Developmental trajectories of the corpus callosum in attention-deficit/hyperactivity disorder.

Child Psychiatry Branch, National Institute of Mental Health, Bethesda, Maryland 20892, USA.
Biological psychiatry (Impact Factor: 8.93). 01/2011; 69(9):839-46. DOI: 10.1016/j.biopsych.2010.11.024
Source: PubMed

ABSTRACT It was recently found that the development of typical patterns of prefrontal, but not posterior, cortical asymmetry is disrupted in right-handed youth with attention-deficit/hyperactivity disorder (ADHD). Using longitudinal data, we tested the hypothesis that there would be a congruent disruption in the growth of the anterior corpus callosum, which contains white matter tracts connecting prefrontal cortical regions.
Areas of five subregions of the corpus callosum were quantified using a semiautomated method from 828 neuroanatomic magnetic resonance scans acquired from 236 children and adolescents with ADHD (429 scans) and 230 typically developing youth (399 scans), most of whom had repeated neuroimaging. Growth rates of each diagnostic group were defined using mixed-model linear regression.
Right-handed participants with ADHD showed a significantly higher rate of growth in the anterior-most region of the corpus callosum (estimated annual increase in area of .97%, SEM .12%) than their typically developing peers (annual increase in area of .32% SEM .13%; t = 3.64, p = .0003). No significant diagnostic differences in growth rates were found in any other regions in right-handed participants, and no significant diagnostic differences were found in non-right-handed participants.
As hypothesized, we found anomalous growth trajectories in the anterior corpus callosum in ADHD. This disrupted anterior callosal growth may reflect, or even drive, the previously reported disruption in the development of prefrontal cortex asymmetry. The finding documents the dynamic, age-dependent nature of callosal and congruent prefrontal cortical abnormalities characterizing ADHD.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Emotion perception forms an integral part of social communication, and is critical to attain developmentally appropriate goals. This skill, which emerges relatively early in development is driven by increasing connectivity among regions of a distributed socio-cognitive neural network, and may be vulnerable to disruption from early childhood TBI. The present study aimed to evaluate the very long-term impact of childhood TBI on emotion perception, as well as examine the contribution of injury and non-injury related risk and resilience factors to variability in socio-cognitive outcomes. 34 young adult survivors of early childhood TBI (M age= 20.62 years; M time since injury: 16.55 years) and 16 typically developing controls matched for age, gender and socio-economic status (SES) were assessed using tasks that required recognition and interpretation of facial and prosodic emotional cues. Survivors of severe childhood TBI were found to have significantly poorer emotion perception than controls and young adults with mild to moderate injuries. Furthermore, poorer emotion perception was associated with reduced volume of the posterior corpus callosum, the presence of frontal pathology, lower socio-economic status (SES), and a less intimate family environment. Our findings lend support to the vulnerability of the immature 'social brain' network to early disruption, and underscore the need for context-sensitive rehabilitation that optimizes early family environments to enhance recovery of emotion perception skills after childhood TBI.
    Journal of neurotrauma 10/2013; · 4.25 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Attention-deficit/hyperactivity disorder (ADHD) is a common chronic neurodevelopmental disorder with a high heritability. Much evidence of hemisphere asymmetry has been found for ADHD probands from behavioral level, electrophysiological level and brain morphology. One previous research has reported possible association between BAIAP2, which is asymmetrically expressed in the two cerebral hemispheres, with ADHD in European population. The present study aimed to investigate the association between BAIAP2 and ADHD in Chinese Han subjects. A total of 1,397 ADHD trios comprised of one ADHD proband and their parents were included for family-based association tests. Independent 569 ADHD cases and 957 normal controls were included for case-control studies. Diagnosis was performed according to the DSM-IV criteria. Nine single nucleotide polymorphisms (SNPs) of BAIAP2 were chosen and performed genotyping for both family-based and case-control association studies. Transmission disequilibrium tests (TDTs) for family-based association studies showed significant association between the CA haplotype comprised by rs3934492 and rs9901648 with predominantly inattentive type (ADHD-I). For case-control study, chi-square tests provided evidence for the contribution of SNP rs4969239, rs3934492 and rs4969385 to ADHD and its two clinical subtypes, ADHD-I and ADHD-C. However, only the associations for ADHD and ADHD-I retained significant after corrections for multiplicity or logistic regression analyses adjusting the potential confounding effect of gender and age. These above results indicated the possible involvement of BAIAP2 in the etiology of ADHD, especially ADHD-I.
    Behavioral and Brain Functions 12/2013; 9(1):48. · 2.79 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: A deletion on human chromosome 16p11.2 is associated with autism spectrum disorders. We deleted the syntenic region on mouse chromosome 7F3. MRI and high-throughput single-cell transcriptomics revealed anatomical and cellular abnormalities, particularly in cortex and striatum of juvenile mutant mice (16p11(+/-)). We found elevated numbers of striatal medium spiny neurons (MSNs) expressing the dopamine D2 receptor (Drd2(+)) and fewer dopamine-sensitive (Drd1(+)) neurons in deep layers of cortex. Electrophysiological recordings of Drd2(+) MSN revealed synaptic defects, suggesting abnormal basal ganglia circuitry function in 16p11(+/-) mice. This is further supported by behavioral experiments showing hyperactivity, circling, and deficits in movement control. Strikingly, 16p11(+/-) mice showed a complete lack of habituation reminiscent of what is observed in some autistic individuals. Our findings unveil a fundamental role of genes affected by the 16p11.2 deletion in establishing the basal ganglia circuitry and provide insights in the pathophysiology of autism.
    Cell Reports 05/2014; · 7.21 Impact Factor

Full-text (2 Sources)

Available from
May 17, 2014