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11 Articles in Volume 14, Issue #1
The WHO Pain Ladder: Do We Need Another Step?
History of Pain: The Psychosocial Assessment of Pain
Lyme Disease: A Short Primer for Pain Practitioners
Opioid Prescribing Part 1: A Practical Guide to Appropriate Documentation
Pain, Impairment, Whiplash, and the New AMA Guides: What Clinicians Need to Know
The 5 Coping Skills Every Chronic Pain Patient Needs
Demystifying Benzodiazepine Urine Drug Screen Results
Practical Pain Management: The Nation’s Premier Teaching Journal for Pain Practitioners
PPM’s Editorial Board Weighs In on WHO Ladder
Are patients taking acetaminophen (Tylenol) at risk for developing serious skin conditions?
What are some home exercises and tips to help patients manage rotator cuff injuries and pain?

Lyme Disease: A Short Primer for Pain Practitioners

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, with 14 states accounting for over 96% of cases reported.1 In the United States, Lyme disease is most common in northeastern states, from Virginia to Maine; Upper Midwest states, mostly Wisconsin and Minnesota; and the West Coast, mainly in the northwest.

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.

Cause of LD

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 ticks pick up the bacteria, called Borrelia burgdorferi (B. burgdorferi) or Borrelia mayonii (B. mayonil) when they bite deer or mice that are infected. When infected ticks bite humans, they spread the bacteria. Ticks can attach themselves to any part of the human body, but are most commonly found in the groin, armpits and scalp.

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.

Pain therapy for these individuals may require a vigorous analgesic program, because autoimmune processes tend to be progressive and cause tissue destruction. Electromagnetic measures (eg, acupuncture, ultrasound, radio wave, infrared, laser) may help muscles, tendons, and joints stay flexible and mobile. Range of motion and stretching exercises are necessary to keep joints mobile and prevent contractures. Water therapy is very comforting. Corticosteroid injections or topical applications may be essential for treatment, especially if joint swelling is present and patients have limited mobility.

The Patient Who Suspects Chronic Lyme Infection

LD is so prevalent and well known that the public is well aware of its symptoms. Many patients, particularly those who have been diagnosed with fibromyalgia, degenerative arthritis, or neuropathies of unknown origin, believe they may have had unrecognized and undiagnosed LD. They may request recurrent LD testing and even antibiotic therapy, despite negative Lyme serologic tests.

In reality, some of these patients may be correct. The authors have encountered several patients who presented with a chronic pain syndrome such as fibromyalgia who were later found to have disseminated LD or PTLDS. At this juncture, we are not prepared to set out any specific diagnostic or treatment protocols. We do, however, believe that pain practitioners must consider LD as an underlying cause of pain in patients who present without a clear event or cause of chronic muscle, nerve, or joint pain. In addition to diffuse musculoskeletal and joint pathologies, cranial neuropathy (particularly facial palsy), and radiculoneuritis (motor or sensory or both) are 2 of the most common presentations of acute, early neurologic LD. Given what appears to be an epidemic of LD, we will carefully monitor the situation and bring you updates through Practical Pain Management.


There are approximately 300,000 new LD cases reported each year. The disease is reaching near epidemic proportions, especially in the Northeast and upper Midwest, where LD cases appear to cluster. It is unknown, however, whether this rate of new cases signals a true increase in infection or instead is a reflection of enlightened awareness and new testing technology. It is clear, however, that patients with suspected (or diagnosed) LD are showing up in pain practices in increasing numbers. These patients tend to fall into 4 categories (Table 4). The first category encompasses patients who have pain and documented LD by virtue of serologic test results. The second category is composed of patients with pain without an identifiable, obvious cause, in whom serologic testing later documents the presence of disseminate LD. The third category includes patients who investigated LD on their own and determined they may have it based on symptoms that are compatible with disseminated LD (unconfirmed). The fourth category encompasses pain patients with PTLDS, which presents as an autoimmune disorder that progressively destroys tissue, such as joint cartilage.

Pain treatment of LD generally follows the step-up regimen of multimodal analgesic therapy with oral and topical agents. A chronic infectious or autoimmune disorder always is accompanied by inflammation, making NSAIDs essential. Clinicians are reminded to incorporate physical and complementary modalities to improve function, diminish pain, and enhance patient well-
being. All pain practitioners should educate themselves about LD and its treatment, and stay abreast of future clinical recommendations.

Editor's Note: Online version updated July 2019.

Last updated on: July 30, 2019
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