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piątek, 27 maja 2016

Udar mozgu - Borelioza - j.angielski

 Case Report

Stroke as an Unusual First Presentation of Lyme Disease

 

Abstract

Introduction. Lyme neuroborreliosis is a nervous system infection caused by spirochete Borrelia burgdorferi with diverse neurological complications. Stroke due to cerebral vasculitis is a rare consequence of neuroborreliosis and has been described in just a few case reports. Case Presentation. Here, we report the case of a 43-year-old patient who presented with discrete left-sided hemiparesis and amnestic cognitive impairment. Brain magnetic resonance imaging showed a thalamic infarct, and serological and cerebrospinal fluid (CSF) tests confirmed the diagnosis of active neuroborreliosis. The antibiotic treatment with intravenous ceftriaxone for three weeks led to an improvement of the symptoms and remarkable regression of radiological findings, but not to full recovery of the amnestic cognitive disorder. Conclusion. Lyme neuroborreliosis should be suspected in patients with cerebrovascular events without obvious risk factors, especially those living in endemic areas such as northern Europe or those who have been exposed to ticks and those with clinical or radiological findings suggesting Lyme neuroborreliosis, in order to establish the diagnosis and start a proper antibiotic therapy.

1. Background

Lyme borreliosis is a multisystem infection caused by the spirochete Borrelia burgdorferi sensu lato species, which are transmitted by the bite of infected Ixodes ricinus ticks. While Borrelia burgdorferi sensu stricto is the sole pathogen in North America, five different species, most often Borrelia afzelii and Borrelia garinii, can cause the disease in Europe and Asia.
Lyme borreliosis is an endemic widespread in the northern global hemisphere. In Germany, an analysis of health insurance data showed an annual incidence of 261 per 100,000 [1, 2]. The clinical manifestations of Lyme disease are diverse and vary with its stage, from erythema migrans (EM) in early localized stage to neurologic and/or cardiac complications in the early disseminated stage. Late Lyme disease occurs months to a few years after the primary infection and is typically associated with arthritis and/or neurologic problems. Acrodermatitis chronica atrophicans is a cutaneous manifestation of late Lyme disease. However, some patients may present in later stage without any signs or symptoms of earlier Lyme disease [3]. Moreover, nonspecific symptoms, including fatigue, anorexia, headache, neck stiffness, and myalgias, may appear in each stage. This wide variety of clinical manifestations is partly due to differences in the infecting species of the bacterium and can lead to a late diagnosis of the disease [4]. The involvement of the central or peripheral nervous system secondary to systemic infection with Borrelia bacterium is called Lyme neuroborreliosis (LNB). Approximately, 13% of patients with Lyme disease develop neurological complications such as meningitis, meningoencephalitis, facial palsy, cranial neuritis and radiculoplexitis, rarely stroke, intracerebral hemorrhage, and sinus thrombosis [2, 510].
Herein, we report cerebral ischemic stroke as a rare and an unusual first manifestation of LNB.

http://www.hindawi.com/journals/crinm/2015/389081/

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Optic Neuritis in Acute Neuroborreliosis

(Lyme Disease) in the U.S.-Mexican

Border: Case Report*



Abstract

Objective: We describe a patient diagnosed with acute neuroborreliosis presenting with anterior

optic neuritis (papillitis) in a non-endemic region. Case Presentation: A 43-year-old previously

healthy right handed man admitted due to an insidious onset of severe headache and spells of ascending

paresthesias from his right foot into his right arm and face followed by speech arrest and

clumsiness of his right hand. His neurologic exam was significant for somnolence, nuchal rigidity

and Kernig and Brudzinski signs were present. MRI of the brain with gadolinium showed diffuse

hyperintense signal involving the supra and infratentorial cortical sulci, with associated faint diffuse

leptomeningeal enhancement, consistent most likely with diffuse leptomeningoencephalitis.

EEG: normal. CSF VDRL was negative. Dilated fundus exam revealed mild optic nerve edema more

significant to the left than to the right eye, confirmed and measured by spectral domain OCT (Optical

Coherence Tomography). There was an evidence of posterior uveitis with an early vitreous

hemorrhage superficial to the left optic nerve. Lyme disease serum antibody (IgM) Immunoblotting

was positive in 2 bands confirming the diagnosis of neuroborreliosis. Conclusion: Optic nerve

involvement in Lyme disease is an uncommon complication that should be confirmed by specific

diagnostic criteria to establish its causal relation.

http://file.scirp.org/pdf/WJNS_2016051116214680.pdf
 
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