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Ernest H. Friedman, MD
Departments of Medicine and Psychiatry Case Western Reserve University 1831 Forest Hills Blvd Cleveland, OH 44112

Arch Pediatr Adolesc Med. 1995;149(10):1178-1179.

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

The neurobiological manifestations of sustained arrhythmias in children prenatally exposed to cocaine¹ are suggested by reports linking brainstem cardiovascular control to dopamine lateralized to the right hemisphere.² This hypothesis is supported by a study demonstrating that prenatal stress reduces dopamine turnover in the right nucleus accumbens, leading to depression in adult offspring.³ The fact that delay-dependent speeding of reaction time, indicating motor readiness, is abolished by depletion of dopamine subserving cardiovascular reactivity in challenging tasks² prompts identification of a subset of children who are at increased risk for significant arrhythmias under conditions of stress¹ by monitoring vocal hesitation and switching pauses.² This noninvasive method is supported by immobility in behavioral despair,³ lengthy pause times, and shortened reaction times following cocaine administration.⁴ It is also supported by the construct validity of response latencies, easily obtainable through microcomputer testing of spontaneous speech in emotionally . . . [Full Text PDF of this Article]

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