Transcript Fibromyalgia: Is it real?

Fibromyalgia: Is it real?
Melissa Tucker
Gilbert Boissonneault
March 24, 2006
Outline of objectives
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What is Fibromyalgia?
Speculated mechanisms of actions
Current treatment
How does it effect us as practionars
What is Fibromyalgia?
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A syndrome
characterized by:
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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
What is Fibromyalgia?
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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.
How does FM effect the body?
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Pain isn’t releated to actual tissue damage
Beyond this there are no known causes
Studies concentrate on
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Serotonin dysfunctions
Hypothalamic-pituitary-adrenal axis
Hypothalamic-pituitary-thyroid axis
Growth hormone
Neuromediators
Serotonin’s Role
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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
Hypothalamic-pituitary-adrenal Axis
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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.
Hypothalamus-pituitary-thryoid axis
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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
Growth Hormone
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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
Endorphins, Enkephalins and
Neuromodulators
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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
Cytokines
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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
Pharmacologic
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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
Nonpharmacologic Therapies
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Physical therapy include stretching, deep
tissue massage, transcutaneous
electrical nerve stimulation
Acupuncture showed short term benefit
Low impact exercise such as Yoga
Chiropractic manipulation
References
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Anderberg, U., Lui Z., Bergland L., Nyberg F. Elevated plasma levels of the Neuropeptide Y in female
fibromyalgia patients. Europe Journal Of 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 Program At a Tertiary Care Center. Mayo
Clinical Procedures. 2005; 80: 55-60.
Bayazit Y., Gursoy S., Karakurum G., Madenci E., and Ozer E. Neurotologic Manifestations of the
fibromyalgia syndrome. Journal of the Neurological
Sciences. 2002; 196: 77-80.
Bennett R., and Rao S. Pharmacolgoical therapies in fibromyalgia. Best practice And Research Clinial
Rheumatology. 2003; 17: 611-627.
Bradley L., and McKendree-Smith N. Central nervous system mechanisms of pain In 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-axis Function. Life Science. 1996; 58:
1683-1694.
References
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Hamaty D. Valentine J.L., Howard J., et. al. The plasma endorphin, prostaglandin And
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 growth Hormone 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 of The
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Staud R. Fibromyalgia pain: do we know the source? Current Opinion in Rheumatology.
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