Abstract
Perinatal asphyxia is an important cause of neonatalmortality and of neurological disabilities among survi-vors. Infants who sustain perinatal asphyxia severeenough to result in long-term neurological disabilitiesinvariably exhibit anovert neonatal encephalopathy andother organ system involvement in the ”rst few days oflife (1). The main concerns of families and medicalteams taking care of these neonates include not only theimmediate problems of management, but the need foran accurate evaluation of the severity of brain damage,and therefore the prediction of neurological outcome ofthese patients. Recent advances in neuroprotectiveinterventions emphasize even more the importance ofan early identi” cation of those infants at highest risk oflate neurological morbidity.Several methods have been used for early estimationof the damage and prediction of outcome. The mostavailable tools include clinical grading of the encepha-lopathy, electrophysiological assessments such as elec-troencephalogram and evoked responses, neuroimagingand cerebral blood ‘ow studies. However, uncertaintyregarding the eventual neurological outcome remainsduring the ” rst hours after birth; with the exception ofassessment of the electrical activity by means of anamplitude-integrated EEG, the other tools have alimited prognostic value in the earliest hours of life(2, 3).Brain damage induces the release of several sub-stances into the cerebrospinal ‘uid (CSF), e.g. metab-olic products (4, 5), neuro aminoacids (6,7), brain-speci” c proteins (BSPs) (8–11), nerve growth factor(12) and interleukin-6 (13). BSPs seem to be the bestbiochemical markers of brain damage after hypoxic-ischaemic injury. Those such as creatine kinase brainisoenzyme (8), neuron-speci”c enolase (9, 10), myelinbasic protein (10) and glial ” brillary acidic protein (11)in CSF may re‘ect the extent of ongoing brain damageand have shown to be of value in predicting outcome inasphyxiated infants. In this issue of
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