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Neurophysiological dysfunction in relation to the concentration of glucose in the blood
Early Human Development, 17 (1988) 287--295
287
Elsevier Scientific Publishers Ireland Ltd. EHD 00912
Abstracts of papers presented at the Neonatal Society Meeting November 1987
Neurophysioiogical dysfunction in relation to the concentration of glucose in the blood. T.H.H.G. Koh*, J.A. Eyre, M. Tarbit and A. Aynsley-Green, Department of Child Health, University of Newcastle upon Tyne, U.K. That hypoglycaemia can cause brain damage cannot be disputed. There is, however, controversy over the definition of hypoglycaemia in neonates and children and over its significance when asymptomatic. We have measured sensory evoked potentials and correlated them to blood glucose concentrations in 16 children aged 1 day--15 years. Eleven (two newborns) were fasted during investigations for recurrent hypoglycaemia; three (all newborns) were studied during spontaneous hypoglycaemia and two had insulin provocation for the investigation of short stature. Serial brainstem evoked potentials (EPs) were measured in 11 and somatosensory EPs in five. A blood glucose level (<2.5 mmol/1 was recorded in ten children, nine of whom showed abnormal changes in EPs; only four were symptomatic. Following restoration of the blood glucose > 2.5 mmol/1 EPs returned immediately to normal in six, but in three (all neonates) the EPs remained abnormal for 1 h, 1 day and 2 days respectively. The only subject with no change in EPs had hyperketonaemic hypoglycaemia. No change was recorded in serial EPs in the six children who maintained blood glucose levels > 2.5 mmol/1. We conclude: (1) EPs allow an objective measurement of neural function ;n relation to intermediary metabolism; (2) asymptomatic hypoglycaemia is associated with neurophysiological dysfunction; (3) more detailed studies will allow a functional definition of hypoglycaemia in different groups of neonates and children. *Support from the M.R.C. is gratefully acknowledged. The effects of systemic glucose administration on brain metabolism and intracellular pH (pHi) during cerebral ischaemia studied by in vivo 31p and tH magnetic resonance spectroscopy in the lamb. P.L. Hope, E.B. Cady, D.T. Delpy, N.K. Ives, R.M. Gardiner and E.O.R. Reynolds, Department of Medical Paediatrics and Medical Physics and Bioengineering, University College London, Rayne Institute, London WC1E 6J J, U.K. There is evidence that accumulation of lactate with concomitant intracellular acidosis is an important mediator of neuronal damage during cerebral ischaemia, and that hyperglycaemia may have a deleterious effect by accelerating anaerobic glycolysis. The aim of these experiments was to further investigate the influence of blood glucose concentration on brain metabolism during ischaemia. Observations were made in nine lambs under sodium pentobarbitone anaesthesia. Brain phosphorus metabolites, pH i and brain lactate were measured by 3~p and ~H-MRS under control conditions, during 40 min cerebral ischaemia, and in the postischaemic period. Measurements were also made of arteriocerebral venous concentration differences for oxygen, glucose and lactate. Three animals were normoglycaemic during ischaemia (Group A, plasma glucose 8.5 _+ S.E.M. 2.5 mM/1) and in six animals IV glucose was infused (Group B, plasma glucose 17.7 _ 1 mM/l).
287
Elsevier Scientific Publishers Ireland Ltd. EHD 00912
Abstracts of papers presented at the Neonatal Society Meeting November 1987
Neurophysioiogical dysfunction in relation to the concentration of glucose in the blood. T.H.H.G. Koh*, J.A. Eyre, M. Tarbit and A. Aynsley-Green, Department of Child Health, University of Newcastle upon Tyne, U.K. That hypoglycaemia can cause brain damage cannot be disputed. There is, however, controversy over the definition of hypoglycaemia in neonates and children and over its significance when asymptomatic. We have measured sensory evoked potentials and correlated them to blood glucose concentrations in 16 children aged 1 day--15 years. Eleven (two newborns) were fasted during investigations for recurrent hypoglycaemia; three (all newborns) were studied during spontaneous hypoglycaemia and two had insulin provocation for the investigation of short stature. Serial brainstem evoked potentials (EPs) were measured in 11 and somatosensory EPs in five. A blood glucose level (<2.5 mmol/1 was recorded in ten children, nine of whom showed abnormal changes in EPs; only four were symptomatic. Following restoration of the blood glucose > 2.5 mmol/1 EPs returned immediately to normal in six, but in three (all neonates) the EPs remained abnormal for 1 h, 1 day and 2 days respectively. The only subject with no change in EPs had hyperketonaemic hypoglycaemia. No change was recorded in serial EPs in the six children who maintained blood glucose levels > 2.5 mmol/1. We conclude: (1) EPs allow an objective measurement of neural function ;n relation to intermediary metabolism; (2) asymptomatic hypoglycaemia is associated with neurophysiological dysfunction; (3) more detailed studies will allow a functional definition of hypoglycaemia in different groups of neonates and children. *Support from the M.R.C. is gratefully acknowledged. The effects of systemic glucose administration on brain metabolism and intracellular pH (pHi) during cerebral ischaemia studied by in vivo 31p and tH magnetic resonance spectroscopy in the lamb. P.L. Hope, E.B. Cady, D.T. Delpy, N.K. Ives, R.M. Gardiner and E.O.R. Reynolds, Department of Medical Paediatrics and Medical Physics and Bioengineering, University College London, Rayne Institute, London WC1E 6J J, U.K. There is evidence that accumulation of lactate with concomitant intracellular acidosis is an important mediator of neuronal damage during cerebral ischaemia, and that hyperglycaemia may have a deleterious effect by accelerating anaerobic glycolysis. The aim of these experiments was to further investigate the influence of blood glucose concentration on brain metabolism during ischaemia. Observations were made in nine lambs under sodium pentobarbitone anaesthesia. Brain phosphorus metabolites, pH i and brain lactate were measured by 3~p and ~H-MRS under control conditions, during 40 min cerebral ischaemia, and in the postischaemic period. Measurements were also made of arteriocerebral venous concentration differences for oxygen, glucose and lactate. Three animals were normoglycaemic during ischaemia (Group A, plasma glucose 8.5 _+ S.E.M. 2.5 mM/1) and in six animals IV glucose was infused (Group B, plasma glucose 17.7 _ 1 mM/l).