Developmental Trajectories of Brain Volume Abnormalities in Children and Adolescents With Attention-Deficit/Hyperactivity Disorder

Castellanos, F. Xavier; Lee, Patti P.; Sharp, Wendy; Jeffries, Neal; Greenstein, Deanna; Clasen, Liv S.; Blumenthal, Jonathan D.; James, Regina S.; Ebens, Christen L.; Walter, James M.; Zijdenbos, Alex P.; Evans, Alan C.; Giedd, Jay N.; Rapoport, Judith L.

doi:10.1001/jama.288.14.1740

Cited by 1,401 publications

(1,104 citation statements)

References 43 publications

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“…The changes observed in the study controls are in line with findings of longitudinal studies of typically developing children. Similar to longitudinal findings in healthy children and adolescents (Castellanos et al, 2002;Giedd et al, 1999;Lenroot and Giedd, 2006;Rapoport et al, 1999;Sowell et al, 2003), our control group showed an increase in cerebral WM/GM ratio, decrease in caudate volume, and no change in amygdala and hippocampus volumes.…”

Section: Discussionsupporting

confidence: 88%

“…Supporting this view, the STG GM reaches it maximal volume later than all other cortical regions after the age of 16 years . The typical caudate development has been observed to increase in childhood and then begins to decrease in size during adolescence (Castellanos et al, 2002). Thus it seems that in 22q11.2DS adolescents pruning of the STG GM and caudate nucleus lags behind that of typically developing adolescents.…”

Section: Discussionmentioning

confidence: 98%

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Developmental trajectories of brain structure in adolescents with 22q11.2 deletion syndrome: A longitudinal study

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Penniman

et al. 2007

Schizophrenia Research

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The 22q11.2 deletion syndrome (22q11.2DS) is associated with very high rates of schizophrenialike psychosis and cognitive deficits. Here we report the results of the first longitudinal study assessing brain development in individuals with 22q11.2DS. Twenty-nine children with 22q11.2DS and 29 age and gender matched controls were first assessed during childhood or early adolescence; Nineteen subjects with 22q11.2DS and 18 controls underwent follow-up during late adolescenceearly adulthood. The 22q11.2DS subjects showed greater longitudinal increase in cranial and cerebellar white matter, superior temporal gyrus, and caudate nucleus volumes. They also had a more robust decrease in amygdala volume. Verbal IQ (VIQ) scores of the 22q11.2DS group that developed psychotic disorders declined significantly between assessments. Decline in VIQ in 22q11.2DS was associated with more robust reduction of left cortical grey matter volume. No volumetric differences were detected between psychotic and nonpsychotic subjects with 22q11.2DS. Brain maturation associated with verbal cognitive development in 22q11.2DS varies from that observed in healthy controls. Further longitudinal studies are likely to elucidate brain developmental trajectories in 22q11.2DS and their association to psychotic disorders and cognitive deficits in this population.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 98%

Developmental trajectories of brain structure in adolescents with 22q11.2 deletion syndrome: A longitudinal study

Gothelf

Penniman

et al. 2007

Schizophrenia Research

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“…Additionally, the specificity of our mental rotation fMRI task allows our interpretations to be constrained by known brain-behaviour relationships that exist from nonhuman primate work on spatial working memory. 24,25 The caudate nucleus remains a brain area of significant interest in the pathophysiology of ADHD-CT: decreased caudate nucleus size is a replicated finding in children with ADHD-CT, 43,44 although no difference in size is evident during adolescence. 44 Structural lesion and functional imaging animal data support the association of caudate nucleus dysfunction with core ADHD-CT symptoms, working memory and response inhibition dysfunction.…”

Section: Discussionmentioning

confidence: 99%

“…24,25 The caudate nucleus remains a brain area of significant interest in the pathophysiology of ADHD-CT: decreased caudate nucleus size is a replicated finding in children with ADHD-CT, 43,44 although no difference in size is evident during adolescence. 44 Structural lesion and functional imaging animal data support the association of caudate nucleus dysfunction with core ADHD-CT symptoms, working memory and response inhibition dysfunction. 1,45 The caudate nucleus has a high concentration of dopaminergic synapses underpinning its functions, dopamine being a key neurotransmitter known to be functionally aberrant in ADHD.…”

Section: Discussionmentioning

confidence: 99%

Right parietal dysfunction in children with attention deficit hyperactivity disorder, combined type: a functional MRI study

et al. 2007

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Attention deficit hyperactivity disorder, combined type (ADHD-CT) is associated with spatial working memory deficits. These deficits are known to be subserved by dysfunction of neural circuits involving right prefrontal, striatal and parietal brain regions. This study determines whether decreased right prefrontal, striatal and parietal activation with a mental rotation task shown in adolescents with ADHD-CT is also evident in children with ADHD-CT. A crosssectional study of 12 pre-pubertal, right-handed, 8-12-year-old boys with ADHD-CT and 12 prepubertal, right-handed, performance IQ-matched, 8-12-year-old healthy boys, recruited from local primary schools, was completed. Participants underwent functional magnetic resonance imaging while performing a mental rotation task that requires spatial working memory. The two groups did not differ in their accuracy or response times for the mental rotation task. The ADHD-CT group showed significantly less activation in right parieto-occipital areas (cuneus and precuneus, BA 19), the right inferior parietal lobe (BA 40) and the right caudate nucleus. Our findings with a child cohort confirm previous reports of right striatal-parietal dysfunction in adolescents with ADHD-CT. This dysfunction suggests a widespread maturational deficit that may be developmental stage independent.

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“…Gene association studies have related allelic variants of SNAP25 with attention deficit hyperactivity disorder (ADHD) [Brophy et al, 2002;Mill et al, 2002;Barr et al, 2000]. Although there is no formal evidence supporting a synaptogenesis deficit in ADHD, diminished brain volumes have been reported [Castellanos et al, 2002]. Because of this converging evidence, we investigate the influence of this gene on normal executive attention.…”

Section: Molecular Genetic Studies On Snap25 and Its Potential Role Imentioning

confidence: 97%

Synaptogenesis and heritable aspects of executive attention

Fossella

Sommer

Fan

et al. 2003

Ment. Retard. Dev. Disabil. Res. Rev.

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In humans, changes in brain structure and function can be measured non-invasively during postnatal development. In animals, advanced optical imaging measures can track the formation of synapses during learning and behavior. With the recent progress in these technologies, it is appropriate to begin to assess how the physiological processes of synapse, circuit, and neural network formation relate to the process of cognitive development. Of particular interest is the development of executive function, which develops more gradually in humans. One approach that has shown promise is molecular genetics. The completion of the human genome project and the human genome diversity project make it straightforward to ask whether variation in a particular gene correlates with variation in behavior, brain structure, brain activity, or all of the above. Strategies that unify the wealth of biochemical knowledge pertaining to synapse formation with the functional measures of brain structure and activity may lead to new insights in developmental cognitive psychology.

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Developmental Trajectories of Brain Volume Abnormalities in Children and Adolescents With Attention-Deficit/Hyperactivity Disorder

Cited by 1,401 publications

References 43 publications

Developmental trajectories of brain structure in adolescents with 22q11.2 deletion syndrome: A longitudinal study

Developmental trajectories of brain structure in adolescents with 22q11.2 deletion syndrome: A longitudinal study

Right parietal dysfunction in children with attention deficit hyperactivity disorder, combined type: a functional MRI study

Synaptogenesis and heritable aspects of executive attention

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