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The dopaminergic hypothesis of attention-deficit/hyperactivity disorder needs re-examining.

机译:注意缺陷/多动障碍的多巴胺能假说需要重新研究。

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摘要

Although psychostimulants alleviate the core symptoms of attention-deficit/hyperactivity disorder (ADHD), recent studies confirm that their impact on the long-term outcomes of ADHD children is null. Psychostimulants enhance extracellular dopamine. Numerous review articles assert that they correct an underlying dopaminergic deficit of genetic origin. This dopamine-deficit theory of ADHD is often based upon an overly simplistic dopaminergic theory of reward. Here, I question the relevance of this theory regarding ADHD. I underline the weaknesses of the neurochemical, genetic, neuropharmacological and imaging data put forward to support the dopamine-deficit hypothesis of ADHD. Therefore, this hypothesis should not be put forward to bias ADHD management towards psychostimulants.
机译:尽管精神兴奋剂减轻了注意力缺陷/多动症(ADHD)的核心症状,但最近的研究证实,它们对ADHD儿童长期结局的影响是无效的。精神刺激药可增强细胞外多巴胺。许多评论文章断言他们纠正了遗传来源的潜在多巴胺能缺陷。这种多动症的多巴胺缺乏理论通常基于过于简单的奖励多巴胺能理论。在这里,我质疑这一理论与多动症的相关性。我强调了神经化学,遗传,神经药理学和影像学数据的弱点,这些数据为支持多动症的多巴胺缺乏症假说提供了支持。因此,不应提出这一假说来使多动症治疗偏向精神兴奋剂。

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