Central Sensitization in Neurological, Psychiatric, and Pain Disorders: A Multicenter Case-Controlled Study, Suzuki et al, 2021

Andy

Andy

Retired committee member
Abstract
Background. The role of central sensitization in refractory pain-related diseases has not yet been clarified.

Methods. We performed a multicenter case-controlled study including 551 patients with various neurological, psychological, and pain disorders and 5,188 healthy controls to investigate the impact of central sensitization in these patients. Symptoms related to central sensitization syndrome (CSS) were assessed by the Central Sensitization Inventory (CSI) parts A and B. Patients were categorized into 5 groups based on CSI-A scores from subclinical to extreme. The Brief Pain Inventory (BPI), addressing pain severity and pain interference with daily activities, and the Patient Health Questionnaire (PHQ)-9, assessing depressive symptoms, were also administered.

Results. CSI-A scores and CSI-B disease numbers were significantly greater in patients than in controls (). Medium effect sizes (r = 0.37) for CSI-A scores and large effect sizes (r = 0.64) for CSI-B disease numbers were found between patients and control groups. Compared with the CSI-A subclinical group, the CSI-A mild, moderate, severe, and extreme groups had significantly higher BPI pain interference and severity scores, PHQ-9 scores, and CSS-related disease numbers based on ANCOVA. Greater CSI-B numbers resulted in higher CSI-A scores () and a higher odds ratio ( for trend <0.001). CSS-related symptoms were associated with pain severity, pain interference with daily activities, and depressive symptoms in various pain-related diseases.

Conclusions. Our findings suggest that CSS may participate in these conditions as common pathophysiology.
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Open access, https://www.hindawi.com/journals/prm/2021/6656917/

2.2. Clinical Assessments
Participants completed questionnaires including smoking, caffeine intake, alcohol consumption, and body mass index. CSS-related symptoms were assessed by the Japanese version of the CSI, comprising parts A and B [19]. CSI-A scores 25 items for health-related and CSS-related somatic symptoms (score, 0–100), and CSI-B screens whether subjects have previously been diagnosed with 10 specific CSS diagnoses: restless legs syndrome, chronic fatigue syndrome, fibromyalgia, temporomandibular joint disorder, migraine or tension headaches, irritable bowel syndrome, and multiple chemical sensitivity. Cronbach’s α coefficients of CSI-A scores were 0.902 in the patient group and 0.894 in the control group in the present study. Patients were categorized into 5 groups based on CSI-A scores: subclinical, 0–29; mild, 30–39; moderate, 40–49; severe, 50–59; and extreme, 60–100 [19, 20]. A CSI-A score of ≥40 is reportedly the optimal cutoff for distinguishing subjects with CSS and those without [19]. Patients completed the Brief Pain Inventory (BPI) Japanese version, consisting of a pain severity score (means of items 3–6), assessing pain severity, and a pain interference score (mean of items 9A-9G), addressing pain interference with daily activities [21]. The Japanese version of the Patient Health Questionnaire (PHQ)-9, assessing depressive symptoms (scores, 0–27), was also completed [22].
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Only read the abstract, but this looks like a good example of the inappropriate use of questionnaires.

I could make a diabetes questionnaire with nonspecific symptoms that occur in patients with diabetes such as thirst, fatigue etc.

I then offer the diabetes questionnaire to a group of CFS patients

"Our results suggest that CFS patients have diabetes".
 
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I might be wrong, but in my understanding, "central senzitation" does not imply in itself any mental causation.

Therefore, the paper might be of interest.
 
Snow Leopard said:
Who cares? We're pointing out the methodology sucks.
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Admittedly, I don´t see the point.

Why would it be inappropriate to compare fever from a cold with fever from, say, dengue fever?

Why should this not lead to any further knowledge, whatever it might be?


So, in "CSS" it may turn out some day that the dopamine system is affected, or whatever.
 
Well the questionnaire is the Central Sensitisation Inventory - how much more evidence do you need that CSS exists??? :banghead:
It’s amazing that you can put together a list of symptoms that commonly co-occur, give the list a label and hey presto, you have a diagnosis - even better you can then add a hypothesis for the diagnosis and people will quote your paper as the basis for all sorts of studies into your new diagnosis. Then it is beyond doubt...
 
Snow Leopard said:
But they're not actually measuring any real evidence of "CSS" they're just using questionnaires and pretending this is evidence.
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I still don´t see the point.

Should it be as unscientific forbidden to ask ppl how it feels?


I would agree though, that it cannot not compete with objective knowledge like, say, about neurotransmitters. But this alone doesn´t say much as well.
 
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Daisybell said:
Well the questionnaire is the Central Sensitisation Inventory - how much more evidence do you need that CSS exists??? :banghead:
It’s amazing that you can put together a list of symptoms that commonly co-occur, give the list a label and hey presto, you have a diagnosis - even better you can then add a hypothesis for the diagnosis and people will quote your paper as the basis for all sorts of studies into your new diagnosis. Then it is beyond doubt...
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To be fair, this is the precise criticism I see medics make of ME *constantly.*
Difference is, they don't know that ME has a distinct (generally postviral) aetiology, symptomology, and trajectory, and we do not make any claims of identifying any underlying disease process with our clinical diagnosis, whereas CSS is just to fibro what impaired connectivity is to FND.
Or, what serotonin imbalance was to depression, before they figured out themselves they needed something a bit more sophisticated than that one.
 
