Mayes Linda C, Grillon Christian, Granger Richard, Schottenfeld Richard
Yale Child Study Center, Yale School of Medicine, New Haven, Connecticut 06520, USADepartment of Psychiatry, Yale School of Medicine, New Haven, Connecticut 06520, USA.
Ann N Y Acad Sci. 1998 Jun;846(1):126-143. doi: 10.1111/j.1749-6632.1998.tb09731.x.
Four lines of evidence suggest a plausible link between prenatal cocaine exposure (CE) and specific effects on the mechanisms subserving arousal and attention regulation in infants and preschool-aged children. These are (1) the association of prenatal CE with alterations in monoaminergic system ontogeny; (2) neurobehavioral effects of prenatal CE in animals consistent with an enduring increased level of activity in response to novelty and inhibited exploration and altered responses to stress, suggesting overarousal in the face of novel/stressful situations and disrupted attention and exploration; (3) altered norepinephrine system function in cocaine-exposed human infants; and (4) neurobehavioral findings in infants and preschool-aged children suggestive of disrupted arousal regulation in the face of novelty, increased distractibility, and consequent impaired attention to novel, structured tasks. This paper summarizes findings on response to novel challenges from a cohort of prenatally cocaine-exposed infants and preschool-aged children followed longitudinally since birth. Arousal regulation in the face of novel challenges is operationalized behaviorally as state and emotional reactivity and neurophysiologically as the startle response and heart rate variability. Across different ages and tasks, behavioral and neurophysiological findings suggest that prenatally cocaine-exposed children are more likely to exhibit disrupted arousal regulation. Because the regulation of arousal serves as a gating mechanism to optimize orientation and attention, arousal regulation has important implications for ongoing information processing, learning, and memory. Furthermore, impaired arousal regulation predisposes children to a lower threshold for activation of "stress circuits" and may increase their vulnerability to the developmentally detrimental effects of stressful conditions particularly when such children are also exposed to the chaotic environmental conditions often characterizing substance-abusing families.
有四条证据表明，产前接触可卡因（CE）与对婴儿和学龄前儿童唤醒及注意力调节机制的特定影响之间存在合理联系。这些证据包括：（1）产前接触可卡因与单胺能系统个体发育改变之间的关联；（2）产前接触可卡因对动物的神经行为影响，表现为对新奇事物的反应持续增加、探索受抑制以及对应激反应改变，这表明在面对新奇/应激情况时过度唤醒，注意力和探索能力受到干扰；（3）接触可卡因的人类婴儿去甲肾上腺素系统功能改变；（4）婴儿和学龄前儿童的神经行为学研究结果表明，面对新奇事物时唤醒调节受到干扰，注意力分散增加，进而对新奇的结构化任务的注意力受损。本文总结了一组自出生起就纵向跟踪的产前接触可卡因的婴儿和学龄前儿童对新奇挑战的反应研究结果。面对新奇挑战时的唤醒调节在行为上表现为状态和情绪反应性，在神经生理学上表现为惊跳反应和心率变异性。在不同年龄和任务中，行为和神经生理学研究结果表明，产前接触可卡因的儿童更有可能表现出唤醒调节紊乱。由于唤醒调节作为一种门控机制，用于优化定向和注意力，因此对正在进行的信息处理、学习和记忆具有重要意义。此外，唤醒调节受损使儿童更容易激活“应激回路”，可能增加他们对压力条件下发育有害影响的易感性，特别是当这些儿童还暴露于吸毒家庭常见的混乱环境条件时。
