Brain-specific proteins in the cerebrospinal fluid of severely asphyxiated newborn infants

Upcoming trials of neuroprotective strategies in severely asphyxiated newborn infants emphasize the need for early and objective markers of both good and bad long‐term prognosis. Traditional markers such as neurological depression and seizures are not specific. Aim: To study whether measurement in t...

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Bibliographic Details
Published inActa Paediatrica Vol. 90; no. 10; pp. 1171 - 1175
Main Authors Blennow, M, Sävman, K, Ilves, P, Thoresen, M, Rosengren, L
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.10.2001
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Summary:Upcoming trials of neuroprotective strategies in severely asphyxiated newborn infants emphasize the need for early and objective markers of both good and bad long‐term prognosis. Traditional markers such as neurological depression and seizures are not specific. Aim: To study whether measurement in the cerebrospinal fluid of some proteins known to be specific to the central nervous system was in covariance with the clinical course and long‐term prognosis. Methods: Twenty‐two asphyxiated infants were included in the study and compared with a control group of 8 infants without signs of perinatal asphyxia. Cerebrospinal fluid (CSF) was collected during the first 4 d of life and analysed for neurofilament protein (NFp), glial fibrillary acidic protein (GFAp), protein S‐100 and neuron‐specific enolase (NSE). Results: The concentrations of all four proteins were significantly increased in the CSF of asphyxiated infants. The concentrations correlated significantly with other indicators of long‐term prognosis and to neurological impairment at 1 y of age, or death before that time. Specifically, concentrations were excessively high in the five infants who died. Conclusions: High concentrations of brain‐specific proteins are released into the CSF of asphyxiated infants. It might therefore be useful to measure these concentrations when excluding patients with the gravest prognosis from neuroprotective trials.
Bibliography:ark:/67375/WNG-XZH0348Q-0
ArticleID:APA1171
istex:757E92E3CAAF50A38AC3B2447B917ED8C0F5FB98
ISSN:0803-5253
1651-2227
DOI:10.1111/j.1651-2227.2001.tb03249.x