Attention-deficit/hyperactivity disorder is characterized by a delay in cortical maturation
Open accessAbstract
There is controversy over the nature of the disturbance in brain development that underpins attention-deficit/hyperactivity disorder (ADHD). In particular, it is unclear whether the disorder results from a delay in brain maturation or whether it represents a complete deviation from the template of typical development. Using computational neuroanatomic techniques, we estimated cortical thickness at >40,000 cerebral points from 824 magnetic resonance scans acquired prospectively on 223 children with ADHD and 223 typically developing controls. With this sample size, we could define the growth trajectory of each cortical point, delineating a phase of childhood increase followed by adolescent decrease in cortical thickness (a quadratic growth model). From these trajectories, the age of attaining peak cortical thickness was derived and used as an index of cortical maturation. We found maturation to progress in a similar manner regionally in both children with and without ADHD, with primary sensory areas attaining peak cortical thickness before polymodal, high-order association areas. However, there was a marked delay in ADHD in attaining peak thickness throughout most of the cerebrum: the median age by which 50% of the cortical points attained peak thickness for this group was 10.5 years (SE 0.01), which was significantly later than the median age of 7.5 years (SE 0.02) for typically developing controls (log rank test χ( 1 ) 2 = 5,609, P < 1.0 × 10 −20 ). The delay was most prominent in prefrontal regions important for control of cognitive processes including attention and motor planning. Neuroanatomic documentation of a delay in regional cortical maturation in ADHD has not been previously reported.
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Slower maturation or decreased size of the PFC and diminished PFC, caudate or cerebellum activation have been found in patients with ADHD.
“Slower maturation or decreased size of the PFC and also diminished PFC, caudate or cerebellum activation have been found in patients with ADHD [77, 78].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [78]
The Discussion reports that cortical maturation delay in ADHD was most prominent in the lateral prefrontal cortex and describes prefrontal hypoactivation in children with ADHD. It does not establish decreased PFC size or diminished caudate or cerebellar activation; the study measured cortical thickness and its maturation, not activation in those regions. (LLM, conf=0.86)
Experimental — accuracy not yet measuredADHD is associated with slowed or impaired development of the right lateral PFC.
“ADHD is associated with slowed (Shaw et al., 2007) or impaired (Shaw et al., 2009) development of the right lateral PFC, the PFC region needed for inhibiting inappropriate actions and attention to distractors (Aron, Robbins, & Poldrack, 2004).”
From Guanfacine’s mechanism of action in treating prefrontal cortical disorders: Successful translation across species (2020) · cites this paper as Shaw et al., 2007
The Discussion (page unavailable in our copy) says cortical maturation delay in ADHD was most prominent in the lateral prefrontal cortex, supporting the 'slowed' development attributed to Shaw et al. (2007). It does not specify the right lateral PFC, so the right-sided localization is not established by the passages found. The sentence attributes 'impaired' development to a different citation. (LLM, conf=0.82)
Experimental — accuracy not yet measuredADHD is associated with delayed maturation of the cerebral cortex.
“ADHD is also associated with delayed maturation of the cerebral cortex.”
From Attention-deficit/hyperactivity disorder (2015) · cites this paper as [88]
In one study, the age of attaining peak cortical thickness was 10.5 years for patients with ADHD and 7.5 years for unaffected individuals; this delay was most prominent in the prefrontal regions important for executive functioning, attention and motor planning.
“In one study, the age of attaining peak cortical thickness was 10.5years for patients with ADHD and 7.5years for unaffected individuals; this delay was most prominent in the prefrontal regions that are important for executive functioning, attention and motor planning 88 .”
From Attention-deficit/hyperactivity disorder (2015) · cites this paper as [88]
The delay in cortical maturation is prominent in children with ADHD, but findings in adults are more heterogeneous.
“While this delay (e.g., in reaching peak cortical thickness) is prominent in children [73], findings in adults are more heterogeneous.”
From ADHD in Adulthood: Clinical Presentation, Comorbidities, and Treatment Perspectives (2025) · cites this paper as [73]
There is evidence of delayed maturation of the PFC in children with ADHD.
“There is evidence of delayed maturation of the PFC in children with ADHD (Shaw et al., 2007).”
From Catecholamine influences on prefrontal cortical function: Relevance to treatment of attention deficit/hyperactivity disorder and related disorders (2011) · cites this paper as Shaw et al., 2007
In a longitudinal study of cerebral cortex thickness, psychostimulant treatment normalized the ADHD-associated excess cortical thinning during adolescence.
“In a longitudinal study of cerebral cortex thickness, psychostimulant treatment normalized the ADHD-associated excess cortical thinning during adolescence (Shaw et al., 2007, Shaw et al., 2009, van der Marel et al., 2014).”
From Sensitive periods of substance abuse: Early risk for the transition to dependence (2017) · cites this paper as Shaw et al., 2007
Patients with ADHD show a regional delay in the maturation of cortical thickness, especially in regions responsible for cognitive control such as attention, working memory, inhibition and evaluation of reward contingencies in the prefrontal cortex, and a slightly earlier maturation of the primary motor cortex.
