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Objective: We questioned whether neuron-specific enolase (NSE) and myelin basic protein (MBP) concentrations in cerebrospinal fluid (CSF) in the first 72 hours of life are correlated with the neurologic condition of asphyxiated full-term infants in the neonatal period and at 1 year of age., Patients and Methods: Sixty-nine asphyxiated infants were studied with serial neurologic examination, cranial ultrasonography, and neurologic follow-up. CSF samples were obtained by lumbar puncture at 12 and 72 hours of life. NSE was measured by enzyme immunoassay, and MBP was measured by radioimmunoassay., Results: Twenty infants had no neonatal encephalopathy and 49 exhibited different stages of encephalopathy. NSE and MBP concentrations in CSF at 12 and 72 hours of life were related to the degree of neonatal encephalopathy. Neither NSE nor MBP levels were correlated with any perinatal factors. Infants with documented brain injury had the highest concentrations of both NSE and MBP. The concentrations of these two biochemical markers at both 12 and 72 hours correlated with adverse outcome (death or cerebral palsy at 1 year). Based on a receiver operating characteristics curve analysis for any given specificity, NSE at 12 hours was a more accurate marker than MBP at either 12 or 72 hours for distinguishing infants with motor impairment at age 1 year from infants with normal outcome at the same age., Conclusions: Our findings suggest that NSE and MBP are reliable biochemical markers for early estimates of hypoxic-ischemic brain damage in asphyctic full-term newborns, NSE being superior to MBP.

Determination of CSF lactate levels were performed in 150 nonasphyxiated and 46 asphyxiated high risk neonates. Statistical analysis of log lactate levels of nonasphyxiated infants showed significant relationship to gestational and postnatal ages (P < .0001 and < .0002, respectively). CSF lactate elevation was seen in 16/29 infants studied within eight hours of asphyxia in contrast to 0/17 infants studied after eight hours (P < .001). Higher incidence of CSF lactate elevation was seen in term infants (7/8), infants with fetal distress (13/17), and very low Apgar scores (11/18). Seven of eight infants with markedly elevated lactate levels had both fetal distress and very low Apgar scores. CSF lactate determination in the immediate postasphyxial period appears to be an objective way of assessing the severity of cerebral hypoxia.