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Updated: Jul 19, 2026

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Chronic polyneuropathy and Lyme disease.

A Mygland1, T Skarpaas, U Ljøstad

  • 1Department of Neurology, Sørlandet Sykehus, Kristiansand, Norway. aase.mygland@sshf.no

European Journal of Neurology
|October 14, 2006
PubMed
Summary

In European Lyme disease-endemic areas, Borrelia burgdorferi antibodies are not a common cause of chronic polyneuropathy (PN) without other Lyme symptoms. This study found similar antibody prevalence in PN patients and healthy donors, suggesting infection rarely causes isolated PN.

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Area of Science:

  • Neurology
  • Infectious Diseases
  • Immunology

Background:

  • Borrelia burgdorferi infection can manifest in the peripheral nervous system (PNS) as cranial neuropathy, radiculopathy, or asymmetric peripheral neuropathy with acrodermatitis chronica atrophicans (ACA).
  • North American studies suggest Lyme disease can also present as symmetric chronic polyneuropathy (PN) without ACA or other typical Lyme manifestations.
  • The clinical presentation of Lyme neuroborreliosis varies, necessitating investigation into less common presentations like isolated chronic PN in different geographic regions.

Purpose of the Study:

  • To determine the prevalence of Borrelia burgdorferi antibodies in patients with isolated chronic polyneuropathy (PN) in a high-incidence Lyme disease region of Europe (Vest-Agder County, Norway).
  • To assess whether Borrelia burgdorferi infection is a significant cause of chronic PN presenting without ACA or other characteristic Lyme disease symptoms in this European population.

Main Methods:

  • Sera from 209 patients diagnosed with chronic PN and 247 healthy blood donors from Vest-Agder County, Norway, were tested for Borrelia burgdorferi antibodies.
  • Statistical analysis was used to compare antibody prevalence between PN patients and healthy controls, and between subgroups of PN patients (cryptogenic vs. identified etiologies).
  • Clinical and electrophysiological data were compared between antibody-positive and antibody-negative PN patients. Response to antimicrobial treatment was assessed in antibody-positive cases.

Main Results:

  • Borrelia burgdorferi antibodies were detected in 21% of PN patients and 18% of healthy blood donors, a statistically similar prevalence (P = 0.553).
  • Antibody prevalence was comparable between cryptogenic PN (24%) and PN of identified etiologies (18%) (P = 0.311).
  • PN patients with Borrelia burgdorferi antibodies exhibited normal cerebrospinal fluid (CSF) findings and did not differ clinically or electrophysiologically from those without antibodies. None of the 20 antibody-positive patients showed improvement with antimicrobial treatment.

Conclusions:

  • In a European region with high Lyme disease incidence, chronic distal peripheral neuropathy (PN) without acrodermatitis chronica atrophicans (ACA) or other Lyme manifestations is rarely caused by Borrelia burgdorferi infection.
  • The similar prevalence of Borrelia burgdorferi antibodies in PN patients and healthy controls suggests that isolated chronic PN is an atypical presentation of Lyme neuroborreliosis in this European setting.
  • Further research may be needed to elucidate the causes of cryptogenic chronic PN in Lyme-endemic areas, as Borrelia burgdorferi appears to be an infrequent etiology for this specific presentation.