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Cited by 257Attention Deficit Hyperactivity DisorderNeurotransmitter Receptor Influence on BehaviorNeural and Behavioral Psychology Studies

The DOI matches its Crossref record; 50 of the 52 references it cites were found in a registry or an index.

High Midbrain [ 18 F]DOPA Accumulation in Children With Attention Deficit Hyperactivity Disorder

Ernst, Monique, Zametkin, Alan J., Matochik, John A., Pascualvaca, Daisy, Jons, Peter H., Cohen, Robert M.·1999·American Journal of Psychiatry
DOI 10.1176/ajp.156.8.1209
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Abstract

OBJECTIVE: Attention deficit hyperactivity disorder (ADHD) is a highly prevalent childhood psychiatric disorder characterized by impaired attention, excessive motor activity, and impulsivity. Despite extensive investigation of the neuropathophysiology of ADHD by a wide array of methodologies, the neurobiochemical substrate of this disorder is still unknown. Converging evidence, however, suggests a primary role of the dopaminergic system. METHOD: This study examined the integrity of presynaptic dopaminergic function in children with ADHD through use of positron emission tomography and the tracer [18F]fluorodopa ([18F]DOPA). Accumulation of [18F]DOPA in synaptic terminals, a measure of dopa decarboxylase activity, was quantified in regions rich in dopaminergic innervation, including caudate nucleus, putamen, frontal cortex, and midbrain (i.e., substantia nigra and ventral tegmentum). RESULTS: Accumulation of [18F]DOPA in the right midbrain was higher by 48% in 10 children with ADHD than in 10 normal children. Despite its magnitude, this difference would not have reached statistical significance if corrected by the Bonferroni test for multiple comparisons. However, [18F]DOPA in the right midbrain was correlated with symptom severity. No other dopamine-rich regions significantly differed between groups. CONCLUSIONS: These findings are suggestive of dopaminergic dysfunction at the level of the dopaminergic nuclei in children with ADHD. Abnormality in dopa decarboxylase activity may be primary or secondary to deficits in other functional units of the dopamine pathway (e.g., receptor, uptake transporter, vesicular transporter, degradation enzymes). Efforts toward defining the origin of this abnormality should help delineate mechanisms of midbrain control of attention and motor behavior important for the understanding of the causes and treatment of ADHD.

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  1. Ullmann RK, Sleator EK, Sprague RL: Introduction to the use of ACTeRS. Psychopharmacol Bull 1985; 21:915–920

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Metadata

Authors
Ernst, M., Zametkin, A. J., Matochik, J. A., Pascualvaca, D., Jons, P. H., & Cohen, R. M.
Affiliations
National Institutes of Health (US)
Venue
American Journal of Psychiatry
Publisher
American Psychiatric Association Publishing
Published
1999-08-01
Volume
156
Issue
8
Pages
1209-1215
ISSN
  • 0002-953X (ISSN-L)
  • 1535-7228
DOI
10.1176/ajp.156.8.1209
OpenAlex
W2148955566
Cited by
256
References
52
Citations by year
2026: 4 · 2025: 7 · 2024: 5 · 2023: 2 · 2022: 3 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 3 · 2016: 6 · 2015: 2 · 2014: 7 · 2013: 6 · 2012: 13
FWCI
10.94
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Psychiatry (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
Keywords
attention deficit hyperactivity disorder, [18F]fluorodopa, midbrain, substantia nigra, ventral tegmental area, dopaminergic dysfunction, symptom severity, children
MeSH terms
Adolescent, Attention Deficit Disorder with Hyperactivity, Caudate Nucleus, Child, Dihydroxyphenylalanine, Dopa Decarboxylase, Dopamine, Female, Fluorine Radioisotopes, Frontal Lobe, Humans, Functional Laterality, Male, Mesencephalon, Putamen, Severity of Illness Index, Tomography, Emission-Computed, Presynaptic Terminals

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