Central sensitisation theory - discussion thread

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anniekim

Senior Member (Voting Rights)
I know central sensitisation theory is the new buzzword by many of the bps brigade, Per Fink refers to it a lot in his slides, and has no evidence.

May I ask as well as I think them suggesting central sensitisation is the cause of pain in pwme, are they also trying to claim it’s the cause of the severe sensory sensivitity problems in ME?

Also what is their explanation for the neuro signalling to become amplified? Is it the catch all stress cause? Many thanks.
 
It's one of those things that seems plausible but I'm not sure to what extent it's proven and it could be as unhelpful as the deconditioning/fear avoidance model in that it looseLy gives an explanation and then the idea would be desensitisation is an option or treatment, rather similar to reconditioning, this can still discourage biomedical research if people believe it enough along with the usual 'No other cause has be found'.

The sensory sensitivity in ME is very interesting but little looked at. It's been masked by the fatigue model and also it's much more an issue in severe ME than milder forms. However even when mild to moderate and getting as much daily light and sun as the next i had odd sensitivities to sun and lights at night. I guess the central sensitisation model would cover that, I don't know how sophisticated a model it is beyond the surface idea though, I also don't understand why MS wheelchair and bedridden people don't have it and we do, if inactivity being reclined etc is partly blamed for symptoms generally. From a biological explanation I saw Michael ElZakker say he finds low thalamus activity which he thinks could be causing light sensitivity.
It's a phenomenon in head injury and I read them talking about over excitable areas/pathways in that, but there is not treatment interestingly, just ways to manage, despite that recently a nurse suggested I try desensitisation (increased exposure) which shows how in CFS it is viewed as reversible without actually treating the illness.

I'd be interested in the explanation of their theories too as it's going to be influencing our health professionals. I saw an article by white where he uses it, it sounded plausible but AFAIC only really makes sense if CFS was really reversible by retraining /desensitisation which it doesn't seem to be. Maybe it's true as a theory but the body is not easily healed , maybe it's not true at all and is another red herring /psychological preferred garden path, convenient excuse for low funding.
 
@anniekim Central Sensitisation explains "everything". That is the "beauty" of the philosophy. (Can you see my ironic use of quotation marks? :whistle:)

The core of the symptoms, according to this philosophy (I refuse to call it a theory or a hypothesis), is pain and fatigue, but secondary consequences can be things like light or sound sensitivity. It's basically a new MUS dustbin.

Their "proof" consists of beautifully drawn circles that capture a bunch of unexplained symptoms (hence they must be related!).

(I've hidden the images under spoilers to make this post less visually taxing.)

1-s2.0-S0049017207001473-gr1.jpg

01.jpg

Clinical+Features+of+Central+Sensitization%2FDysfunctional+Pain.jpg

As you can see, CSS diagrams capture possible life events of pretty much every single human being alive.
Yunusfibro1.png
 
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As always, it's overly simplistic. I think they're latching onto things like evidence of primed glial cells in the brain, and low level neuroinflammation, and mangling it with a biopsychosocial agenda. They expect to desensitize with rehabilitation, of course.

What they fail to ignore is the actual biological part of their model. Yet again. The emphasis for them is on loosely defined 'sensitization' and 'stress', which you can bet they treat as primarily psychological.
 
One of the things i find problematic is the assumption that pwME are 'not used to it', so desensitisation could work.

But what about the experience of people whose problems with sound & light are the reverse of this theory... ie that when they're well rested AND anxious they can tolerate a great deal more sensory input than when depleted & calm.
So for example starting off by enjoying some music in the sunshine but as they begin to "tire" (after maybe 10-30mins depending on how much other demand there is on the system -eg standing or lying down)) it becomes more & more intrusive - the sound getting louder & louder, & also light getting brighter & brighter until it's unbearable. And eventually the sound of just a whisper & even dim light becomes excruciating, not just to the eyes & head but to the entire body... to the point where they (disappointedly) have to go inside where it is dark & quiet.
What about those people? - the idea that it's an exposure/sensitivity thing just doesnt fit with that experience does it? it's backwards.

EDITED - to make suitable for thread moving to public space
 
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The notion of central sensitisation syndrome is in a sense more insidious even than the notion of MUS because it gives the impression that we are no longer in the "unexplained" area. We have an explanation now: Your CNS is "sensitised"! Which explains everything! And nothing…

Maybe such sensitised states do exist, but in the wrong hands, i.e that of a doctor unwilling to take you seriously, that theory lends itself so easily to be used to deny the physiological reality of your sufferings. That doctor will look at you and reassure you but when speaking to you of the fancy notion of CSS, the message basically translates to:

"Don't worry, I don't think you're hysterical. It's your brain that's hysterical."
 