“Regarding age, it has been shown that patients with ADHD show a regional delay in the maturation of cortical thickness, especially in regions responsible for cognitive control such as attention, working memory, inhibition and evaluation of reward contingencies in the prefrontal cortex (Shaw et al. 2007), and a slightly earlier maturation of the primary motor cortex.”
From The neurobiological link between OCD and ADHD (2014) · cites this paper as Shaw et al. 2007
The abnormal development of cognitive control and motor areas may drive the poor control of motor activity.
“The authors thus suggested that the abnormal development of cognitive control and motor areas may drive the poor control of motor activity (Shaw et al. 2007).”
From The neurobiological link between OCD and ADHD (2014) · cites this paper as Shaw et al. 2007
Structural characteristics of the anterior cingulate have been found to be related to self-regulation in a number of neurodevelopmental conditions.
“its structural characteristics have been found to be related to self-regulation in a number of neurodevelopmental conditions (9–13, 32, 50, 51).”
From Multimodal imaging of the self-regulating developing brain (2012) · cites this paper as [10]
Structural differences in prefrontal and cingulate cortices have repeatedly been identified in children with a range of psychopathological conditions related to self-regulation and attention, including ADHD, conduct disorder, and prenatal substance exposure.
“structural differences in prefrontal and cingulate cortices have repeatedly been identified in children with a range of different psychopathological conditions related to self-regulation and attention, including Attention Deficit Hyperactivity Disorder, conduct disorder, and prenatal substance exposure (10–13, 29–34).”
From Multimodal imaging of the self-regulating developing brain (2012) · cites this paper as [10]
The differential increases for children with ADHD may be a byproduct of their underdeveloped cortical structures that support working memory.
“The differential increases for children with ADHD may be a byproduct of their underdeveloped cortical structures that support working memory (Shaw et al., 2007).”
From Are Episodic Buffer Processes Intact in ADHD? Experimental Evidence and Linkage with Hyperactive Behavior (2018) · cites this paper as Shaw et al., 2007
ADHD is associated with underdevelopment or hypoactivation in right frontal/prefrontal and temporoparietal regions thought to support cross-modality binding in adults.
“as well as evidence of ADHD-related underdevelopment/hypoactivation (Shaw et al., 2007; Smith et al., 2006) in right frontal/prefrontal and temporoparietal regions thought to support cross-modality binding in adults (Prabhakaran et al., 2000; Zhang et al., 2004).”
From Are Episodic Buffer Processes Intact in ADHD? Experimental Evidence and Linkage with Hyperactive Behavior (2018) · cites this paper as Shaw et al., 2007
Longitudinal fMRI evidence shows a 3-5 year delay in the development of prefrontal/frontal regions in children with ADHD compared with typically developing children.
“Longitudinal fMRI evidence, however, reveals a 3–5 year delay in the development of these same prefrontal/frontal regions in children with ADHD relative to typically developing children (Shaw et al., 2007).”
From Improving Outcomes for Youth with ADHD: A Conceptual Framework for Combined Neurocognitive and Skill-Based Treatment Approaches (2014) · cites this paper as Shaw et al., 2007
Longitudinal fMRI studies show that prefrontal cortical regions tied to central executive working memory mature 3-5 years later in ADHD.
“longitudinal fMRI investigations reveal a 3–5 year delay in the maturation of prefrontal cortical regions associated with central executive working memory functioning (Shaw et al., 2007).”
From Improving Outcomes for Youth with ADHD: A Conceptual Framework for Combined Neurocognitive and Skill-Based Treatment Approaches (2014) · cites this paper as Shaw et al., 2007
Delayed peaks in cortical thickness in ADHD lead to increased cortical thickness in ADHD during late childhood and early adolescence.
“For example, delayed peaks in cortical thickness in Attention-Deficit/Hyperactivity Disorder (ADHD) (64), a disorder associated with visuospatial WM impairments (65), lead to increased cortical thickness in ADHD during late childhood and early adolescence.”
From Influence of the COMT genotype on working memory and brain activity changes during development (2011) · cites this paper as [64]
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- Authors
- Shaw, P., Eckstrand, K., Sharp, W., Blumenthal, J., Lerch, J. P., Greenstein, D., Clasen, L., Evans, A., Giedd, J., & Rapoport, J. L.
- Affiliations
- National Institutes of Health (US)
- Montreal Neurological Institute and Hospital (CA)
- Corresponding author
- Shaw, P.
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2007-12-04
- Volume
- 104
- Issue
- 49
- Pages
- 19649-19654
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC2148343
- OpenAlex
- W2156645869
- Cited by
- 1,819
- References
- 63
- Citations by year
- 2026: 90 · 2025: 89 · 2024: 97 · 2023: 83 · 2022: 89 · 2021: 93 · 2020: 101 · 2019: 115 · 2018: 73 · 2017: 134 · 2016: 114 · 2015: 107 · 2014: 112 · 2013: 100 · 2012: 111
- FWCI
- 41.94
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Keywords
- attention deficit hyperactivity disorder, cortical maturation, cortical thickness, brain development, prefrontal cortex
- MeSH terms
- Adolescent, Attention Deficit Disorder with Hyperactivity, Cerebral Cortex, Child, Female, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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