Central sensitization latest articles (Chronic Whidespread Pain/Fibromyalgia)

pattismith

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Published online 2020 Mar 11. doi: 10.1093/rheumatology/keaa042

Enthesitis in psoriatic arthritis (Part 3): clinical assessment and management
Philip Measek1,k2
Author information Article notes Copyright and License information Disclaimer
k1 Rheumatology Division, Swedish Medical Center/Providence St. Joseph Health, Seattle, WA, USA
k2 University of Washington School of Medicine, Seattle, WA, USA
....The focus of this article is on the assessment of enthesitis by physical examination, the impact of enthesitis on function and quality of life, the impact of concomitant FM on clinical assessment, and the evidence for therapy of enthesitis....

Effect of central sensitization on assessment of enthesitis
Physical examination detects tenderness.

Physical examination does not discriminate between the true presence of inflammation (i.e. enthesitis) vs tenderness attributable to other factors, including what we label FM/CWP/central sensitization, which are conditions with overlapping definitions and features.

These are relatively common chronic central pain syndromes, which arise in individuals with genetic, biological and psychosocial predisposing factors and are characterized by CWP, often accompanied by fatigue, sleep disturbance and other symptoms.

These conditions occur more commonly in patients with chronic pain and inflammatory conditions.

We might use the term enthesalgia to describe this phenomenon when it influences tenderness at entheseal insertion points.

It is possible that in some individuals, tenderness is attributable only to -itis, in others only to -algia and in others, a combination of the two.


The phenomenon of coexistent central pain syndromes accompanying chronic rheumatic diseases has become an item of research and clinical importance because of its influence on disease severity measures and determination of treatment response in clinical trials and in practice.

Numerous studies of cohorts of patients with various rheumatological conditions, including RA, SLE, SS, OA, PsA and AS, have demonstrated that 15–20% of these cohorts, on average, will have a concomitant diagnosis of FM based on various classification criteria [5].

Brikman et al. [6] noted, in a Tel Aviv cohort of PsA patients, that concomitant FM was present in 18% and that all of the disease severity measures that included a subjective element reported by the patient, such as pain or patient global, such as Disease Activity in PsA (DAPSA), minimal disease activity (MDA), HAQ and LEI, were twice as severe as the same measures in patients without concomitant FM.

Højsgaard et al. [7] studied 69 PsA patients initiating treatment with physical and US examination of joints and entheses and also performed measures for FM/CWP, such as the widespread pain index (WPI) and Pain Detect questionnaire.

Responses consistent with FM/CWP on the WPI were seen in 35%.
These patients were not able to achieve a state of MDA, and there was little correlation between examination of joints and entheses and US findings.

These findings emphasize the importance of evaluating patients for concomitant FM/CWP in order to contextualize our assessment of disease severity and treatment response better in individual patients.
 

pattismith

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Already posted articles about it here:

Assessment of enthesis in patients with psoriatic arthritis and fibromyalgia using clinical examination and ultrasound | Phoenix Rising ME/CFS Forums

another article in 2021

Background:

Central sensitization (CS) is a condition characterized by a disproportionate response to pain stimuli. We sought to investigate the prevalence of CS in patients with inflammatory arthritides and its association with measures of disease activity and functional disability.

Methods:

We conducted an observational retrospective study in psoriatic arthritis (PsA) and rheumatoid arthritis (RA) patients. We administered to all the subjects in the study the CS inventory (CSI), a questionnaire that has been used for the diagnosis of CS.

Demographic and clinical characteristics were collected as well as measures or disease activity [i.e. Simple Disease Activity Index, Disease Activity Score in PsA (DAPSA)] and functional disability [Health Assessment Questionnaire Disability Index (HAQ-DI)]. Patients with fibromyalgia were excluded from the analyses. The primary outcome measure was the presence of functional disability as assessed by HAQ-DI >1.

Results:

We enrolled 150 patients with inflammatory arthritides (78 PsA and 72 RA).

