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  • Updated 03.24.2024
  • Released 05.08.1995
  • Expires For CME 03.24.2027

Lyme disease



Historically, Lyme disease, an infection with the tick-borne spirochete Borrelia burgdorferi (Bb), has been said to involve the nervous system in 10% to 15% of infected individuals–both in Europe and the U.S.–although data suggest this proportion may be decreasing with earlier diagnosis and treatment. Controlled studies indicate that neuroborreliosis is generally curable with oral antibiotics, particularly doxycycline, often with relatively rapid resolution of neurologic deficits. Although much is said about “neurologic” symptoms, symptoms such as fatigue, “brain fog,” and concentration difficulty, which present after microbiological cure of this infection, studies indicate that months after treatment these symptoms are not only unrelated to nervous system infection but occur with essentially the same frequency in treated patients and in healthy controls. Lyme disease diagnosis generally relies on 2-tier serologic testing, with positive or equivocal ELISAs validated by either a Western blot or by a second, independent ELISA. Demonstrated synthesis of anti-Bb antibody in the CSF (intrathecal antibody production; ITAb) is considered necessary to make a diagnosis of definite CNS Lyme neuroborreliosis, a diagnosis that may be further supported by demonstrated elevation of CSF CXCL13 concentration.

Key points

• Lyme disease, an infection with the tick-borne spirochete B burgdorferi, historically has been reported as affecting the central or peripheral nervous system in up to 10% to 15% of patients–a number that may be declining with earlier diagnosis and treatment.

• Clinical phenomena associated with Lyme neuroborreliosis (LNB) typically include one or more of the following: cranial neuropathy (most often the facial nerve), radiculopathy, and lymphocytic/monocytic meningitis.

• Diagnosis of definite CNS Lyme neuroborreliosis requires demonstration of a CSF pleocytosis and intrathecal production of anti-Bb antibody. If either is absent, cases are considered possible/probable, not definite.

• Serodiagnosis after the first month of infection has high sensitivity and specificity.

• Treatment with 2- to 4-week courses of oral antibiotics is curative in most; parenteral treatment is recommended either if there is evidence of parenchymal brain or spinal cord involvement or if objectively demonstrable active disease persists after appropriate oral treatment.

• Persisting difficulties after treatment, often referred to as “post-treatment Lyme disease syndrome,” may occur but are not associated with nervous system infection and, in most studies, are no more common than in controls.

• Misinterpretation of testing and clinical observations results in many patients being treated unnecessarily for what is incorrectly thought to be Lyme disease, with considerable potential for side effects and patient expense.

Historical note and terminology

The term "Lyme arthritis" was first introduced in 1977 and was subsequently broadened to "Lyme disease" when it was recognized that the disorder commonly involved multiple organ systems in addition to joints (73). However, the syndrome was described much earlier in the 20th century. In 1910, Afzelius first reported the typical cutaneous lesion, erythema migrans (formerly known as erythema chronicum migrans). In 1922, Garin and Bujadoux described tick bite-associated meningoradiculitis, the most typical neurologic presentation in this disorder. Following a more detailed description of this syndrome by Bannwarth, the notion that bites of Ixodes ticks could lead to a syndrome of lymphocytic meningitis with painful radiculoneuritis became widely accepted by European clinicians. The first reports of Lyme arthritis described cases of what had been thought to be juvenile rheumatoid arthritis among children in the region of Lyme, Connecticut (73). Detailed epidemiologic studies led to the association of this disorder with bites of Ixodes ticks. In 1979, Reik and colleagues described a neurologic syndrome in American patients with Lyme disease virtually identical to that described by Garin and Bujadoux (62). In 1983, the responsible spirochete, Borrelia burgdorferi, was identified as the causative agent in American patients with Lyme disease. Shortly thereafter, closely related microorganisms were identified in European patients. Subsequent work has both broadened the scope of the neurologic disorders recognized as associated with this infection (known collectively as "Lyme neuroborreliosis") and refined the microbiological understanding of the responsible organisms. Advances in genomics have led to a proposed change in taxonomy, differentiating the organisms responsible for Lyme disease and related disorders, with the recommended name Borreliella, from the relapsing fever Borrelia (07)--a proposal that has yet to gain widespread acceptance. The broad group formerly termed B burgdorferi sensu lato would be termed Borreliella burgdorferi, with corresponding changes in the names for B afzelii and B garinii.

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