Chris said:
Don't worry, I don't think you're hysterical. It's your brain that's hysterical."
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Once I had somethimg pretty similar said to me. I was told, by a doc who had just met me and seen I had been diagnosed with ME, well some people are just weaker than others, can't handle life's pressures, etc., etc. Don't worry it's not your fault, your brain is just wired that way.

There were words. He got a surprise how much this little, frail weakling had to say for herself. We agreed not to see each other again.
 
Briefly, the paper below gave me the clearest explanation yet how CSS dismisses the idea of actual disease or injury but from the paper the ‘idea of direct psychological causality to symptoms is regarded too simplistic to account for most MUS’. It’s so sneaky. BPS model upgraded from fear avoidance argument but still nonsense.

Below from the paper:

“What causes MUS, if not disease?

Bodily symptoms arise from both peripheral and central processes [4]. While disease-based medicine has focused on peripheral triggers (i.e., disease or injury in an organ), recent work has demonstrated the importance of central symptom processing [9, 10]. “Central sensitisation” is an example of central processes involved in the persistence or amplification of symptoms. This was first elaborated in relation to pain, but also appears to play a role for other symptoms [9].

Symptom processing can be considered at the psychological level (as described in cognitive-behavioural models of MUS [11]) and increasingly also at the neuro-physiological level [12]. Furthermore, altered central symptom processing may give rise to increased peripheral symptom production (e.g., autonomic arousal). Previous models of MUS have emphasized the idea of “somatisation”, i.e., the presence of bodily symptoms as indirect markers of psychological distress [13]. Although considerable comorbidity has been found between both moderate and severe MUS and common mental disorders, the idea of direct psychological causality to symptoms is regarded too simplistic to account for most MUS [14].

In this paper we will use the term MUS to refer to symptoms which are primarily influenced by central processes rather than peripheral organ disease or injury. Some clinicians and researchers use the term “functional symptoms” instead of MUS, but this is still used disparagingly by some doctors and is probably not yet suitable for widespread use in primary care settings.”

https://bmcfampract.biomedcentral.com/articles/10.1186/s12875-017-0592-6

(I also note the lead author in the paper above may be on the WHO ICD 11 Primary Care Group for Mental Health that is asking to include a version of Fink’s BDS - that uses CSS theory -renamed BSS in PC arm) https://www.vumc.nl/afdelingen-themas/49661/20678990/4.3_Rosendal_MUS_BSS_WHO.pdf
 
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Autopsies done on people with severe ME like Sofia Mirza showed nodules on the spinal cord that could be related to herpes viruses. As usual, I can't remember the details but at the time it was said that these could well account for the fact that all sensory inputs were amplified. I know that they have found that if a nerve is damaged it can heal by forming little "nervelets" (think of your fingers on the end of your arm) Since each of these sends a signal, pain is amplified.

Just saying that the central nervous system is sensitised means nothing where is the mechanism and the evidence? It riles me that they keep dismissing our experience as "anecdotal" when their theories are al conjectures with no solid evidence.
 
Mithriel said:
Autopsies done on people with severe ME like Sofia Mirza showed nodules on the spinal cord that could be related to herpes viruses. As usual, I can't remember the details but at the time it was said that these could well account for the fact that all sensory inputs were amplified. I know that they have found that if a nerve is damaged it can heal by forming little "nervelets" (think of your fingers on the end of your arm) Since each of these sends a signal, pain is amplified.

Just saying that the central nervous system is sensitised means nothing where is the mechanism and the evidence? It riles me that they keep dismissing our experience as "anecdotal" when their theories are al conjectures with no solid evidence.
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Yes I think Dr Chaudhuri gave a talk saying that Also the dorsal root ganglionitis found- outside the SC - could be causing an amplification of sensation and signals causing the brain to respond with feeling of fatigue. That all sounds plausible but we have not had enough research. The CSS seems more theoretical assumed to be true which I dislike couched in to much jumbo jumbo talk to my reading. AFAIU theyre not looking for the cause of the CSS but no doubt are still mainly in the business of rehabilitation for it?
 
A fatigue clinic in Holland using CCS model based on Jo Nijs’work. Google translation below from their page:

Physiotherapy in patients with chronic fatigue syndrome

ME / CFS and fibromyalgia are unexplained, no cause is known. Patients have especially severe fatigue and many other complaints that only get worse by physical exertion; the immune system is (further) disrupted.

