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- Anqi Qiu, Deana Crocetti, Marcy Adler, E Mark Mahone, Martha B Denckla, Michael I Miller, and Stewart H Mostofsky.
- Division of Bioengineering, National University of Singapore, 7 Engineering Dr. 1, Block E3A #04-15, Singapore. bieqa@nus.edu.sg
- Am J Psychiatry. 2009 Jan 1; 166 (1): 74-82.
ObjectiveVolumetric abnormalities of basal ganglia have been associated with attention deficit hyperactivity disorder (ADHD), especially in boys. To specify localization of these abnormalities, large deformation diffeomorphic metric mapping (LDDMM) was used to examine the effects of ADHD, sex, and their interaction on basal ganglia shapes.MethodThe basal ganglia (caudate, putamen, globus pallidus) were manually delineated on magnetic resonance imaging from 66 typically developing children (35 boys) and 47 children (27 boys) with ADHD. LDDMM mappings from 35 typically developing children were used to generate basal ganglia templates. Shape variations of each structure relative to the template were modeled for each subject as a random field using Laplace-Beltrami basis functions in the template coordinates. Linear regression was used to examine group differences in volumes and shapes of the basal ganglia.ResultsBoys with ADHD showed significantly smaller basal ganglia volumes compared with typically developing boys, and LDDMM revealed the groups remarkably differed in basal ganglia shapes. Volume compression was seen bilaterally in the caudate head and body and anterior putamen as well as in the left anterior globus pallidus and right ventral putamen. Volume expansion was most pronounced in the posterior putamen. No volume or shape differences were revealed in girls with ADHD.ConclusionsThe shape compression pattern of basal ganglia in boys with ADHD suggests that ADHD-associated deviations from typical brain development involve multiple frontal-subcortical control loops, including circuits with premotor, oculomotor, and prefrontal cortices. Further investigations employing brain-behavior analyses will help to discern the task-dependent contributions of these circuits to impaired response control that is characteristic of ADHD.
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