Cerebral metabolism is known to be highly dependent upon glucose utili
sation. In the neonate, severe hypoglycaemia is now recognized to be a
ssociated with subsequent adverse neurodevelopment and in extremis gli
al and neuronal cell death. However, the level at which hypoglycaemia
becomes clinically important is not well understood. Clinical methods
for assessing effects of hypoglycaemia are at best crude. Noninvasive
assessment of neuronal function suggests that cerebral dysfunction occ
urs at blood glucose levels well above clinical action levels. Thus, w
e appear to ignore apparently asymptomatic hypoglycaemia at our and in
deed the patient's peril. Furthermore, glycaemic status invariably is
interpreted with scant regard to alternative catabolic substrates. In
the neonate, recent evidence suggests this approach is unfounded. This
presentation will review evidence that glycaemic status in neonates s
hould no longer be considered as an entity in itself, but rather in th
e light of compensatory metabolic processes and treated accordingly.