title: The neural correlates of attention deficit hyperactivity disorder: an ALE meta-analysis.
abstract: 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.
authors.affiliation: NYU Child Study Center, New York, NY 10016, USA.
authors.forename: Steven G
authors.initials: SG
authors.lastname: Dickstein
authors.forename: Katie
authors.initials: K
authors.lastname: Bannon
authors.forename: F Xavier
authors.initials: FX
authors.lastname: Castellanos
authors.forename: Michael P
authors.initials: MP
authors.lastname: Milham
mesh_terms: D000293:Adolescent; D001289:Attention Deficit Disorder with Hyperactivity / Q000503:physiopathology* / Q000523:psychology*; D001479:Basal Ganglia / Q000378:metabolism / Q000503:physiopathology; D002648:Child; D003342:Corpus Striatum / Q000378:metabolism / Q000503:physiopathology; D005625:Frontal Lobe / Q000378:metabolism / Q000503:physiopathology; D006179:Gyrus Cinguli / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D008279:Magnetic Resonance Imaging; D009415:Nerve Net / Q000098:blood supply* / Q000503:physiopathology*; D010296:Parietal Lobe / Q000378:metabolism / Q000503:physiopathology; D049268:Positron-Emission Tomography; D013788:Thalamus / Q000378:metabolism / Q000503:physiopathology