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*O* Myalgic Encephalomyelitis vs Fibromyalgia by Jodi Bassett
Do M.E. and Fibromyalgia really have as much in common as some people claim? The reality is that the similarities between the two illnesses are minimal and superficial at best but their differences are truly profound. Even if they do share one or two symptoms is this really significant when in so many much more important ways they are so VERY different and have so very little in common? The idea of these two very different patient groups being mixed up and treated as if they represented the exact same patient group is utterly terrifying, the results could only be disastrous for all concerned.
Fibromyalgia and Myalgic Encephalomyelitis are distinct and unique illnesses and it is vitally important that they are always seen that way for the benefit of all patients involved.
Similar lists could also be created to show the differences between Myalgic Encephalomyelitis and; Lupus, Lyme disease, multiple sclerosis or Gulf War Syndrome. Although M.E. does have far more in common with all of these illnesses than with Fibromyalgia, these illness are all (more significantly) unique and distinct illnesses with different symptoms, core characteristics, aetiology’s, and pathologies which it would be equally unwise (and unscientific) to treat as if they represented the same illness.
It is only due to the flawed Fukada and other CFS criteria that these illnesses are falsely claimed to be almost interchangeable. But these criteria do not describe M.E., or any other distinct illness and are virtually meaningless.
What follows is a brief selection of some of the many research studies and articles which show that despite sharing some symptoms, ME and Fibromyalgia (and Gulf War Illness and many others) are undoubtedly, separate illnesses.
Smoke and Mirrors by Jodi Bassett
This paper looks at the lack of evidence (and financial and political motivations) behind the 'behavioural' model of M.E. and outlines a strategy for the resolution of the confusion caused by the 'CFS' disease category
'The disease category ‘CFS’ must be abandoned completely
Patients with fatigue (and other symptoms) caused by a variety of different illnesses need to be diagnosed correctly with these illnesses if they are to have any chance of recovery; not given a meaningless Oxford or Fukuda ‘CFS’ misdiagnosis. (Some of the conditions commonly misdiagnosed as ‘CFS’ are very well defined and well-known illnesses and very treatable – but ONLY once they have been correctly diagnosed). Patients with M.E. need this same opportunity. Each of the patient groups involved must be correctly diagnosed and then treated as appropriate based on legitimate and unbiased science involving the SAME patient group. Dr Byron Hyde MD explains that doctors must return to the age-old medical principals of correct diagnosis (a) careful history, (b) detailed physical examination and (c) appropriate investigation. (2006, [Online])
The name Myalgic Encephalomyelitis must be fully restored (to the exclusion of all others) and the WHO classification of M.E. must be accepted and adhered to in all official documentations and government policy. There were sound medical reasons for the creation of the name in 1956, and for the classification of the illness by the WHO in 1969; neither of which has changed in the interim. Professor Malcolm Hooper explains: The term myalgic encephalomyelitis (means muscle pain, my-algic, with inflammation of the brain and spinal cord, encephalo-myel-itis, brain spinal cord inflammation) was first coined by Ramsay and Richardson and has been included by the World Health Organisation (WHO) in their International Classification of Diseases (ICD), since 1969. The currently version ICD-10 lists ME under G.93.3 - neurological conditions. It cannot be emphasised too strongly that this recognition emerged from meticulous clinical observation and examination. (Hooper 2006, [online])'
The effects of CBT and GET on patients with Myalgic Encephalomyelitis by Jodi Bassett
'As (bad) luck would have it, graded exercise programs are probably the single most inappropriate treatment that a M.E. sufferer could be recommended to undertake. This is because one of the unique features of authentic M.E. is exercise intolerance – that patients worsen with even trivial levels of activity or exercise.
