. Because CS is unrelated to actual injury or tissue damage, the pain it causes is regarded as unreliable information, signaling that is best to be ignored. Hence a time-contingent form of graded activity is recommended [42]. As a prominent Belgian research group explained (translated from Dutch):

“due to central sensitization being present, it is no longer possible to rely on symptoms such as pain or fatigue. These are not an accurate representation of what is happening in the bodies of persons with fibromyalgia/CFS.” [43]​

Instead of CBT, ‘pain physiology education’ is advised to accompany graded activity [44] and to explain to patients why they should ignore what their body is telling them. “The innovative aspect of pain physiology education”, one paper explained, “is the use of physiology (i.e., the mechanism of central sensitization) to change perceptions and cognitions. This makes it appropriate even for CFS cases reluctant to the biopsychosocial model.” [45]

Another matter of concern is the central sensitization inventory (CSI), a questionnaire constructed to detect symptoms associated with central sensitization syndromes. As it mostly lists vague and common symptoms such as headaches, concentration difficulties and a lack of energy, many patients with ill-defined diseases will score more than the 40-point cutoff that warns clinicians for the presence of CS. The authors of the CSI explain what should happen next:

“For patients who report a wide range of comorbid symptoms within the CSS family, the clinician may choose to pursue fewer expensive diagnostic tests and, instead, gear treatment toward biopsychosocial symptom management strategies and toward more appropriate and effective medications.” [46]​

In summary: despite limited evidence, central sensitization provides a promising opportunity to tackle the devastating pain many ME/CFS patients suffer. By connecting this hypothesis to graded exercise therapy - for which there is convincing evidence it causes more harm than good in ME/CFS patients [47] - researchers are hindering the CS-theory to reach its full potential. There is no evidence that graded exercise therapy ‘desensitizes’ the nervous system of ME/CFS patients and one can only hope that patient organizations, researchers and clinicians around the world, will see through these illusory arguments.

By Michiel Tack. August 11, 2018.

The author wishes to thank ScottTriGuy from the Science for ME-forum for reviewing and commenting on this article before publication.

 

References:

1. Fordyce W, McMahon R, Rainwater G, Jackins S, Questad K, Murphy T, et al. Pain complaint-exercise performance relationship in chronic pain. Pain. 1981; 10(3): 311-21.
2. Linton SJ. The relationship between activity and chronic back pain. Pain. 1985; 21: 289-294.
3. Lethem J, Slade PD, Troup JD, Bentley G. Outline of a Fear-Avoidance Model of exaggerated pain perception I. Behav Res Ther. 1983; 21(4): 401-8.
4. Vlaeyen JW, Linton SJ. Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art. Pain. 2000; 85(3): 317-32.
5. Knapik A, Saulicz E, Gnat R. Kinesiophobia – Introducing a New Diagnostic Tool. J Hum Kinet. 2011; 28: 25–31.
6. Philips HC. Avoidance behaviour and its role in sustaining chronic pain. Behav Res Ther. 1987; 25(4): 273-9.
7. Malec J, Glasgow RE, Ely R et al. Coping with pain: a self-management approach. JSAS Catalog of selected documents in psychology 1977; 7: 113 (MS NO 1601). Cited in: Lauwerier E. Coping with chronic pain: problem solving and acceptance (Doctoral dissertation). Retrieved from: https://biblio.ugent.be/publication/4100366
8. Wessely S, David A, Butler S, Chalder T. Management of chronic (post-viral) fatigue syndrome. J R Coll Gen Pract. 1989; 39(318): 26-9.
9. Vercoulen JH, Swanink CM, Galama JM, Fennis JF, Jongen PJ, Hommes OR, et al. The persistence of fatigue in chronic fatigue syndrome and multiple sclerosis: development of a model. J Psychosom Res. 1998; 45(6): 507-17.
10. Institute of Medicine. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Redefining an Illness. Washington, D.C.: The National Academies Press, 2015.
11. https://www.cdc.gov/me-cfs/healthca...clinical-course/etiology-pathophysiology.html
12. Woolf CJ, Thompson SW, King AE. Prolonged primary afferent induced alterations in dorsal horn neurones, an intracellular analysis in vivo and in vitro. J Physiol (Paris). 1988-1989; 83(3): 255-66
13. Hansson P. Translational aspects of central sensitization induced by primary afferent activity: what it is and what it is not. Pain. 2014; 155(10): 1932-4.
14. Gracely RH, Schweinhardt P. Programmed symptoms: disparate effects united by purpose. Curr Rheumatol Rev. 2015; 11(2): 116-30.
15. Yunus MB. Central sensitivity syndromes: a unified concept for fibromyalgia and other similar maladies. JIRA 2000; 8: 27-33.
16. Yunus MB. Central sensitivity syndromes: a new paradigm and group nosology for fibromyalgia and overlapping conditions, and the related issue of disease versus illness. Semin Arthritis Rheum. 2008; 37(6): 339-52.
17. Nijs J, Meeus M, Van Oosterwijck J, Ickmans K, Moorkens G, Hans G, De Clerck LS. In the mind or in the brain? Scientific evidence for central sensitisation in chronic fatigue syndrome. Eur J Clin Invest. 2012; 42(2): 203-12.
18. Meeus M, Nijs J, Huybrechts S, Truijen S. Evidence for generalized hyperalgesia in chronic fatigue syndrome: a case control study. Clin Rheumatol. 2010; 29(4): 393-8.
19. Winger A, Gunnvald K, Wyller VB, Sulheim D, Fagermoen E, Småstuen MC, et al. Pain and pressure pain thresholds in adolescents with chronic fatigue syndrome and healthy controls: a cross-sectional study. BMJ Open 2014; 4(10): e005920.
20. Whiteside A, Hansen S, Chaudhuri A. Exercise lowers pain threshold in chronic fatigue syndrome. Pain. 2004; 109(3): 497-9.
21. Meeus M, Roussel NA, Truijen S, Nijs J. Reduced pressure pain thresholds in response to exercise in chronic fatigue syndrome but not in chronic low back pain: an experimental study. J Rehabil Med. 2010; 42(9): 884-90.
22. Van Oosterwijck J, Nijs J, Meeus M, Lefever I, Huybrechts L, Lambrecht L, et al. Pain inhibition and postexertional malaise in myalgic encephalomyelitis/chronic fatigue syndrome: an experimental study. J Intern Med. 2010; 268(3): 265-78.
23. Nijs J, Malfliet A, Ickmans K, Baert I, Meeus M. Treatment of central sensitization in patients with 'unexplained' chronic pain: an update. Expert Opin Pharmacother. 2014; 15(12): 1671-83.
24. Meeus M, Nijs J, Van de Wauwer N, Toeback L, Truijen S. Diffuse noxious inhibitory control is delayed in chronic fatigue syndrome: an experimental study. Pain. 2008; 139(2): 439-48.
25. Meeus M, Ickmans K, Struyf F, Hermans L, Van Noesel K, Oderkerk J, et al. Does acetaminophen activate endogenous pain inhibition in chronic fatigue syndrome/fibromyalgia and rheumatoid arthritis? A double-blind randomized controlled cross-over trial. Pain Physician. 2013; 16(2): E61-70.
26. Ickmans K, Meeus M, De Kooning M, Lambrecht L, Pattyn N, Nijs J. Associations Between Cognitive Performance and Pain in Chronic Fatigue Syndrome: Comorbidity with Fibromyalgia Does Matter. Pain Physician. 2015; 18(5): E841-52.
27. Collin SM, Nijs J, Meeus M, Polli A, Willekens B, Ickmans K. Endogenous Pain Facilitation Rather Than Inhibition Differs Between People with Chronic Fatigue Syndrome, Multiple Sclerosis, and Controls: An Observational Study. Pain Physician. 2017; 20(4): E489-E497.
28. Hermans L, Nijs J, Calders P, De Clerck L, Moorkens G, Hans G, et al. Influence of Morphine and Naloxone on Pain Modulation in Rheumatoid Arthritis, Chronic Fatigue Syndrome/Fibromyalgia, and Controls: A Double-Blind, Randomized, Placebo-Controlled, Cross-Over Study. Pain Pract. 2018; 18(4): 418-430.