Prevalence of CS was observed in 35.3% of the overall sample (29% in RA, 42.9% in PsA).


Binary logistic regressions showed a strong, independent and linear association between functional disability and CS in both PsA and RA patients. The strength of this association was greater in PsA than in RA.

Conclusion:

CS is an important determinant of functional disability in patients with chronic inflammatory arthritides.

PsA appeared to be more vulnerable to CS.


In addition, in the presence of CS, DAPSA did not adequately capture the occurrence of functional disability.

Therefore, special attention should be paid to PsA patients, in whom the concomitant diagnosis of CS should be routinely ruled out.
 

pattismith

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Thanks @pattismith !

You may want to read the attached articles. They describe why many people feel that the term "central sensitization" is an unscientific term when applied to humans, especially in the context of widespread pain.

Best wishes.
Thank you, I understand your concern.

However, I prefer the name "central sensitization" than the name "pain catastrophizing", if you see what I mean :lol:

I understand CS is often used for pain that may be either really central (spine or brain related) or peripheral (nerve related), so hyperalgesia or hypersensitivity may be better names or maybe neuropathic pain, why not?

Despite of that, I read interesting articles about CS, and I think they mostly consider CS to be linked to brain neuroinflammation and cytokines related, and it may be right!

Central Pain Syndrome (CPS) is a CS with objectivable lesion in the Central nervous system.

researchers now know that damage to the pain-conducting pathways anywhere along the neural axis, from the spinal cord to the sensory cortex, can cause central pain syndrome, including cases following injury or a stroke.

Consequently, the current name for this group of disorders is central pain syndrome to acknowledge that damage to various areas of the CNS (and not predominantly the thalamus) can cause central pain and that a stroke is not necessarily the primary cause.

Central pain syndrome can be broken down into central pain of brain or brainstem origin or central pain of spinal cord origin.

The term for the specific subtype of central pain syndrome caused by CNS damage due to a stroke is central post-stroke pain.

I like to read that more articles make no difference between CS and CPS...:xeyes:

Central Pain Syndrome Article (statpearls.com)



The neuropathic pain questionnaire does exist, it doesn't tel if the origin is central neuropathic or peripheral neuropathic:

Microsoft Word - DN4 Document.doc (myvmc.com)

The Central Sensitization Inventory CSI

The Central Sensitization Inventory (CSI) was developed to assess the overlapping health-related symptom dimensions of CS/CSSs. Part A has 25 items scored from 0 to 4. Total scores range from 0-100. Part B (which is not scored) asks if one has previously been diagnosed with one or more specific disorders, including seven separate CSSs and three CSS-related disorders.
A CSI-9 has been proposed as a shorter version of the CSI-25

Development and psychometric properties of short form of central sensitization inventory in participants with musculoskeletal pain: A cross-sectional study (plos.org)

(In my own case, I have SFN, but most of my pain/sleepiness/exercice intolerance vanish if I take methylphenidate, so I came to the conclusion that my symptoms are related to a central disruption of my mesolimbic dopamine pathway.

So my CS does not rule out peripheral nerve injury, nor even concomitante connectivitis... it's just a brick in my wall.)
 

Pyrrhus

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I understand CS is often used for pain that may be either really central (spine or brain related) or peripheral (nerve related), so hyperalgesia or hypersensitivity may be better names or maybe neuropathic pain, why not?
Yes, pain can originate in the central nervous system. The terms "hyperalgesia" and "neuropathic pain" are good helpful words to describe this. But that is NOT what "central sensitization" means.

The term "central sensitization" is a physiological concept that only refers to the ability of a single neuron or small group of neurons located in a very small area, in laboratory animals, to fire more spontaneously in response to certain stimulation.

The term "central sensitization" has nothing to do with the central nervous system of humans.

The confusion started with Yunus's illogical and pseudoscientific publications in the 1980's, which misrepresented the physiological concept of "central sensitization". His misrepresentation was ignored by most doctors, except for psychiatrists.

