Hello fellow members !
A handy document to reference to maybe?
3.1. No single specific cause of FMS has yet been identified. The absence of any peripheral pathology and the presence of widespread tissue hyperalgesia suggest a central mechanism for the syndrome rather than some pathological process in the muscles themselves. Patients with the condition experience allodynia, i.e. pain on normally painless (non-nociceptive) stimulus, such as touch or light pressure; another pointer to a central mechanism.
3.2. Abnormalities in sensory processing A number of investigators have found that while patients with FMS are not able to detect nociceptive stimuli at lower levels than normal subjects, (e.g. heat, electrical current, pressure), the threshold at which these stimuli induce a sensation of pain is lower. This observation is interpreted by some as being attributable to an abnormality in the normal pain-suppressing neural pathways between brain and spinal cord.4
3.3. Neuroendocrine aberrations Several studies have identified subtle abnormalities of the hypothalamic-pituitary-adrenal axis along with a loss of the normal rhythmic diurnal fluctuation in blood cortisol levels. Other evidence emerging from this line of enquiry includes low blood levels of serotonin relative to healthy controls, and unusually high levels of substance P (a peptide involved in the transmission of pain impulses) in the cerebrospinal fluid. Changes have also been noted in the growth hormone axis that suggest abnormal hypothalamic function. However these and other related anomalies have not led to greater understanding of the cause of the condition and their significance is not yet clear.5
3.4. Psychological factors Although some symptoms of FMS suggest a psychological component, careful studies have revealed no consistent relationship between the condition and psychological status. However in a number of studies an increased frequency of life stress has been found, accompanied in a significant proportion of patients by anxiety, low mood and poor coping skills. Most patients are not depressed and any onset of depression does not correlate with an alteration in the level of pain.6,7,8
3.5. Genetic factors A number of studies have suggested familial aggregation and so possibly an as yet unidentified genetic link.9
3.6. Sleep abnormalities One of the original proposals with regard to causation was that patients suffering from the syndrome exhibited abnormal alpha-wave activity on electro-encephalography during certain phases of sleep. However the specificity of this observation has been queried and its reproducibility and causal significance challenged.10,11
3.7. Other investigators have proposed that there may be impairment of the normal 24-hour
5 variability of heart rate, and postulate that excessive nocturnal sympathetic activity may result in non-restorative sleep and ensuing fatigue.12
3.8. However, although sleep abnormalities and morning fatigue are common in FMS, it is well-recognised that disrupted sleep, of whatever variety, and of whatever origin may result in muscle pain, fatigue and poor concentration.
3.9. Peripheral mechanisms A large number of investigators have attempted to identify abnormalities in the muscle tissue in FMS. However despite isolated abnormal findings no consistent relationships have been found.
3.10. Reactive or secondary fibromyalgia Fibromyalgia may arise insidiously and unheralded in an otherwise healthy individual, but in a proportion of cases there appears to be an initiating factor; for example a stressful event, or physical trauma, such as a whiplash injury or surgical operation. In some, there is a history of an influenza-like illness but immunological investigation in such patients has produced inconclusive or inconsistent results and there is at present no clear evidence that FMS is attributable to an infective process.
3.10.1. Trauma Between 14 and 23 per cent of patients with FMS associate the onset of their symptoms with physical trauma. However no convincing evidence has been produced that there is any consistent causative link between traumatic events and fibromyalgia.13,14,15
3.10.2. A number of studies suggest that patients with so-called reactive fibromyalgia have more perceived disability, self-reported pain and affective distress than those in whom no initiating event was identified.
3.10.3. There is however no single environmental exposure that is likely to trigger this illness. Instead, data from a wide variety of sources has led many investigators to conclude that when certain people who are genetically predisposed are exposed to any of a wide variety of stressors, including infections or other types of immune stimulation, drugs, physical trauma, infections or emotional stress – acute or chronic – they will develop a multisystem illness of this type. 6
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Emma 
FibroAction Administrator
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