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OBJECTIVE: To document perinatal events, brain imaging, neurophysiology and clinical outcome in term infants with early postnatal collapse (PNC). DESIGN: Tertiary referral centre, retrospective case review (1993-2006). PATIENTS: Infants born at > or =36 weeks' gestation with early (<72 h) PNC. Peri-partum and post-collapse data were collated with clinical, electrophysiological, neuroimaging and autopsy data and neurodevelopmental outcome. RESULTS: Twelve infants were studied; median gestation 39 weeks (36-41), birth weight 3150 g (1930-4010). Ten were born vaginally (including occipitoposterior (1), breech (2), water birth (2), ventouse/forceps (3)), and two by emergency caesarean section. Median Apgar scores were 9 (3-9) and 10 (8-10) at 1 and 5 min; median cord pH was 7.29 (7.18-7.34). All were thought to be well after birth. The median age at PNC was 75 min (10 min to 55 h). All infants required extensive resuscitation. The median pH after PNC was 6.75 (6.39-7.05). Seven infants became severely encephalopathic, with severely abnormal EEG/aEEG recorded within 12 h. MRI showed acute severe hypoxic-ischaemic injury. All died. One infant showed rapid recovery, had mild encephalopathy, and good outcome. Four infants had severe respiratory illness, normal background EEG, and MRI showing slight white matter change (n = 3) or a small infarction (n = 1). All had a good 2-year outcome. CONCLUSIONS: In this term cohort, early PNC was generally followed by severe encephalopathy, acute central grey matter injury and poor outcome, or severe respiratory illness, slight white matter change and good outcome. Early EEG and MRI predicted outcome accurately. However, no antepartum, intrapartum or other aetiological factors were identified. Further investigation is needed in larger PNC cohorts.

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Well constructed and carefully analysed trials of hypothermic neural rescue therapy for infants with neonatal encephalopathy have recently been reported. The data suggest that either selective head cooling or total body cooling reduces the combined chance of death or disability after birth asphyxia. However, as there are still unanswered questions about these treatments, many may still feel that further data are needed before health care policy can be changed to make cooling the standard of care for all babies with suspected birth asphyxia.

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In this study we present a design for a multi-frequency microwave radiometer aimed at prolonged monitoring of deep brain temperature in newborn infants and suitable for use during hypothermic neural rescue therapy. We identify appropriate hardware to measure brightness temperature and evaluate the accuracy of the measurements. We describe a method to estimate the tissue temperature distribution from measured brightness temperatures which uses the results of numerical simulations of the tissue temperature as well as the propagation of the microwaves in a realistic detailed three-dimensional infant head model. The temperature retrieval method is then used to evaluate how the statistical fluctuations in the measured brightness temperatures limit the confidence interval for the estimated temperature: for an 18 degrees C temperature differential between cooled surface and deep brain we found a standard error in the estimated central brain temperature of 0.75 degrees C. Evaluation of the systematic errors arising from inaccuracies in model parameters showed that realistic deviations in tissue parameters have little impact compared to uncertainty in the thickness of the bolus between the receiving antenna and the infant's head or in the skull thickness. This highlights the need to pay particular attention to these latter parameters in future practical implementation of the technique.

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Introduction of hypothermia therapy as a neuroprotection therapy after hypoxia-ischemia in newborn infants requires appraisal of cooling methods. In this numerical study thermal simulations were performed to test the hypothesis that cooling of the surface of the cranium by the application of a cooling bonnet significantly reduces deep brain temperature and produces a temperature differential between the deep brain and the body core. A realistic three-dimensional (3-D) computer model of infant head anatomy was used, derived from magnetic resonance data from a newborn infant. Temperature distributions were calculated using the Pennes heatsink model. The cooling bonnet was at a constant temperature of 10 degrees C. When modeling head cooling only, a constant body core temperature of 37 degrees C was imposed. The computed result showed no significant cooling of the deep brain regions, only the very superficial regions of the brain are cooled to temperatures of 33-34 degrees C. Poor efficacy of head cooling was still found after a considerable increase in the modeled thermal conductivities of the skin and skull, or after a decrease in perfusion. The results for the heatsink thermal model of the infant head were confirmed by comparison of results computed for a scaled down adult head, using both the heatsink description and a discrete vessel thermal model with both anatomy and vasculature obtained from MR data. The results indicate that significant reduction in brain temperature will only be achieved if the infant's core temperature is lowered.

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This study addressed the hypothesis that in human infants severe in utero insults induce a significant proportion of brain cells to undergo apoptosis. Morphologic criteria were used to quantify apoptosis and necrosis in the cingulate gyrus of two groups of infants: six infants who died after severe birth asphyxia with hypoxic-ischemic encephalopathy, and six others who suffered unexpected and apparently sudden intrauterine death at or close to term. The fraction of apoptotic cells was much higher than basal levels determined in animal experiments, and within both groups increased in proportion to the severity of injury as determined by total cell death (p < 0.05). The mean fraction of apoptotic cells was similar in asphyxiated infants, 8.3% (95% confidence interval for the population, 3.7-12%), and in stillbirths, 6.7% (0.2-13.6%). In the asphyxiated group, 20.8% (11-30.6%) of cells were necrotic, but significantly less necrosis, 3% (0.4-5.6%), was seen in stillborn infants (p < 0.05). Cell death was apoptotic after birth asphyxia in 26% (1-51%) and 78% (41-100%) in stillborn infants. In situ end labeling studies confirmed the presence of DNA fragmentation in apoptotic cells. These results demonstrate that infants who die after intrauterine insults, both those with evidence of delayed cerebral injury after hypoxia-ischemia and those without, have a significant number of cells in the brain with the morphologic characteristics of apoptosis. They confirm that apoptosis contributes significantly to cerebral damage in the perinatal period.

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