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The common link between functional somatic syndromes may be central sensitisation (PD White and Co.)

Dolphin

Senior Member
Messages
17,567
J Psychosom Res. 2015 Mar;78(3):228-36. doi: 10.1016/j.jpsychores.2015.01.003. Epub 2015 Jan 9.
The common link between functional somatic syndromes may be central sensitisation.
Bourke JH1, Langford RM2, White PD3.
Author information

Abstract
OBJECTIVES:
Functional somatic syndromes are common and disabling conditions that all include chronic pain, and which may be related to central nervous system sensitisation. Here, we address the concept of central sensitisation as a physiological basis for the functional somatic syndromes.

METHODS:
A narrative review of the current literature on central sensitisation and physiological studies in the functional somatic syndromes.

RESULTS:
Central sensitisation may be a common neurophysiological process that is able to explain non-painful as well as painful symptoms in these disorders. Furthermore, central sensitisation may represent an endophenotypic vulnerability to the development of these syndromes that potentially explains why they cluster together.

CONCLUSIONS:
Further research is needed to verify these findings, including prospective studies and the standardisation of combined methods of investigation in the study of central sensitisation in functional somatic syndromes. In turn, this may lead to new explanatory mechanisms and treatments being evaluated. Our conclusions add to the debate over the nomenclature of these syndromes but importantly also provide an explanation for our patients.

Copyright © 2015 Elsevier Inc. All rights reserved.

KEYWORDS:
Central sensitisation; Chronic pain; Functional somatic syndromes; Neurophysiology; Pathophysiology

PMID:

25598410

[PubMed - indexed for MEDLINE]
 

Dolphin

Senior Member
Messages
17,567
I am not a fan of such theories. I think it's too easy for them to say that patients' symptoms are not important: the body is sending them incorrect symptoms but there's nothing really wrong.

And I feel we now that ignoring symptoms is not a good strategy in ME/CFS.

Anyway, can't say I'm a fan of what is done in this paper. Having a large selection of illnesses allows them to find something to say to back up a point they want to make when it may not have relevance to the other illnesses. Sometimes I know that the research doesn't apply to other illnesses in the group
e.g.
Spinal sensitisation may follow the activation of nociceptive pathways by peripheral injury, such as that caused by trauma or inflammation, resulting in the release of substance P and pro-inflammatory cytokines[24]and the activation of spinal cord glial cells[25].
Increased levels of substance P have been found in Fibromyalgia but not CFS.
Pain. 1998 Nov;78(2):153-5.
Chronic fatigue syndrome differs from fibromyalgia. No evidence for elevated substance P levels in cerebrospinal fluid of patients with chronic fatigue syndrome.
Evengard B1, Nilsson CG, Lindh G, Lindquist L, Eneroth P, Fredrikson S, Terenius L, Henriksson KG.
Author information

Abstract
Levels of substance P were determined in the cerebrospinal fluid (CSF) in 15 patients with chronic fatigue syndrome (CFS). All values were within normal range. This is in contrast to fibromyalgia (FM). The majority of patients with FM have increased substance P values in the CSF. The results support the notion that FM and CFS are different disorders in spite of overlapping symptomatology.

PMID: 9839828 [PubMed - indexed for MEDLINE]
 

Dolphin

Senior Member
Messages
17,567
I thought it was interesting what happens with central sensitisation in migraine and osteoarthritis:

