Abstract
2391
Introduction: The brain primarily utilizes glucose for ATP generation. However, in situations where glucose is lacking, e.g. prolonged fasting, ketone bodies such as b- hydroxybutyrate and acetoacetate become an important energy source for the brain. The brain’s utilization of ketones depends mainly on the concentration in the blood, thus many dietary approaches such as ketogenic diets, ingestion of ketogenic medium-chain fatty acids or exogenous ketones, facilitate significant changes in the brain’s metabolism.
Ketosis has been variously described previously as causing increased or decreased brain glucose utilisation with multiple animal studies and case reports providing conflicting results.
The analysis of regional cerebral glucose metabolism (FDG uptake) is an important component of the interpretation of paediatric brain scans. Regional differences may be seen in a wide variety of pathologies such as seizures, developmental disorders, encephalitis, genetic and injuries.
The analysis of cerebral uptake may involve comparison to a normal age appropriate uptake database. It has been previously demonstrated that glucose uptake in brain regions varies with age and maturation.
We set out to examine whether the ketosis generated by the fasting state for a FDG PET scan was sufficient to create a significant change in cerebral regional FDG uptake that may change the interpretation of brain FDG studies.
Methods: Children and adolescents between the ages of 5- 18 who underwent a PET MRI study were identified using the Royal Childrens Hospital database.
Only patients who were awake (non-anaesthetised) for uptake were included.
Patients were examined for a variety of indications including seizure disorders, oncological, infection and inflammatory conditions.
Patients with known cerebral tumours/ pathologies were excluded.
Fasting ranged from 4 hours to 24 hours.
Blood sugar level and blood ketones were measured prior to FDG injection.
All patients underwent PETMR imaging on a Seimens Biograph scanner.
Automated regions were obtained for the frontal, parietal, temporal and occipital lobes, as well as the basal ganglia. Regional SUVmax for each region was measured using the Seimens Syngovia Neuroanalysis application.
SUV max for the respective regions was plotted against blood ketone levels with trend lines generated.
The analysis was made in two groups 4-10 and 11-18 as it has been shown previously that regional cerebral metabolism changes with maturity.
Results: There were 55 individual patients available for analysis.
18 were between 4-10 years of age and 37 from 11-18.
Blood glucose levels were in the normal range in all patients.
Ketone levels ranged from 0-3.8 mmol/l in the 4-10 age group with an average of 0.51, and from 0.1 to 1.4 in the 11-18 group with an average of 0.3.
SUV max 4-10 years: basal ganglia mean 12.4: range 7.3-19.1, frontal lobe mean 12.59:range 6.8-17.6, parietal lobe mean 12.7: range 6.2 - 20.5.
SUV max 11-18 years: basal ganglia mean 14.8: range 8.6- 27.5, frontal lobe mean 16.2:range 6.9-28.2, parietal lobe mean 15.6: range 6.4-24.1.
This slight increase in SUVmax is in keeping with the expected change in uptake with maturation.
Plotting regional uptake against ketone levels showed a non significant change in SUV as blood ketone levels rose.
Conclusions: Our analysis confirms the normal increase in regional cerebral glucose usage with maturation.
The degree of ketosis associated with a short fast of 24 hours or less does not significantly affect the uptake of FDG sufficiently to require correction in the analysis of cerebral PET scans.
It should not be assumed that children on more prolonged ketogenic diets would also show this pattern.
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