Conflict of interest statement: No conflicts declared.
The neural correlates of attention deficit hyperactivity disorder: an ALE meta-analysis
Version of Record online: 26 OCT 2006
Journal of Child Psychology and Psychiatry
Volume 47, Issue 10, pages 1051–1062, November 2006
How to Cite
Dickstein, S. G., Bannon, K., Xavier Castellanos, F. and Milham, M. P. (2006), The neural correlates of attention deficit hyperactivity disorder: an ALE meta-analysis. Journal of Child Psychology and Psychiatry, 47: 1051–1062. doi: 10.1111/j.1469-7610.2006.01671.x
- Issue online: 26 OCT 2006
- Version of Record online: 26 OCT 2006
- Manuscript accepted 1 June 2005
- Attention deficit/hyperactivity disorder (ADHD);
- functional magnetic resonance imaging (fMRI);
- positron emission tomography (PET);
- executive function
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.