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Updated: Aug 19, 2026

Non-invasive Optical Measurement of Cerebral Metabolism and Hemodynamics in Infants
Published on: March 14, 2013
Cerebral oxygen metabolism in newborns
D I Altman1, J M Perlman, J J Volpe
1Department of Neurology, Washington University School of Medicine, St Louis, MO 63110.
Insights
Newborn brain energy needs are lower than adults, with minimal cerebral metabolic rate for oxygen (CMRO2) observed in healthy infants. This suggests newborns may utilize nonoxidative metabolism to meet brain energy demands.
Area of Science:
- Neonatal neuroscience
- Developmental neurobiology
- Pediatric critical care
Background:
- Understanding neonatal brain energy metabolism is crucial for treating sick newborns.
- Developmental changes in brain metabolism impact nutrient supply and therapeutic interventions.
Purpose of the Study:
- To investigate developmental changes in brain energy metabolism in human neonates.
- To measure cerebral metabolic rate for oxygen (CMRO2) in sick newborns.
Main Methods:
- Positron emission tomography (PET) was used to measure CMRO2.
- The study included 11 sick newborns of varying gestational ages.
Main Results:
- Preterm infants showed CMRO2 ranging from 0.06 to 0.54 mL/100g/min.
- Term infants exhibited CMRO2 between 0.0 and 1.3 mL/100g/min.
- Newborns with minimal brain injury had CMRO2 below adult viability thresholds.
Conclusions:
- Neonatal brain energy requirements are significantly lower than in adults.
- The fetal and newborn brain may meet energy needs through nonoxidative metabolism.
- CMRO2 levels in healthy newborns suggest unique metabolic adaptations.
Objective:
A better understanding of the developmental changes in brain energy metabolism that occur in human neonates is critically important for designing rational treatment strategies that ensure an adequate supply of nutrients to the brain and minimize deleterious side effects of therapeutic interventions in sick newborns.
Methods:
Cerebral metabolic rate for oxygen (CMRO2) was measured with positron emission tomography in 11 sick newborns of different gestational ages.
Results:
In five preterm infants, mean hemispheric CMRO2 was 0.06 to 0.54 mL 100 g-1 min-1. Two of these preterm infants with virtually absent CMRO2 (0.06 mL 100 g-1 min-1) had minimal or no evidence of parenchymal brain injury detected in the newborn period. In six term infants, mean hemispheric CMRO2 was 0.0 to 1.3 mL 100 g-1 min-1. Two with no neurological disease had mean hemispheric CMRO2 of 0.4 and 0.7 mL 100 g-1 min-1 and were normal at 6 and 7 months, respectively.
Conclusions:
CMRO2 in four newborns who had minimal or no detectable brain injury was considerably below the threshold for brain viability in adults of 1.3 mL 100 g-1 min-1. This indicates that energy requirements in fetal and newborn brain are minimal or can be met by nonoxidative metabolism.
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