Exercise or exertion intolerance is one of the many things which separates Myalgic Encephalomyelitis so distinctly from various post-viral fatigue states or other illnesses involving 'chronic fatigue' as the defining or primary feature. People with M.E. do not improve with exercise. They cannot; exercise intolerance is a large and essential part of what M.E. is. Veteran M.E. expert Dr Ramsay explained that this unique characteristic: ‘is virtually a sheet-anchor in the diagnosis of Myalgic Encephalomyelitis and without it a diagnosis should not be made.’ (1986, [Online]).
This essential feature of M.E. is characterised by a unique form of paralytic muscle weakness whereby muscles perform normally to begin with but after even a minor degree of physical effort; three, four or five days, or longer, elapse before full muscle power is restored. This is quite distinct from the ‘chronic fatigue’ seen in many other illnesses. This paralytic muscle weakness in M.E. affects all muscles including the heart and causes what is commonly known as exercise intolerance; that patients relapse with physical and mental exertion. These features are a core part of what M.E. is as they are responsible for causing much of the symptomatology and disability associated with the illness. (Ramsay 1986, [Online]) (Hyde 2003, [Online]) (Hyde 1992 p. xi) (Hyde & Jain 1992 pp. 38 - 43) (Dowsett 2001, 2000, 1999.b, b [Online])
Doctors who have experience with M.E. (and can tell the difference between authentic M.E. and various unrelated fatigue states) and the leading M.E. experts all concur; exercise can have many harmful effects on patients both in the short- and long-term.'
This unique symptom is ONLY seen in M.E. patients.
*O*O* A New and Simple Definition of Myalgic Encephalomyelitis and a New Simple Definition of Chronic Fatigue Syndrome & A Brief History of Myalgic Encephalomyelitis & An Irreverent History of Chronic Fatigue Syndrome by Dr Byron Hyde MD (an extract, PDF format)
‘Do not for one minute believe that CFS is simply another name for Myalgic Encephalomyelitis (M.E.). It is not. Though CFS is based upon a typical M.E. epidemic, in my opinion it has always been a confused and distorted view of reality. The invention of Chronic Fatigue Syndrome has to be one of the most curious cases of inventive American scientific imperialism that one could imagine. It is my opinion that the CDC 1988 definition of CFS describes a non-existing chimera based upon inexperienced individuals who lack any historical knowledge of this disease process. The CDC definition is not a disease process.’
*HIGHLY RECOMMENDED*
*O* Information on Myalgic Encephalomyelitis (M.E.)/Chronic Fatigue Syndrome (CFS) by Jill McLaughlin
ME/CFS is similar to other illnesses such as multiple sclerosis, lupus, Lyme disease, mononucleosis, Gulf War Syndrome. CFS may overlap or co-exist with fibromyalgia, multiple chemical sensitivities, irritable bowel syndrome.
However, these may co-exist with other conditions as well and are viewed as separate entities which stand on their own, regardless of whether a person has other medical problems. Even though there are similarities or overlap does not mean that they represent the same etiological or pathobiological process.
*O* SCIENCE or SEMANTICS? By Margaret Williams
"In spite of some overlap, FM and ME/CFS do not represent the same syndrome."
*O* Dr Paul Cheney on heart issues and ME/ICD-CFS
'Next, the NJ team looked to see if there were any symptoms that were 100% observable in the group of disabled cases, but not in the others. They found that there was only one symptom (among the loooong list of CFIDS symptoms) that was seen in 100% of the patients with the Q problem. Only one. Post-exertional [illness exacerbation and realpse]. That is, when you push yourself physically, you get worse.
What distinguishes CFIDS from FM? Post-exertional [illness exacerbation and realpse]. Patients who have FM, but not CFIDS, can exercise—it helps them. FM patients do not have a Q problem. MCS patients do not have a Q problem. They do have other issues that overlap with CFIDS. However, Q is what separates them. CFIDS patients have a big Q problem, and post-exertional [illness exacerbation and realpse] is the one symptom that correlates with Q.