Central sensitisation as a vulnerability endophenotype for the functional somatic syndromes The component parts of CS have been demonstrated in the FSS (Table 2) and suggest that CS may represent an underlying vulnerable pathophysiology for FSS in general. By way of its effects on sleep, neuroendocrine axes and the ANS, CS may provide the physiological basis for symptoms other than pain in FSS. Furthermore, although further work is required in those that recover from FSS, CS in FSS appears to be a constant state. This is important, as CS has been demonstrated in other disorders, the pathophysiology of which has been more clearly defined. Two prominent examples are migraine and osteoarthritis [166,167]. As such, CS would not seem to be sufficiently specific to FSS. However, in both migraine and osteoarthritis, CS seems to be an induced and as such a temporary state. In migraine, 79% of sufferers have been reported to demonstrate allodynia, predominantly ipsilateral to the migrainous head pain during an attack, with no sufferers demonstrating allodynia between attacks[166]. As such, CS in migraine seems dependent upon the presence of active pathophysiology. In osteoarthritis, CS appears to return to a non-centrally sensitised state after successful surgical replacement of the affected joint and elimination of the osteoarthritis pain[167]. This would suggest that CS in osteoarthritis is an effect rather than a cause. Currently it is therefore unclear as to whether an‘over-processed’ input in the periphery is required for a centrally sensitised state to prevail. Data from osteoarthritis patients [167]might suggest that this is essential and that CS can be reversed with the removal of this input. However, in FSS it is potentially possible that normal pathways exist to the level of the brainstem (by way of example) and that it is the supraspinal networks that are dysfunctional, without the need for an over-processed peripheral input. In turn, this might allow for a concept of central augmentation of higher brain centres that is autonomous and independent of peripheral input—a central rather than peripheral over-processing. Further work is required in this area in order to elucidate the final contribution of supra versus subtentorial components to the experience of pain.
 

Dolphin

Senior Member
Messages
17,567
They try to link functional somatic syndromes with psychiatric disorders.
Comorbid psychiatric disorders and pain perception

Comorbid mood disorders are more likely in those with FSS compared to those without[111]. Susceptibility to major depressive disorder (MDD) and anxiety disorders is a known risk marker for the development of FSS[112]. The difficulty here is that a previous mood disorder may represent the risk of developing a FSS when accompanied by a comorbid mood disorder, rather than being specific for a FSS alone [113]. The risk might be related to abnormal central processing leading to both mood disorders and FSS. This would seem feasible, with their shared neuroanatomical and neurobiological substrates[114].

[111] Henningsen P, Zimmermann T, Sattel H. Medically unexplained physical symptoms, anxiety, and depression: a meta-analytic review. Psychosom Med 2003;65: 528–33.

[112] Goodwin L, White PD, Hotopf M, Stansfeld SA, Clark C. Psychopathology and physical activity as predictors of chronic fatigue syndrome in the 1958 British birth cohort: a replication study of the 1946 and 1970 birth cohorts. Ann Epidemiol
2011;21:343–50.

[113] Clark C, Goodwin L, Stansfeld SA, Hotopf M, White PD. Premorbid risk markers for chronic fatigue syndrome in the 1958 British birth cohort. Br J Psychiatry 2011;199: 323–9.

[114] Adler G, Gattaz WF. Pain perception threshold in major depression. Biol Psychiatry 1993;34:687–9.

Some comments: diagnosis of various functional somatic syndromes can be delayed for years. In the meantime, patients can be under stress and thus develop secondary psychiatric disorders or else there symptoms can be misinterpreted as psychiatric disorders.

Ref. 112 only applies to CFS and I don't think it shows what it claims to in this sentence.
 

duncan

Senior Member
Messages
2,240
Central sensitisation.

Never did sound very scientificky.

Sounds a little like a construct that helps explain away pain that is perceived not to have an ongoing cause, or perhaps more accurately, to have a cause that wouldn't trigger such a response level in 'normal' people.
 

Dolphin

Senior Member
Messages
17,567
Augmented responses to painful stimuli have been shown in several different FSS (see Table 2) and the concept of multimodality is evident in these conditions. For example, in both FM[44]and CFS[45], neuroimaging studies have shown increased neural recruitment (as demonstrated by increased regional activation) with cognitive tasks, reflecting a centrally mediated state of multimodal hyper-responsivity, whilst in FM, low thresholds to auditory tones correlate with pressure pain thresholds suggesting that these are in part due to a shared variance between pressure pain and auditory thresholds[46].

[45] Lange G, Steffener J, Cook DB, Bly BM, Christodoulou C, Liu WC, et al. Objective evidence of cognitive complaints in chronic fatigue syndrome: a BOLD fMRI study of verbal working memory. Neuroimage 2005;26:513–24.
Lange et al. is usually used as a sign that the brains of patients with CFS have to work harder to do the same level of cognitive tasks as others rather than what they say here.
 

