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CARL E. HUNT, MD
Department of Pediatrics Medical College of Ohio CS 10008 Toledo, OH 43699

Am J Dis Child. 1990;144(2):138-139.

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

Sir.—We recently reported an increased incidence of respiratory pattern abnormalities in infants with prenatal cocaine exposure.¹ A deficient sleep arousal response to asphyxia may be a fundamental abnormality^2,3 in infants at risk for sudden infant death syndrome, and at least part of the interrelationship among intrauterine cocaine exposure, subsequent cardiorespiratory pattern abnormalities, and risk for sudden infant death syndrome may be deficient arousal responsiveness.

In the "Comment" section, we suggested a possible relationship among prenatal cocaine exposure, norepinephrine, and the locus coeruleus, the putative center of arousal in the brain stem. Specific references are now available that discuss in full detail the hypothesis originally proposed by Gingras and Weese-Mayer⁴ that cocaine-induced alterations in norepinephrine in the locus coeruleus may be secondary to an effect on neural transmitter homeostasis. Furthermore, this hypothesis is now being tested in an animal model⁵ and in a human model.⁶ . . . [Full Text PDF of this Article]

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