Abstract
Background: Cognitive control, defined as the ability to suppress inappropriate thoughts and actions, is compromised in attention-deficit/hyperactivity disorder (ADHD). This study examines the neural basis of this deficit. Methods: We used a paradigm that incorporates a parametric manipulation within a go/nogo task, so that the number of go trials preceding a nogo trial is varied to tax the neural systems underlying cognitive control with increasing levels of interference. Results: Using this paradigm in combination with event-related functional magnetic resonance imaging (fMRI), we show that children without ADHD have increased susceptibility to interference with increasing numbers of go trials preceding a nogo trial, but children with ADHD have difficulty even with a single go trial preceding a nogo trial. In addition, children with ADHD do not activate frontostriatal regions in the same manner as normally developing children, but rather rely on a more diffuse network of regions, including more posterior and dorsolateral prefrontal regions. Conclusions: Normal immature cognition may be characterized as being susceptible to interference and supported by the maturation of frontostriatal circuitry. ADHD children show a slightly different cognitive profile at 6 to 10 years of age that is paralleled by a relative lack of or delay in the maturation of ventral frontostriatal circuitry.
Original language | English (US) |
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Pages (from-to) | 871-878 |
Number of pages | 8 |
Journal | Biological psychiatry |
Volume | 53 |
Issue number | 10 |
DOIs | |
State | Published - May 15 2003 |
Externally published | Yes |
Bibliographical note
Funding Information:This work was supported in part by grants from the John Merck Fund and Charles Dana Foundation to BJC and by the Netherlands Royal Academy of the Arts and Sciences (KNAW), the Netherlands Organization for Scientific Research (NWO), foundation ‘De Drie Lichten’ and the Dutch Society for Neuropsychology to SD.
Keywords
- ADHD
- Development
- Event-related fMRI
- Parametric
- Response inhibition
- Striatum