Discussion in 'PsychoSocial ME/CFS Research' started by Andy, Nov 20, 2020.
Open access, https://mcpiqojournal.org/article/S2542-4548(20)30153-3/fulltext
Here we go again. Mayo Clinic and 'central sensitisation'.
And it gets worse. The whole article is about how people with FM and ME/CFS are vulnerable to stressors since our illness is caused by central sensitisation (so they say).
Their conclusion, which sounds good at first, is that medical people should keep in touch with us during the stressful time of the pandemic, and support us.
But there's a sting in the tail:
I had to look up "central sensitisation". It looks like some scientific terms mushed together in a way that sounds impressive, but doesn't actually mean anything, or rather, that it can be used to explain nearly anything without providing any useful techniques for dealing with it. I don't think it fits ME either.
I love that whenever people dismiss ME because we don't know the etiology, they have no issues pushing made-up stuff like CSS as being the etiology, despite there being no evidence whatsoever that it exists, is merely another turtle down, itself explaining nothing.
Almost like they're not arguing honestly and feelings trump facts here. Almost.
Real evidence does not have to have its utility rhetorically "reinforced". Treatment is not a negotiation with reality. Reality doesn't give a damn about feelings and beliefs.
Though in the case of fibromyalgia pain, the purported cascade of known pain signal amplications (such as Substance P enhancement) that result in a sort of centrally maintained pain sensitization, is, in my opinion, a useful theoretical construct for now, until we have more molecular mechanism evidence.
I don't see the central sensitization theory as useful/accurate in ME, and it may turn out not to be in fibro as well.
But in any case, it is a theory, not proven.
more eminence based tosh i am not sure if i remember this properly but some one working in pain clinics came up with this term central sensitivity as far as i am concerned it is just a marketing buzzword and has no place in any medical text . not in a diagnosis it sounds purely like the tripe ambiguous words that b p s ers come up with and then refuse to show any evidence for .
Pain and pain amplification (central sensitivity theory) by a researcher who discovered the deficit of growth hormone levels in fibro patients
I thought it’s been shown in multiple studies that the prevalence of mood disorders in ME/CFS and FM are no more than that of the general population? So how do they get off just stating “high comorbidity” BS, without any reference?
There are papers to support both views simply because of the questionnaires they use. If "feeling fatigue" is taken as a sign of depression then they can find 100% of CFS patients are depressed. In MS studies they have used modified scales so that the physical aspects of the disease are not taken to be signs of depression, but we should be so lucky.
From my reading of fibro research in the past 23 years, there are studies that show that in fibro, at least, a higher level of mood disorders than the general public.
However, I had not critiqued these research reports (prior to my participation in Science4me). I suspect that the research had some representative sampling error, in that the patients studied were from tertiary care (major hospital referral centers) centers which attract the most complex cases (those with co-morbities of fibro+ autoimmune disorders+other illnesses+mood disorders).
Understandably, these people, with multiple illnesses and pain sources, you would expect to have higher depression scores, or other mood disorders.
The fibro patients in the community (not seen at major referral hospitals) are, in the early years of the illness, understandably depressed and anxious until they are able to adapt and have at least an illusion of control over some of it. That can take a good ten years, depending on levels of pain and disability.
If these patients in the community are sampled for research of mood disorders during the ten-years adjustment period, they will probably show a much higher incidence of mood disorder. Also, life situation is involved. Older age at onset is usually associated with less adjustment (i.e. at age 50, one is closer to retirement age and doesn't have to deal as much with multiple role losses).
A researcher with the Oregon Health Sciences Center, a noted fibro research group a few years ago, found a higher incidence of child abuse in the history of fibro patients at that hospital-based clinic. Again, this may be the non-representational sampling at a tertiary care center error. Or, it may be a valid point--in that severe childhood stress primes the brain somehow for fibro.
The controveries persist, but association does not mean causation.
When they talk about mood disorders in ME they bring in a lot of confusion as they always seem to do to make psychology more important than it actually is.
They use terms such as dysthymia (persistent mild depression) and alexithymia (a broad term to describe problems with feeling emotions. In fact, this Greek term used in Freudian psychodynamic theories loosely translates to “no words for emotion.”) which are very loosely defined and often artifacts of the questionnaires where they are used for people who score a bit higher than usual but not enough to be called depressed.
Then they talk about the extent of psychological problems in a way that makes the listeners think they have found something severe and disabling.
People can feel devastating grief and despair because of the losses involved in ME but, to a large extent, these could be lifted if ME was considered like any other disease. I do not think that major depression, independent of life events, is very common in ME.
The way these people bandy about words like depression is the same as the way they talk about fatigue. They devalue the word for their own ends. And the true state of physically induced depression and fatigue in these diseases is lost so there is no hope of treatment.
But how is it any better than a peripheral mechanism account, for example, the idea that the pain is related to proinflammatory cytokines, or the like? That sounds way more plausible to me. If I were an FM patient, I'd be fighting at least for the parity for these two accounts until better evidence comes along, because once everyone rolls over and agrees to the CS idea,then begins the inevitable slide into "psychological".
It used to be that if an illness couldn't be explained medically, then it would be put down to psychological factors. Because psychology is sort of vague and difficult to define, so its useful to fill that "gap" when we don't have another explanantion. Now increasingly, we;'re seeing the same thing being done with neuroscience explanations. We don't know what physiological mechanisms are responsible for the pain in FM, so we will infer that all the action must be going on in the brain. The brain is so vast and difficult to pin down, and the only route that it really ever leads to is exercise and cognitive reeducation.
Separate names with a comma.