Fibromyalgia: Is it real?

1. Fibromyalgia: Is it real? Melissa Tucker Gilbert Boissonneault March 24, 2006

2. Outline of objectives • What is Fibromyalgia? • Speculated mechanisms of actions • Current treatment • How does it effect us as practionars

3. What is Fibromyalgia? • A syndrome characterized by: • Chronic, widespread musculoskeletal pain • Pain on palpation in 11 of the 18 tender points • Pain must last longer than 3 months • Not associated with arthritis, inflammation, or degenerative disorders

4. What is Fibromyalgia? • Commonly associated symptoms include sleep disturbances, anxiety, depression, headaches, and IBS. • Onset usually following an injury, infection, stress, or emotional trauma • Affects women between 30-60 years of age.

5. How does FM effect the body? • Pain isn’t releated to actual tissue damage • Beyond this there are no known causes • Studies concentrate on • Serotonin dysfunctions • Hypothalamic-pituitary-adrenal axis • Hypothalamic-pituitary-thyroid axis • Growth hormone • Neuromediators

6. Serotonin’s Role • 5-HT is speculated to have lower levels in the serum in FM patients • Inhibits the pathways that control sensations and excite the pathways that are involved in muscle control

7. Hypothalamic-pituitary-adrenal Axis • Help explain the fatigue, sleep disturbances and pain components • Buskila’s (2001) idea is that there is an exaggerated adrenocoricotropin hormone response to corticotropin releasing hormone. • HPA axis to CRH found in the FM patients closely resembles that seen in psychiatric disorders especially those with anxious depression.

8. Hypothalamus-pituitary-thryoid axis • Coincidence of FM with Hashimoto thyroiditis similarities, sensitivity to cold, low blood pressure and constipation • Research found basal TSH and thyroid hormone levels, with the exception of free thyroxine, were all in the low-normal range, and the secretion of free T4 in response to TRH was poor • thyroid hormone dysfunctions can also contribute to depression in FM

9. Growth Hormone • Controlled by GH-releasing hormone and somatostain • A significantly lower secretion of GH in FM patients was found • Pulsatile secretion of GH is closely releated to stage 4 sleep in which almost 80% of its daily production is secreted

10. Endorphins, Enkephalins and Neuromodulators • Act as receptor sites for opiate drugs, which play an important role in regulating pain • Hyperalgesia of FM patients could be explained by lowered endorphin levels • Descending pathways selectively inhibit the transmission of information originating in nociceptors and release certain endogenous opioids. • These endogenous opiates respond to a variety of stressful situations

11. Cytokines • In the immune system cells release a substantial amount of protein messengers that regulate host cell division and function of the immune defenses • In response to trauma, inflammation, or infection immune cells release proinflammatory cytokines • proinflammatory cytokines provide signals to the central nervous system thereby creating exaggerated pain as well as a number of physiologic, behavioral, and hormonal changes • Cytokine signaling could correspond to a vital means of interlinking the chronic pain of FM to the relevance of stressors

12. Pharmacologic • First approach is with an anitdepressent, commonly amitriptyline or fluoxetine. • Muscle relaxants show some assistance in the management of FM, cyclobenzaprine • Other classes of drugs used are NSAIDs and analgesics

13. Nonpharmacologic Therapies • Physical therapy include stretching, deep tissue massage, transcutaneous electrical nerve stimulation • Acupuncture showed short term benefit • Low impact exercise such as Yoga • Chiropractic manipulation

15. References • Anderberg, U., Lui Z., Bergland L., Nyberg F. Elevated plasma levels of theNeuropeptide Y in female fibromyalgia patients. Europe JournalOf Pain. 1999; 3: 19-30 • Bauer A., Elkin P., Loehrer L., Mandrekar J., Oh T., Thompson J., Vinent A., and Wahner-Roedler D. Use of Complementary and Alternative Medical Therapies by Patients Referred to a Fibromyalgia Treatment ProgramAt a Tertiary Care Center. Mayo Clinical Procedures. 2005; 80: 55-60. • Bayazit Y., Gursoy S., Karakurum G., Madenci E., and Ozer E. NeurotologicManifestations of the fibromyalgia syndrome. Journal of the Neurological Sciences. 2002; 196: 77-80. • Bennett R., and Rao S. Pharmacolgoical therapies in fibromyalgia. Best practiceAnd Research Clinial Rheumatology. 2003; 17: 611-627. • Bradley L., and McKendree-Smith N. Central nervous system mechanisms of painIn fibromyalgia and other musculoskeletal disorders: behavioral and Psychological treatment approaches. Current Opinion in Rheumatology. 2002; 14: 45-51. •  Buesing A. A conservative, cost effectie approach to fibromyalgia. JAAPA. 2005; 18: 32-37. • Buskila D. and Press J. Neuroendocrine mechanisms in fibromyalgia-chronic Fatigue. Best Practice and Research Clinical Rheumatology. 2001; 15: 747-758. • Dinan, T.G. Serotonin and the regulation of hypothalamic-pituitary-axisFunction. Life Science. 1996; 58: 1683-1694.

16. References • Hamaty D. Valentine J.L., Howard J., et. al. The plasma endorphin, prostaglandinAnd catecholamine profile of patients with birositis treated with cyclobenzaprine and placebo:a 5-month study. Journal of Rheumatology.1989; 16: 164-168.  • Landis, C.A., Lentz, M.J., Rothermel, J., Riffle, S.C., Chapman, D., Buchwald, D., Shaver, J.L. Decrease nocturnal levels of prolactin and growthHormone in women with fibromyalgia. Journal Clinical Endocrinol Metab. 2001; 86: 1672-1678.  • Neeck G. Pathogenic mechanisms of fibromyalgia. Department of Rheumatology. 2001; 1: 243-255.  • Neeck, G., Riedel, W. Thyroid function in patients with fibromyalgia syndrome.Journal of Rheumatology. 1992; 19: 1120-1122.  • Pongratz D. and Sievers M. Fibromyalgia- symptom or diagnosis: A definition ofThe position. Scand J Rheumatol. 2000; 29: 3-7.  • Staud R. Fibromyalgia pain: do we know the source? Current Opinion in Rheumatology. 2004; 16: 157-163.