Changes of positron emission tomography in newborn infants at different gestational ages, and neonatal hypoxic-ischemic encephalopathy.

Cerebral glucose metabolism was measured by (18)F-fluorodeoxyglucose position emission tomography in infants at different gestational ages and with neonatal hypoxic-ischemic encephalopathy. Thirty-six preterm and term infants at different gestational ages without brain injury were divided into four subgroups: ≤32 weeks (n = 4), 33-34 weeks (n = 5), 35-36 weeks (n = 12), and ≥37 weeks (n = 15). Twenty-four newborn infants with hypoxic-ischemic encephalopathy were divided into three subgroups: mild (n = 13), moderate (n = 7), and severe (n = 4). Cerebral glucose metabolism manifested a trend toward increase, and the structure of cranial (18)F-fluorodeoxyglucose positron emission tomography images became clear with increased gestational age, especially at ≥37 weeks. Uptakes of (18)F-fluorodeoxyglucose in the ≥37-week group were significantly higher than in the ≤32-week group (P < 0.01). Cerebral glucose metabolism changed significantly in neonatal hypoxic-ischemic encephalopathy, and was either unbalanced bilaterally or relatively low at all sites. Moreover, uptakes of (18)F-fluorodeoxyglucose were significantly lower in severe than in mild and medium hypoxic-ischemic encephalopathy (P < 0.05). Cerebral glucose metabolism, as measured by (18)F-fluorodeoxyglucose positron emission tomography, may prove useful for estimating brain development and injury in newborn infants, and its clinical values need further investigation.

Brain positron emission tomography in preterm and term newborn infants.

OBJECTIVE: To study the clinical values of positron emission tomography (PET) in preterm and term newborn infants through observing brain glucose metabolism by (18)F-fluorodeoxyglucose ((18)F-FDG) PET. METHOD: To observe the brain (18)F-FDG PET imaging in 9 term and 7 preterm newborn infants in the same condition after administration of 0.1 mCi/kg (18)F-FDG. RESULT: The brain (18)F-FDG PET imaging showed that the uptake of (18)F-FDG was relatively more in the thalamus, and less in the cerebral cortex in preterm and term newborn infants. The uptake of (18)F-FDG of cerebral cortex in preterm infants was less than that in term infants, so the structure of brain (18)F-FDG PET imaging was a little fainter in preterm neonates as compared with that in term newborns. CONCLUSION: (18)F-FDG PET imaging could show different glucose metabolisms of brain in preterm and term infants. Brain (18)F-FDG PET imaging might be a useful tool for estimating the brain function in newborn infants, and its clinical values need further investigation.