ADHD: increased dopamine receptor availability linked to attention deficit and low neonatal cerebral blood flow

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

ADHD: increased dopamine receptor availability linked to attention deficit and low neonatal cerebral blood flow. / Lou, Hans; Rosa, Pedro; Pryds, Ole; Karrebaek, Hanne; Lunding, Jytte; Cumming, Paul; Gjedde, Albert.

In: Developmental Medicine and Child Neurology, Vol. 46, No. 3, 2004, p. 179-83.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Lou, H, Rosa, P, Pryds, O, Karrebaek, H, Lunding, J, Cumming, P & Gjedde, A 2004, 'ADHD: increased dopamine receptor availability linked to attention deficit and low neonatal cerebral blood flow', Developmental Medicine and Child Neurology, vol. 46, no. 3, pp. 179-83.

APA

Lou, H., Rosa, P., Pryds, O., Karrebaek, H., Lunding, J., Cumming, P., & Gjedde, A. (2004). ADHD: increased dopamine receptor availability linked to attention deficit and low neonatal cerebral blood flow. Developmental Medicine and Child Neurology, 46(3), 179-83.

Vancouver

Lou H, Rosa P, Pryds O, Karrebaek H, Lunding J, Cumming P et al. ADHD: increased dopamine receptor availability linked to attention deficit and low neonatal cerebral blood flow. Developmental Medicine and Child Neurology. 2004;46(3):179-83.

Author

Lou, Hans ; Rosa, Pedro ; Pryds, Ole ; Karrebaek, Hanne ; Lunding, Jytte ; Cumming, Paul ; Gjedde, Albert. / ADHD: increased dopamine receptor availability linked to attention deficit and low neonatal cerebral blood flow. In: Developmental Medicine and Child Neurology. 2004 ; Vol. 46, No. 3. pp. 179-83.

Bibtex

@article{24baca80b31511debc73000ea68e967b,
title = "ADHD: increased dopamine receptor availability linked to attention deficit and low neonatal cerebral blood flow",
abstract = "Attention-deficit-hyperactivity disorder (ADHD), while largely thought to be a genetic disorder, has environmental factors that appear to contribute significantly to the aetiopathogenesis of the disorder. One such factor is pretern birth with vulnerable cerebrovascular homeostasis. We hypothesised that cerebral ischaemia at birth could contribute to persistent deficient dopaminergic neurotransmission, which is thought to be the pathophysiological basis of the disorder. We examined dopamine D(2/3) receptor binding with positron emission tomography (PET) using [11C] raclopride as a tracer, and continuous reaction times (RT) with a computerized test of variables (TOVA) in six adolescents (12-14 years of age, one female) who had been examined with cerebral blood flow (CBF) measurements at preterm birth and had a subsequent history of attention deficit. We found that high dopamine receptor availability ('empty receptors') was linked with increased RT and RT variability, supporting the concept of a dopaminergic role in symptomatology. High dopamine receptor availability was predicted by low neonatal CBF, supporting the hypothesis of cerebral ischaemia as a contributing factor in infants susceptible to ADHD.",
author = "Hans Lou and Pedro Rosa and Ole Pryds and Hanne Karrebaek and Jytte Lunding and Paul Cumming and Albert Gjedde",
year = "2004",
language = "English",
volume = "46",
pages = "179--83",
journal = "Developmental medicine and child neurology. Supplement",
issn = "0419-0238",
publisher = "Wiley-Blackwell",
number = "3",

}

RIS

TY - JOUR

T1 - ADHD: increased dopamine receptor availability linked to attention deficit and low neonatal cerebral blood flow

AU - Lou, Hans

AU - Rosa, Pedro

AU - Pryds, Ole

AU - Karrebaek, Hanne

AU - Lunding, Jytte

AU - Cumming, Paul

AU - Gjedde, Albert

PY - 2004

Y1 - 2004

N2 - Attention-deficit-hyperactivity disorder (ADHD), while largely thought to be a genetic disorder, has environmental factors that appear to contribute significantly to the aetiopathogenesis of the disorder. One such factor is pretern birth with vulnerable cerebrovascular homeostasis. We hypothesised that cerebral ischaemia at birth could contribute to persistent deficient dopaminergic neurotransmission, which is thought to be the pathophysiological basis of the disorder. We examined dopamine D(2/3) receptor binding with positron emission tomography (PET) using [11C] raclopride as a tracer, and continuous reaction times (RT) with a computerized test of variables (TOVA) in six adolescents (12-14 years of age, one female) who had been examined with cerebral blood flow (CBF) measurements at preterm birth and had a subsequent history of attention deficit. We found that high dopamine receptor availability ('empty receptors') was linked with increased RT and RT variability, supporting the concept of a dopaminergic role in symptomatology. High dopamine receptor availability was predicted by low neonatal CBF, supporting the hypothesis of cerebral ischaemia as a contributing factor in infants susceptible to ADHD.

AB - Attention-deficit-hyperactivity disorder (ADHD), while largely thought to be a genetic disorder, has environmental factors that appear to contribute significantly to the aetiopathogenesis of the disorder. One such factor is pretern birth with vulnerable cerebrovascular homeostasis. We hypothesised that cerebral ischaemia at birth could contribute to persistent deficient dopaminergic neurotransmission, which is thought to be the pathophysiological basis of the disorder. We examined dopamine D(2/3) receptor binding with positron emission tomography (PET) using [11C] raclopride as a tracer, and continuous reaction times (RT) with a computerized test of variables (TOVA) in six adolescents (12-14 years of age, one female) who had been examined with cerebral blood flow (CBF) measurements at preterm birth and had a subsequent history of attention deficit. We found that high dopamine receptor availability ('empty receptors') was linked with increased RT and RT variability, supporting the concept of a dopaminergic role in symptomatology. High dopamine receptor availability was predicted by low neonatal CBF, supporting the hypothesis of cerebral ischaemia as a contributing factor in infants susceptible to ADHD.

M3 - Journal article

C2 - 14995087

VL - 46

SP - 179

EP - 183

JO - Developmental medicine and child neurology. Supplement

JF - Developmental medicine and child neurology. Supplement

SN - 0419-0238

IS - 3

ER -

ID: 14945137