Published online August 1, 2008
PEDIATRICS Vol. 122 No. 2 August 2008, pp. 440-441 (doi:10.1542/peds.2008-1417)
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COMMENTARY

How Low Can I Go? The Impact of Hypoglycemia on the Immature Brain

Terrie Inder, MBChB, MD, FRACP

Department of Pediatrics, St Louis Children's Hospital, Washington University, St Louis, Missouri

Abbreviations: EAA—excitatory amino acid

The first 20% of the full text of this article appears below.

Cerebral metabolism and function depends on adequate blood glucose, which provides for >90% of cerebral energy.1 Although the newborn brain is less vulnerable than the adult brain to the immediate functional and electrophysiological impact of hypoglycemia, epidemiologic and experimental evidence has confirmed cerebral injury related to isolated hypoglycemia in the newborn brain.2 In the July 2008 of Pediatrics, Burns et al3 described the neuroimaging findings and neurodevelopmental outcomes of 35 term infants with symptomatic hypoglycemia (86% of infants with a blood glucose of <35 mg/dL).


   NATURE AND MECHANISMS OF CEREBRAL INJURY
 
The impact of isolated hypoglycemia on the developing brain has been well documented in animal experiments, including those on primates.2,4 These experiments have defined 3 important principles in relation to hypoglycemia-mediated cerebral injury in the newborn. First, prolonged and severe, rather than transient or minor, hypoglycemia was required for . . . [Full Text of this Article]

Address correspondence to Terrie Inder, MBChB, MD, FRACP, Washington University School of Medicine, Department of Neurology, 660 S Euclid Ave, St Louis, MO 63110. E-mail: inder_t@wustl.edu