Fibromyalgia
Just as he dismisses ME/CFS as a somatisation disorder, Professor Wessely likewise asserts that fibromyalgia (FM) also is a somatisation disorder - indeed, he asserts that it is the same somatisation disorder (Lancet 1999:354:936-939). He clearly believes this, but where is his evidence? There is none.
The scientific evidence, especially the more recent evidence, continues to mount and it does not support Professor Wessely's beliefs. He, however, rejects this substantial body of evidence that he is wrong.
The WHO classifies FM as a discrete disorder in ICD-10 at M79 under soft tissue disorders, not as a somatisation disorder.
The Mayo Clinic recently published "Fibromyalgia myths: The truth about 9 common myths", which stated "Fibromyalgia is a specific diagnosis" ( http://www.mayoclinic.com/health/fibromyalgia/AR00056 ).
Illustrations of research findings in FM include the following:
In 1997 it was shown that levels of somatomedin C are lower in FM patients (AL Bennett et al. J Psychiat Res 1997:31:1:91-96).
In 1998 researchers showed that levels of Substance P are elevated in FM patients (Evengaard B et al. Pain 1998:78:2:153-155). In 2003 it was shown that endothelin-1 is raised in FM patients (Pache M et al. Rheumatology 2003:42:493-494).
Research in 2005 indicated that FM is the result of internal biochemical imbalances that cause the physical symptoms (Co-Cure MED: 2nd January 2005: Fibromyalgia: new insights into a Misunderstood Ailment).
Different research in 2005 found elevated N(epsilon)-carboxymethyllysine levels in muscular tissue and in serum of patients with FM, with more intensive staining in the interstitial connective tissue of fibromyalgic muscles (Ruster M et al. Scand J Rheumatol 2005:34(6):460-463).
Again in 2005, more serious abnormalities were demonstrated by histologic studies particularly on electron microscopy, revealing disorganisation of Z bands and abnormalities in the number and shape of mitochondria: biochemical studies and P31 magnetic resonance spectroscopy showed inconstant abnormalities of ATP and phosphocreatine levels. The authors noted that "Mitochondrial abnormalities, reduced capillary circulation and thickened capillary endothelium may result in decreased availability of oxygen and impaired oxidative phosphorylation as well as ATP synthesis" and commented that these abnormalities do not seem to be the consequences of de-conditioning (Le Goff P. Joint Bone Spine 2005, November 9th).
In 2006, an important review in the Annals of the New York Academy of Sciences (Sarzi-Puttini P et al, Ann N Y Accad Sci 2006:1069:109-117) demonstrated orthostatic intolerance in FM, suggesting underlying abnormalities in cardiovascular neural regulation: "Research suggests that various components of the central nervous system are involved, including the HPA axis, pain-processing pathways, and the autonomic nervous system".
Again in 2006, research showed a greater prevalence of FM in HTLV-1 (human T cell lymphotrophic virus) infected individuals, suggesting that FM may be associated with this viral infection (Cruz BA et al: J Rheumatol: 2006:33(11):2300-2303).
In 2007, researchers at Yale University School of Medicine showed muscle hypoperfusion induced by regional vasomotor dysregulation in FM, noting that this vasoconstriction in muscle would lead to low-level ischaemia and its metabolic sequelae (Katz DL et al. Med Hypotheses 2007: March 19th).
More research into FM in 2007 demonstrated bladder symptomatology (Brand K et al. Clin Rheumatol 2007: May 3rd).
Further research in 2007 showed that autoimmune thyroiditis is present in an elevated percentage of FM patients and that patients with thyroid autoimmunity showed a higher percentage of dry eyes, burning or pain with urination, allodynia, blurred vision and sore throat (Bazzichi L et al. Clin Rheumatol 2007: May 9th).
In 2007, Bazzichi et al also showed evidence of abnormal levels of cytokines in FM: "The higher levels of cytokines found in FM patients suggest the presence of an inflammatory response system (IRS) and highlight a parallel between the clinical symptoms and biochemical data" (Clin Exp Rheumatol 2007:25(2):225-230). Another paper in 2007 revealed a conspicuous pattern of altered brain morphology, suggesting that FM is associated with structural changes in the central nervous system of patients (Schmidt-Wilcke T et al. Pain: 2007: June 21st).
In January 2008 researchers provided compelling evidence of a demyelinating polyneuropathy in FM, with electrodiagnostic (EDX) evidence of both polyneuropathy and demyelination. The authors concluded that 33% of FM patients have clinical and EDX findings of chronic inflammatory demyelinating polyneuropathy / CIDP. (Caro XJ et al. Rheumatology (Oxford) 2008:47(2):208-211).