Amw66 said:
CSS will follow on from FND as an additional diagnosis
The subverting of language by whatever means is usually the first step.
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I clearly say: No, this is not already a subverting of language.

You can come up with the idea that in a variety of symptoms any so far unknown dysfunction of nerves takes place and give it a label. This is in fact science in its progress.

You also can come up with a description of symptoms and put them together with a term, which interprets them as a "senzitisation in the CNS".


This is perfectly fine, so far. If you put critic on this, you make it easy for your enemies not to be taken seriously.


The problem arises when you come up with the interpretation, that symptoms and the guessed dysfunction or (more specifically) the guessed senzitation would be psychologically caused, without that there is any good evidence for nor that it is even of more likely possibility over physiological causes. But if you are doing premature critics, you will have shot you arrow already.
 
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Sphyrna said:
To be fair, this is the precise criticism I see medics make of ME *constantly.*
Difference is, they don't know that ME has a distinct (generally postviral) aetiology, symptomology, and trajectory, and we do not make any claims of identifying any underlying disease process with our clinical diagnosis, whereas CSS is just to fibro what impaired connectivity is to FND.
Or, what serotonin imbalance was to depression, before they figured out themselves they needed something a bit more sophisticated than that one.
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To my knowledge, the causes of any diseases her, interpreted as FND or CSS, is not known.

Only b/c ME/CFS begins in about 66% of cases apparently with a trigger, it´s not excluded that eg depression is not a physiologically caused disease, or at least has physiological components (which may be in disabling depression major contributers, at least).


So you make no point in favour of ME/CFS.
 
I was making a point in favour of demarcating clinical constructs in absence of understood pathology via the clinical picture, but I also believe that inferring a *hypothetical* pathology from the same examination is ass-backwards.
spinoza577 said:
Only b/c ME/CFS begins in about 66% of cases apparently with a trigger, it´s not excluded that eg depression is not a physiologically caused disease, or at least has physiological components (which may be in disabling depression major contributers, at least).
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I didn't claim that it doesn't. I brought up the serotonin hypothesis as an example of an explanatory model that is embryonic at best, and holds equally little predictive value and explanatory power in theory as well as in clinical practice. Just like the other models I mentioned.
Unlike many medics who merely pay lip service to the idea of abolishing mind-body dualism, I'm actually interested in multi-pronged approaches.
The problem is that the brain-behaviour divide isn't exactly trivial to bridge, and I don't think that applying one explanatory model to multiple conditions, when it hasn't even borne fruit for *any* of them, is the key.

I'd like for anyone to look at my friend with fibro and myself and tell me we are suffering from two manifestations of the same condition. The only similarities are the demographic and absence of a biomarker that is easily detectable via standard bloodwork. Yet, I always see medics equating FND/Fibro/ME/what-have-you, and I just want to tell them to stop.
 
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spinoza577 said:
I clearly say: No, this is not already a subverting of language.

You can come up with the idea that in a variety of symptoms any so far unknown dysfunction of nerves takes place and give it a label. This is in fact science in its progress.

You also can come up with a description of symptoms and put them together with a term, which interprets them as a "senzitisation in the CNS".


This is perfectly fine, so far. If you put critic on this, you make it easy for your enemies not to be taken seriously.


The problem arises when you come up with the interpretation, that symptoms and the guessed dysfunction or (more specifically) the guessed senzitation would be psychologically caused, without that there is any good evidence for nor that it is even of more likely possibility over physiological causes. But if you are doing premature critics, you will have shot you arrow already.
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Not my idea.i recall Mike Ekzakker flagged this up a couple of years ago, how the term was being bastardised to shift agendas

I didn't bookmark the reference, but it seemed pertinent.
CSS seems to have taken off since in BPS world
 
Sphyrna said:
I was making a point in favour of demarcating clinical constructs in absence of understood pathology via the clinical picture, but I also believe that inferring a *hypothetical* pathology from the same examination is ass-backwards.
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Without hypothesis no science. Ok, here its more about the clinical picture which is given an underlying hypothetical vague mechanism, but I daresay, or I find, the guess is reasonable or at least reasonable enough.

I didn't claim that it doesn't. I brought up the serotonin hypothesis as an example of an explanatory model that is embryonic at best, and holds equally little predictive value and explanatory power in theory as well as in clinical practice. Just like the other models I mentioned.
Unlike many medics who merely pay lip service to the idea of abolishing mind-body dualism, I'm actually interested in multi-pronged approaches.
The problem is that the brain-behaviour divide isn't exactly trivial to bridge, ...
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I agree, and there is all in all not much fantasy or imagination at work. As we could learn from Einstein, without fantasy, no good science.

...and I don't think that applying one explanatory model to multiple conditions, when it hasn't even borne fruit for *any* of them, is the key.
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Here I disagree and say, it´s a fruitful approach to search for similarities, even if they may turn out then not to take place.
 
spinoza577 said:
I still don´t see the point.

Should it be as unscientific forbidden to ask ppl how it feels?
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It can be problematic if researchers have never bothered to ask patients if they believe the questionnaires are relevant or of high quality. (which an unfortunate flaw of most questionnaire based studies)

If it is about how patients feel, I'd prefer a qualitative study, not a bunch of questionnaires that have not been properly validated by the patient group themselves.
 
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