Background: Knowledge about the effects of GH treatment on cognitive functioning in children with Prader-Willi syndrome (PWS) is limited.

Background: Midazolam sedation and morphine analgesia are commonly used in ventilated premature infants. Objectives: To evaluate the effects of midazolam versus morphine infusion on cerebral oxygenation and hemodynamics in ventilated premature infants. Methods: 11 patients (GA 26.6–33.0 weeks, BW 780–2,335 g) were sedated with midazolam (loading dose 0.2 mg/kg, maintenance 0.2 mg/kg/h) and 10 patients (GA 26.4–33.3 weeks, BW 842–1,955 g) were sedated with morphine (loading dose 0.05 mg/kg, maintenance 0.01 mg/kg/h). Changes in oxyhemoglobin (ΔcO₂Hb) and deoxyhemoglobin (ΔcHHb) were assessed using near infrared spectrophotometry. Changes in cHbD (= ΔcO₂Hb – ΔcHHb) reflect changes in cerebral blood oxygenation and changes in concentration of total hemoglobin (ΔctHb = ΔcO₂Hb + ΔcHHb) represent changes in cerebral blood volume (ΔCBV). Changes in cerebral blood flow velocity (ΔCBFV) were intermittently measured using Doppler ultrasound. Heart rate (HR), mean arterial blood pressure (MABP), arterial oxygen saturation (saO₂) and transcutaneous measured pO₂ (tcpO₂) and pCO₂ (tcpCO₂) were continuously registered. Statistical analyses were carried out using linear mixed models to account for the longitudinal character study design. Results: Within 15 min after the loading dose of midazolam, a decrease in saO_2, tcpO₂ and cHbD was observed in 5/11 infants. In addition, a fall in MABP and CBFV was observed 15 min after midazolam administration. Immediately after morphine infusion a decrease in saO_2, tcpO₂ and cHbD was observed in 6/10 infants. Furthermore, morphine infusion resulted in a persistent increase in CBV. Conclusions: Administration of midazolam and morphine in ventilated premature infants causes significant changes in cerebral oxygenation and hemodynamics, which might be harmful.

Our study shows that the primordial follicle pool and number of small antral follicles are conserved in girls and female adolescents with PWS. We found no classical hypogonadotropic hypogonadism. However, maturation of follicles and progression of pubertal development are impaired, which might be due to dysregulation of LH secretion. Because these impairments are not absolute, ovulation and thus conception cannot be ruled out in individual female adolescents with PWS.

Background: Sodium bicarbonate (NaHCO₃) is often used for correction of metabolic acidosis in preterm infants. The effects of NaHCO₃ administration on cerebral hemodynamics and oxygenation are not well known. Furthermore, there is no consensus on infusion rate of NaHCO₃. Objectives: To evaluate the effects of rapid versus slow infusion of NaHCO₃ on cerebral hemodynamics and oxygenation in preterm infants. Methods: Twenty-nine preterm infants with metabolic acidosis were randomized into two groups (values are mean ±SD): In group A (GA 30.5 ± 1.7 weeks, b.w. 1,254 ± 425 g) NaHCO₃ 4.2% was injected as a bolus. In group B (GA 30.3 ± 1.8 weeks, b.w. 1,179 ± 318 g) NaHCO₃ 4.2% was administered over a 30-min period. Concentration changes of oxyhemoglobin (cO₂Hb) and deoxyhemoglobin (cHHb) were assessed using near infrared spectrophotometry. Changes in HbD (= cO₂Hb – cHHb) represent changes in cerebral blood oxygenation and changes in ctHb (= cO₂Hb + cHHb) reflect changes in cerebral blood volume. Cerebral blood flow velocity was intermittently measured using Doppler ultrasound. Longitudinal data analysis was performed using linear mixed models (SAS procedure MIXED), to account for the fact that the repeated observations in each individual were correlated. Results: Administration of NaHCO₃ resulted in an increase of cerebral blood volume which was more evident if NaHCO₃ was injected rapidly than when infused slowly. HbD and cerebral blood flow velocity did not show significant changes in either group. Conclusion: To minimize fluctuations in cerebral hemodynamics, slow infusion of sodium bicarbonate is preferable to rapid injection.