Lyme Disease and Fibromyalgia

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Lyme disease is a bacterial infection that is transmitted by the bite of infected blacklegged ticks. The symptoms associated with Lyme disease typically progress through three stages. Stage one is marked by flu-like symptoms such as fever, chills, headache, lightheadedness, muscle pain, stiff neck, and itching. A rash or red spot at the site of the tick bite may also be visible on some individuals. If it is diagnosed in the early stages, Lyme disease can usually be effectively treated with antibiotics such as doxycycline or amoxicillin. If left untreated, Lyme disease will continue to progress and cause more serious and widespread complications. Stage two symptoms include weakness or paralysis in the facial muscles, muscle pain or swelling in the large joints, and heart palpitations. Symptoms of the third and final stage include abnormal muscle movements, muscle weakness, numbness and tingling, and difficulty speaking. Lyme disease shares obvious symptoms with fibromyalgia, along with certain forms of arthritis and other conditions. Therefore, it may need to be considered during the diagnostic process among individuals who have a high likelihood of exposure to infected blacklegged ticks (due to geographic location, occupation, or other factors).

Fortunately, specific blood tests can effectively detect Lyme disease if performed at the correct time. Blood tests to detect Lyme disease measure antibodies that the body makes in response to the infection; however, it can take several weeks following contraction of the infection for the body to produce enough antibodies to show up on a blood test. Because of this, individuals who have Lyme disease but who are tested in the first few weeks following infection will frequently test negative for Lyme disease. For those who have had the disease longer than four to six weeks, blood tests will almost universally be positive. Therefore, if symptoms persist in an individual who initially tests positive, the blood test should be repeated after several weeks. Those who have been ill for months or years and who have negative blood test results will almost always not have Lyme disease.

Research on Lyme Disease and Fibromyalgia

There is some evidence to suggest that certain infections, such as that which causes Lyme disease, may play a role in the development of fibromyalgia and related syndromes. In a 1992 observational study, researchers found that 8% of 287 Lyme disease patients developed fibromyalgia over a period of three and a half years. Further examination and analysis of blood samples, onset of symptoms, and response to antibiotic therapy among this cohort led researchers to conclude that Lyme disease may trigger the onset of fibromyalgia (Dinerman & Steele, 1992). However, most researchers agree that more detailed evidence is needed to support a causal association (Buskila et al., 2008).

Of more concern is the extreme symptomatic overlap between fibromyalgia and Lyme disease, which can make effective diagnosis extremely difficult. Often, in the past, individuals were mistakenly diagnosed as having “chronic” or “refractory” Lyme disease, which did not respond to repeated cycles of antibiotic therapy, when in reality they actually had fibromyalgia.

In an early study published on the association between Lyme disease and fibromyalgia, 100 patients who were seen at a Lyme disease referral center were evaluated. Researchers found that of these individuals, only 37 patients actually had Lyme disease. Furthermore, 25 patients met the diagnostic criteria for fibromyalgia (Sigal, 1990).

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References -

1.        Buskila D, Atzeni F, Sarzi-Puttini P. Etiology of fibromyalgia: The possible role of infection and vaccination. Autoimmun Rev. 2008;8(1):41-43.

2.        Sigal L. Summary of the first 100 patients seen at a Lyme disease referral center. Am J Med. 1990;88(6):57-81.

3.        Dinerman H, Steere A. Lyme disease associated with fibromyalgia. Ann Intern Med. 1992;117(4):281-285.

Ablin JN, Shoenfeld Y, Buskila D. Fibromyalgia infection and vaccination: two more parts in the etiological puzzle. J Autoimmun. 2006;27:145-152.

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