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Spectral EEG analysis using automated quantification of total absolute band power (tABP) expresses brain function. We hypothesized that pCO2 or blood glucose affects tABP during the critical first days of life in premature infants.To use automated tABP quantification to determine whether EEG background activity in premature infants during the first 3 days of life is influenced by pCO2 or blood glucose levels.Preterm infants, group 1 [gestational age (GA) = 24-27 weeks] and group 2 (GA = 28-30 weeks), underwent continuous EEG monitoring for 3 days after birth. Biochemical data were extracted from the observational datasheet used during monitoring. Blood samples were taken at the request of the attending physician. Statistical analyses were performed as repeated measurements using linear mixed models with a random intercept. The effect of time was treated as a fixed covariate and the GA groups as a fixed factor in all models. Continuous data were described using the mean ± SD or median and range, and categorical data were described using the number of patients and percentages unless otherwise indicated.There was an association between increased pCO2 and tABP and between increased blood glucose and tABP. Further, there were no differences in the responses between groups 1 and 2.Both hyperglycemia and hypercapnia showed a negative effect on brain activity decreasing tABP during the first 3 days of life in premature infants.

Although dexamethasone (DEX) is used widely in neonates with chronic, and even recently with acute respiratory disease, its potential side-effects on human cerebral and ocular haemodynamics remain unknown. The effects of DEX on cerebral and ocular blood flow velocities were assessed in preterm infants with lung disease and mechanical ventilation. Ten ventilated preterm infants received DEX (0.25 mg/kg/12 h) for ongoing chronic lung disease or extubation failure. Colour Doppler flow imaging studies of the internal carotid, anterior cerebral and ophthalmic arteries were made before and 10, 30, 60, 120 and 240 min after the 1st, 3rd, and 5th doses of DEX. Peak systolic, temporal mean, and end-diastolic flow velocities and the resistance index (RI) of Pourcelot were determined. The brain was examined by ultrasonography before and at the end of each Doppler study. All patients were continuously monitored for transcutaneous blood gases and blood pressure. All flow velocities and the RI of the internal carotid, anterior cerebral and ophthalmic arteries showed a similar trend throughout the study. The means of the values averaged for the 240 min of cerebral and ocular blood flow velocity with each dose were progressively higher and the values of the RI progressively lower up to the 5th dose. The most significant changes occurred in end-diastolic flow velocity and consisted of a percentage increase between the 1st and 5th dose of 72% in the internal carotid artery, 102% in the anterior cerebral artery and 84% in the ophthalmic artery. Changes in arterial blood pressure followed a pattern similar to that of changes in blood flow velocity.Dexamethasone increments cerebral and ocular blood flow velocity. We speculate that this finding may be relevant to the development of brain and retinal injury.

39 children with brachial plexus palsy during the period 1/1 1990 30/6 1995 were identified retrospectively. The incidence was 1.8/1,000 (95% confidence interval 1.3-2.5/1,000). Shoulder dystocia was noted in 74%, and 44% were delivered by vacuum or forceps. Mean birth weight was 4,300 g. The outcome is known for all children. Seven children show permanent sequelae; in three of these there is marked loss of function. In the remaining children, normalization occurred within one month in 41%, within three months in 69% and within six months in 83%. Surgical repair is now a treatment option if elbow flexion is still impossible at three months of age.

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.