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Neurobiology of Arrhythmias in Children Prenatally Exposed to Cocaine

Ernest H. Friedman, MD
Arch Pediatr Adolesc Med. 1995;149(10):1178-1179. doi:10.1001/archpedi.1995.02170230132028.
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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


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