The neural correlates of attention deficit hyperactivity disorder: an ALE meta-analysis
The neural correlates of attention deficit hyperactivity disorder: an ALE meta-analysis
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DOI：
10.1111/j.1469-7610.2006.01671.x
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发表时间：
2006-10-01
影响因子：
7.6
通讯作者：
Milham, Michael P.
中科院分区：
文献类型：
--
作者：
Dickstein, Steven G.;Bannon, Katie;Milham, Michael P.
背景资料：注意力缺陷多动障碍（ADHD）是儿童和青少年中最普遍和最常研究的精神病理学形式之一。ADHD的因果模型长期以来一直涉及支持执行功能的额-纹状体和额-顶叶网络的功能障碍，这一假设现在可以使用功能性神经成像系统地进行检查。目前的工作提供了一个客观的，公正的，基于经验的荟萃分析发表的功能性神经影像学研究多动症。研究方法：最近开发的一种称为激活似然估计（ALE）的体素定量荟萃分析技术应用于16项神经影像学研究，检查和对比ADHD患者和健康对照组的神经活动模式。使用p <0.05的统计阈值报告逐体素结果，校正。鉴于大量研究检查了反应抑制，纳入了额外的荟萃分析，特别关注抑制的神经相关性的组间差异。结果如下：在所有研究中，在ADHD患者中检测到显著的额叶活动减退模式，影响前扣带、背外侧前额叶和下前额叶皮质，以及相关区域，包括基底神经节、丘脑和部分顶叶皮质。当只关注反应抑制的研究时，观察到的组间差异更为有限，包括下前额叶皮层、内侧壁区域和中央前回。相比之下，对反应抑制以外的结构的研究分析显示，ADHD患者的功能减退模式比反应抑制更广泛。结论：迄今为止，在ADHD的神经影像学文献中最一致的发现是额-纹状体和额-顶叶回路内的神经活动缺陷。这些结果的分布性质不支持模型强调功能障碍，在任何一个额叶子区域。虽然我们的研究结果表明，在基于额叶的神经回路缺陷的ADHD的基础上的首要地位，我们讨论了潜在的偏见，在这样的结论可以完全接受之前，需要解决的文献。
Background: Attention deficit/hyperactivity disorder (ADHD) is one of the most prevalent and commonly studied forms of psychopathology in children and adolescents. Causal models of ADHD have long implicated dysfunction in fronto-striatal and frontal-parietal networks supporting executive function, a hypothesis that can now be examined systematically using functional neuroimaging. The present work provides an objective, unbiased statistically-based meta-analysis of published functional neuroimaging studies of ADHD. Methods: A recently developed voxel-wise quantitative meta-analytic technique known as activation likelihood estimation (ALE) was applied to 16 neuroimaging studies examining and contrasting patterns of neural activity in patients with ADHD and healthy controls. Voxel-wise results are reported using a statistical threshold of p < .05, corrected. Given the large number of studies examining response inhibition, additional meta-analyses focusing specifically on group differences in the neural correlates of inhibition were included. Results: Across studies, significant patterns of frontal hypoactivity were detected in patients with ADHD, affecting anterior cingulate, dorsolateral prefrontal, and inferior prefrontal cortices, as well as related regions including basal ganglia, thalamus, and portions of parietal cortex. When focusing on studies of response inhibition alone, a more limited set of group differences were observed, including inferior prefrontal cortex, medial wall regions, and the precentral gyrus. In contrast, analyses focusing on studies of constructs other than response inhibition revealed a more extensive pattern of hypofunction in patients with ADHD than those of response inhibition. Conclusions: To date, the most consistent findings in the neuroimaging literature of ADHD are deficits in neural activity within fronto-striatal and fronto-parietal circuits. The distributed nature of these results fails to support models emphasizing dysfunction in any one frontal sub-region. While our findings are suggestive of the primacy of deficits in frontal-based neural circuitry underlying ADHD, we discuss potential biases in the literature that need to be addressed before such a conclusion can be fully embraced.