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Lyme Disease: A Short Primer for Pain Practitioners

“It was obvious to participants at the workshop that a significant impasse has developed in the world of Lyme disease. Lines in the sand have been drawn, sides have been taken, and frustration prevails. The ‘walk in the woods’ process of conflict resolution seems necessary for creating a new environment of trust and a better environment for more constructive dialogue to help focus research needs and achieve better outcomes. Such a process does not imply a compromise of the science but rather is needed to shift to a more positive and productive environment to optimize critical research and promote new collaborations.” —Excerpts from Institute of Medicine Committee on Lyme Disease and Other Tick-Borne Diseases: The State of the Science: 2011
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Recently, the Centers for Disease Control and Prevention (CDC) dramatically increased the estimate of the annual number of new cases of Lyme Disease (LD) in the United States from 30,000 to 300,000.1 The number of new LD cases each year certainly qualifies this infection as an epidemic or at least a highly endemic disease. Consequently, pain practitioners must familiarize themselves with the signs and symptoms of LD. This article is a short primer on LD to give the pain practitioner some basic information and guidance. Given the magnitude of LD, Practical Pain Management will seek to expand on LD research in future issues.

Painful Sequelae

Many of patients with active or previously treated LD infection will develop painful sequelae.2-7 In addition, many patients who are initially diagnosed with myopathies, neuropathies, or arthropathies later prove to have LD.2-4 Many pain patients who have investigated LD on their own believe their pain may have resulted from an unrecognized LD infection. To complicate active disease, there is an autoimmune, painful condition called Post-Treatment Lyme Disease Syndrome (PTLDS) that may follow the eradication of an active infection.

Origin and Cause of LD

LD was named after the coastal town in Connecticut, Old Lyme, where it was first reported in 1977. Although now found around wooded areas throughout the United States, 96% of reported cases of LD are clustered in 13 states in the Northeast and upper Midwest: Connecticut, Delaware, Maine, Maryland, Massachusetts, Minnesota, New Hampshire, New Jersey, New York, Pennsylvania, Vermont, Virginia, and Wisconsin.1

LD is caused by the spirochete bacteria Borrelia burgdorferi.8-12 It is the most common vector-borne illness in the United States and is transmitted by a bite by an infected black-legged tick of the Ixodes family. The tick is sometimes called the deer tick, because it is carried by deer and other animals.

Three Stages of Active Infection

Infection following a tick bite causes 3 stages of disease (Table 1). The early localized infection causes a rash called “erythema migrans,” commonly called a “bull’s-eye rash,” which eventually resolves, even without antibiotic treatment. Although diagnostic following a tick bite, the rash only occurs in about half of LD cases. In the early stages of infection, the spirochete can spread to other tissues and organs (eg, skin, nervous system, joints, and heart), causing more severe symptoms.8 LD has a predilection to attack the facial nerve and cause Bell’s palsy.13-16 The disease also commonly affects the neck and cervical spine, causing pain, stiffness, headache, and possible radicular symptoms. Joint, muscle, and nerve pain begin to occur during active infection, with the knee being a favored site of joint pain.4-6

The late, disseminated stage of infection is characterized by neurologic manifestations and severe arthritic pain in joints.2-16 There may be shooting pains, myalgias, numbness or tingling in the hands or feet, insomnia, and problems with short-term memory. Tragically, the spirochete may have a predilection for the central nervous system (CNS).13-16 Once infected, CNS LD may cause a number of symptoms that may mimic other neurologic diseases, including multiple sclerosis, Parkinson’s disease, and Alzheimer’s disease. Many physicians refer to CNS infection by LD as “neuroborreliosis.”6,10,13-16

Testing and Antibiotic Treatment

Diagnosis of LD usually is confirmed by serologic testing. Once LD is diagnosed, treatment of the infection requires antibiotics. There is some controversy surrounding diagnostic testing and antibiotic therapy. Ideally, antibiotic management of LD should be supervised by a physician with expertise or specialization in LD. Antibiotics commonly used for oral treatment include doxycycline (currently in short supply nationwide), amoxicillin, and cefuroxime axetil.17 Patients with certain neurologic or cardiac forms of illness may require intravenous treatment with drugs such as ceftriaxone or penicillin.17 [Editor’s Note: The specifics of antibiotic therapy will not be covered here]. If a specialist is not available and the treating pain clinician tests and treats, we recommend you consult “Clinical Practice Guidelines” or another up-to-date manual.17

Pain Treatment of Active Disease

Pain may be severe enough to require specific analgesic therapy at any stage of LD. The first line of pain treatment is anti-inflammatory agents, because inflammation is always present with LD.4-6 The agents can be delivered topically (diclofenac; PennSaid, Voltaren, others) or systemically. Topical anesthetics such as lidocaine (Lidoderm, others) also are helpful for managing joint pain (Table 2). In addition to anti-inflammatory agents, standard, step-wise multimodal pain treatment is recommended—starting with agents such as acetaminophen, muscle relaxants (when needed), various neuropathic drugs, and complementary therapies. Opioid analgesics may be required for severe pain if non-opioid measures are ineffective. Hypnotic agents may be necessary for insomnia, and anxiolytics often are required as well.

Post-Treatment LD Syndrome

Approximately 10% to 20% of patients with LD have symptoms that may last months to years after treatment with antibiotics.2,3,7,9,12 These symptoms can include muscle and joint pain, cognitive defects, sleep disturbances, and fatigue. The cause of these symptoms is not precisely known, since there is no evidence that there is ongoing infection with the spirochete. As noted, this condition is referred to as PTLDS. It is apparently an autoimmune disorder in which a person’s immune system continues to respond, doing damage to the body’s tissues even after the infection has been cleared. Further antibiotic therapy is not helpful.

PTLDS appears to be similar to other infections that produce an autoimmune condition after the active infection has resolved. Included here are Campylobacter jejuni (polyneuropathy, Guillain-Barre Syndrome), chlamydia (reactive arthritis, Reiter’s Syndrome), Streptococcus (glomerulonephritis), and Epstein-Barr virus (infectious mononucleosis) (Table 3). These post-infectious syndromes are of great importance to pain practitioners because they may produce severe pain in joints, nerves, and muscles that require potent analgesics. Also, many patients who are given a diagnosis of fibromyalgia, myofacial pain syndrome, or degenerative joint disease may, in fact, have PTLDS.

Last updated on: April 14, 2015
First published on: February 1, 2014