Attention-deficit/hyperactivity disorder (ADHD) as a noradrenergic disorder

Attention-deficit/hyperactivity disorder (ADHD) as a noradrenergic disorder
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DOI:
10.1016/s0006-3223(99)00192-4
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发表时间:
1999-11-01
影响因子:
10.6
通讯作者:
Spencer, T
Spencer, T
中科院分区:
医学1区
文献类型:
--
作者:
Biederman, J;Spencer, T

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本文回顾了中枢去甲肾上腺素能网络失调可能是ADHD病理生理学的基础这一论点。我们回顾了有关ADHD的神经生物学和药理学文献。去甲肾上腺素能系统与高级皮质功能的调节密切相关,包括注意力、警觉性、警觉性和执行功能。已知去甲肾上腺素能激活深刻影响注意力的表现,特别是唤醒的维持,这是一种已知在ADHD中缺乏的认知功能。来自家庭、收养、双胞胎和种族隔离分析的数据强烈支持这种疾病的遗传假说。虽然ADHD的分子遗传学研究相对较新,而且还远未确定,但一些重复的报告已经发现ADHD与DAT和D4受体基因之间的关联。脑成像研究很好地符合这样的想法,即额皮质下通路功能障碍发生在ADHD与ifs潜在的去甲肾上腺素能功能失调。丰富的药理学数据(在兴奋剂文献中和没有兴奋剂文献)为具有去甲肾上腺素能和多巴胺能药理学特征的药物在ADHD中的选择性临床活性提供了强有力的证据,现有的研究为ADHD是一种可能具有遗传病因学和病理生理学异质性的脑部疾病的概念提供了令人信服的理论、基础生物学和临床支持,神经生物学和药理学数据为ADHD的去甲肾上腺素能假说提供了令人信服的支持,并表明具有去甲肾上腺素能活性的药物可能在这种疾病的治疗中发挥重要作用。(C)1999年生物精神病学学会。
This review revisits the thesis that a dysregulation of the central noradrenergic networks may underlie the pathophysiology of ADHD. We review the pertinent neurobiological and pharmacological literature on ADHD. The noradrenergic system has been intimately associated with the modulation of higher cortical functions including attention, alertness, vigilance and executive function, Noradrenergic activation is known to profoundly affect the performance of attention, especially the maintenance of arousal, a cognitive function known to be deficient in ADHD. Data from family, adoption, twin, and segregation analysis strongly support a genetic hypothesis for this disorder. Although molecular genetic studies of ADHD are relatively new and far from definitive, several replicated reports have found associations between ADHD with DAT and D4 receptor genes. Brain imaging studies fit well with the idea that dysfunction in fronto-subcortical pathways occurs in ADHD with ifs underlying dysregulation of noradrenergic function. A wealth of pharmacological data (within and without the stimulant literature) provides strong evidence for selective clinical activity in ADHD for drugs with noradrenergic and dopaminergic pharmacological profiles, Available research provides compelling theoretic, basic biologic and clinical support for the notion that ADHD is a brain disorder of likely genetic etiology with etiologic and pathophysiologic heterogeneity, NL Neurobiological and pharmacological data provide compelling support for a noradrenergic hypothesis of ADHD and suggest that drugs with noradrenergic activity may play an important role in the therapeutics of this disorder. (C) 1999 Society of Biological Psychiatry.