Evoked potentials were used to measure neural function in relation to blood glucose concentration in 17 children at the Department of Child Health, University of Newcastle upon Tyne. Thirteen children were admitted for investigation of metabolic or endocrine disorders and hypoglycemia was provoked by fasting or insulin administration; 4 had recurrent episodes of spontaneous hypoglycemia. Abnormal brainstem auditory evoked potentials were recorded in 9 and abnormal somatosensory evoked potentials in 1 of the 11 children whose blood glucose concentration remained above 2.6 mmol/1; 5 of these 10 children were asymptomatic and 5 became drowsy. No change in evoked potentials was recorded in the 6 children whose blood glucose concentration remained above 2.6 mmol/1. Of the 10 children with abnormal evoked potentials, 6 had normal latencies immediately after the IV administration of 25% dextrose (2ml/kg) or the IM administration of glucagon (20 ug/kg), whereas 4 had persistently prolonged I-V latencies or absent wave V for 1 hr, 1.5 hrs, 16 hrs, and 2 days. The authors suggest that blood glucose concentration should be maintained above 2.6 mmol/1 to ensure normal neural function in newborns and children irrespective of the presence or absence of abnormal clinical signs. [1]

COMMENT. A prospective controlled study of neonates with episodes of hypoglycemia has shown that long term follow up may reveal impairments in intellectual function [2]. Short term follow up studies of infants who have suffered hypoglycemia may be misleading. Clinical signs of hypoglycemia and disturbances of neural function in the newborn baby may be subtle and difficult to recognize, and the distinction between “symptomatic“ and “asymptomatic“ hypoglycemia may require recordings of evoked potentials to demonstrate neural dysfunction. Whether the transient abnormalities in evoked potentials demonstrated in the above study can be predictive of permanent neural damage remains to be determined. The neurological signs resulting from abnormal cerebral metabolism secondary to hypoglycemia may depend on the rate of fall of blood sugar, the duration and degree of hypoglycemia, and the age of the patient [3]. Alternative substrates, particularly ketone bodies, can be used for energy by the brain and may have a protective effect during episodes of hypoglycemia. [4]