ME/CFS can be distinguished from FMS patients by the confirmed breakdown of one of the body's antiviral defense pathways. It is interesting that if a patient meets both the criteria for ME/CFS and FMS, her/his test results will be that of an ME/CFS patient.
While approximately 75% of ME/CFS patients also meet the criteria for FMS, only a relatively small number of FMS patient meet the criteria for ME/CFS. This is reflected in the much higher prevelance of FMS. Appoximately 422 per 100,000 or 0.42% of adults meet the criteria for ME/CFS, whereas 3 - 10 % (depending on the study) of the adult population have FMS.
Dr Darrel Ho-Yen of Scotland, (a well respected M.E. researcher and virologist) was published in the British Medical Journal in 1994:
The distribution and number of tender points in fibromyalgia are different from the chronic fatigue syndrome, and the management of the two conditions is different. Patients with (ME/CFS) should be advised not to increase their activities gradually until they feel 80% of normal, whereas patients with fibromyalgia may benefit from a regime of increasing activity. (BMJ 1994:309:1515).
Myalgic Encephalomyelitis / Chronic Fatigue Syndrome and Fibromyalgia:additional considerations for the MRC in relation to the PACE trials by Margaret Williams, 5th January 2005
Of foremost significance is the fact that fibromyalgia is classified as a distinct entity in ICD-10 at section M79.0 under Soft Tissue Disorders and it is not permitted for the same condition to be classified to more than one rubric, since ICD categories are mutually exclusive. The literature itself is quite clear about this distinction, stating that up to 70% of those with ME/CFS have concurrent FM, and those who have both FM and ME/CFS have worse physical functioning than those who have ME/CFS alone.
Some illustrations from the literature make these distinctions clear:
1991: in spite of some overlap, FM and ME/CFS do not represent the same syndrome. (Primary fibromyalgia and the chronic fatigue syndrome. AJ Wysenbeek et al Rheumatology Int 1991:10:227-229)
1996: “fibromyalgia appears to represent an additional burden of suffering amongst those with (ME)CFS” (Fibromyalgia and Chronic Fatigue Syndrome – similarities and differences. Dedra Buchwald and Deborah Garrity. Rheum Dis Clin N Am 1996:22:2:219-243)
1997: levels of somatomedin C are lower in FM patients but higher in ME/CFS patients (Somatomedin C (insulin-like growth factor) levels in patients with CFS. AL Bennett, AL Komaroff et al. J psychiat Res 1997:31:1:91-96)
1998: “recent studies suggest that (co-existent FM and (ME)CFS) may bode much more poorly for clinical outcome than CFS alone. In contrast to (significantly) elevated CBG (cortisol binding globulin) levels in patients with CFS, no differences were observed in FM patients. Differences in secretion of AVP may explain the divergence of HPA axis function in FM and (ME)CFS” (Evidence for and Pathophysiologic Implications of HPA Axis Dysregulation in FM and CFS. Mark A Demitrack and Leslie J Crofford. Ann New York Acad Sci 1998:840:684-697)
1998: there is no evidence for elevated Substance P in patients with ME/CFS, whereas levels are elevated in patients with FM (CFS differs from FM. No evidence for altered Substance P in cerebrospinal fluid of patients with CFS. Evengaard B et al Pain 1998:78:2:153-155)
2001: patients with FM are *NOT* acetylcholine sensitive (Investigation of cutaneous microvascular activity and flare response in patients with fibromyalgia. AW Al-Allaf, F Khan, J Moreland, JJF Belch. Rheumatology 2001:40:1097-1101)
2004: patients with ME/CFS *ARE* acetylcholine sensitive (Acetlycholine mediated vasodilatation in the microcirculation of patients with chronic fatigue syndrome. VA Spence, F Khan, G Kennedy, NC Abbot, JJF Belch Prostaglandins, Leukotrienes and Essential Fatty Acids 2004:70:403-407)
2003: endothelin-1 is *RAISED* in fibromyalgia (Increased plasma endothelin-1 in fibromyalgia syndrome. Pache M, Ochs J et al Rheumatology 2003:42:493-494)
2004: endothelin-1 is *NORMAL* in ME/CFS (Plasma endothelin-1 levels in chronic fatigue syndrome. Kennedy G, Spence V, Khan F, Belch JJF Rheumatology 2004:43:252-253)
Consultant rheumatologists who have sufficient experience with both syndromes have observed clinically that in FM, the muscle pain is helped by gentle stretching and exercise, whereas in ME/CFS, exercise makes muscle pain worse.
