We don't know that they "Reduce central sensitisation". We know that they have positive psychiatric effects (on mood or other symptoms) and this leads to a change in how people rate their level of pain on self-report questionnaires.
The rest is just speculation.
Yes, those drugs are tested by observing the patient's reduced pain response, etc, so I agree it is not a direct measure of the drug's ability to reduce central sensitization.
In my mind, a simple model of how central sensitization might occur is by too much NMDA receptor activation on neurons, or too little GABA receptor activation. This is because NMDA activation turns up the sensitivity of neurons, and GABA activation turns the sensitivity down.
Dr Paul Cheney has long proposed that in ME/CFS, neurons are oversensitive to firing because their NMDA receptors more activated than their GABA receptors. High NMDA activation, as well as low GABA activation, lowers a neuron's threshold for firing, thus making neurons more sensitive to stimuli.
Dr Cheney uses
benzodiazepines to treat the
oversensitive neurons in ME/CFS. Ref:
1
High dose transdermal magnesium, which many ME/CFS patients find useful, likely works because it is a potent NMDA receptor inhibitor, and so will reduce oversensitivity of neurons.
I have never heard any objections to Dr Cheney's view and treatment on oversensitive neurons in ME/CFS, and I have never heard any objections to Dr Jay Goldstein's concept of neurosomatic disorders. They are very similar ideas to central sensitization.
I am going to agree that we disagree on this subject matter of using psych meds to treat Fibromyalgia. Per your profile, I am glad you are having success with Amisulpride which Wikipedia says is "
atypical antipsychotic used to treat
psychosis in
schizophrenia and episodes of
mania in
bipolar disorder"
https://en.wikipedia.org/wiki/Amisulpride
The sort of argument that "
if you use an antidepressant, it must be a mental treatment" tends to come from those with not much knowledge of biochemistry. Drugs can have many effects and uses other than the main use for which they are labelled. Dr Chia for example is using Prozac on ME/CFS patients because this antidepressant has antiviral effects against enteroviruses.
How do you provide evidence that something (CSS) doesn't exist? It's incumbent upon them to prove the model, but they haven't and they aren't even trying.
Certainly a theory of the mechanism of CSS must be set up in such a way that it can be falsified or verified. If there is no possibility of falsifying or verifying an idea, then it is not a scientific theory.
I agree that there does seem to be little research on central sensitization, especially given that it is proposed to occur in a wide range of diseases.
Which makes you wonder how seriously central sensitization is actually taken as a scientific idea. Seems like the researchers are a bit lazy.
Then again, none of us here have bothered to read up about the detailed mechanisms of central sensitization. I tried to read one complex paper, but I am a bit brain dead in recent days.
CSS, as used to relabel MUS, is full blown BPS.
It may well be the case that the Wessely and the somatoform brigade try to hijack CSS and turn it into another "all in the mind" etiology. I can definitely see there is a danger of that.
However, the originator of CSS, Prof Yunus, developed this concept to try to
counter the views that ME/CFS, fibromyalgia, IBS, etc were "all in the mind".
Rather than being a causal mechanism, it is more likely to be an aspect of different syndromes/diseases. But the BPS school will attempt to sell it as much more than this.
I agree. It's more likely to be an aspect of ME/CFS and related diseases, rather than an explanation of the full picture. CSS may potentially be the cause of some of the symptoms in ME/CFS, but other ME/CFS symptoms may have a different etiological basis.
And CSS itself may not be the first cause of ME/CFS, but a downstream effect (which then causes its own symptoms). As part of the pathophysiology of ME/CFS, CSS itself might for example be caused by a viral infection in the brain, which then increases neuronal sensitivity by an inflammatory mechanism (inflammation in the brain pumps out lots of extracellular glutamate).
@Daffodil and
@lizw118 had almost full remission from brain fog etc a day or two after taking Rocephin, an antibiotic drug which significantly ramps up glutamate clearance from the brain, thereby likely reducing neuronal oversensitivity. See here:
Rocephin shots
So the glutamate / neuronal oversensitivity theory should not be dismissed out of hand.
But I do think it is premature to label ME/CFS and related diseases as CSS.
