Abstract

ObjectivesTo examine whether post-treatment Lyme disease syndrome (PTLDS) defined by fatigue, cognitive complaints and widespread pain following the treatment of Lyme disease is associated with small fiber neuropathy (SFN) manifesting as autonomic and sensory dysfunction.MethodsThis single center, retrospective study evaluated subjects with PTLDS. Skin biopsies for assessment of epidermal nerve fiber density (ENFD), sweat gland nerve fiber density (SGNFD) and functional autonomic testing (deep breathing, Valsalva maneuver and tilt test) were performed to assess SFN, severity of dysautonomia and cerebral blood flow abnormalities. Heart rate, end tidal CO2, blood pressure, and cerebral blood flow velocity (CBFv) from middle cerebral artery using transcranial Doppler were monitored.Results10 participants, 5/5 women/men, age 51.3 ± 14.7 years, BMI 27.6 ± 7.3 were analyzed. All participants were positive for Lyme infection by CDC criteria. At least one skin biopsy was abnormal in all ten participants. Abnormal ENFD was found in 9 participants, abnormal SGNFD in 5 participants, and both abnormal ENFD and SGNFD were detected in 4 participants. Parasympathetic failure was found in 7 participants and mild or moderate sympathetic adrenergic failure in all participants. Abnormal total CBFv score was found in all ten participants. Low orthostatic CBFv was found in 7 participants, three additional participants had abnormally reduced supine CBFv.ConclusionsSFN appears to be associated with PTLDS and may be responsible for certain sensory symptoms. In addition, dysautonomia related to SFN and abnormal CBFv also seem to be linked to PTLDS. Reduced orthostatic CBFv can be associated with cerebral hypoperfusion and may lead to cognitive dysfunction. Autonomic failure detected in PTLDS is mild to moderate. SFN evaluation may be useful in PTLDS.

Highlights

  • Lyme disease is a transmittable tick-borne infection caused by the spirochete Borrelia burgdorferi [1,2,3]

  • small fiber neuropathy (SFN) appears to be associated with post-treatment Lyme disease syndrome (PTLDS) and may be responsible for certain sensory symptoms

  • Dysautonomia related to SFN and abnormal cerebral blood flow velocity (CBFv) seem to be linked to PTLDS

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Summary

Introduction

Lyme disease is a transmittable tick-borne infection caused by the spirochete Borrelia burgdorferi [1,2,3]. Lyme disease is a serious public health problem. It is estimated that approximately 300,000 cases occur annually in the US [2]. The reported annual incidence ranges from 20–100 cases per 100,000 people in endemic areas. Neurologic sequelae of Lyme disease, termed Lyme neuroborreliosis, occurs in 10–15% of patients with untreated Lyme disease [2,4,5]. The spirochete can invade peripheral and central nervous system and may cause aseptic meningitis, cranial neuropathy, painful radiculitis or encephalo-myelo-radiculitis and various forms of peripheral neuritis

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