29. Evengard B, Nilsson CG, Lindh G, Lindquist L, Eneroth P, Fredrikson S, et al. Chronic fatigue syndrome differs from fibromyalgia. No evidence for elevated substance P levels in cerebrospinal fluid of patients with chronic fatigue syndrome. Pain. 1998; 78(2): 153-5.
30. Nijs J, Van de Velde B, De Meirleir K. Pain in patients with chronic fatigue syndrome: does nitric oxide trigger central sensitisation? Med Hypotheses. 2005; 64(3): 558-62.
31. Meeus M, Van Eupen I, Hondequin J, De Hauwere L, Kos D, Nijs J. Nitric oxide concentrations are normal and unrelated to activity level in chronic fatigue syndrome: a case-control study. In Vivo. 2010; 24(6): 865-9.
32. Yunus MB. Editorial review: an update on central sensitivity syndromes and the issues of nosology and psychobiology. Curr Rheumatol Rev. 2015; 11(2): 70-85.
33. The Cochrane review (Larun et al. 2017) for example writes: “Evidence has also been found for central sensitisation contributing to hyperresponsiveness of the central nervous system to a variety of visceral inputs. The most replicated finding in patients with CFS is an increased sense of effort during exercise, which is consistent with this model. Graded exercise therapy may reduce this extra sense of effort, perhaps by reducing central sensitisation.” Retrieved from: http://cochranelibrary-wiley.com/doi/10.1002/14651858.CD003200.pub7/full
34. Sandler CX, Hamilton BA, Horsfield SL, Bennett BK, Vollmer-Conna U, Tzarimas C, et al. Outcomes and predictors of response from an optimised, multidisciplinary intervention for chronic fatigue states. Intern Med J. 2016; 46(12): 1421-29.
35. http://www.virology.ws/2018/05/14/trial-by-error-australias-online-get-cbt-education-program/
36. https://www.sst.dk/da/udgivelser/2018/~/media/1CE89F3206874263888BA4719419B844.ashx
37. https://www.me-gids.net/module-ME_CVS_docs-viewpub-tid-1-pid-1982.html
38. In 2012 Nijs et al. wrote: “it is tempting to speculate that exercise can indeed desensitize the central nervous system. However, this hypothesis is not (yet) supported by scientific evidence.” Retrieved from: http://www.painphysicianjournal.com/current/pdf?article=MTcxNw==&journal=68
39. http://www.virology.ws/2018/08/06/trial-by-error-mayo-still-champions-get/
40. This is a quote taken from a 2016 article on the treatment of cancer pain by Nijs et al. The authors suggest screening for the presence of central sensitization, as this might reduce the effectiveness of exercise therapy: “Another important consideration when prescribing exercise is the presence of signs of central sensitization. The presence of central sensitization may reduce the effectiveness of exercise interventions.” Nijs J, Leysen L, Pas R, Adriaenssens N, Meeus M, Hoelen W, et al. Treatment of pain following cancer: applying neuro-immunology in rehabilitation practice. Disabil Rehabil. 2018; 40(6): 714-721.
41. Nijs J, Malfliet A, Ickmans K, Baert I, Meeus M. Treatment of central sensitization in patients with 'unexplained' chronic pain: an update. Expert Opin Pharmacother. 2014; 15(12): 1671-83.
42. This paper (Nijs et al. 2014) for example explains: “Why preferring a time-contingent approach (‘Perform the exercise for 5 min, regardless of the pain’) over a symptomcontingent approach (‘Stop the exercise once it hurts’)? As indicated above, CS implies that the brain can produce pain and other ‘warning signs’ even when there is no real tissue damage. A symptom-contingent approach may facilitate the brain in its production of nonspecific warning signs like pain, whereas a time-contingent approach may deactivate brain-orchestrated top-down pain facilitatory pathways.” Retrieved from: https://www.researchgate.net/profil...s-with-unexplained-chronic-pain-An-update.pdf
43. Kos D, Nijs J, Meeus M, Salhi B. Chronische vermoeidheid: een praktische handleiding voor de revalidatie van kanker, MS, fibromyalgie en CVS. Leuven: Acco; 2012. P.157. The full passage reads as follows (in Dutch): “Vooral door de aanwezige centrale sensitisatie is een tijdcontingente aanpak aangewezen. Immers, door de aanwezige centrale sensitisatie kan men niet langer vertrouwen op symptomen zoals pijn of vermoeidheid. Die zijn immers geen accurate weergave van wat zich in het lichaam van personen met fibromyalgie/CVS afspeelt. Aan de andere kant mag dit geen alibi zijn om de ziekte(toestand) van de patiënten te negeren, en moet men andere methoden toepassen om de belastbaarheid van de patiënt te respecteren.”
44. This was noticed in 2011 by Tom Kindlon who wrote: “it seems questionable, and indeed possibly unethical, to have adherence to such an intervention as the goal of any educational program.” Retrieved from: https://www.archives-pmr.org/article/S0003-9993(11)00158-4/pdf
45. Nijs J, Crombez G, Meeus M, Knoop H, Damme SV, Cauwenbergh V, Bleijenberg G. Pain in patients with chronic fatigue syndrome: time for specific pain treatment? Pain Physician. 2012; 15(5): E677-86.
46. Mayer TG, Neblett R, Cohen H, Howard KJ, Choi YH, Williams MJ, et al. The development and psychometric validation of the central sensitization inventory. Pain Pract. 2012; 12(4): 276-85.
47. Kindlon T. Reporting of Harms Associated with Graded Exercise Therapy and Cognitive Behavioural Therapy in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Bulletin of the IACFS/ME. 2011; 19(2): 59-111. Retrieved from: http://iacfsme.org/PDFS/Reporting-of-Harms-Associated-with-GET-and-CBT-in.aspx

