FUNCTIONAL
MATURATION OF LIMBIC SYSTEM. Harry T. Chugani,
Departments of Pediatrics, Neurology and Radiology,
Children's Hospital of Michigan, Wayne State University
School of Medicine, Detroit, Michigan.Using positron
emission tomography (PET) and the tracer
2-deoxy-2(18F)fluoro-D-glucose (FDG), we have shown that
the pattern of glucose metabolism in the human newborn
brain is fairly consistent, with the highest degree of
activity in primary sensory and motor cortex, cingulate
cortex, medial temporal region, thalamus, brainstem and
cerebellar vermis. Increases of glucose utilization are
seen by two to three months in the parietal, temporal and
primary visual cortex, basal ganglia, and cerebellar
hemispheres. These changes in glucose metabolism coincide
with improved skills involving visuo-spatial and
visuo-sensorimotor integration, the disappearance or
reorganization of brainstem reflex neonatal behaviors,
and increasing cortical contribution to the
electroencephalogram. Starting between 6 and 8 months,
lateral and inferior portions of frontal cortex become
more functionally active and eventually, between 8 and 12
months, the dorsal and med ial frontal regions also show
increased glucose utilization. These changes of frontal
cortex metabolism come at a time when cognitively-related
behaviors, such as the phenomenon of stranger anxiety,
and improved performance on the delayed response task
begin to appear. Increased glucose requirement in frontal
cortex also coincides with the expansion of dendritic
fields and the increased capillary density observed in
frontal cortex during the same period of development. By
approximately one year of age, the infant's pattern of
glucose utilization resembles qualitatively that of the
adult.
At birth,
the regional or local cerebral metabolic rates of glucose
utilization (LCMRglc) are about 30% lower than those seen
in adults. Between birth and approximately 3 years, the
cerebral cortex shows a dramatic increase in LCMRglc to
reach levels that exceed adult rates by over two-fold.
Such changes in LCMRglc are not observed in brainstem,
but a less dramatic increase is seen in basal ganglia and
thalamus. Between 3 years and about 10 years, the LCMRglc
for cerebral cortex is essentially at a high plateau of
over two-fold the glucose utilization seen in adults.
Subsequently, LCMRglc for cerebral cortex begins to
decline and gradually reaches adult values by 16-18
years. Based on the temporal relationship between these
developmental changes of LCMRglc and synaptogenesis in
humans, as well as on similar studies performed in our
laboratory on developing cat and monkey, we believe that
the ontogenetic changes of LCMRglc described above
provide an indirect measure of synaptogenesis in the
human brain.
[Abstract Titles] [Anderson] [Bolz] [Olson] [Levitt] [Zhou]