FIBROMYALGIA

 Presented by

Morris Jagodowicz, M.S., M.D.

 

Learning Objectives: After reading this article you should be able to:

 

This lecture is approved for 2 credit hour

 

 

 

 

 

 

Fibromyalgia is a very complex disorder that was first described in the medical literature as far back as the 17th century.  Even today, many physicians question the existence of fibromyalgia.  Since there are no laboratory tests that can confirm the diagnosis, it remains a poorly understood disorder that has been labeled as a “wastebasket” diagnosis.  In 1987 the American Medical Association, as well as the World Health Organization recognized fibromyalgia as a discrete clinical entity.

 

The pathophysiology of fibromyalgia centers on a central pain processing disorder. The most marked abnormality associated with fibromyalgia is a low serotonin level.  Serotonin is a neurotransmitter involved in pain perception and mood disorders, as well as sleep.  Most studies involving low serotonin levels were derived from measuring levels of tryptophan, a precursor to serotonin; and 5-hydroxyindole acetic acid, a metabolic byproduct; in the cerebrospinal fluid of patients. Other studies report the presence of substance P in the spinal fluid twice the normal level.  Substance P is a neurotransmitter released when axons are stimulated.  The more Substance P available, the more sensitivity of nerves to pain.  Studies involving the hypothalamic-pituitary-adrenal system indicate that this axis is partly regulated by serotonin levels. Since Fibromyalgia patients typically show low levels, this may also explain the hypothalamic-pituitary-adrenal dysfunction in these patients. Changes in this axis usually are associated with a low free cortisol in 24 hour urine measurements, insulin induced hypoglycemia with overproduction of pituitary ACTH, elevated cortisol in the evening, low level of growth hormone, and over stimulation of ACTH secretion leading to insufficient adrenal release of glucocorticoids.  Nerve growth factor has also been documented to be elevated in the cerebrospinal fluid of patients with fibromyalgia.  This is important since NGF enhances substance P production, thereby increasing sensitivity to pain.

 

The epidemiology of the disease usually affects up to 6% of the United States population including children.  Women meet the criteria of fibromyalgia four times more than men. There is little gender difference in children.  When the disease strikes, it tends to be more severe in men.  The typical age at diagnosis is between 20-60 years of age. There is no racial propensity in fibromyalgia.  Fibromyalgia coexists with other conditions such as chronic fatigue syndrome, depression, dysmenorrheal, irritable bowl syndrome, myofascial pain syndrome, rheumatoid arthritis, systemic lupus erythematosus, tension/migraine headaches, tempero-mandibular joint (TMJ) disorders, thyroid dysfunction, and sleep disorders.

 

When it comes to making a diagnosis of fibromyalgia, one must first exclude other conditions since no single x-ray or lab test can pinpoint this ailment.  Since hypothyroidism shares many of the same symptoms, a thyroid panel should be ordered. Antinuclear antibodies are important in differentiating fibromyalgia from conditions such as systemic lupus erythematosus.  Rheumatoid factor should be obtained to differentiate rheumatoid arthritis from fibromyalgia.  Finally the physician should obtain an erythrocyte sedimentation rate to rule out inflammatory diseases and polymyalgia rheumatica.  Polymyalgia rheumatica is a myalgic syndrome that involves pain in the neck, shoulder and pelvic girdle.  The syndrome has a dramatic response to corticosteroids. Patients with polymyalgia rheumatica have an elevated ESR, whereas, fibromyalgia patients have a normal value.

The American College of Rheumatology has defined guidelines for diagnosis of fibromyalgia.  These guidelines are as follows:

 Two prominent associated conditions deserve mention.  The first is depression.  It remains uncertain as to which came first similar to the “chicken or the egg”.  It is unclear whether depression is a result of fibromyalgia or part of the disease process.  Depression is usually treated with a regimen of selective serotonin reuptake inhibitors such as Prozac, Paxil, Zoloft, Luvox, Serzone, and Effexor.  Studies involving women with fibromyalgia indicate that Prozac and Effexor are effective and well tolerated.  The second prominent associated condition is sleep disorder. These patients experience an unrefreshing sleep associated with morning fatigue.  Medication such as Xanax, Ambien, Sonata, or Ativan may be helpful.

 

Treatment of fibromyalgia does not only center on medication, but also involves physical therapy and use of trigger point injections.  Any successful rehabilitation program should involve a psychologist, physical therapist, and exercise physiologist.  A combination of aerobic, flexibility and strength training has been shown to have beneficial effects on the symptoms of fibromyalgia.  Trigger point injections have resulted in a reduction of pain and an increase in range of motion and exercise tolerance.  Long-term outcomes improve when trigger point injections are used together with physical therapy.  There are a wide range of techniques used.  They involve use of 1% Lidocaine or use of Botulinum Toxin A (Botox) and B (Myobloc).  Corticosteroids are usually not recommended for trigger point injections in patients with fibromyalgia.

 

In conclusion, fibromyalgia is a multi-symptom, chronic pain condition that disrupts and impedes the lives of millions of people every day. The most effective treatment program is one where the patient and the doctor establish a partnership, with good communication and a well-defined treatment approach.

 

TAKE THE TEST! 

 

 

References

 

  1. Russell IJ, Orr MD, Littman B. Elevated cerebrospinal fluid levels of substance P in patients with the fibromyalgia syndrome. Arthritis Rheum 1994; 37:1593-1601.
  2. Chaitow L. Conditions associated with fibromyalgia. In: Fibromyalgia Syndrome: A Practitioner’s Guide to Treatment. Edinburgh: Churchill Livingston; 2000: 31-59.
  3. Griep EN, Boersma JW, de Kloet ER. Altered reactivity of the hypothalamic-pituitary-adrenal axis in the primary fibromyalgia syndrome. J Rheumatology 1993; 20: 469-474.
  4. Gevirtz C. Pain management in patients with fibromyalgia. Topics in Pain Management 2004; 20: 1-6.
  5. Lue FA. Sleep and fibromyalgia. J Musculoskeletal Pain 1994; 2: 89-100.
  6. Arnold LM, Hess EV, Hudson JI, et al. A randomized, placebo-controlled, double-blind, flexible-dose study of fluoxetine in the treatment of women with fibromyalgia. American J  of Medicine 2002; 112: 191-197
  7. Lang, Amy M. Botulinum toxin type A for the management of cervicothoracic and cervicobrachial pain: Treatment rationale and open-label results in 25 patients. Amer J of Pain Management2003, Vol 14: 13-23