Longitudinal Mapping of Cortical Thickness and Clinical Outcome in Children and Adolescents With Attention-Deficit/Hyperactivity Disorder

Shaw, Philip; Lerch, Jason P.; Greenstein, Deanna; Sharp, Wendy; Clasen, Liv S.; Evans, Alan C.; Giedd, Jay N.; Castellanos, F. Xavier; Rapoport, Judith L.

doi:10.1001/archpsyc.63.5.540

Cited by 602 publications

(500 citation statements)

References 68 publications

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“…In addition, we had follow-up information on a large proportion of the ADHD sample (n ¼ 107) and had DNA on 69 of these 107. We categorized the follow-up sample as having ''good'' or ''poor'' outcome based on a median split of scores at follow-up on the Children's Global Assessment Scale (CGAS) [Shaffer et al, 1983;Shaw et al, 2006]. There was a higher frequency of the 7-repeat allele in the good outcome group as compared to the poor outcome group (28% vs. 18%, respectively), though this difference did not reach statistical significance, likely due to the small sample size (P ¼ 0.11).…”

Section: Resultsmentioning

confidence: 99%

Association of the dopamine receptor D4 (DRD4) gene 7‐repeat allele with children with attention‐deficit/hyperactivity disorder (ADHD): An update

Gornick¹,

Addington²,

Shaw³

et al. 2006

American J of Med Genetics Pt B

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Polymorphisms of the dopamine receptor D4 gene DRD4, 11p15.5, have previously been associated with attention-deficit/hyperactivity disorder (ADHD) [Bobb et al., 2005; Am J Med Genet B Neuropsychiatr Genet 132:109-125;Faraone et al., 2005; Biol Psychiatry 57:1313-1323Thapar et al., 2005; Hum Mol Genet 14 Spec No. 2:R275-R282]. As a follow up to a pilot study [see Castellanos et al., 1998; Mol Psychiatry 3:431-434] consisting of 41 probands and 56 controls which found no significant association between the DRD4 7-repeat allele in exon 3 and ADHD, a greatly expanded study sample (cases n ¼ 166 and controls n ¼ 282) and long term follow-up (n ¼ 107, baseline mean age n ¼ 9, follow-up mean age of n ¼ 15) prompted reexamination of this gene. The DRD4 7-repeat allele was significantly more frequent in ADHD cases than controls (OR ¼ 1.2; P ¼ 0.028). Further, within the ADHD group, the 7-repeat allele was associated with better cognitive performance (measured by the WISC-III) (P ¼ 0.013-0.07) as well as a trend for association with better long-term outcome. This provides further evidence of the role of the DRD4 7-repeat allele in the etiology of ADHD and suggests that this allele may be associated with a more benign form of the disorder. INTRODUCTIONAttention-deficit/hyperactivity disorder (ADHD) is a common, highly heritable childhood disorder defined by chronic inattention, hyperactivity, and impulsivity based on criteria specified in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV) [American Psychiatric Association, 1994]. Family, twin and adoption studies, as well as linkage and association studies, have shown strong genetic contributions to the etiology of ADHD [Faraone and Biederman, 1998;Fisher et al., 2002;Ogdie et al., 2003; ArcosBurgos et al., 2004]. The most consistently replicated candidate gene in ADHD genetics is the association with the dopamine receptor D4 gene (DRD4) [LaHoste et al., 1996;Smalley et al., 1998;Swanson et al., 1998;Comings et al., 1999;Faraone et al., 1999;Holmes et al., 2000;Muglia et al., 2000;Tahir et al., 2000;Curran et al., 2001;Mill et al., 2001;Roman et al., 2001;Bhaduri et al., 2006]. The majority of these studies have reported on a variable number tandem repeat (VNTR) polymorphism in exon 3 of the DRD4 gene. Despite a few inconsistencies in reported associations of this VNTR and ADHD [Eisenberg et al., 2000;Hawi et al., 2000;Sunohara et al., 2000;Marino et al., 2003;Purper-Ouakil et al., 2005] the majority of reports and several meta-analyses have found positive support for the association [LaHoste et al., 1996;Smalley et al., 1998;Comings et al., 1999;Curran et al., 2001;Mill et al., 2001;Roman et al., 2001;Holmes et al., 2002;Bobb et al., 2005;Faraone et al., 2005;Bhaduri et al., 2006].In the present study, we used both case-control and familybased designs to test the association between ADHD and the DRD4 7-repeat allele using an expanded sample from a previous pilot study [Castellanos et al., 1998] of ADHD patients recruited as part of a d...

