Longitudinal mapping of cortical thickness and clinical outcome in children and adolescents with attention-deficit/hyperactivity disorder.

By P. Shaw, Jason P. Lerch, Deanna K. Greenstein, W. Sharp, Liv S. Clasen, Alan C. Evans, Jay N. Giedd, F. X. Castellanos, Judith L. Rapoport. Archives of General Psychiatry, 2006

726 citations recorded by the source corpus.

Subfields: Cognitive Neuroscience, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/65fa75580e71dad32c476f06100f9d87b296c91c

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Citations in the corpus

Mindboggling morphometry of human brains (2016, background): “Volume measurement is almost ubiquitous in such studies, and cortical thickness measures derived from structural MRI data have been reported to help characterize a variety of disorders [30] such as mild cognitive impairment and Alzheimer’s disease [31–33], multiple sclerosis [34], schizophrenia [35]”
The NKI-Rockland Sample: A Model for Accelerating the Pace of Discovery Science in Psychiatry (2012, background): “…by a comprehensive phenotypic characterization (e.g., psychiatric, neurocognitive, psychological, and behavioral), to facilitate identification of developmental patterns (Evans and Brain Development Cooperative Group, 2006; Shaw et al., 2006a,b; Giedd and Rapoport, 2010; Giedd et al., 2010).”
Cingulate-precuneus interactions: a new locus of dysfunction in adult attention-deficit/hyperactivity disorder. (2008, background): “In summary, we found strong evidence of disconnection between an anterior cingulate control region implicated in ADHD (32,37) and posterior components of the default-mode network, i.”
Development of the Cerebral Cortex across Adolescence: A Multisample Study of Inter-Related Longitudinal Changes in Cortical Volume, Surface Area, and Thickness (2017, background): “…et al., 2007, 2008; Raznahan et al., 2011), while others show widespread monotonic decreases during childhood and adolescence (Sowell et al., 2004; Shaw et al., 2006; van Soelen et al., 2012; Mutlu et al., 2013; AlexanderBloch et al., 2014; Mills et al., 2014a; Wierenga et al., 2014; Zielinski et…”
Structural MRI of Pediatric Brain Development: What Have We Learned and Where Are We Going? (2010, positive): “We have demonstrated this for the cortex, where right parietal cortical normalization accompanied clinical improvement (Shaw et al., 2006b)—and for the cerebellum, where progressive volume loss of the inferior posterior lobes mirrors persistence of ADHD (Mackie et al., 2007).”
Etiologic Subtypes of Attention-Deficit/Hyperactivity Disorder: Brain Imaging, Molecular Genetic and Environmental Factors and the Dopamine Hypothesis (2007, methodology): “An important finding is based on a study of the assessment over time (Castellanos et al., 2002; Shaw et al., 2006), which tracked changes in anatomical size with development in a large sample of ADHD cases (n = 152) and non-ADHD (n = 139) controls.”
Spontaneous attentional fluctuations in impaired states and pathological conditions: a neurobiological hypothesis. (2007, result): “Imaging studies, both structural and functional, provide some support for this model with evidence of reduced volumes in dorsolateral prefrontal cortex and the neostriatum (caudate/putamen; Castellanos et al., 2002; Shaw et al., 2006) and reduced activations during executive performance in the ventr”
Response Inhibition and Response Selection: Two Sides of the Same Coin (2008, background): “Cortical thickness map from Shaw et al. (2006) showing significant differences between children with ADHD and typically developing controls.”
Wake EEG oscillation dynamics reflect both sleep pressure and brain maturation across childhood and adolescence (2024, unknown): “…because SWA reflects the overall synchronicity of the brain, which decreases with age following decreasing synaptic density across adolescence (Campbell & Feinberg, 2009; Hut-tenlocher, 1979; Jenni & Carskadon, 2004), and may be lower in ADHD due to reduced cortical thickness (Shaw et al., 2006).”