No evidence for elevated Substance P levels in cerebrospinal fluid of patients with CFS
Background: Substance P (SP) is a neuropeptide involved in the neurotransmission of pain from periphery to the central nervous system. It has been reported that SP in the cerebrospinal fluid is markedly elevated in patients with Fibromyalgia. As Fibromyalgia and CFS are conditions which share some symptoms, we wanted to investigate the levels of SP in the cerebrospinal fluid of CFS patients. Methods: Cerebrospinal fluid was obtained from 15 patients (9 women, average age 39.3 years) fulfilling CDC-criteria for CFS but not for Fibromyalgia. The sample was immediately centrifuged at +4°C for 10 min. at 1000g to remove cells. Rapid cooling was performed. The sample was stored in plastic cryogenic tubes and stored frozen at -70°C. An radioimmunoassay was used to analyze the sample. For comparison, cerebrospinal fluid drawn from 13 patients with cerebrovascular disease (7 women, average age 65 years) was treated and analyzed in the same manner. All samples were analyzed blindly. Results: All values of SP of the CFS patients were within previously reported normal range of SP in cerebrospinal fluid. In the control group, 2 patients had slightly increased values. Conclusion: The results support the notion that FM and CFS are different disorders in spite of overlapping symptomatology.
Specific oxidative alterations in vastus lateralis muscle of CFS patients Fulle S, Mecocci P, Fano G, Vecchiet I, Vecchini A, Racciotti D, Cherubini A, Pizzigallo E, Vecchiet L, Senin U, Beal MF Free Radic Biol Med 2000 Dec 15;29(12):1252-1259 Lab. Interuniversitario di Miologia, Dip. Biologia Cellulare e Molecolare, Universita di Perugia, Perugia, Italy
Although a specific defect in muscle metabolism has not been clearly defined, yet several studies report altered oxidative metabolism. In this study, we detected oxidative damage to DNA and lipids in muscle specimens of CFS patients as compared to age-matched controls, as well as increased activity of the antioxidant enzymes catalase, glutathione peroxidase, and transferase, and increases in total glutathione plasma levels.
From these results we hypothesize that in CFS there is oxidative stress in muscle, which results in an increase in antioxidant defenses. Furthermore, in muscle membranes, fluidity and fatty acid composition are significantly different in specimens from CFS patients as compared to controls and to patients suffering from fibromyalgia.
These data support an organic origin of CFS, in which muscle suffers oxidative damage.
Peripheral cholinergic function in humans with chronic fatigue syndrome, Gulf War syndrome and with illness following organophosphate exposure Khan F, Kennedy G, Spence VA, Newton DJ and Belch JJF Vascular Diseases Research Unit, The Institute of Cardiovascular Research, University of Dundee
Aims: In the present study, we have investigated whether the peripheral cholinergic abnormalities that we have reported previously [Spence et al. Am J Med 2000; 108: 736–9] in patients with chronic fatigue syndrome (CFS) are also present in those with Gulf War syndrome (GWS) and agricultural workers exposed to organophosphate pesticides, where cholinesterase inhibition is specifically implicated. We also looked at whether these abnormalities might be due to a reduction in the activity of cholinesterase expressed on the vascular endothelium. Methods and Results: We used laser Doppler imaging to measure the forearm skin blood flow responses to iontophoresis of acetylcholine and of methacholine (which is resistant to breakdown by cholinesterase) in patients with CFS, GWS and those with a history of ill health after definite organophosphate exposure, as well as in matched healthy controls. The response to acetylcholine was significantly higher in patients with CFS than in controls (P=0.029, repeated-measures ANOVA), but was normal in those with GWS and those exposed to organophosphates. The methacholine response was higher than the acetylcholine response in all patient groups except for those with CFS, where there was no difference between the responses. Conclusions: Although there are many clinical similarities between these three illnesses, our results indicate peripheral cholinergic abnormalities in the vascular endothelium of only patients with CFS, suggesting that this syndrome has a different aetiology, which might involve inhibition of vascular cholinesterase.