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Section: Resultsmentioning

confidence: 99%

Association of the dopamine receptor D4 (DRD4) gene 7‐repeat allele with children with attention‐deficit/hyperactivity disorder (ADHD): An update

Gornick¹,

Addington²,

Shaw³

et al. 2006

American J of Med Genetics Pt B

View full text Add to dashboard Cite

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“…Mixed effect models, which would have been the gold standard technique to combine cross-sectional and longitudinal data, commonly encompass more than 500 scans (Shaw et al, 2006a(Shaw et al, , 2006b(Shaw et al, , 2007a(Shaw et al, , 2007b(Shaw et al, , 2008 or 3-4 time-points Greenstein et al, 2006). Given the limited size of our sample, we preferred the use of repeated-measures at each cortical vertex, to identify significant differences in thickness changes over the 3 year period.…”

Section: Longitudinal Analysesmentioning

confidence: 99%

“…Moreover, cortical thickness studies have an exquisite resolution, allowing for the identification of local alterations with high precision. Consequently, a growing amount of studies apply thickness measurement as an index of development in patients with various conditions, such as attention deficit/hyperactivity disorder (ADHD) (Shaw et al, 2007a(Shaw et al, , 2006b, autism (Chung et al, 2005;Hadjikhani et al, 2007;Hardan et al, 2006), or schizophrenia Greenstein et al, 2006;Kuperberg et al, 2003). In 22q11DS, previous studies by Bearden and colleagues in 21 affected children and adolescents compared to 13 controls reported thinner superior parietal, right parieto-occipital and ventro-medial occipito-temporal cortices (Bearden et al, 2007;Bearden et al, 2009).…”

mentioning

confidence: 99%

Deviant trajectories of cortical maturation in 22q11.2 deletion syndrome (22q11DS): A cross-sectional and longitudinal study

Schaer

Debbané

Cuadra

et al. 2009

Schizophrenia Research

106

129

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22q11.2 deletion syndrome (22q11DS) is associated with an increased susceptibility to develop schizophrenia. Despite a large body of literature documenting abnormal brain structure in 22q11DS, cerebral changes associated with brain maturation in 22q11DS remained largely unexplored. To map cortical maturation from childhood to adulthood in 22q11.2 deletion syndrome, we used cerebral MRI from 59 patients with 22q11DS, aged 6 to 40, and 80 typically developing controls; three year follow-up assessments were also available for 32 patients and 31 matched controls. Cross-sectional cortical thickness trajectories during childhood and adolescence were approximated in age bins. Repeated-measures were also conducted with the longitudinal data. Within the group of patients with 22q11DS, exploratory measures of cortical thickness differences related to COMT polymorphism, IQ, and schizophrenia were also conducted. We observed deviant trajectories of cortical thickness changes with age in patients with 22q11DS. In affected preadolescents, larger prefrontal thickness was observed compared to age-matched controls. Afterward, we observed greater cortical loss in 22q11DS with a convergence of cortical thickness values by the end of adolescence. No compelling evidence for an effect of COMT polymorphism on cortical maturation was observed. Within 22q11DS, significant differences in cortical thickness were related to cognitive level in children and adolescents, and to schizophrenia in adults. Deviant trajectories of cortical thickness from childhood to adulthood provide strong in vivo cues for a defect in the programmed synaptic elimination, which in turn may explain the susceptibility of patients with 22q11DS to develop psychosis.

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“…The pre-SMA area is connected to the anterior prefrontal areas (Dum and Strick 1991) and striatal projections from the pre-SMA largely extend to the caudate nucleus and the middle and rostral putamen (Lehericy et al 2004). Anatomic imaging studies of children with ADHD reported localized anomalies in pre-SMA area, including reduced volume (Mostofsky et al 2002) and thickness when compared with control children (Shaw et al 2006). This area plays an important role in motor planning and switching from automatic to voluntary controlled actions (Hoshi and Tanji 2004).…”

Section: Role Of Cerebral Cortex In Inhibitory Controlmentioning

confidence: 99%

Pathophysiology of NSS in ADHD

Pasini

D’Agati

2009

The World Journal of Biological Psychiatry

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Attention deficit/hyperactivity disorder (ADHD) is the behavioural disorder most commonly diagnosed in childhood. In addition to the main symptoms of inattention, impulsiveness and hyperactivity, neurological soft signs (NSS) are often associated with ADHD. NSS are discrete motor and sensory disorders that cannot be linked to specific cerebral lesions. We review all the scientific contributions on NSS in ADHD. The conclusions support the presence of an alteration in the neural networks for motor control inhibition, at the base of the pathophysiology of NSS in children with ADHD, as well as a possible central role of dopamine in these neural circuits.

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Longitudinal Mapping of Cortical Thickness and Clinical Outcome in Children and Adolescents With Attention-Deficit/Hyperactivity Disorder

Cited by 602 publications

References 68 publications

Association of the dopamine receptor D4 (DRD4) gene 7‐repeat allele with children with attention‐deficit/hyperactivity disorder (ADHD): An update

Association of the dopamine receptor D4 (DRD4) gene 7‐repeat allele with children with attention‐deficit/hyperactivity disorder (ADHD): An update

Deviant trajectories of cortical maturation in 22q11.2 deletion syndrome (22q11DS): A cross-sectional and longitudinal study

Pathophysiology of NSS in ADHD

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