The psychiatrists thought that the misrepresentation of "central sensitization" was a more acceptable way of describing psychosomatic mental illnesses, by pretending that they believed the patient. In reality, these psychiatrists used a dishonest misrepresentation of Yunus's own misrepresentation of the physiological concept of "central sensitization" to deceive patients.

Despite of that, I read interesting articles about CS, and I think they mostly consider CS to be linked to brain neuroinflammation and cytokines related, and it may be right!
These are definitely very interesting ideas, but these ideas have nothing to do with "central sensitization".

The neuropathic pain questionnaire does exist, it doesn't tel if the origin is central neuropathic or peripheral neuropathic:
"Central neuropathic pain" is probably the correct term that you are looking for!

I hope this clarifies.
 
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pattismith

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These are definitely very interesting ideas, but these ideas have nothing to do with "central sensitization".



"Central neuropathic pain" is probably the correct term that you are looking for!

I hope this clarifies.
I do prefer the term central neuropathic pain. However, I doesn't systematically reject articles using central sensitization, if they are written in a way were you can see that obviously, the writer refers to possible neuroinflammation.

I think the fact psychologists misused the sensitization term might not discredit all the articles where you find this term.

For example, this article about neuropathic pain in RA written in 2017, also use the sensitization term, but you can read also:

Sustained nociceptive input can lead to changes in central pain processing, and nociceptive input is increased following local sensitisation of peripheral nerves within the joint.

Synovitis generates bioactive lipids, kinins, cytokines (e.g., TNF-α, IL-1 and IL-6), neuropeptides (e.g., calcitonin generelated peptide (CGRP)) (77-79) and neurotrophins (e.g., nerve growth factor (NGF) (80), each of which can sensitise peripheral nerves.

Immune cells within the CNS directly contribute to developing central sensitisation through the generation of cytokines such as IL-1 (81, 82). Furthermore, RA is associated with systemic features of inflammation.

Circulating cytokines might gain access to the CNS, particularly given that the blood brain barrier might be compromised in chronic inflammation (83).

A causative relationship between synovitis and augmented central pain processing is further suggested by research in rodent models.

Inflammatory arthritis in rats is associated with central sensitisation, with behavioural, electrophysiological and histological evidence of altered spinal and supraspinal pain processing that can begin even before clinical features of arthritis become apparent (81, 84).

Spinal exposure to TNF-α, IL-6 and IL-1β leads to allodynia and hyperalgesia (85).

TNF-α inhibition might act in part through central actions to reduce pain processing in people with RA,
although few adequately controlled studies have been reported to date (86, 87). RA treatment focuses on suppression of synovitis and the immune response.

Changes in clinical practice now enable rapid access by patients to immunomodulatory treatments but, unfortunately, suppression of synovitis often does not lead to pain-free remission.

The maintenance of pain despite successful remission of synovitis in established RA suggests that, once established, central sensitisation is not reversed by standard RA treatments.

Analgesic benefit from DMARDs might depend in part on specific interruption of neuroimmune mechanisms that drive central sensitisation, which would mean that different DMARDs might have different effects on pain, despite similar suppression of synovitis.

Cytokine candidates that impact upon central neuronal mechanisms might not be those traditionally developed as targets for treating synovitis itself (36, 37), and there remains potential for new regulators of central pain mechanisms to be uncovered.

Preventing the development of central sensitisation during the earlier phases of RA, and identifying mechanisms by which central sensitisation might persist in established disease despite suppression of synovitis, has huge potential to reduce the long term burden of pain in this disease.
article (4).pdf
 

Pyrrhus

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However, I doesn't systematically reject articles using central sensitization, if they are written in a way were you can see that obviously, the writer refers to possible neuroinflammation.

I think the fact psychologists misused the sensitization term might not discredit all the articles where you find this term.
Yes, good point!