The latter is not seen to the extent with other disorders, as physical effort often has a 'complaining-damping' effect.

Patients often have unrealistic expectations and / or incorrect beliefs about the origin of their chronic complaints, the usefulness of rest and the fear of movement. Stress causes extra stress, sleep is an important point of interest (a scientific study of 350 sleep study results among our fatigue patients gave a significant disturbance to the effectiveness of sleep at 100%).

In the treatment by the psychosomatic physical therapist, we refer to the explanatory model of Prof. Dr. Jo Nijs (VU Brussels): the mechanism of central sensitization (named after the patient: 'hypersensitive nervous system'). The information supply of the nervous system is disrupted. Not activating the damping system gives increased sensitivity of fatigue / pain signal or disturbing the sensitivity of sensory signals. Therefore, management of activities and exercise must be treated very carefully. Together with the ME / CVS Foundation these are set out in a folder.

It seems a paradox: exercise gives an increase in symptoms versus it is important to move. But it is only the "exaggerated" forms of physical exertion that lead to malaise (such as performing a (sub) maximum exercise test or long-term work in the garden). Therapy must be tailored to the possibilities: with low intensity and short periods of exertion, alternated with rest breaks. This requires a great deal of expertise from the therapists, and in the case of Fatigue & Pain Center, therapists and patients are supported by the Activity and Motion Weigher.

Measuring is knowing

With the help of the "Beweegweger", which makes the load on the activity measurable, the patient learns to build up the loadability in a responsible manner. Prior to this, a study is taking place with the Sensewear, which measures, among other things, metabolism throughout the day. The motion scale then calculates how many METs (metabolic equivalent of a task) is an operation. The physiotherapist and patient thus have insight into whether the patient advances in energy. The ultimate goal is to increase the load capacity. A second measurement with Sensewear objectifies the result.

https://vermoeidheidenpijncentrum.n...herapie-bij-chronisch-vermoeidheids-syndroom/
 
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anniekim said:
This pic sums up the steps in development of CSS well!
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So true.
Thanks for the "scientific" CSS stuff. Here's the peter white etc article where they talk about retraining the brain to accept activity, I think css is part of the idea

https://www.theguardian.com/society...ried-alive-victim-of-chronic-fatigue-syndrome

Michael van elzakkar has said the thalamus is responsible for filtering out stuff which I think gets through in ME and could lead to signal amplification. The difference is that with the psychologists they are more aboutjust saying a theory which supports their supposed success with treatment, rather than trying to understand the illness mechanisms. They would say that's not their job but with the type of headlines and papers they've published they've, I would say, discouraged others from feeling there's a need.
 
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Have just found this interesting bit of research from 2014 on
The Role of the Dorsal Root Ganglion in the Development of Neuropathic Pain
Abstract
Background
The dorsal root ganglion (DRG), in the not too distant past, had been thought of as a passive organ not involved in the development of abnormal aberrent neuropathic pain (NP), but merely metabolically “supporting” physiologic functions between the peripheral nervous system (PNS) and the central nervous system (CNS). New information regarding metabolic change within the DRG has dispelled this supportive passive role and suggests that the DRG is an active, not a passive, organ, in the process of the development of chronic pain.

Methods
A review of the anatomic and physiologic literature utilizing PubMed and Google Scholar was performed to create a review of the anatomic and physiologic foundations for the development of NP after peripheral afferent fiber injury.

Conclusions
The DRG is as involved in the process of generating NP as is the nociceptor and the dorsal horn of the spinal cord.
Click to expand...

full text here : https://academic.oup.com/painmedicine/article/15/10/1669/1939615


the whole CSS thing is another example of hijacking a biological problem and presenting/treating it as psychogenic.
 
Still confused by a lot of this. In the BMC paper I linked to above, it is written:

In this paper we will use the term MUS to refer to symptoms which are primarily influenced by central processes rather than peripheral organ disease or injury.
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Am I right they are dismissing the idea of disease even in the brain (as I take it the brain would be described as the only non peripheral organ?), though they only refer to disease or injury in the peripheral organs?

EDIT:

My knowledge of medical language is extremely limited. When the sentence above referred to ‘peripheral organ disease’ I thought a peripheral organ had to be something other than the brain organ. However, i think in this context peripheral means in relation to the organ as earlier in the the paper it said “While disease-based medicine has focused on peripheral triggers (i.e., disease or injury in an organ)”. Oh dear, my head gets easily scrambled.
 
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