Cardiovascular response to upright tilt in fibromyalgia differs from that in chronic fatigue syndrome. Naschitz JE, Rozenbaum M, Rosner I, Sabo E, Priselac RM, Shaviv N, Ahdoot A, Ahdoot M, Gaitini L, Eldar S, Yeshurun D. Departments of Internal Medicine A, Rheumatology, Anesthesiology, and Surgery, Bnai Zion Medical Center and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
OBJECTIVE: To compare the cardiovascular response during postural challenge of patients with fibromyalgia (FM) to those with chronic fatigue syndrome (CFS). METHODS: Age and sex matched patients were studied, 38 with FM, 30 with CFS, and 37 healthy subjects. Blood pressure (BP) and heart rate (HR) were recorded during 10 min of recumbence and 30 min of head-up tilt. Differences between successive BP values and the last recumbent BP, their average, and standard deviation (SD) were calculated. Time curves of BP differences were analyzed by computer and their outline ratios (OR) and fractal dimensions (FD) were measured. HR differences were determined similarly. Based on the latter measurements, each subject's discriminant score (DS) was computed. RESULTS: For patients and controls average DS values were: FM: -3.68 (SD 2.7), CFS: 3.72 (SD 5.02), and healthy controls: -4.62 (SD 2.24). DS values differed significantly between FM and CFS (p < 0.0001). Subgroups of FM patients with and without fatigue had comparable DS values. CONCLUSION: The DS confers numerical expression to the cardiovascular response during postural challenge. DS values in FM were significantly different from DS in CFS, suggesting that homeostatic responses in FM and CFS are dissimilar. This observation challenges the hypothesis that FM and CFS share a common derangement of the stress-response system.
Somatomedin C (insulin-like growth factor I) levels in patients with chronic fatigue syndrome. Bennett AL, Mayes DM, Fagioli LR, Guerriero R, Komaroff AL. Journal of Psychiatric Research 1997; 31(1): 91-96.
Abstract: Chronic fatigue syndrome is a disorder clinically quite similar to fibromyalgia syndrome, and it is of interest to examine if these two syndromes have pathogenetic as well as clinical features in common. Somatomedin C levels have been found to be lower in patients with fibromyalgia syndrome than in healthy controls. An attractive hypothesis relating sleep disturbance, altered somatotropic neuroendocrine function and fibromyalgia symptoms has been put forward as a plausible pathogenic mechanism for fibromyalgia syndrome. We therefore sought to investigate the level of somatomedin C in patients with chronic fatigue syndrome. Somatomedin C levels were determined by radioimmunoassay in frozen serum specimens from 49 patients with CFS and 30 healthy blood donor control subjects of similar age and gender. Somatomedin C levels were higher in patients with CFS than in healthy control subjects (255.3 ± 68.5 vs 211.9 ± 76.2, P = 0.01). There was no effect of gender, use of nonsteroidal anti-inflammatory drugs or tricyclic drugs on levels of somatomedin C. There was a tendency for somatomedin C levels to fall with age. In contrast to patients with fibromyalgia, in whom levels of somatomedin C have been found to be reduced, levels in patients with CFS were found to be elevated. Thus, despite the clinical similarities between these two conditions, they may be associated with different abnormalities of sleep and/or of the somatotropic neuroendocrine axis.
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