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William E. Bell, MD; Naguib A. Samaan, MD, PhD; Daniel S. Longnecker, MD

Arch Neurol. 1970;23(4):330-339.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

HYPOGLYCEMIA in the neonate or young infant is recognized to be a metabolic error with potentially devastating effects on the brain. Neurologic sequelae may occur in the adult, but susceptibility to hypoglycemia is much greater in the immature, poorly myelinated brain of the infant. In addition, the general metabolic immaturity of the neonate allows disturbances of carbohydrate metabolism in a variety of circumstances, such as cold exposure,¹ congestive heart failure,² or idiopathic respiratory distress of the newborn.³

Hypoglycemia in the young infant may be defined as true blood glucose level less than 20 mg/100 ml in the premature infant; less than 30 mg/100 ml in the full-term infant in the first 48 hours of life; and less than 40 mg/100 ml thereafter.⁴ Manifestations suggestive of hypoglycemia include pallor, lethargy, limpness, absent Moro reflex, rolling of the eyes or the abrupt appearance of internal strabismus, . . . [Full Text PDF of this Article]

Author Affiliations
Iowa City

From the departments of pediatrics and neurology (Dr. Bell) and pathology (Dr. Longnecker), University Hospitals, and the Veterans Administration Hospital (Dr. Samaan), Iowa City. Dr. Samaan is now with the M.D. Anderson Hospital, University of Texas, Houston, and Dr. Longnecker is now with the Department of Pathology, St. Louis University School of Medicine, St. Louis.

Footnotes
Accepted for publication May 14, 1970.

Reprint requests to Department of Pediatrics, University Hospitals, Iowa City 52240 (Dr. Bell).

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