(Much of my following post may be not relevant to the article this thread is discussing as it relates to 'central sensitisation' as an explanation for ME which may or may not be intended by the article.
Also sorry it has become a very long and rambling. I probably should have saved it elsewhere and then rewritten it later in a much more digestible format, so I do not expect many or even anyone to read it.)
I may be being very stupid but I still have no idea what 'central sensitisation' means, or if anyone has actually proposed something that is actually measurable. Are they postulating a neurological or a psychological phenomenon?
Is it suggesting that somewhere in people's sensory system/systems the normal neurological signals are somehow amplified? Presumably, given the word 'central' they are presumably locating it in the brain and saying everything is fine in the rest of the nervous system. Why is the amplification happening in one part of the nervous, eg say the cerebral cortex but not in another part eg the lower motor neurones? Why does this process impact on signals coming to the brain but not signals coming from the brain? Is it modality specific, eg just pain, just vision, just sound or is it a feature of the entire brain? Is it a feature the whole brain or of just part of the brain, eg the brain stem, specific cerebral lobes?
Are they saying saying that hypersensitivity to light is the same as smells triggering PEM and the same as ideopathic pain? If so presumably they are postulating it involves multiple neurological pathways (sorry my neuroanatomy and neurophysiology have been unused for over thirty years old and interestingly much more effected by brain fog than my neuropsychology or cognitive psychology).
Presumably this is different from the evidence that exists for inflammation of the brain? Presumably it does not explain the co-occurrence of such as motor symptoms, IBS, cognitive problems, balance issues?
Are they predicting consistent relationships between the experience of say pain and the peripheral phenomenon that triggers the pain? (The abstract above does seem to suggest this.) If so why are they not trying to map pattern in the relationship between say the stimuli that trigger pain and the subjective experience of pain? How does this explain for example during PEM I may experience severe chostrochondritis, a localised pain arround the breast bone that can be so severe as to be totally incapacitating, combined with my intercostal muscles being tender to the touch, whilst simultaneously my subjective response to say stubbing my toe remains unchanged?
Why do they tend to support the use of therapies designed to 'desensitise', when without a clear understanding of the underlying mechanism, this may be as likely to worsen the condition as to lessen it? For example most of us experience a worsening of our symptoms following exertion and a lessening of our symptoms with rest. How then can you assert without evidence that exposure to the triggering stimuli, eg exertion, even if it is a graded exposure, will desensitise? Presumably this at present is a post hoc justification for a belief in the efficacy of such as GET
Is their belief in systematic desensitisation advocating a physiological process as might happen in some treatments of allergies or a psychological one as in the treatment of phobias? Presumably advocating the use of CBT and GET suggests they believe it to be a psychological process, or do they like Crawley believe that behavioural changes can work like a magic 'pill' to modify neurophysiological processes?
Is this desensitisation best conducted in a modality specific way, eg if some one is sensitive to pain then they should be exposed to pain? I would argue that with my chostrochondritis I might be able to learn to be more stoical through exposure to pain, though given rest completely relieves it and exertion is its trigger, being stoical is of no practical value as pushing through the pain is undoubtedly counterproductive?
If they are suggesting it is a psychological phenomenon are they are also suggesting some level of awareness of the issue is required. For example in this situation hypersensitivity to light would not necessarily be related to objective measures of brightness but rather to whether the person is focusing on the light. The phobia analogy would be that if a person was in the presence of say a spider but had not noticed it it would not cause distress. The problem with spiders is not that the spider is in a person's visual field, but that they are consciously aware of the spider being there. Presumably knowing you are in a room with a spider provokes distress even if you can not see it, but in contrast hypersensitivity to light is not a problem in a darkened room even if you know there is bright sunlight behind the drawn curtains.
Knowledge that my localised ideopathic pain does not relate to structural damage or any obvious disease process in the perceived location may help me endure it, but it has no significant impact on the perceived intensity or, when severe, its debilitating effect. Indeed there may be times when this knowledge is counter productive as it encourages me to disregard the pain push through it, when as symptom of PEM, the most productive response is rest.
Similarly my gluten intolerance triggered migraine, vomiting and a worsening of my general ME symptoms for years before I knew I had any food intolerances. My awareness that food intolerances can be an issue in ME is irrelevant to the effect exposure to certain food stuffs has on me. No matter what my illness beliefs are, how much sleep I get, my food intolerances can only be managed by controlling my exposure to the relevant food stuff. Desensitisation does not work as
I continued eating gluten for years after the onset of the symptoms before I was aware of the issue. Conversely avoiding gluten has not so far impacted on the underlying intolerance, as accidental exposure, eg eating an onion bhaji that subsequently turns out to have been made with wheat flour rather than gram flour, still triggers the symptoms.
In this article recommendations for intervention are a very bizarre ragbag. If they believe central sensitisation is neurophysiological why recommend lifestyle changes. How do they expect changing a person's illness beliefs will impact on the firing of neurones in the visual cortex in the example of hypersensitivity to light? Why should diet, except in cases of malnutrition, impact on the parts of the cerebral cortex mediating pain perception? Conversely if it is psychological, why do people treating phobias not advocate a special anti spider diet or an anti psychosis exercise regime?
Personally I believe that some form of central sensitisation as a result of something like neurological inflammation may be a factor in understanding some of the symptoms of such as ME, but that it makes no sense as primary explanation of a multi system condition like ME or even of ideopathic pain. Further the choice of treatment approaches in this article for central sensitisation, whatever is meant by this, seem totally arbitrary.
[Added - just realised I foolishly ate chocolate today even though I know it triggers insomnia and a brief spell of euphoria. Hence this night time splurge. Soon the crash, perhaps then a bout of IBS and a migraine as I go into the withdrawal symptoms. So obviously a sign of my false illness beliefs.]