Dolphin

Senior Member
Messages
17,567
Central sensitisation and risk factors for functional somatic syndromes

A variety of environmental and psychosocial factors are recognised as risks for FSS[82]. These include childhood adversity and personality traits as predisposing factors, and physical trauma and infections as triggers[83]. Any kind of early life adversity is more commonly reported in all the FSS[10,11,84], although this association may vary across FSS [85]. This predisposition may be governed by the effects of such events on the neuroendocrine stress axis[86], as demonstrated by the association between adverse childhood experiences with hypocortisolism in FSS and chronic pain[87,88]. HPA axis involvement has been implicated by nucleotide polymorphisms in sub-groups of CFS[89], which supports its role in predisposition or cause rather than effect of these disorders. Such a mechanism may affect the consequences of events experienced as an adult, such as a precipitating infection or other stressors. The biological mechanism involved appears related to centrally sensitising phenomena, with early adversity being associated with neuroendocrine sensitisation [87], limbic system hyper-responsiveness and reduced hippocampal volumes[90]. These may be governed by epigenetic changes[91,92]and not only confer susceptibility to infections or their immune response, but also to stress related illnesses such as affective disorders and the FSS[87,93].
The longitudinal studies in CFS have not consistently found that early life adversity is a risk factor.

Other types of studies can be affected by recall bias and similar biases (patients remembering things that also happened to other healthy people who don't recall them). Also, some of these types of studies e.g. the two Heim studies cited used the CDC's empiric criteria (Reeves et al., 2005).
 
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Kyla

ᴀɴɴɪᴇ ɢꜱᴀᴍᴩᴇʟ
Messages
721
Location
Canada
This paper looks to be a steaming pile of horse turds.

On the plus side it looks like the research and awareness has gotten to the point that they feel they can't just ignore it anymore. Instead they will apparently just cobble together a bunch of jargon-filled pseudoscience.

..and I'm sure osteoarthritis patients will be thrilled to find out their pain has been declared psychosomatic :confused:
 

Kati

Patient in training
Messages
5,497
Thank you so much for keeping track, @Dolphin and for explaining things.

Unfortunately Central sensitization is mentioned here at the local ME clinic, and the influence from UK is showing at different levels of governments as well in Canada when it comes to ME and FM.
 
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15,786
Do they get around to explaining the two-day CPET results in a central sensitization context? Or swollen lymph nodes? Or blood pressure & heart rate that might be pretty normal one week and really bad the following week?

Come on guys, don't hold back ... hypothesize how our supposedly overly sensitive CNS manages all of that :rolleyes:
 

Dolphin

Senior Member
Messages
17,567
Do they get around to explaining the two-day CPET results in a central sensitization context? Or swollen lymph nodes? Or blood pressure & heart rate that might be pretty normal one week and really bad the following week?

Come on guys, don't hold back ... hypothesize how our supposedly overly sensitive CNS manages all of that :rolleyes:
No, they don't mention any of that.
 
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30
I like how one can turn opinion into "research" simply by getting it published in a friendly journal....

Especially when it's the friendly Journal of Psychosomatic Research on whose editorial board sit several familiar names, including:

P.D. White
Queen Mary, University of London (QMUL), London, UK

M. Sharpe
Warneford Hospital, Headington, Oxford, UK

S. Wessely
King's College London, London, UK

:eek: http://www.journals.elsevier.com/journal-of-psychosomatic-research/editorial-board/
 
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jimells

Senior Member
Messages
2,009
Location
northern Maine
Especially when it's the friendly Journal of Psychosomatic Research on whose editorial board sit several familiar names, including:

:jaw-drop:

What a good find! These people truly are shameless and have no honor. When I am looking at PubMed articles and I see this journal name, I know the study is junk without even reading it. I wonder how many subscribers they have besides the Wessely School and medical libraries...

I also wonder if PD White "pal reviewed" his own study before he published it in his own journal.