In February 2008 researchers from McGill University, Montreal, Canada, presented evidence that "neurotransmitter studies show that FM patients have abnormalities in dopaminergic, opioidergic, and serotonergic systems" and that "studies of brain anatomy show structural differences between the brains of FM patients and healthy individuals" (Schweinhardt P et al. Neuroscientist 2008: February 12th).
Also in 2008, in a blinded study, skin biopsy samples showed electron microscopic evidence of unusual patterns of unmyelinated nerve fibres as well as associated Schwann cells, which the researchers considered may contribute to the lower pain threshold seen in FM patients (Kim SH et al. Clin Rheumatol 2008:27(3):407-411).
In a study published in March 2008, US researchers noted that previously, functional magnetic resonance imaging (fMRI) had shown that the insula displays augmented activity in FM, which means that neurons in FM patients are more active in this part of the brain. This linked to their own findings that pain decreased when levels of the brain molecule glutamate went down, glutamate being a neurotransmitter that conveys information between neurons in the nervous system (Clauw D et al. Arthritis and Rheumatism 2008:58:3).
Such research findings cannot rationally be dismissed, yet Wessely et al still insist that fibromyalgia is a somatisation disorder and they have deliberately included FM patients in the Medical Research Council's behavioural intervention trials on patients with "CFS/ME" in which "Wessely School" psychiatrists are the investigators, a diagnostic inaccuracy that would seem to make a mockery of the MRC's claim that it funds only studies of the highest scientific calibre, especially as in July 2004 a Minister of State (Dr Stephen Ladyman MP) made it known at a House of Commons All Party Parliamentary Group on FM that doctors were to be offered financial incentives to persuade patients with fibromyalgia to enter these MRC trials.
...
It cannot have been overlooked by Wessely et al that the work of Dr Jonathan Kerr of St Georges, London, has linked ME/CFS to OPs (J Clin Path 2005:58:826-832). Kerr et al suggest that patients with (ME)CFS "have reproducible alterations in gene regulation", noting that "sixteen genes were confirmed as having an expression profile associated with (ME)CFS. These genes can be grouped according to immune, neuronal, mitochondrial and other functions. These findings are consistent with previous work showing that patients with (ME)CFS have evidence of immune activation, such as increased number of activated T cells and cytotoxic T cells, and raised circulating cytokine concentrations. NTE (neuropathy target esterase) is a target for organophosphates and chemical warfare agents, both of which may precipitate (ME)CFS. EIF2B4 is a mitochondrial translation initiation factor and one of the EIFB2 family, within which mutations have been shown to be associated with central nervous system hypomyelination and encephalopathy. The involvement of genes from several disparate pathways suggests a complex pathogenesis involving T cell activation and abnormalities of neuronal and mitochondrial function, and suggests possible molecular bases for the recognised contributions of organophosphate exposure and virus infection".
In his subsequent paper referred to above (J Clin Pathol 2007), Kerr stated: "We have previously documented upregulation of NTE in (ME)CFS. NTE is the primary site of action of organophosphate (OP) compounds. Exposure to OP compounds may trigger CFS/ME and Gulf War Illness".
...
It is a matter of note that the 1996 findings of neurologist Professor Peter Behan from the University of Glasgow linking ME/CFS to chronic low-dose OP exposure were excluded from the Report of the Royal Colleges, given that Behan found ME/CFS to be clinically identical to chronic low-dose OP exposure and that such OP exposure "in some way prepared the patients for the later development of (ME)CFS". Behan reported that the abnormalities found in both ME/CFS and in OP poisoning were "compatible with a decreased responsiveness of CNS type II glucocorticoid receptors, (confirming) the hypothesis of brain steroid receptor resistance in patients with the delayed response to OPs and in (ME)CFS" (J Nutrition & Environmental Medicine 1996:6:341-350).
...
In ME/CFS specifically, there is evidence that the disorder is accompanied by an increased transloctaion of endotoxins of gram-negative enterobacteria through the gut wall, with signs of activation of the inflammatory response system and IgG3 subclass deficiency (Maes M et al. Neuro Endocrinol Lett 2007:28:6).
Clearly, the out-dated hypothesis that IBS is a psychosomatic disorder has been abandoned by those who fulfil their contractual obligations to keep up-to-date with medical science, yet Professor Wessely et al seem unaware of this progress in medicine.
No comments:
Post a Comment