The interactions between premature birth and the caregiving environment on infants' cognitive and social functioning were examined. Participants were 150 infants (83 preterm, 67 full-term) and their parents. When infants were 6 months old, parents reported on their levels of emotional distress, and triadic family interactions were filmed and coded. At 12 months of age, the infants' cognitive and social functioning was assessed. Prematurity moderated the effects of maternal (but not paternal) emotional distress and triadic interactions on infants' cognitive and social outcomes. Whereas for cognitive functioning the interactions were consistent with a diathesis-stress approach, for social functioning the interactions were consistent with a differential susceptibility approach. The differential effects of the caregiving environment between groups and outcomes are discussed.

A characteristic of perinatal encephalopathies are the distinct patterns of neuronal and glial cell loss. Cerebral hypoperfusion is thought to be a major cause of these lesions. Gestational age is likely to influence outcome. This study compares the cortical electrophysiologic and histopathologic responses to hypoperfusion injury between preterm and near term fetuses. Chronically instrumented 0.65 (93-99-d, n = 9) and 0.9 (119-133-d, n = 6) gestation fetal sheep underwent 30 min of cerebral hypoperfusion injury. The parasagittal cortical EEG and impedance (measure of cytotoxic edema) responses plus histologic outcome (3 d) were compared. The acute rise in impedance was similar in amplitude, but the onset was delayed (5.0 +/- 0.7 versus 9.1 +/- 1.1 min, p < 0.05) in the preterm fetuses relative to those near term. In contrast the extent of the secondary rise was reduced (p < 0.01) and peaked earlier in the preterm fetuses (19.8 +/- 1.0 versus 40.5 +/- 3.5 h, p < 0.01). Both groups had a similar fall in EEG spectral edge frequency. The preterm fetuses had a milder loss of EEG intensity at 72 h (-7.7 +/- 1.5 versus -12.8 +/- 0.9 dB, p < 0.05). At both ages there was a predominantly parasagittal cortical distribution of damage with a similar pattern of neuronal loss in the thalamus and striatum. There was extensive selective neuronal loss within the upper layers of the cortex in those near term. In contrast the preterm fetuses developed subcortical infarcts (p < 0.05). The cortical response to injury altered during the last trimester. The results suggest the severity of the delayed phase of cortical neuronal injury and selective neuronal loss increased near term. In contrast, the preterm fetuses had a more rapidly evolving injury leading to necrosis of the subcortical white matter.

Cerebral blood flow (CBF) measurement by near infrared spectroscopy (NIRS) using oxyhemoglobin (HbO2) as a tracer (CBF-HbO2) needs rapid changes in arterial oxygen saturation (SaO2) which often cannot be achieved in many sick infants. An alternative method based on the same adaptation of the Fick principle using i.v. injection of the dye indocyanine green (ICG) is described (CBF-ICG). Six mechanically ventilated infants (age 26-38 wk, birth weight 0.885-3.730 kg) requiring supplementary oxygen therapy were studied within 72 h of birth. For CBF-ICG measurements, ICG (0.1 mg x kg-1 was injected via an umbilical venous catheter, and blood ICG concentration was measured by an optical umbilical artery catheter and brain ICG concentration was measured by NIRS. For CBF-HbO2 measurements the inspired oxygen concentration was rapidly increased, blood HbO2 concentration was calculated from SaO2 measured by pulse oximetry, and brain HbO2 concentration was measured by NIRS. A series of CBF measurements were performed using each method before and after altering the arterial carbon dioxide tension (PaCO2). Mean CBF values from repeated measurements by each method at any given PaCO2 were used to compare the methods. The SD of single measurements within an individual subject by CBF-ICG was 15%, and by CBF-HbO2, 24%. The relationship between the methods was mean CBF-ICG = (1.13 x mean CBF-HbO2) - 2.76 mL x 100 g-1 x min-1 HbO2 (r = 0.93, p < 0.001). The mean difference between the methods (CBF-ICG - CBF-HbO2) was -0.25 mL x 100 g-1 x min-1 (95% confidence interval 6.30 to -6.80). The methods were in good agreement, and the use of i.v. ICG permitted rapid and repeated CBF measurements in the sickest infants at greatest risk of cerebral injury.

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