 

Very good - has it been published (yet)?

 

Yeah, let’s not spend any money on investigating patients with vague symptoms. (Hear my sarcasm)
Let’s put the patients in group therapy so they get educated about CSS and the fact they need to go on a merry-go-round of alternative therapies including psych therapies, so instead of getting access to and providing experience to phyisicans which will lead them to research questions and hypothesis, the patients is simply told ‘ not my problem, get therapy’.

This is a horrible, expensive and vicious circle to put patients in, and it has been going on for decades. We know there are biological abnormalities. We need science and effective treatments, and BPS is not it.

 

No

 

Terrific summary!

 

I'd like to see an experiment where some of those supporting the sensitivised hypothesis were strapped down on to a bed, along with me, and we were all subjected to some form of electrical pain, under my control. I'm certainly not the big brute type, but I reckon that 20 years of ME has made me much more used to pain than they will be.

This is where the promise not to deliberately cause patients unnecessary suffering hampers research.

 

Thanks for your response Graham. I do however disagree. The word sensitization in CS doesn’t refer to coping with pain or being less tough in dealing with it. It refers to changes in the excitability of the nervous system. If you for example break your leg or cut your arm, the area surrounding the site of injury will be more sensitized to pain (this is called secondary hyperalgesia), reflecting changes in the CNS. This sensitization probably helps in keeping you still and steady so the wound can heal – at least from an evolutionary point of view. Anyone who has experienced such an injury knows that stimuli that normally don’t hurt will now hurt in the area surrounding the cut or broken bone. This is sensitization; it refers to a biochemical phenomenon and normally has nothing to do with psychological processes or being though or not. The International association for the study of pain (IASP) defines sensitization as a neurophysiological term, referring to an “increased responsiveness of nociceptive neurons to their normal input.” So this was one argument in my essay: central sensitization isn’t necessarily a bad theory, it’s the biopsychosocial interpretation of it that is flawed.

 

I must be misunderstanding something here @Michiel Tack , or I didn't explain myself clearly enough. If I have become sensitized to pain, in the way that is suggested by the theory, then doesn't that mean than I will react to particular level of pain more strongly than the average person? The body sends out stronger pain signals, much more easily? The implication is that we feel the everyday knocks and aches that most people get, but our systems react much more strongly to them, giving us higher pain levels? The theory is then that we react to that, thinking it is a cue to take care?

Given that ME has had such a dramatic effect upon my life, if this is true, then the sensitization must be quite large. In which case, if my reactions to similar levels of inflicted pain are so much greater than that of healthy folk, it would be relatively easy to see.

As the various pains associated with ME happen all over my body, and in all sorts of guises, it would be hard to argue that it is a sensitization that has specific locations.

I have always been the practical sort – gardening, DIY etc. – and cuts, bruises, knocks and "pulled" muscles have always been part of that. I still do a little, and still suffer the same consequences. I also used to suffer from sinus headaches, and still do. I can't see that I am in any way more sensitive to such problems, wherever they occur.

My suggestion is that, if anything, over time we become more used to pain: when I fell and broke my hip a few years back, there was a lot of surprise in medical quarters that I wasn't complaining about it a lot more. So in fact if we and healthy folk are exposed to comparative levels of pain, I suspect we will feel it the same, but it would bother us less.

Why can't this be tested, if that is a correct interpretation?

