Central sensitisation theory - discussion thread

To be fair the (null) hypothesis that symptoms of ME are generated in the brain irrespective of peripheral tissues is falsifiable in principle. Science does not require that you have a slam dunk way to falsify ready and waiting - just that in principle you might have some fairly good options one day.

 

How would you change my experiment to make it proper science? Before I thought of this experiment I always thought somatization was unfalsifiable but now I think in the case of peripheral pain we could (at least in some cases) prove that the pain is not generated by the brain.

 

We can't start with fitting an experiment to an hypothesis - that would be circular. One has to start with a clear statement of what the question(s) to be answered are in the context of an unambiguous hypothesis - the problem you identify (somatisation) (in the context of this thread) has been conflated with a proposition (central sensitisation) without either being expressed in terms of distinct and falsifiable hypotheses - so the first thing that has to happen is to separate these two conceptions.

I would start by setting somatisation to one side, it is not readily set within a falsifiable hypothesis and that makes it scientifically dubious and as such should be resisted as a diagnosis - you can't show a null hypothesis for a proposition that isn't adequately formulated.

Central Sensitisation is well formulated and has been subject to experiment, it's important not to confuse that well formulated proposition with its appropriation to the cause of a somatisation argument; as @adambeyoncelowe wrote earlier in this thread:

"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 recognise 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."
----------------

Whether Central Sensitisation has a role in ME/CFS is an interesting question, but there is nothing in the core ideas around Central Sensitisation that suggest anything other than identifiable biology:

Neuroinflammation and Central Sensitization in Chronic and Widespread Pain

Abstract

"Chronic pain is maintained in part by central sensitization, a phenomenon of synaptic plasticity, and increased neuronal responsiveness in central pain pathways after painful insults. Accumulating evidence suggests that central sensitization is also driven by neuroinflammation in the peripheral and central nervous system. A characteristic feature of neuroinflammation is the activation of glial cells, such as microglia and astrocytes, in the spinal cord and brain, leading to the release of proinflammatory cytokines and chemokines. Recent studies suggest that central cytokines and chemokines are powerful neuromodulators and play a sufficient role in inducing hyperalgesia and allodynia after central nervous system administration. Sustained increase of cytokines and chemokines in the central nervous system also promotes chronic widespread pain that affects multiple body sites. Thus, neuroinflammation drives widespread chronic pain via central sensitization. We also discuss sex-dependent glial/immune signaling in chronic pain and new therapeutic approaches that control neuroinflammation for the resolution of chronic pain."

Full: https://pubs.asahq.org/anesthesiolo...euroinflammation-and-Central-Sensitization-in

Edited to correct Adam's quote in line with his post below.

 

And by "fail to ignore" I meant "fail to recognise", but I can't go back and edit my typo now.

 

Well I thought the double negative worked in the context of the psyc Looking Glass world - but have changed your quote in my post with a strike though and italic.