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1. Initially it was thought to be an inflammatory condition. When no evidence of inflammation could be found and an association was noted with depression and stress, the concept of "psychogenic rheumatism" 11 was advanced, but a number of studies have established that Fibromyalgia is neither a psychosomatic nor somatiform disorder and that when present, anxiety and depression are more likely to be the result than the cause of Fibromyalgia.

2. Microtrauma to the muscle leading to development of trigger points & muscle spasm is another hypothesis which may explain Myofascial pain but not fibromyalgia.

3. There is already evidence of a strong familial pattern in many cases of FM, with fibromyalgia often following the female side of the family. Exciting new genetic studies are now underway to investigate genetics and fibromyalgia.

4. Fibromyalgia is actually a CNS myalgia which is the result of central sensitization. Decreased CNS serotonin, increased SubP, increased nerve growth factor supports it & many features of fibromyalgia can be explained by this theory. But some has questioned that central sensitization may be secondary to other effect.

5. Fibromyalgia may be due to non-restorative deep sleep. Patients often report insomnia or light sleep as well as an increase in symptoms after disturbed sleep. Abnormal amounts of alpha activity on the electroencephalogram of during deep sleep have been reported. Fibromyalgia-like symptoms can be induced in normal volunteers by depriving them of deep sleep. 12

6. Cellular function is deranged due to less production of ATP. This reduction may be due excessive accumulation of phosphate which is not cleared due to faulty excretion in fibromyalgia. ATP is required in sufficient amount to clear intracellular Ca following muscle contraction. These leads to sustained muscle contraction found in Fibromyalgia. Less than normal ATP explains other symptoms of fibromyalgia like fatigue & other CNS changes.

With all these discussion we can easily understand that there is no single clear pathophysiological explanation which can explain all clinical & biochemical abnormality. This is the reason behind of so many hypotheses. But based on present knowledge we may draw the following conclusions.

� Fibromyalgia is a systemic disease and Myofascial Pain Syndrome is a localized problem. In both condition there is muscle tenderness (called trigger points/tender points) which is more pronounced and widespread in fibromyalgia.

� On muscle biopsy no abnormality is found except for low ATP levels.

� In Fibromyalgia central sensitization is the key feature responsible for persistence of pain which makes it difficult to treat.

� Fibromyalgia is triggered and unmasked by stressful events.

TREATMENT OPTIONS:

1. If trigger points develop secondary to other known conditions, it must be treated adequately.

2. Neutralization /Inactivation of trigger points with local anaesthetic drugs/steroids/ etc. or even by dry needling may be done which gives very good results. It can be done with laser also.

3. Drugs acting on central sensitization should be taken. It is particularly important for fibromyalgia. Drugs commonly prescribed are antidepressants (e.g. Amitryptilin, duloxetine etc.) & anticonvulsants (e.g. gabapentine, pregabalone etc.)

4. Analgesics like Tramadol, NSAIDs, paracetamol etc. Combination of Tramadol & Paracetamol have important role as these drugs acts on central sensitization.

5. Different muscle relaxants.

6. Different form of physiotherapy.



REFERENCES:

1. Wolfe F. The epidemiology of fibromyalgia. J Musculoskel Pain 1(3/4):137, 1993.

2. Frederick Wolfe, M.D., et al., "The American College of Rheumatology 1990 Criteria for the Classification of Fibromyalgia: Report of a Multicenter Criteria Committee," Arthritis & Rheumatism,33, No. 2,160-172,1990.

3. D. Buskila, M.D., et al., "Increased Rates of Fibromyalgia Following Cervical Spine Injury: A Controlled Study of 161 Cases of Traumatic Injury," Arthritis & Rheumatism, 40, No. 3, 446-52,1997.

4. Stuart Donaldson, Ph.D., et al., �Fibromyalgia: A Retrospective Study of 252 Consecutive Referrals,� Canadian Journal of Clinical Medicine, 5, 6, 1998.

5. I. Jon Russell, M.D., Ph.D., et al., "Elevated Cerebrospinal Fluid Levels of Substance P in Patients with the Fibromyalgia Syndrome," Arthritis & Rheumatism,37, No. 11, 1593-1601,1994.

6. "Cerebrospinal Fluid (CSF) Substance P (SP) in Fibromyalgia (FM): Changes in CSP SP Over Time, Parallel Changes in Clinical Activity," Arthritis & Rheumatism, Abstract Supplement,41, #9, 1998.

7. Russell IJ. Neurochemical pathogenesis of fibromyalgia syndrome. J Musculoskel Pain 4(1/2):61-92, 1996.

8. Leslie J. Crofford, M.D., et al, "Neurohormonal Perturbations in Fibromyalgia," Baillieres Clin Rheumatology, Vol. 10, No. 2, May 1996, pp. 365-78.

9. Leslie J. Crofford, M.D., "The Hypothalamic-Pituitary-Adrenal Stress Axis in the Fibromyalgia Syndrome," Journal of Musculoskeletal Pain, The Haworth Press, Vol. 4, No. 1/2, 1996.

10. Boland EW. Psychogenic rheumatism: the musculoskeletal expression of psychoneurosis. Ann Rheum Dis 6:195, 1947.

11. Moldofsky HD. A chronobiologic theory of fibromyalgia. J Musculoskel Pain 1(3/4):49, 1993.

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