 

Thank you @Michiel Tack for writing this excellent explanation of the dangers of the central sensitisation theory for ME. It beggars belief that once again clinical guidelines across different countries are promoting harmful graded exercise for patients with ME overlaying another theory with a nonsense bps approach. I note Belgium Professor of Physiotherapy, Jo Nijs, has his name on a lot of the CS papers.

 

To add, UK author, Jo Marchant, in her book called Cure - A Journey into the Science of Mind over Body - published in 2016 discussed how a well known South African sports physiologist, Tim Noakes, is claiming the fatigue in ‘CFS’ is mediated through sensitised faulty brain signals telling the body it is fatigued before it actually is. He too claims these faulty brain signals can be normalised by gradually increasing exercise. I think he has done some small studies on athletes who developed fatigue.

This theory ignores CFS patients who meet ME criteria have much more than fatigue going on and there is other research out there showing other possible reasons for the energy problems in ME as well as the myriad of other symptoms in the illness.

 

It can and has been done, I mention it in the text: "Some studies [18, 19] have shown a generalized hyperalgesia (increased sensitivity to pain) in ME/CFS patients that was not present in controls." One can however question the validity of these studies. In my opinion the question is unresolved.

You make a good point here, but it only applies to your personal situation. I think it is possible that a subset of ME/CFS patients do display hyperalgesia/allodynia.

Another point is that CS usually doesn't come alone, but accompanies another kind of pain. The first time it was studied (and in fact the only situation in which it has been demonstrated and proven) was in reaction to a periperhal noxious stimulus. So there was something to explain the pain. CS was merely one aspect in the body's response to that threatening information (i.e. lasting changes in the susceptibility of the CNS created lower pain thresholds in the area surrounding the injury). So one must not think pain is either caused by CS or something else. CS is more like an aspect of the body's pain response and its existence, independent of a peripheral injury, remains to be demonstrated.

 

Thanks for that information. This is of course the main problem: researchers have to prove that brain signals are false, before exclaiming this to be the case or using this hypothesis in clinical guidelines. When it comes to CS (the extended definition) evidence points towards just the opposite: it looks like those 'brain signals' are telling something important and need to be taken into consideration:

 

@Michiel Tack, fully agree. There is no way they should be pushing this theory and desentisation treatment in the form of graded exercise/activity in clinical guidelines with no firm evidence and whilst there is other research showing possible other causes for the symptoms including the energy problems. Also as you said, if central fatigue is a contributor it may be a protective mechanism.

 

@Michiel Tack, in case it is of interest I will attach screenshots of the pages in the Jo Marchant book discussing Tim Noakes theory on CFS. It has developed from his earlier theory that fatigue in exercise is not due to muscles reaching their limit but writes Jo Marchant ‘that the brain acts in advance of this limit, making us feel tired and forcing us to stop exercising well before any peripherals sign of damage occur... They (Noakes and his colleague) called the brain system that does this the central governor’.

 

And the final two pages on Noakes theory of CFS from Marchant’s book.

 

Thanks. I run a local ME support group, and in my experience, the majority of people with ME would be more like me. It is possible that a subset of ME/CFS patients do have that sensitization, but it is also possible that a subset of ME/CFS patients are one-legged Inuits with hearing problems. Surely the effect is only worth mentioning if (a) it is a significant effect (as ME is a significant handicap), and (b) it affects at least a sizeable proportion of people with ME/CFS.

Once again though, the theory that we get signals from our muscles way before they reach our limit is looking at ME from a very restricted point of view. The types of pain suffered varies tremendously: muscle pain is only one component, and often muscles can ache as a result of too much cognitive effort. There is also a wide variety of what I would call "nerve" pain – electrical tingling, over-sensitivty, stabbing etc. Add to that various forms of head pain and digestive disorders.

It's as though these folk have no real concept of the full-body impact of ME, and are taken off track by the term "chronic fatigue syndrome".

I forgot to say though – thanks for the article. You raise some good and challenging points.

 

Thanks. It was intended as a warning for ME/CFS patient organizations around the world. I hope MEAction or the ME Global Chronicle will publish it.

 

We are living this nightmare in my community. The local program is rebranding ME, fm and post Lyme as CSS. While they dropped the ‘exercise as treatment’, they are very focused on group therapy, meditation, acceptance therapy and anything but medical care. In fact they are even saying that POTS is a form of CSS.