The objective of our study was to describe PET performed in term AGA infants at 36 mo who were diagnosed to have perinatal asphyxia defined as cord ph <7.1, 5 min Apgar ≤4, need for CPR at birth and presence of hypoxic ischemic encephalopathy. Surviving infants had serial neurological examinations categorized at 36 mo as normal, neuromotor impairment with no developmental delay, or cerebral palsy (CP with developmental delay). Infants had neonatal CT and magnetic resonance imaging (MRI) at 6 mo. At 36 mo infants underwent PET to assess glucose metabolism using Siemens EXACT-HR tomograph with IV administration of 0.143 mCi/kg of 18-fluoro-2-deoxyglucose (FDG). PET and neurologic exams were performed by independent examiners.

Results: 14 study infants survived to 36 mo, 3 refused consent for PET. Of the 11 infants with PET, 5 had normal neurologic exams, 1 had neuromotor impairment and 5 had CP (spastic quadriplegia). PET revealed normal glucose metabolism in 2 infants, both of whom had normal neurologic exams. Decreased glucose metabolism was noted in 4 of 11 infants. One infant who had hypometabolism in thalamus and cerebellum had a normal neurologic exam, another with hypometabolism in posterior frontal, anterior parietal and superior temporal cortex bilaterally, also had a normal neurologic exam. The third infant with hypometabolism in the superior temporal cortex and thalamus had a normal neurological exam while the remaining infant with mild hypometabolism in metabolism in the temporal cortex had a normal neurological exam. The remaining 5 infants had severe hypometabolism of the entire cerebral cortex ± hypometabolism of thalamus ± sparing of the occipital cortex. Brain stem metabolism remained intact in all. All 5 infants had severe CP. The sensitivity of PET for documenting CP/impairment was 100%; specificity was 40%. CT, MRI did not correlate with outcome. Absolute glucose metabolic rates and correlation of PET with neuropsychological outcome are being performed.