Evidence from:
A.Hakkinen et al. Annals of Rheumatic Disease (2001) Vol. 60 #1, p. 21.
Muscle strength training works just as well for FM as for health people. This very small study shows that people with FM may have completely normal muscle health. If so, some other cause must be sought.
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Evidence from:
R.Kwaitek et al. Arthritis and Rheumatism (Dec 2000) Vol. 43 #12.
Small reductions in blood flow were detected in the thalamus of the Fibromyalgia cases. These were not sufficiently distinct to be diagnostic.
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Evidence from:
V.Hadhazy et al. Journal of Rheumatology (2000) Vol.27 p.2911.
Strenuous exercise improves quality of life for FM cases. But doesn’t cure FM. The suggestion is that there is no organic disease sufficient to negate the effects of fitness improvement.
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Evidence from:
Fibromyalgia Conference. Bristol 15th – 17th May 2001
Much of the medico legal interest in FM arises in connection with mechanical injury events, in particular; whiplash events. So-called ‘reactive’ FM was the intended focus of this conference, though much of what could be learnt from the conference would also be applicable to those medical histories that include no trauma.
It is scientifically unsatisfactory in the case of a subjective condition for causation to be based solely on temporality.
Symptom syndromes do not easily fit with the pathology based medical model.
It is claimed that CNS sensitisation or “wind-up” should occur within hours or days of the initiating event. Proponents of this model of pathogeneses find it difficult to explain delayed FM (i.e. FM that manifests months after the alleged causative event).
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Evidence from:
JE Naschitz et al. Journal of Rheumatology. June (2001) Vol. 28 #6 p 1356.
FM, chronic fatigue syndrome and healthy controls were compared. Blood pressure effects were the same in FM and controls. Pain free CFS cases were distinct from both.
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Evidence from:
J Elert et al. Journal of Rheumatology. June (2001) Vol. 28 #6 p 1361.
FM, chronic WAD and healthy controls were compared. Disease cases tended to have slightly increased resting muscle tension and significantly slower recruitment.
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Evidence from:
AM Mengshoel et al. Journal of Rheumatology. September (2001) Vol. 28 #9 p 2085.
18 years after diagnosis with FM, 79% were still diagnosable but had not deteriorated. This adds strength to the view that when FM occurs it was essentially a flip into a new normal state, timing of flip essentially arbitrary.
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Evidence from:
N Galeotti et al. Journal of Rheumatology. October (2001) Vol. 28 #10 p 2298.
Lymphocytes were extracted from blood samples from 17 healthy normal controls, 19 cases of severe FM, and 12 cases with diagnosable chronic pain states e.g. arthritis or carpal tunnel syndrome.
Proteins known as Gi proteins were found to be hypofunctional (i.e. their effect was under-active) in FM but not in the other two groups.
Comment
A possible genetic vulnerability factor.
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Evidence from:
AW Al-Allaf et al. Rheumatology. October (2001) Vol.40 #10 p 1097.
15 FM cases 15 age and sex matched healthy normal controls took part.
No differences were found in either; cutaneous vascular response or, flare response.
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