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Astroglial and neuronal proteins in cerebrospinal fluid as markers of CNS involvement in Lyme neuroborreliosis
Author(s) -
DoteVall Leif,
Hagberg Lars,
Karlsson JanErik,
Rosengren Lars E.
Publication year - 1999
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.1999.tb00010.x
Subject(s) - neuroborreliosis , cerebrospinal fluid , medicine , enolase , lyme neuroborreliosis , glial fibrillary acidic protein , pathology , lyme disease , central nervous system , parenchyma , borrelia burgdorferi , immunology , immunohistochemistry , antibody
Is Lyme neuroborreliosis, even in its early phase, a parenchymatous disorder in the central nervous system (CNS), and not merely a meningitic process? We quantified cerebrospinal fluid (CSF) levels of four nerve and glial cell marker proteins in Lyme neuroborreliosis patients with pretreatment durations of 7–240 days. AH 23 patients had meningo‐radiculitis, and six had objective signs of encephalopathy. Glial fibrillary acidic protein (GFAp) pretreatment levels in CSF, and the light subunit of neurofilament protein (NFL) levels were related to clinical outcome and declined significantly after treatment ( P < 0.001 and P < 0.01, respectively). NFL was detectable in 11 out of 22 patients, and pre‐and post‐treatment NFL levels were associated with the duration of neurological symptoms within 100 days prior to treatment. Neuron‐specific enolase (NSE) concentrations also decreased after therapy ( P < 0.001), while CSF levels of glial S‐100 protein remained unchanged. The pretreatment duration of disease was related to postinfectious sequelae. GFAp, NSE and NFL levels in CSF are unspecific indicators of astroglial and neuronal involvement in CNS disease. The findings in the present study are in agreement with the hypothesis that early and late stages of Lyme neuroborreliosis damage the CNS parenchyma.