Nervous System Involvement in Lyme Borreliosis
Katarina Ogrinc, Vera Maraspin*
Identifiers and Pagination:Year: 2016
Issue: Suppl 1: M5
First Page: 44
Last Page: 54
Publisher ID: TODJ-10-44
Article History:Received Date: 22/10/2015
Revision Received Date: 16/12/2015
Acceptance Date: 16/12/2015
Electronic publication date: 28/03/2016
Collection year: 2016
open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
Lyme neuroborreliosis (involvement of the central and/or peripheral nervous system due to infection with B. burgdorferi sensu lato) is the second most frequent manifestation of Lyme borreliosis in Europe, while it comprises the third most common expression of the disease in North America. Early Lyme neuroborreliosis, which is much better defined and far more common than late Lyme neuroborreliosis, is in Europe caused mainly by B. garinii and comprises the classic triad of meningitis, radiculoneuritis and/or cranial neuropathy, while in American patients subacute meningitis with or without cranial neuropathy is the most common manifestation. Among chronic forms of European Lyme neuroborreliosis peripheral neuritis associated with acrodermatitis chronic atrophicans is most frequently observed. A reliable diagnosis of borrelial central nervous system infection requires demonstration of lymphocytic pleocytosis and the evidence of borrelial infection of the central nervous system, established by intrathecal synthesis of specific antibodies and/or isolation of Borreliae from the cerebrospinal fluid. Treatment with oral doxycycline, or parenteral penicillin or third generation cephalosporins (most frequently ceftriaxone) for 2-4 weeks is efficient in the majority of patients..